Nadpłytkowość
Etiologia i przyczyny

Nadpłytkowość, definiowana jako liczba płytek krwi >450 000/µl (450 × 10⁹/l), dzieli się na pierwotną (trombocytemia esencjalna, ET) i wtórną (reaktywną). ET jest klonalnym nowotworem mieloproliferacyjnym charakteryzującym się autonomiczną proliferacją megakariocytów w szpiku, najczęściej związanym z mutacjami JAK2V617F (50-60% przypadków), CALR i MPL, prowadzącymi do nadaktywności szlaku JAK/STAT i zaburzeń trombopoezy. Nadpłytkowość wtórna, stanowiąca 80-90% przypadków, jest reakcją na stany zapalne, infekcje (np. zapalenie płuc, RSV, HRV), niedokrwistość z niedoboru żelaza, nowotwory (płuca, przewód pokarmowy, piersi, jajnik, chłoniaki), splenektomię oraz inne czynniki (urazy, leki, choroby nerek). Mechanizm wtórnej nadpłytkowości opiera się na zwiększonej produkcji trombopoetyny stymulowanej przez cytokiny prozapalne, zwłaszcza IL-6. U dzieci nadpłytkowość wtórna jest niemal zawsze związana z infekcjami, a ET jest rzadkością.

Etiologia nadpłytkowości

Nadpłytkowość, określana również jako trombocytoza, to stan charakteryzujący się zwiększoną liczbą płytek krwi powyżej 450 000/µl (450 × 10⁹/l). W zależności od przyczyny wyróżnia się dwa główne typy nadpłytkowości: pierwotną (esencjalną) oraz wtórną (reaktywną), przy czym ta druga występuje znacznie częściej, stanowiąc 80-90% wszystkich przypadków nadpłytkowości.12

Nadpłytkowość pierwotna

Nadpłytkowość pierwotna, nazywana również trombocytemią esencjalną (ET), jest chorobą szpiku kostnego, w której dochodzi do autonomicznej produkcji płytek krwi. Przyczyna tego schorzenia nie jest do końca poznana, często jednak wiąże się ze zmianami w określonych genach, które kontrolują produkcję płytek krwi w szpiku kostnym.34

Badania genetyczne wykazały, że ponad połowa pacjentów z nadpłytkowością pierwotną ma mutację genu JAK2 (JAK2V617F), która prowadzi do nadaktywności szlaku sygnałowego JAK/STAT, zwiększając produkcję płytek krwi.56 Inne częste mutacje dotyczą genów CALR i MPL, które również uczestniczą w regulacji trombopoezy.78

W nadpłytkowości pierwotnej szpik kostny produkuje nie tylko zbyt dużą liczbę płytek krwi, ale płytki te często nie funkcjonują prawidłowo, co zwiększa ryzyko powikłań zakrzepowych lub krwotocznych.910

Nadpłytkowość pierwotna należy do grupy nowotworów mieloproliferacyjnych (MPN), obok czerwienicy prawdziwej (polycythemia vera), pierwotnego zwłóknienia szpiku (myelofibrosis) i przewlekłej białaczki szpikowej. Charakterystyczną cechą tych zaburzeń jest klonalna proliferacja komórek szpiku kostnego.1112

Nadpłytkowość wtórna

Nadpłytkowość wtórna (reaktywna) występuje jako reakcja organizmu na inny stan lub chorobę podstawową. W przeciwieństwie do nadpłytkowości pierwotnej, płytki krwi w nadpłytkowości wtórnej są zazwyczaj funkcjonalnie prawidłowe, a ryzyko powikłań zakrzepowych jest znacznie niższe.1314

Nadpłytkowość wtórna jest często określana według koncepcji „5 I” – infekcja, niedokrwienie (ischemia), zapalenie (inflammation), zawał (infarction) i niedobór żelaza (iron deficiency).15

Infekcje jako przyczyna nadpłytkowości wtórnej

Zarówno ostre jak i przewlekłe zakażenia bakteryjne, wirusowe czy pasożytnicze mogą prowadzić do wzrostu liczby płytek krwi. Mechanizm tego zjawiska wiąże się ze zwiększoną produkcją interleukiny 6 (IL-6) i innych cytokin prozapalnych, które stymulują wytwarzanie trombopoetyny, głównego regulatora produkcji płytek krwi.1617

Badania wykazały, że infekcje stanowią jedną z najczęstszych przyczyn nadpłytkowości wtórnej, szczególnie u dzieci, gdzie odpowiadają za 37-78% przypadków.18 Najczęstszą infekcją prowadzącą do nadpłytkowości jest zapalenie płuc.19

W badaniu retrospektywnym obejmującym 3156 dzieci z infekcjami dróg oddechowych, u 817 (25,9%) stwierdzono nadpłytkowość wtórną (≥500 × 10⁹ płytek/l).20 Badania wykazały również, że wirusowe infekcje dróg oddechowych mogą być przyczyną nadpłytkowości wtórnej, przy czym najczęściej izolowanymi wirusami były RSV (39,5%) i HRV (22,6%).21

Stan zapalny i choroby zapalne

Przewlekłe choroby zapalne, takie jak reumatoidalne zapalenie stawów, zapalenie naczyń, sarkoidoza, nieswoiste zapalenia jelit czy inne choroby autoimmunologiczne, mogą powodować nadpłytkowość wtórną poprzez zwiększoną produkcję cytokin prozapalnych, szczególnie IL-6.2223

W przypadku reumatoidalnego zapalenia stawów, przewlekły stan zapalny prowadzi do ciągłej stymulacji produkcji płytek krwi, co może skutkować utrzymującą się nadpłytkowością. Wysoki poziom płytek może być wskaźnikiem aktywności choroby i postępu stanu zapalnego.24

Podobnie, w wrzodziejącym zapaleniu jelita grubego, podczas zaostrzeń choroby często obserwuje się zwiększoną liczbę płytek krwi, co jest związane z reakcją organizmu na stan zapalny, traktowany jako uraz lub infekcja.25

Niedobór żelaza

Niedokrwistość z niedoboru żelaza jest częstą przyczyną nadpłytkowości wtórnej. Mechanizm tego zjawiska nie jest w pełni poznany, ale może wiązać się z bezpośrednim wpływem niedoboru żelaza na megakariopoezę lub z działaniem erytropoetyny.2627

Badania wykazały istotny związek między nadpłytkowością a niedokrwistością z niedoboru żelaza. Niedobór żelaza zwiększa tendencję organizmu do wytwarzania większej liczby płytek krwi i tworzenia zakrzepów.2829

Jedna z teorii tłumaczących ten mechanizm sugeruje, że rozwój nadpłytkowości u osób z niedokrwistością z niedoboru żelaza może być wynikiem ewolucyjnej adaptacji do niedoboru żelaza spowodowanego utratą krwi w wyniku urazu.30

Interesującym faktem jest to, że nadpłytkowość wtórna u pacjentów z niedokrwistością z niedoboru żelaza wiąże się z dwukrotnie wyższym ryzykiem zakrzepicy w porównaniu z pacjentami z samą niedokrwistością z niedoboru żelaza.31

Nowotwory

Różne rodzaje nowotworów mogą powodować nadpłytkowość wtórną. Około 35% osób z wysoką liczbą płytek krwi ma również nowotwór, najczęściej płuc, przewodu pokarmowego, piersi, jajnika lub chłoniaka.3233

Czasami wysoka liczba płytek krwi może być pierwszym objawem nowotworu. Nowotwory mogą powodować wzrost liczby płytek krwi poprzez wydzielanie cytokin lub poprzez uszkodzenie tkanek, powodowanie utraty krwi.3435

Najnowsze badania wykazały, że nadpłytkowość jest silnym markerem ryzyka występowania nowotworów, w szczególności raka płuca, endometrium, żołądka, przełyku i jelita grubego (akronim LEGO-C).36

Splenektomia i hiposplenizm

Śledziona odgrywa kluczową rolę w filtracji i usuwaniu płytek krwi z krążenia. U pacjentów po splenektomii (chirurgicznym usunięciu śledziony) lub z hiposplenizmem (zmniejszoną funkcją śledziony) często obserwuje się nadpłytkowość.3738

Nawet do 90% pacjentów po splenektomii doświadcza nadpłytkowości pooperacyjnej z powodu utraty sekwestracji śledzionowej.39 Po splenektomii obserwuje się gwałtowny wzrost liczby płytek krwi, która następnie powoli zmniejsza się do wartości referencyjnych.40

W przypadku pacjentów po usunięciu śledziony, nadpłytkowość może utrzymywać się przez całe życie, jednak rzadko wymaga leczenia, ponieważ ryzyko powikłań zakrzepowych jest niskie.41

Inne przyczyny nadpłytkowości wtórnej

Do innych przyczyn nadpłytkowości wtórnej należą:4243

  • Uszkodzenie tkanek (np. oparzenia, urazy, złamania)
  • Krwawienie i utrata krwi
  • Niedokrwistość hemolityczna
  • Zabiegi chirurgiczne
  • Wpływ leków (np. glikokortykosteroidy, adrenalina, erytropoetyna)
  • Odstawienie leków mielosupresyjnych
  • Efekt odbicia po chemioterapii mielosupresyjnej
  • Efekt odbicia po niedokrwistości z niedoboru żelaza
  • Efekt odbicia w fazie zdrowienia po małopłytkowości
  • Choroby nerek (np. zespół nerczycowy, zapalenie nerek)
  • Wysiłek fizyczny
  • Ciąża i poród (nadpłytkowość fizjologiczna)
  • Wstrząs elektryczny
  • Niedokrwistość aplastyczna

4445

Leki mogące powodować nadpłytkowość

Niektóre leki mogą wywoływać nadpłytkowość wtórną poprzez różne mechanizmy. Jednym z proponowanych mechanizmów jest uwalnianie cytokin, szczególnie IL-6, co prowadzi do nadpłytkowości.46

Do leków, które mogą powodować nadpłytkowość, należą:4748

  • Glikokortykosteroidy
  • Adrenalina
  • Winkrystyna
  • Erytropoetyna
  • Siarczan żelaza
  • Cyprofloksacyna
  • Piperacylina/tazobaktam
  • Kwas retinowy
  • Klozapina
  • Heparyna drobnocząsteczkowa
  • Enoksaparyna

49

Nadpłytkowość wtórna może również występować w trakcie antybiotykoterapii zakażeń, szczególnie u dzieci. Może pojawić się jako laboratoryjny efekt uboczny po leczeniu karbapenemami (np. imipenem/cilastatyna, meropenem) i cefalosporynami (np. ceftriakson i ceftazydym) w przypadku zakażeń ośrodkowego układu nerwowego lub dróg oddechowych u noworodków i dzieci, z częstością występowania około 10% u leczonych pacjentów.50

Nadpłytkowość rodzinna

Nadpłytkowość rodzinna to bardzo rzadkie schorzenie, w którym występuje skrajnie wysoka liczba płytek krwi u wielu osób w kolejnych pokoleniach. Dotyka obu płci i zwykle jest przekazywana w sposób autosomalny dominujący.51

Wyróżnia się dwa typy nadpłytkowości rodzinnej. Pierwszy dotyczy pojedynczej linii komórkowej (płytek), z dominującym dziedziczeniem mendeliańskim, wysoką penetracją i poliklonalną hematopoezą.52

Znane są co najmniej dwie klasy mutacji molekularnych prowadzących do nadpłytkowości rodzinnej. Jedna obejmuje mutacje genu THPO, które powodują zwiększoną produkcję trombopoetyny poprzez różne mechanizmy. Druga obejmuje mutacje genu c-MPL, które w jakiś sposób konstytutywnie utrzymują aktywowaną transdukcję sygnału, prowadząc do ciągłej sygnalizacji dla proliferacji megakariocytów.5354

Diagnostyka opiera się na obserwacji podwyższonych poziomów płytek krwi (ponad 450 × 10⁹/l) i wykluczeniu wtórnych przyczyn nadpłytkowości. Badania genetyczne są konieczne do potwierdzenia diagnozy.55

Czynniki ryzyka i epidemiologia

Nadpłytkowość wtórna jest znacznie częstsza niż nadpłytkowość pierwotna, stanowiąc 80-90% wszystkich przypadków.5657

U dorosłych, najczęstszymi przyczynami nadpłytkowości wtórnej są ostre infekcje, uszkodzenie tkanek, przewlekłe choroby zapalne i nowotwory, przy czym jeden lub więcej z tych czynników występuje w ponad 75% przypadków.58

U dzieci, nadpłytkowość wtórna jest prawie zawsze przyczyną podwyższonej liczby płytek krwi, a najczęstszą jej przyczyną są infekcje.59 Występowanie nadpłytkowości u dzieci zależy od wieku: najwyższą częstość występowania stwierdza się u noworodków (szczególnie wcześniaków) i niemowląt do 24 miesiąca życia, która stopniowo zmniejsza się do 10 roku życia.60

Nadpłytkowość pierwotna (trombocytemia esencjalna) jest rzadka u dzieci, występując ponad 60 razy częściej u dorosłych.61 Epidemiologia molekularna trombocytemii esencjalnej u dzieci różni się od jej odpowiednika u dorosłych, z mniejszą częstością występowania mutacji JAK2V617F.62

Mechanizmy patofizjologiczne nadpłytkowości

Zrozumienie mechanizmów molekularnych leżących u podstaw nadpłytkowości jest kluczowe dla właściwej diagnostyki i leczenia tego schorzenia. Mechanizmy te różnią się w zależności od typu nadpłytkowości – pierwotnej czy wtórnej.63

Patofizjologia nadpłytkowości pierwotnej

Nadpłytkowość pierwotna (trombocytemia esencjalna) charakteryzuje się klonalną proliferacją megakariocytów w szpiku kostnym, co prowadzi do zwiększonej produkcji płytek krwi. Kluczową rolę w patogenezie tego schorzenia odgrywają mutacje genów odpowiedzialnych za regulację trombopoezy.6465

Mutacja JAK2V617F jest najczęstszą zmianą genetyczną związaną z trombocytemią esencjalną, występującą u około 50-60% pacjentów. Jest to mutacja typu gain-of-function, prowadząca do nadwrażliwości lub nawet niezależności wewnątrzkomórkowego szlaku sygnałowego JAK-STAT na zewnętrzną stymulację receptorów MPL, EPO i G-CSF przez krążące cytokiny i czynniki wzrostu.6667

Kiedy mutacja JAK2-V617F występuje w stanie heterozygotycznym, preferencyjnie stymuluje megakariopoezę i w większości przypadków objawia się jako trombocytemia esencjalna. Homozygotyczna JAK2-V617F zmniejsza megakariopoezę na korzyść zwiększonej erytropoezy, prowadząc do czerwienicy prawdziwej i/lub zwłóknienia szpiku.68

Inne częste mutacje związane z nadpłytkowością pierwotną dotyczą genów CALR i MPL. Mutacje te prowadzą do zaburzenia regulacji układu trombopoetyna (TPO) – receptor c-MPL, co sugeruje ich rolę w patogenezie trombocytemii esencjalnej.6970

Pierwszym dowodem na monoklonalność w trombocytemii esencjalnej były badania klonalności wykorzystujące analizę izoenzymu dehydrogenazy glukozo-6-fosforanowej (G6PD) w latach 80. XX wieku. Obserwacje te zostały następnie potwierdzone przez analizę DNA sprzężonego z chromosomem X.71

W przeciwieństwie do przewlekłej białaczki szpikowej, pierwotna anomalia molekularna w trombocytemii esencjalnej nie została jeszcze zidentyfikowana. Zarówno anomalie strukturalne, jak i liczbowe obejmujące wiele poszczególnych chromosomów (w tym trisomie 9 i 8 oraz delecje długiego ramienia chromosomów 5, 7, 13, 17 i 20) zostały powiązane z trombocytemią esencjalną.72

Patofizjologia nadpłytkowości wtórnej

Nadpłytkowość wtórna powstaje w wyniku zwiększonej produkcji płytek krwi w odpowiedzi na różne stany chorobowe lub czynniki zewnętrzne. Mechanizm ten jest regulowany przez cytokiny i czynniki wzrostu, które stymulują megakariopoezę i trombocytopoezę.7374

Wspólnym czynnikiem wśród różnych przyczyn nadpłytkowości wtórnej jest obecność związków zapalnych, takich jak interleukina 6 (IL-6), które zwiększają wydzielanie trombopoetyny, a następnie zwiększają produkcję megakariocytów.75

W przypadku infekcji, zwiększona produkcja IL-6 i innych cytokin prozapalnych stymuluje wytwarzanie trombopoetyny przez wątrobę, co prowadzi do zwiększonej produkcji płytek krwi. W pediatrycznych pacjentach z infekcjami, nadpłytkowość wtórna wynika ze zwiększonej megakariopoezy i trombopoezy, które mogą być stymulowane nawet 10-krotnie.76

W przypadku utraty krwi, odpowiedź szpiku kostnego polega na produkcji nie tylko większej liczby czerwonych krwinek, ale także większej liczby płytek krwi – dzieje się to w odpowiedzi na cytokiny.77

Mechanizm nadpłytkowości wtórnej w niedokrwistości z niedoboru żelaza pozostaje niejasny. Jedna z teorii sugeruje, że niedobór żelaza może wpływać na megakariopoezę lub działanie erytropoetyny, prowadząc do zwiększonej produkcji płytek krwi.78

W przypadku wysiłku fizycznego, badania potwierdziły, że ostry wysiłek prowadzi do przejściowego wzrostu liczby płytek krwi, częściowo z powodu hemokoncentracji i mobilizacji z wątroby, płuc i śledziony. Jednak regularne treningi zmniejszają adhezję i agregację płytek krwi, wywierając tym samym działanie przeciwzakrzepowe.79

Konsekwencje kliniczne nadpłytkowości

Konsekwencje kliniczne nadpłytkowości różnią się znacząco w zależności od tego, czy jest to nadpłytkowość pierwotna czy wtórna. W obu przypadkach możliwe są powikłania zakrzepowe i krwotoczne, jednak ich częstość i nasilenie są różne.8081

Konsekwencje nadpłytkowości pierwotnej

Nadpłytkowość pierwotna (trombocytemia esencjalna) wiąże się z istotnie wyższym ryzykiem powikłań zakrzepowych i krwotocznych niż nadpłytkowość wtórna.82 Powikłania te wynikają nie tylko z wysokiej liczby płytek krwi, ale również z ich nieprawidłowej funkcji.83

Zakrzepica jest najbardziej niepokojącym powikłaniem klonalnej nadpłytkowości. Klasycznie, pacjenci z trombocytemią esencjalną rozwijają zespół Budda-Chiariego, czyli zakrzepową niedrożność żyły wątrobowej i/lub żyły głównej dolnej. Mogą jednak rozwinąć wiele rodzajów niedrożności naczyniowej, w tym niedrożność żylną (np. zakrzepicę żył głębokich, zatorowość płucną) i niedrożność tętniczą (np. udar mózgu, zawał mięśnia sercowego, erytromelalgię).84

Poważne krwawienie w związku z nadpłytkowością powinno budzić podejrzenie rozsianego wykrzepiania wewnątrznaczyniowego (DIC), niedoboru czynników krzepnięcia i nabytej choroby von Willebranda. Skrajna nadpłytkowość występuje w chorobie von Willebranda z powodu nieprawidłowej adsorpcji płytkowej krążącego czynnika von Willebranda.85

U około 50% pacjentów z trombocytemią esencjalną mogą występować objawy mikronaczyniowe, takie jak bóle głowy, zaburzenia widzenia, parestezje, zawroty głowy i erytromelalgia. Uważa się, że objawy te, szczególnie erytromelalgia, są wynikiem interakcji płytek krwi z śródbłonkiem w małych naczyniach, z towarzyszącym stanem zapalnym i przejściową niedrożnością zakrzepową.86

Po wielu latach trwania choroby może rozwinąć się zwłóknienie szpiku kostnego (włóknienie). Niewielki odsetek pacjentów z trombocytemią esencjalną rozwija białaczkę, a ryzyko to wzrasta wraz z długością trwania choroby.8788

Konsekwencje nadpłytkowości wtórnej

W przeciwieństwie do nadpłytkowości pierwotnej, nadpłytkowość wtórna jest zazwyczaj łagodna i rzadko prowadzi do powikłań zakrzepowych lub krwotocznych.8990

Ryzyko powikłań zakrzepowych w nadpłytkowości wtórnej jest uważane za niskie, występujące tylko u 1,6% pacjentów w jednej dużej serii przypadków, przy czym wszystkie zdarzenia zakrzepowe zidentyfikowano jako żylne i występowały u pacjentów z innymi czynnikami ryzyka, takimi jak stan pooperacyjny lub z podstawowym nowotworem.91

Należy jednak zauważyć, że nadpłytkowość wtórna u pacjentów z niedokrwistością z niedoboru żelaza wiąże się z dwukrotnie wyższym ryzykiem zakrzepicy w porównaniu z pacjentami z samą niedokrwistością z niedoboru żelaza.92

Obecność nadpłytkowości wtórnej w infekcjach i nowotworach może być również predyktorem gorszego rokowania. To podwyższone ryzyko śmiertelności zostało potwierdzone w innych badaniach na hospitalizowanych pacjentach, przy czym jedno badanie wykazało 30-dniowe ryzyko śmiertelności 2,5 razy wyższe u osób z nadpłytkowością wtórną o wartości 500 000/µl w porównaniu do osób z prawidłową liczbą płytek krwi.93

U dzieci z nadpłytkowością wtórną w przebiegu infekcji nie odnotowano zdarzeń zakrzepowo-zatorowych, dlatego leczenie inhibitorami agregacji płytek krwi nie jest wymagane, nawet przy wysokiej liczbie płytek krwi (np. ≥1000 × 10⁹/l). Ważne jest, aby pamiętać, że zalecane jest podejście zachowawcze, a leczenie powinno być skierowane na podstawową infekcję, a nie na liczbę płytek krwi.94

Nadpłytkowość wtórna zazwyczaj ustępuje z czasem, po ustąpieniu przyczyny wywołującej.95 Leczenie nadpłytkowości wtórnej powinno być ukierunkowane na leczenie podstawowej przyczyny nadpłytkowości. Po wyleczeniu czynnika przyczynowego, liczba płytek krwi zazwyczaj normalizuje się.96

Podsumowanie etiologii nadpłytkowości

Nadpłytkowość to stan charakteryzujący się zwiększoną liczbą płytek krwi powyżej 450 000/µl. W zależności od przyczyny, można ją podzielić na dwa główne typy: pierwotną (esencjalną) i wtórną (reaktywną).97

Nadpłytkowość pierwotna (trombocytemia esencjalna) jest rzadkim schorzeniem szpiku kostnego, charakteryzującym się klonalną proliferacją megakariocytów i zwiększoną produkcją płytek krwi. Najczęściej związana jest z mutacjami genów JAK2, CALR i MPL, które prowadzą do zaburzenia regulacji trombopoezy.9899

Nadpłytkowość wtórna jest znacznie częstsza, stanowiąc 80-90% wszystkich przypadków nadpłytkowości. Jest ona reakcją organizmu na różne stany chorobowe, takie jak infekcje, stany zapalne, nowotwory, niedokrwistość z niedoboru żelaza, stan po splenektomii i wiele innych.100101

Najczęstszymi przyczynami nadpłytkowości wtórnej są infekcje (zarówno bakteryjne, jak i wirusowe), przewlekłe stany zapalne (np. reumatoidalne zapalenie stawów, nieswoiste zapalenia jelit), niedokrwistość z niedoboru żelaza, krwawienie, nowotwory i stan po splenektomii.102103

Mechanizmy patofizjologiczne nadpłytkowości obejmują zwiększoną produkcję płytek krwi w szpiku kostnym, która w przypadku nadpłytkowości wtórnej jest mediowana przez cytokiny prozapalne, szczególnie IL-6.104105

Konsekwencje kliniczne nadpłytkowości różnią się w zależności od jej typu. Nadpłytkowość pierwotna wiąże się z istotnie wyższym ryzykiem powikłań zakrzepowych i krwotocznych, podczas gdy nadpłytkowość wtórna jest zazwyczaj łagodna i rzadko prowadzi do powikłań.106107

Leczenie nadpłytkowości zależy od jej przyczyny. W przypadku nadpłytkowości wtórnej, leczenie powinno być ukierunkowane na podstawową przyczynę. W przypadku nadpłytkowości pierwotnej, leczenie może obejmować leki obniżające liczbę płytek krwi, takie jak hydroksymocznik, anagrelid lub interferon alfa, szczególnie u pacjentów z wysokim ryzykiem powikłań zakrzepowych.108

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Secondary thrombocytosis, also known as reactive thrombocytosis, is characterized by an abnormally high platelet count due to underlying events, infections or diseases, or certain medications. Secondary thrombocytosis, which is more common than primary thrombocytosis, is typically identified through routine laboratory studies. In most cases, secondary thrombocytosis symptoms are due to an underlying disorder rather than the thrombocytosis itself. Rarely, extreme thrombocytosis may lead to thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism. […] Approximately 80% to 90% of individuals with thrombocytosis are known to have secondary thrombocytosis. Causes of secondary thrombocytosis include transient conditions like acute blood loss or infection, as well as sustained factors such as iron deficiency, asplenia, cancer, chronic inflammation, or infectious diseases. Reactive thrombocytosis is a laboratory anomaly that generally resolves once the underlying causative condition is addressed.
  • #2
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Thrombocytosis, a condition defined as having a platelet count of more than 450,000 per microliter of blood (450 x 109/L), can be either physiologic in nature or due to primary or secondary causes. […] Secondary or reactive thrombocytosis (RT) is far more prevalent than primary or clonal thrombocytosis, and the presence of comorbid conditions in RT, a transient rise in platelets, and lack of genetic mutations favor a secondary etiology. […] Causes of thrombocytosis can be physiologic (exercise, parturition) and can also be primary/clonal (e.g., essential thrombocythemia, polycythemia vera, primary myelofibrosis, and other hematologic malignancies) as well as secondary/reactive (due to infectious and inflammatory diseases, neoplasms, anemia, trauma, surgery, asplenia, and iron deficiency).
  • #3 Thrombocytosis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/thrombocytosis/symptoms-causes/syc-20378315
    The cause of this disorder is unclear. It often appears to be connected to changes in certain genes. The bone marrow produces too many of the cells that form platelets, and these platelets often don’t work properly. This poses a much higher risk of clotting or bleeding complications than does reactive thrombocytosis.
  • #4 Platelet Disorders – Thrombocythemia and Thrombocytosis | NHLBI, NIH
    https://www.nhlbi.nih.gov/health/thrombocythemia-thrombocytosis
    Thrombocythemia and thrombocytosis are conditions that occur when your blood has a higher-than-normal platelet count. […] Thrombocythemia refers to a high platelet count that is not caused by another health condition. This condition is sometimes called primary or essential thrombocythemia. […] Thrombocytosis refers to a high platelet count caused by another disease or condition. This condition is often called secondary or reactive thrombocytosis. Thrombocytosis is more common than thrombocythemia. […] Thrombocythemia occurs when faulty cells in your bone marrow make too many platelets. Your platelets also do not work properly. […] Thrombocythemia is most often caused by your genes. Mutations, or changes, in the genes that control how your bone marrow forms platelets may cause thrombocythemia.
  • #5 Thrombocytosis: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/13350-thrombocytosis
    Thrombocytosis involves having an elevated level of platelets in your blood. […] There are two main types of thrombocytosis: essential thrombocythemia and reactive thrombocytosis. […] Your experience of thrombocytosis, including its seriousness and whether you need treatment, depends on its cause. […] Essential thrombocythemia (ET) and reactive thrombocytosis have different causes. […] Essential thrombocythemia is an acquired genetic condition, meaning you develop it over time. […] With ET, some of the genes that play a role in platelet production change, or mutate. […] As a result, your bone marrow makes too many platelets. […] More than half those with essential thrombocythemia have a genetic variant called JAK2. […] Other common variants affect the CALR or MPL gene. […] Scientists arent sure still what causes the gene mutations, but research is ongoing.
  • #6 Essential thrombocythemia: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/essential-thrombocythemia/
    Essential thrombocythemia is a condition characterized by an increased number of platelets (thrombocythemia). […] The JAK2 and CALR genes are the most commonly mutated genes in essential thrombocythemia. The MPL, THPO, and TET2 genes can also be altered in this condition. […] Mutations in the JAK2, MPL, and THPO genes that are associated with essential thrombocythemia lead to overactivation of the JAK/STAT pathway. […] Although mutations in the CALR and TET2 genes have been found in people with essential thrombocythemia, it is unclear how these gene mutations are involved in development of the condition. […] Some people with essential thrombocythemia do not have a mutation in any of the known genes associated with this condition. Researchers are working to identify other genes that may be involved in the condition.
  • #7 Thrombocytosis: Causes, Symptoms, Treatment, and More
    https://www.verywellhealth.com/thrombocytosis-overview-and-more-5187124
    Essential thrombocytosis (ET) is a dysfunction in the bone marrow that causes too many platelets to be made. The cause of ET is not entirely clear, but about 90% of cases have an acquired mutation in JAK2, CALR, or MPL. […] Reactive thrombocytosis is an elevation in platelet counts for a reason outside of the bone marrow. The platelets increase in reaction to something such as iron deficiency, infection, inflammation, cancer, or bleeding.
  • #8 High Platelet Count (Thrombocytosis): Symptoms, Causes and Treatment
    https://www.citizenshospitals.com/blogs/high-platelet-count-thrombocytosis-symptoms-causes-and-treatment
    Thrombocytosis may be primary, caused by a bone marrow disorder, or secondary, resulting from another medical condition. […] The primary cause of thrombocytosis is a bone marrow disorder known as essential thrombocythemia (ET). In ET, the bone marrow produces excess platelets due to mutations in specific genes, such as JAK2, CALR, or MPL. […] Secondary thrombocytosis is more common than the primary form and occurs as a reaction to an underlying condition. Some of the most prevalent causes include: […] Infections: Bacterial, viral, or fungal infections can stimulate the immune system, leading to increased platelet production. […] Inflammation: Conditions such as rheumatoid arthritis, inflammatory bowel disease (IBD), and lupus can trigger an inflammatory response, resulting in elevated platelet counts.
  • #9 Thrombocytosis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/thrombocytosis/symptoms-causes/syc-20378315
    The cause of this disorder is unclear. It often appears to be connected to changes in certain genes. The bone marrow produces too many of the cells that form platelets, and these platelets often don’t work properly. This poses a much higher risk of clotting or bleeding complications than does reactive thrombocytosis.
  • #10 What Causes Thrombocythemia and Thrombocytosis? | Hematology-Oncology Associates of CNY
    https://www.hoacny.com/what-causes-thrombocythemia-and-thrombocytosis
    Some conditions can lead to a high platelet count that lasts for only a short time. Examples of such conditions include: Recovery from serious blood loss, Recovery from a very low platelet count caused by excessive alcohol use and lack of vitamin B12 or folate, Acute infection or inflammation, Response to physical activity. […] Although the platelet count is high in secondary thrombocytosis, the platelets are normal (unlike in primary thrombocythemia). Thus, people who have secondary thrombocytosis have a lower risk of blood clots and bleeding.
  • #11 Thrombocytosis: Symptoms, Causes, and Treatment | Doctor
    https://patient.info/doctor/thrombocytosis
    There are a number of haematological diseases causing thrombocytosis. Primary thrombocytosis is a chronic myeloproliferative disorder. However, there are other haematological diseases which can cause thrombocytosis, including other myeloproliferative neoplasms (MPNs), myelodysplastic syndromes (MDS) and overlap syndromes. MPNs such as primary thrombocytosis (essential thrombocythaemia), polycythaemia vera and myelofibrosis are Philadelphia-negative clonal disorders of the bone marrow. […] Primary thrombocytosis (also referred to as essential thrombocytosis, essential thrombocythaemia and primary thrombocythaemia) is due to a failure to regulate the production of platelets (autonomous production) and is a feature of a number of myeloproliferative disorders. […] Other haematological diseases which cause thrombocytosis are myeloproliferative, myelodysplastic or a combination of both. It includes some leukaemias.
  • #12 How I Work up the Patient with Thrombocytosis – The ASCO Post
    https://ascopost.com/issues/march-15-2012/how-i-work-up-the-patient-with-thrombocytosis/
    Causes of primary thrombocytosis include myeloproliferative neoplasms, myelodysplastic syndromes, myelodysplastic syndrome/myeloproliferative neoplasm overlap syndromes, and other myeloid malignancies. […] Essential thrombocythemia is currently defined as a persistent thrombocythemic state (platelet count 450 109/L) that is neither reactive nor associated with an otherwise defined myeloid malignancy (including polycythemia vera), primary myelofibrosis (including prefibrotic primary myelofibrosis), CML, and myelodysplastic syndromes. […] The first evidence of monoclonality in essential thrombocythemia was suggested in the early 1980s by clonality studies that utilized glucose-6-phosphate dehydrogenase (G6PD) isoenzyme analysis. These early observations were subsequently confirmed by X-linked DNA analysis. Unlike the situation for CML, the primary molecular abnormality in essential thrombocythemia has not been identified.
  • #13 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Secondary thrombocytosis, also known as reactive thrombocytosis, is characterized by an abnormally high platelet count due to underlying events, infections or diseases, or certain medications. Secondary thrombocytosis, which is more common than primary thrombocytosis, is typically identified through routine laboratory studies. In most cases, secondary thrombocytosis symptoms are due to an underlying disorder rather than the thrombocytosis itself. Rarely, extreme thrombocytosis may lead to thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism. […] Approximately 80% to 90% of individuals with thrombocytosis are known to have secondary thrombocytosis. Causes of secondary thrombocytosis include transient conditions like acute blood loss or infection, as well as sustained factors such as iron deficiency, asplenia, cancer, chronic inflammation, or infectious diseases. Reactive thrombocytosis is a laboratory anomaly that generally resolves once the underlying causative condition is addressed.
  • #14 Thrombocytosis: Symptoms, Causes, and Treatment | Doctor
    https://patient.info/doctor/thrombocytosis
    This can be secondary to a number of conditions. It is an exaggerated physiological response to a primary problem, such as an infection. The trigger factor (eg, infection) results in the release of cytokines which mediate an increase in platelet production. It is often a transient phenomenon which disappears when the underlying cause is resolved. […] Mutations in the key regulators of thrombopoietin, the thrombopoietin receptor MPL and JAK2, are found in 50-60% of patients with essential thrombocythaemia or primary myelofibrosis and in 10-20% of hereditary thrombocytosis. When present in a heterozygous state the JAK2-V617F mutation preferentially stimulates megakaryopoiesis and in most cases manifests as essential thrombocythaemia. Homozygous JAK2-V617F reduces megakaryopoiesis in favour of increased erythropoiesis, resulting in polycythaemia vera and/or myelofibrosis.
  • #15 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    The common factor among the various underlying causes of secondary thrombocytosis is the presence of inflammatory compounds, such as interleukin 6 (IL6), which enhance thrombopoietin secretion and subsequently increase megakaryocyte production. Secondary thrombocytosis etiologies are often categorized under the „5 I’s”—inflammation, ischemia, infection, infarction, and iron deficiency. […] Acute bacterial, viral, or chronic infectious conditions (eg, tuberculosis) can cause secondary thrombocytosis due to increased production of IL6—an inflammatory component that enhances thrombopoietin synthesis. […] The major functions of the spleen are immune activity and blood filtration. Up to 90% of splenectomized patients experience thrombocytosis postoperatively due to the loss of splenic sequestration.
  • #16 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    The common factor among the various underlying causes of secondary thrombocytosis is the presence of inflammatory compounds, such as interleukin 6 (IL6), which enhance thrombopoietin secretion and subsequently increase megakaryocyte production. Secondary thrombocytosis etiologies are often categorized under the „5 I’s”—inflammation, ischemia, infection, infarction, and iron deficiency. […] Acute bacterial, viral, or chronic infectious conditions (eg, tuberculosis) can cause secondary thrombocytosis due to increased production of IL6—an inflammatory component that enhances thrombopoietin synthesis. […] The major functions of the spleen are immune activity and blood filtration. Up to 90% of splenectomized patients experience thrombocytosis postoperatively due to the loss of splenic sequestration.
  • #17
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    In both children and adults, thrombocytosis is usually defined as a platelet count of more than 450 109/L. As there are many primary and secondary causes, as well as false or spurious conditions mimicking thrombocytosis, establishing the cause requires considering clinical features and hematologic parameters. Pediatric primary thrombocytosis is very rare, but reactive thrombocytosis (RT) can be frequently observed in children with infections, iron deficiency, tissue damage, hemolysis, autoimmune diseases, malignancies, and other causes of an acute-phase response. The incidence of secondary forms due to infections is significantly higher in childhood than in adulthood, and infections are the main cause of pediatric RT, with reported incidence rates ranging from 37% to 78%. […] In pediatric patients with infections, RT is due to increased megakaryopoiesis and thrombopoiesis, which can be stimulated up to 10-fold. Under these conditions, platelet production is altered and may be regulated by various cytokines, such as interleukin (IL-)1 alpha, IL-8, IL-6, and tumor necrosis factor. IL-6 plays a major direct and indirect role by stimulating megakaryopoiesis or hepatic thrombopoietin (TPO) production. Many reports indicate that bacterial infections are more frequently associated with childhood RT than viral infections.
  • #18
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    In both children and adults, thrombocytosis is usually defined as a platelet count of more than 450 109/L. As there are many primary and secondary causes, as well as false or spurious conditions mimicking thrombocytosis, establishing the cause requires considering clinical features and hematologic parameters. Pediatric primary thrombocytosis is very rare, but reactive thrombocytosis (RT) can be frequently observed in children with infections, iron deficiency, tissue damage, hemolysis, autoimmune diseases, malignancies, and other causes of an acute-phase response. The incidence of secondary forms due to infections is significantly higher in childhood than in adulthood, and infections are the main cause of pediatric RT, with reported incidence rates ranging from 37% to 78%. […] In pediatric patients with infections, RT is due to increased megakaryopoiesis and thrombopoiesis, which can be stimulated up to 10-fold. Under these conditions, platelet production is altered and may be regulated by various cytokines, such as interleukin (IL-)1 alpha, IL-8, IL-6, and tumor necrosis factor. IL-6 plays a major direct and indirect role by stimulating megakaryopoiesis or hepatic thrombopoietin (TPO) production. Many reports indicate that bacterial infections are more frequently associated with childhood RT than viral infections.
  • #19 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    In severe infections, such as bacterial meningitis, one of the causes may be a rebound phenomenon after initial thrombocytopenia due to the rapid consumption of platelets. […] The most common infection associated with thrombocytosis is pneumonia. […] A retrospective study by Zheng et al found that out of 3156 children with respiratory tract infection, 817 (25.9%) had secondary thrombocytosis (500 X 109 platelets/L or higher). […] In some instances, such as chronic hemolytic anemia, the stimulus (hypoxia) to produce cytokines persists, causing long-term elevation of platelet counts. […] While thrombocytosis in association with iron-deficiency anemia is well documented, the mechanism remains unclear. […] A rare disorder of unknown etiology, idiopathic cyclic thrombocytopenia is characterized by female predominance, fluctuation of platelet count with rebound thrombocytosis (with peak 1 million/L), and a median age of onset of 35 years, although the youngest patient described was aged 1 year.
  • #20 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    In severe infections, such as bacterial meningitis, one of the causes may be a rebound phenomenon after initial thrombocytopenia due to the rapid consumption of platelets. […] The most common infection associated with thrombocytosis is pneumonia. […] A retrospective study by Zheng et al found that out of 3156 children with respiratory tract infection, 817 (25.9%) had secondary thrombocytosis (500 X 109 platelets/L or higher). […] In some instances, such as chronic hemolytic anemia, the stimulus (hypoxia) to produce cytokines persists, causing long-term elevation of platelet counts. […] While thrombocytosis in association with iron-deficiency anemia is well documented, the mechanism remains unclear. […] A rare disorder of unknown etiology, idiopathic cyclic thrombocytopenia is characterized by female predominance, fluctuation of platelet count with rebound thrombocytosis (with peak 1 million/L), and a median age of onset of 35 years, although the youngest patient described was aged 1 year.
  • #21 Association between secondary thrombocytosis and viral respiratory tract infections in children | Scientific Reports
    https://www.nature.com/articles/srep22964
    Secondary thrombocytosis (ST) is frequently observed in children with a variety of clinical conditions. The leading cause of ST is respiratory tract infection (RTI) in children. […] The most frequent cause of ST is respiratory tract infections (RTIs) in childhood; RTIs account for 6080% of ST cases. […] Previous studies have suggested that thrombocytosis may be an early marker of respiratory syncytial virus (RSV) infection and several authors have reported that RSV-positive bronchiolitis in hospitalized young infants is associated with thrombocytosis. […] Our findings showed that childhood ST is related to respiratory viral infections, but the degree of platelet elevation is unrelated to the species of virus. The total virus detection rate was 78.9% (645/817) in patients with ST. RSV (39.5%) was the most commonly detected virus, followed by HRV (22.6%) and PIV (21.8%). From the present data, we found that RSV single infection (especially subtype B) and HRV infection (especially subtype A) were prominent causative agents of thrombocytosis.
  • #22 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Reactive thrombocytosis accompanying iron deficiency anemia can occur independently or in association with erythropoietin or as an additive event related to cytokines. […] Drug-induced thrombocytosis can result from various causative factors. One proposed mechanism is that certain drugs can cause the release of cytokines, particularly IL6, leading to thrombocytosis. […] Rheumatoid arthritis, inflammatory bowel disease, sarcoidosis, and autoimmune antibody-mediated illnesses can cause thrombocytosis through inflammatory effects, particularly involving IL6. […] Most diseases with antibody-mediated hemolysis manifest thrombocytopenia. Conversely, some conditions, including cold agglutinin disease (CAD), cause thrombocytosis. […] Platelets have an established association with malignancies.
  • #23 What Autoimmune Disease Causes High Platelets: Insights & Management | Maggie Yu MD, IFMCP
    https://drmaggieyu.com/blog/what-autoimmune-disease-causes-high-platelets/
    Thrombocytosis refers to an elevated platelet count in the blood. Platelets are small cells that help with clotting when injuries occur. Normally, our bodies balance platelet production and use. In some cases though, this balance is disrupted. This can happen due to various reasons, including autoimmune diseases. […] Autoimmune conditions trigger the body’s defense mechanism against its own tissues. This misdirected attack can affect many processes, including how platelets are made and used up. When the immune system is involved, it often leads to increased production of these clot-forming cells. […] Secondary thrombocytosis, unlike primary, happens as a response to another condition or factor within the body such as inflammation or infection which are common features of autoimmune disorders.
  • #24 What Autoimmune Disease Causes High Platelets: Insights & Management | Maggie Yu MD, IFMCP
    https://drmaggieyu.com/blog/what-autoimmune-disease-causes-high-platelets/
    Several autoimmune conditions may lead to high platelet counts. These include: Rheumatoid arthritis: A chronic inflammatory disorder affecting joints. Lupus: An illness where the immune system attacks healthy tissue throughout your body. Inflammatory bowel disease (IBD): Which includes Crohn’s disease and ulcerative colitis affects gastrointestinal tract lining causing severe inflammation. […] The immune system plays a crucial role in regulating many bodily functions including blood cell production through complex signaling pathways involving cytokines and growth factors among others things too numerous list here now! […] Rheumatoid arthritis (RA) is a chronic inflammatory disorder. It primarily affects joints, but it can also lead to systemic issues. Inflammation in RA often triggers the body to produce more platelets.
  • #25 What Autoimmune Disease Causes High Platelets: Insights & Management | Maggie Yu MD, IFMCP
    https://drmaggieyu.com/blog/what-autoimmune-disease-causes-high-platelets/
    This constant injury signal leads to a high number of circulating platelets in your bloodstream known as thrombocytosis. […] High levels may suggest ongoing inflammation and possibly advancing disease state. […] Treating rheumatoid arthritis involves managing symptoms and slowing down its progress. Treatments aim both at easing pain and reducing swelling in turn affecting thrombocytosis. […] Hughes Syndrome, also known as Antiphospholipid Syndrome (APS), is an autoimmune disorder. Its marked by the body mistakenly attacking normal proteins in the blood. This can lead to high platelet counts, a condition called thrombocytosis. […] Thrombocytosis increases clot risks significantly in those with Hughes Syndrome. […] Ulcerative colitis (UC) is a chronic condition affecting the colon. Its known for causing inflammation and ulcers in the digestive tract. This can have wide-ranging effects, including on blood platelets.
  • #26 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Reactive thrombocytosis accompanying iron deficiency anemia can occur independently or in association with erythropoietin or as an additive event related to cytokines. […] Drug-induced thrombocytosis can result from various causative factors. One proposed mechanism is that certain drugs can cause the release of cytokines, particularly IL6, leading to thrombocytosis. […] Rheumatoid arthritis, inflammatory bowel disease, sarcoidosis, and autoimmune antibody-mediated illnesses can cause thrombocytosis through inflammatory effects, particularly involving IL6. […] Most diseases with antibody-mediated hemolysis manifest thrombocytopenia. Conversely, some conditions, including cold agglutinin disease (CAD), cause thrombocytosis. […] Platelets have an established association with malignancies.
  • #27
    https://healthmatch.io/anemia/thrombocytosis-and-anemia
    Thrombocytosis is a disorder characterized by an increase in the number of platelets in the body. […] There are two main types of thrombocytosis: primary and secondary. […] Secondary or reactive thrombocytosis, on the other hand, occurs when an underlying condition causes an increase in platelet count. […] What causes thrombocytosis? […] There are many different causes of reactive thrombocytosis, including: Cancer, Chronic inflammatory conditions, Iron deficiency anemia, Infections, Trauma or surgical removal of the spleen, Certain medications, After surgery, Some blood disorders. […] In the case of reactive thrombocytosis as a result of iron deficiency anemia, treatment with iron supplements can correct the iron levels and platelet count, resolving the condition. […] Yes, they are! Many studies have reported a significant association between thrombocytosis and iron deficiency anemia.
  • #28
    https://healthmatch.io/anemia/thrombocytosis-and-anemia
    Thrombocytosis is a disorder characterized by an increase in the number of platelets in the body. […] There are two main types of thrombocytosis: primary and secondary. […] Secondary or reactive thrombocytosis, on the other hand, occurs when an underlying condition causes an increase in platelet count. […] What causes thrombocytosis? […] There are many different causes of reactive thrombocytosis, including: Cancer, Chronic inflammatory conditions, Iron deficiency anemia, Infections, Trauma or surgical removal of the spleen, Certain medications, After surgery, Some blood disorders. […] In the case of reactive thrombocytosis as a result of iron deficiency anemia, treatment with iron supplements can correct the iron levels and platelet count, resolving the condition. […] Yes, they are! Many studies have reported a significant association between thrombocytosis and iron deficiency anemia.
  • #29
    https://healthmatch.io/anemia/thrombocytosis-and-anemia
    Iron deficiency increases the tendency of the body to have a higher platelet count and form clots. […] Yes, IDA can lead to increased platelet production, which can cause thrombocytosis. […] The exact pathway of how IDA can lead to thrombocytosis is not fully mapped, but research studies suggest the following: The mother cells of platelets are called megakaryocytes, and the mother cells of red blood cells are called erythroid. […] One additional theory has also been proposed. The development of thrombocytosis in IDA individuals may result from an evolutionary adaptation to an iron deficiency caused by blood loss from an injury. […] In secondary thrombocytosis, which represents the majority of the cases of thrombocytosis, the answer is probably, no. […] More often, thrombocytosis itself wont cause anemia, but its treatments can. […] These include: Plateletpheresis, Medications.
  • #30
    https://healthmatch.io/anemia/thrombocytosis-and-anemia
    Iron deficiency increases the tendency of the body to have a higher platelet count and form clots. […] Yes, IDA can lead to increased platelet production, which can cause thrombocytosis. […] The exact pathway of how IDA can lead to thrombocytosis is not fully mapped, but research studies suggest the following: The mother cells of platelets are called megakaryocytes, and the mother cells of red blood cells are called erythroid. […] One additional theory has also been proposed. The development of thrombocytosis in IDA individuals may result from an evolutionary adaptation to an iron deficiency caused by blood loss from an injury. […] In secondary thrombocytosis, which represents the majority of the cases of thrombocytosis, the answer is probably, no. […] More often, thrombocytosis itself wont cause anemia, but its treatments can. […] These include: Plateletpheresis, Medications.
  • #31
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Interestingly, RT in patients with iron deficiency anemia has been associated with a twofold thrombosis risk compared with patients with iron deficiency anemia alone. […] The presence of RT in infections and cancer may also be predictive of poor outcomes. […] This elevated mortality risk has been validated in other investigations on hospitalized patients, with one study showing a 30-day mortality risk 2.5 times higher in those with RT of 500,000/microL compared to those with normal platelet counts. […] Elevated platelets are associated with worse outcomes in individuals hospitalized with COVID-19.
  • #32 What Causes Thrombocythemia and Thrombocytosis? | Hematology-Oncology Associates of CNY
    https://www.hoacny.com/what-causes-thrombocythemia-and-thrombocytosis
    In this condition, faulty stem cells in the bone marrow make too many platelets. What causes this to happen usually isn’t known. […] A rare form of thrombocythemia is inherited. („Inherited” means the condition is passed from parents to children through the genes.) In some cases, a genetic mutation may cause the condition. […] This condition occurs if another disease, condition, or outside factor causes the platelet count to rise. For example, 35 percent of people who have high platelet counts also have cancer mostly lung, gastrointestinal, breast, ovarian, and lymphoma. Sometimes a high platelet count is the first sign of cancer. […] Other conditions or factors that can cause a high platelet count are: Iron-deficiency anemia, Hemolytic anemia, Absence of a spleen, Inflammatory or infectious diseases, such as connective tissue disorders, inflammatory bowel disease, and tuberculosis, Reactions to medicine.
  • #33 Platelet Disorders – Thrombocythemia and Thrombocytosis | NHLBI, NIH
    https://www.nhlbi.nih.gov/health/thrombocythemia-thrombocytosis
    Thrombocytosis occurs when another disease or condition causes you to have a high platelet count. […] Some conditions that can raise your risk of thrombocytosis are listed below. […] Anemia: Iron-deficiency anemia and hemolytic anemia can cause thrombocytosis. […] Cancer: Many people who have high platelet counts also have cancer mostly lung, gastrointestinal, breast, or ovarian cancer or lymphoma. […] Surgery to remove your spleen: The spleen is an organ in your upper left abdomen. Normally, your spleen stores platelets. Removing your spleen can raise your platelet count. […] Inflammation or infections: Conditions such as connective tissue disorders, inflammatory bowel disease, and tuberculosis can raise your platelet count.
  • #34 Increased number of platelets call for review of thrombocytosis
    https://www.dvm360.com/view/increased-number-platelets-call-review-thrombocytosis
    Some cancers can cause an increased total platelet count either by causing damage to tissues, causing blood loss or by erroneously producing a cytokine that stimulates the bone marrow to produce platelets. […] Essential thrombocytosis, polycythemia vera, chronic myeloid leukemia and myelofibrosis are uncommon conditions that form a group of diseases known as the myeloproliferative disorders. […] The blood disorder that is mostly characterized by an increased total platelet count is primary thrombocytosis – also called essential thrombocythemia.
  • #35 Thrombocytosis – RefHelp
    https://apps.nhslothian.scot/refhelp/guidelines/haematology/thrombocytosis/
    Persistent significant increase in platelet count 450109/L. Reactive causes are much more common than myeloproliferative neoplasms (MPNs). […] Causes of a reactive thrombocytosis include: infection; inflammation; iron deficiency and/or bleeding; recent surgery; hyposplenism; solid organ malignancy. […] Recent evidence has identified thrombocytosis as a strong risk marker for malignancy, in particular lung, endometrial, gastric, oesophageal and colorectal cancer (acronym LEGO-C). […] If malignancy is suspected please follow the recommendations of the Scottish Referral Guidelines for Suspected Cancer, and note the LEGO-C cancers: lung, endometrial, gastric, oesophageal and colorectal cancer.
  • #36 Thrombocytosis – RefHelp
    https://apps.nhslothian.scot/refhelp/guidelines/haematology/thrombocytosis/
    Persistent significant increase in platelet count 450109/L. Reactive causes are much more common than myeloproliferative neoplasms (MPNs). […] Causes of a reactive thrombocytosis include: infection; inflammation; iron deficiency and/or bleeding; recent surgery; hyposplenism; solid organ malignancy. […] Recent evidence has identified thrombocytosis as a strong risk marker for malignancy, in particular lung, endometrial, gastric, oesophageal and colorectal cancer (acronym LEGO-C). […] If malignancy is suspected please follow the recommendations of the Scottish Referral Guidelines for Suspected Cancer, and note the LEGO-C cancers: lung, endometrial, gastric, oesophageal and colorectal cancer.
  • #37 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    The common factor among the various underlying causes of secondary thrombocytosis is the presence of inflammatory compounds, such as interleukin 6 (IL6), which enhance thrombopoietin secretion and subsequently increase megakaryocyte production. Secondary thrombocytosis etiologies are often categorized under the „5 I’s”—inflammation, ischemia, infection, infarction, and iron deficiency. […] Acute bacterial, viral, or chronic infectious conditions (eg, tuberculosis) can cause secondary thrombocytosis due to increased production of IL6—an inflammatory component that enhances thrombopoietin synthesis. […] The major functions of the spleen are immune activity and blood filtration. Up to 90% of splenectomized patients experience thrombocytosis postoperatively due to the loss of splenic sequestration.
  • #38 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    Thrombocytosis, an increased platelet count above the upper limit of normal (ULN) range, is common in infants and children. Unlike in adults, however, the overwhelming majority of pediatric thrombocytosis cases are secondary (also known as reactive). Normally, no treatment is necessary for secondary thrombocytosis. […] Common causes of secondary thrombocytosis include the following: Bacterial, viral, or parasitic infections – Particularly common in infants during the recovery phase of an infection (most often respiratory tract infection) […] Inflammation – For instance, rheumatoid arthritis, inflammatory bowel disease, Kawasaki syndrome, vasculitis, collagen vascular disease […] Surgery, trauma, burns […] Blood loss, hemolytic anemia, iron deficiency anemia […] Asplenia or hyposplenia
  • #39 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    The common factor among the various underlying causes of secondary thrombocytosis is the presence of inflammatory compounds, such as interleukin 6 (IL6), which enhance thrombopoietin secretion and subsequently increase megakaryocyte production. Secondary thrombocytosis etiologies are often categorized under the „5 I’s”—inflammation, ischemia, infection, infarction, and iron deficiency. […] Acute bacterial, viral, or chronic infectious conditions (eg, tuberculosis) can cause secondary thrombocytosis due to increased production of IL6—an inflammatory component that enhances thrombopoietin synthesis. […] The major functions of the spleen are immune activity and blood filtration. Up to 90% of splenectomized patients experience thrombocytosis postoperatively due to the loss of splenic sequestration.
  • #40 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    The spleen is the major organ for the destruction of platelets; therefore, after splenectomy, a sharp rise in the platelet count is routinely observed, although the count subsequently undergoes a slow decrease to the reference range. […] Additional causes of secondary, noninfectious thrombocytosis reported in the literature are listed below: Caffey disease […] Granulocyte-colony stimulating factor treatment in neonates […] Hepatocellular carcinoma […] Lowmolecular-weight heparin […] Malignant ovarian tumors […] Trauma. […] There are two types of familial thrombocytosis. One affects a single cell lineage (platelets), with Mendelian dominant inheritance, high penetrance, and polyclonal hematopoiesis. […] At least two classes of molecular mutations leading to familial thrombocytosis are known. One involves mutations of the THPO gene that result in increased THPO production by various mechanisms.
  • #41 Thrombocytosis – Diagnosis and treatment – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/thrombocytosis/diagnosis-treatment/drc-20378319
    Treatment for this condition depends on the cause. […] If you have a chronic infection or an inflammatory disease, your platelet count likely will remain high until the condition is under control. […] If you’ve had your spleen removed, you might have lifelong thrombocytosis, but you’re unlikely to need treatment. […] You might need to take prescription medicine or have procedures to lower your platelet counts if you: Have a history of blood clots and bleeding. […] Your doctor might prescribe platelet-lowering drugs such as hydroxyurea (Droxia, Hydrea), anagrelide (Agrylin) or interferon alfa (Intron A). […] In emergencies, platelets can be filtered from your blood with a machine. This procedure is called plateletpheresis. The effects are only temporary.
  • #42 Thrombocytosis: Symptoms, Causes, and Treatment | Doctor
    https://patient.info/doctor/thrombocytosis
    Infection (common infective causes are meningitis, infections of the upper and lower respiratory tract, urinary tract infections, gastroenteritis, septic arthritis, osteomyelitis, and generalised sepsis). […] Inflammation (eg, rheumatoid arthritis, Kawasaki disease, Henoch-Schnlein purpura, inflammatory bowel disease). […] Tissue damage (eg, burns, trauma, fracture). […] Hyposplenism. […] Postoperative. […] Haemorrhage. […] Iron deficiency. […] Malignancy (especially soft-tissue sarcoma, osteosarcoma). […] Haemolysis. […] Drug therapy – eg, corticosteroids; adrenaline (epinephrine). […] Cytokine administration (eg, thrombopoietin). […] Rebound following myelosuppressive chemotherapy. […] Rebound from other causes – eg, with iron-deficiency anaemia, recovery phase of idiopathic thrombocytopenic purpura (ITP). […] Post-splenectomy. […] Renal disorders (eg, nephrotic syndrome, nephritis). […] Low birth-weight/preterm infants.
  • #43 Secondary Thrombocytosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/206811-overview
    Platelets are acute-phase reactants; therefore, platelet counts increase in response to various stimuli, including systemic infections, inflammatory conditions, bleeding, and tumors. This phenomenon is called reactive or secondary thrombocytosis, and it is a benign form of thrombocytosis. […] The primary treatment of secondary thrombocytosis should address the underlying cause of the thrombocytosis. Once the causal agent is managed, platelets counts typically normalize. […] Etiologic conditions associated with secondary thrombocytosis (reactive thrombocytosis) include the following: Infection and inflammation, Trauma or surgery, Chronic inflammatory conditions, Hemorrhage, blood loss, or both, Iron-deficiency anemia, Rebound thrombocytosis, Asplenia (anatomic or functional), Hyposplenism or postsplenectomy, Malignancy, Electric shock, Enoxaparin, Idiopathic.
  • #44 What’s Behind Thrombocytosis in Apparently Healthy Patients
    https://www.cliniciansbrief.com/article/thrombocytosis-diagnosis-cause-platelet-count
    Thrombocytosis, an increase in circulating platelets to 500-600 103/L, can be due to a myeloproliferative disorder but is most often a nonspecific finding that is either physiologic or reactive (ie, secondary to an underlying disease). […] Physiologic thrombocytosis results from mobilization of platelets from splenic and, possibly, pulmonary pools. […] Causes of Physiologic Reactive Thrombocytosis include bone fracture, drug therapy (eg, glucocorticoids, epinephrine, vincristine, erythropoietin), endocrine disease (ie, diabetes mellitus, canine hyperadrenocorticism, feline hyperthyroidism), exercise, hemorrhage (acute), hepatobiliary disease, immune-mediated disease, infection (acute or chronic), inflammatory disease (acute or chronic; especially GI and hepatobiliary disease in cats), iron deficiency, neoplasia (especially carcinoma and lymphoma), rebound from thrombocytopenia, splenectomy, surgery, and trauma.
  • #45 What Causes Thrombocythemia and Thrombocytosis? | Hematology-Oncology Associates of CNY
    https://www.hoacny.com/what-causes-thrombocythemia-and-thrombocytosis
    Some conditions can lead to a high platelet count that lasts for only a short time. Examples of such conditions include: Recovery from serious blood loss, Recovery from a very low platelet count caused by excessive alcohol use and lack of vitamin B12 or folate, Acute infection or inflammation, Response to physical activity. […] Although the platelet count is high in secondary thrombocytosis, the platelets are normal (unlike in primary thrombocythemia). Thus, people who have secondary thrombocytosis have a lower risk of blood clots and bleeding.
  • #46 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Reactive thrombocytosis accompanying iron deficiency anemia can occur independently or in association with erythropoietin or as an additive event related to cytokines. […] Drug-induced thrombocytosis can result from various causative factors. One proposed mechanism is that certain drugs can cause the release of cytokines, particularly IL6, leading to thrombocytosis. […] Rheumatoid arthritis, inflammatory bowel disease, sarcoidosis, and autoimmune antibody-mediated illnesses can cause thrombocytosis through inflammatory effects, particularly involving IL6. […] Most diseases with antibody-mediated hemolysis manifest thrombocytopenia. Conversely, some conditions, including cold agglutinin disease (CAD), cause thrombocytosis. […] Platelets have an established association with malignancies.
  • #47 What’s Behind Thrombocytosis in Apparently Healthy Patients
    https://www.cliniciansbrief.com/article/thrombocytosis-diagnosis-cause-platelet-count
    Thrombocytosis, an increase in circulating platelets to 500-600 103/L, can be due to a myeloproliferative disorder but is most often a nonspecific finding that is either physiologic or reactive (ie, secondary to an underlying disease). […] Physiologic thrombocytosis results from mobilization of platelets from splenic and, possibly, pulmonary pools. […] Causes of Physiologic Reactive Thrombocytosis include bone fracture, drug therapy (eg, glucocorticoids, epinephrine, vincristine, erythropoietin), endocrine disease (ie, diabetes mellitus, canine hyperadrenocorticism, feline hyperthyroidism), exercise, hemorrhage (acute), hepatobiliary disease, immune-mediated disease, infection (acute or chronic), inflammatory disease (acute or chronic; especially GI and hepatobiliary disease in cats), iron deficiency, neoplasia (especially carcinoma and lymphoma), rebound from thrombocytopenia, splenectomy, surgery, and trauma.
  • #48 What’s Behind Thrombocytosis in Apparently Healthy Patients
    https://www.cliniciansbrief.com/article/thrombocytosis-diagnosis-cause-platelet-count
    Reactive thrombocytosis is associated with a variety of conditions; can be mild (500-800 103/L), moderate (801-1,000 103/L), or severe (1,000 103/L); and can be transient or persistent. […] Studies have identified inflammation and neoplasia as the most common triggers in dogs and cats with nonphysiologic thrombocytosis, with marked thrombocytosis more likely to occur with neoplasia. […] Thrombocytosis can also occur as a rebound reaction following platelet loss due to blood loss, following surgery or accidental tissue damage, and during recovery from the suppressive effects of chemotherapy. […] Drug-induced thrombocytosis has been associated with glucocorticoids, vincristine, and erythropoietin in animals and iron sulfate, ciprofloxacin, piperacillin/tazobactam, retinoic acid, clozapine, and low-molecular-weight heparin in humans.
  • #49 Secondary Thrombocytosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/206811-overview
    Platelets are acute-phase reactants; therefore, platelet counts increase in response to various stimuli, including systemic infections, inflammatory conditions, bleeding, and tumors. This phenomenon is called reactive or secondary thrombocytosis, and it is a benign form of thrombocytosis. […] The primary treatment of secondary thrombocytosis should address the underlying cause of the thrombocytosis. Once the causal agent is managed, platelets counts typically normalize. […] Etiologic conditions associated with secondary thrombocytosis (reactive thrombocytosis) include the following: Infection and inflammation, Trauma or surgery, Chronic inflammatory conditions, Hemorrhage, blood loss, or both, Iron-deficiency anemia, Rebound thrombocytosis, Asplenia (anatomic or functional), Hyposplenism or postsplenectomy, Malignancy, Electric shock, Enoxaparin, Idiopathic.
  • #50
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    Moreover, some studies have shown that RT can also occur during antibiotic treatment for pediatric infections. It may appear as a laboratory side effect after treatment with carbapenems (ie, imipenem/cilastatin, meropenem) and cephalosporins (ie, ceftriaxone and ceftazidime) in the case of neonatal and childhood central nervous system or respiratory tract infection, and it has an incidence of nearly 10% in treated patients. The occurrence of childhood RT is age dependent: the highest incidence is found among neonates (particularly premature babies) and infants aged up to 24 months, which gradually decreases up to the age of 10 years. […] As thromboembolic events have not been reported in children with RT secondary to infections, treatment with platelet aggregation inhibitors is not required even when the platelet count is high (ie, 1000 109/L). It is important to remember that a conservative approach is recommended and treatment should be aimed at the underlying infection and not the platelet count.
  • #51 Thrombocytosis: Essential Thrombocythemia and Reactive Causes – Clinical Tree
    https://clinicalpub.com/thrombocytosis-essential-thrombocythemia-and-reactive-causes/
    Thrombocytosis may be pragmatically categorized as (1) nonclonal; (2) due to hereditary, reactive, or spurious causes; or (3) an autonomous clonal process in which the elevated platelet count is a manifestation of a primary myeloproliferative neoplasm (MPN). […] The category of spurious thrombocytosis usually represents laboratory artifact, often precipitated by a concurrent disease state. […] RT is caused by increased megakaryocyte production of platelets mediated by a physiologically normal megakaryocyte response to elevated circulating levels of thrombopoietic and inflammatory cytokines. […] In general, RT is a much more common cause of elevated platelet counts than ET or thrombocythemia due to the other MPNs. […] Familial thrombocytosis is a very rare condition in which extremely high platelet counts have been observed in multiple individuals in successive generations; it affects both sexes and is usually transmitted through an autosomal dominant inheritance mode.
  • #52 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    The spleen is the major organ for the destruction of platelets; therefore, after splenectomy, a sharp rise in the platelet count is routinely observed, although the count subsequently undergoes a slow decrease to the reference range. […] Additional causes of secondary, noninfectious thrombocytosis reported in the literature are listed below: Caffey disease […] Granulocyte-colony stimulating factor treatment in neonates […] Hepatocellular carcinoma […] Lowmolecular-weight heparin […] Malignant ovarian tumors […] Trauma. […] There are two types of familial thrombocytosis. One affects a single cell lineage (platelets), with Mendelian dominant inheritance, high penetrance, and polyclonal hematopoiesis. […] At least two classes of molecular mutations leading to familial thrombocytosis are known. One involves mutations of the THPO gene that result in increased THPO production by various mechanisms.
  • #53 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    The spleen is the major organ for the destruction of platelets; therefore, after splenectomy, a sharp rise in the platelet count is routinely observed, although the count subsequently undergoes a slow decrease to the reference range. […] Additional causes of secondary, noninfectious thrombocytosis reported in the literature are listed below: Caffey disease […] Granulocyte-colony stimulating factor treatment in neonates […] Hepatocellular carcinoma […] Lowmolecular-weight heparin […] Malignant ovarian tumors […] Trauma. […] There are two types of familial thrombocytosis. One affects a single cell lineage (platelets), with Mendelian dominant inheritance, high penetrance, and polyclonal hematopoiesis. […] At least two classes of molecular mutations leading to familial thrombocytosis are known. One involves mutations of the THPO gene that result in increased THPO production by various mechanisms.
  • #54 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    The other involves mutations of the c-MPL gene that somehow constitutively maintain activated signal transduction, leading to continuous signaling for megakaryocytic proliferation. […] While a somatic JAK2V617F mutation results in MPN, germline mutations at various loci can result in single-lineage familial thrombocytoses.
  • #55 Orphanet: Familial thrombocytosis
    https://www.orpha.net/en/disease/detail/71493
    Familial thrombocytosis is caused by germline mutations in the THPO gene (3q26.3-q27) or in the MPL (MPL S505N) gene (1p34) […] Diagnosis is based on the observation of elevated levels of platelets (over 450 x 109/L) and the elimination of secondary causes of thrombocythemia. Genetic testing is required to confirm the diagnosis.
  • #56 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Secondary thrombocytosis, also known as reactive thrombocytosis, is characterized by an abnormally high platelet count due to underlying events, infections or diseases, or certain medications. Secondary thrombocytosis, which is more common than primary thrombocytosis, is typically identified through routine laboratory studies. In most cases, secondary thrombocytosis symptoms are due to an underlying disorder rather than the thrombocytosis itself. Rarely, extreme thrombocytosis may lead to thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism. […] Approximately 80% to 90% of individuals with thrombocytosis are known to have secondary thrombocytosis. Causes of secondary thrombocytosis include transient conditions like acute blood loss or infection, as well as sustained factors such as iron deficiency, asplenia, cancer, chronic inflammation, or infectious diseases. Reactive thrombocytosis is a laboratory anomaly that generally resolves once the underlying causative condition is addressed.
  • #57 Primary & Secondary Thrombocytosis | Apollo Hospitals
    https://www.apollohospitals.com/health-library/primary-secondary-thrombocytosis/
    Thrombocytosis occurs when there are too many platelets in your bloodstream. […] Though the bone marrow is known to have certain gene mutations, the cause for primary thrombocytosis is unknown. […] Secondary or reactive thrombocytosis is caused by another underlying condition/infection. This can include acute bleeding, anaemia (iron deficiency), cancer, inflammation disorders such as rheumatoid arthritis, or surgery like splenectomy (spleen removal). […] Essential or primary thrombocythemia poses a much greater risk of clotting or bleeding complications. However, secondary thrombocytosis accounts for 80-90% of the cases.
  • #58
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Given the prevalence of RT in clinical practice (and therefore in underwriting), it is important to understand how it is diagnosed. Several factors point toward a reactive etiology rather than a primary cause. The presence of, for example, comorbid conditions such as an infection, a connective tissue disease, bleeding, splenectomy, trauma, or postoperative state would favor a diagnosis of RT, whereas the absence of these conditions would suggest PT. […] In adults, acute infection, tissue damage, chronic inflammatory disorders, and malignancy are the most common causes of RT, with one or more of these present in more than 75% of RT cases. […] The risk of thrombotic complications from RT is considered to be low, occurring in only 1.6% of patients in one large case series, with all thrombotic events identified as venous and occurring in patients with other risk factors, such as a postoperative state or with underlying malignancy.
  • #59 Thrombocytosis – Don’t Forget the Bubbles
    https://dontforgetthebubbles.com/primary-thromobcytosis/
    Thrombocytosis is very common and is often transient in children when it is a secondary thrombocytosis. […] In children, we frequently see secondary thrombocytosis. In fact, 6-15% of hospitalised children have high platelets. The platelet levels can reach over 900x 109/L even in secondary thrombocytosis. This can occur most frequently with infection but also with inflammatory conditions (e.g. Kawasaki disease, rheumatoid arthritis, inflammatory bowel disease); in acute care (e.g. hypoxia, trauma, blood loss) and in haematology/oncology (e.g.malignancy, iron deficiency). […] In adults, essential thrombocytosis, along with polycythaemia vera and primary myelofibrosis, are part of the family of myeloproliferative neoplasms. Patients can be at risk of thrombosis or bleeding, and also splenomegaly, bone marrow fibrosis, and the potential to transform into acute myeloid leukaemia. Even the hereditary forms have risks of complications.
  • #60
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    Moreover, some studies have shown that RT can also occur during antibiotic treatment for pediatric infections. It may appear as a laboratory side effect after treatment with carbapenems (ie, imipenem/cilastatin, meropenem) and cephalosporins (ie, ceftriaxone and ceftazidime) in the case of neonatal and childhood central nervous system or respiratory tract infection, and it has an incidence of nearly 10% in treated patients. The occurrence of childhood RT is age dependent: the highest incidence is found among neonates (particularly premature babies) and infants aged up to 24 months, which gradually decreases up to the age of 10 years. […] As thromboembolic events have not been reported in children with RT secondary to infections, treatment with platelet aggregation inhibitors is not required even when the platelet count is high (ie, 1000 109/L). It is important to remember that a conservative approach is recommended and treatment should be aimed at the underlying infection and not the platelet count.
  • #61
    https://link.springer.com/article/10.1007/s00277-021-04485-0
    Thus, a recent review described annual incidences of essential thrombocythemia (ET), one of the Philadelphia-negative myeloproliferative neoplasms (MPNs), ranging between 0.004 and 0.11 per 100,000 in children aged 0-16 years, while the meta-analysis in adults showed a pooled annual incidence rate of 1.03 per 100,000 (95% CI: 0.58-1.80). […] Recent research has elucidated the association between MPNs and somatic mutations in the genes JAK 2, MPL, and CALR. […] However, a lower overall incidence of these driver mutations was described in children diagnosed with ET. […] Thus, in a group of 89 children with clinically diagnosed ET, Randi et al. found approximately 75% to be triple-negative and to display non-clonal disease. […] Due to heterogeneity of adult and childhood ET, it has previously been emphasized that specific diagnostic criteria for MPNs in children are necessary.
  • #62
    https://haematologica.org/article/view/6991
    The molecular pathogenesis of ET in childhood is not fully aligned with its adult counterpart. […] Fewer children than adults with ET are JAK2-mutant positive. […] In view of the significant number of JAK2V617F-negative children with ET, a recent study out of Japan looked for alternative causative mutations in pediatric patients. […] ET and hereditary forms of thrombocytosis seem to differ in their pathogenesis as well in pediatric patients.
  • #63 Thrombocytosis: Causes, Symptoms, Diagnosis, and Treatment
    https://neumedix.com/thrombocytosis-causes-symptoms-diagnosis-and-treatment/
    Abnormalities in the bone marrow, such as mutations in the JAK2 gene, lead to the overproduction of platelets, resulting in primary thrombocytosis. […] Underlying conditions or factors, such as infections, inflammation, or anemia, trigger the body to produce more platelets as a reactive response, leading to secondary thrombocytosis.
  • #64 Essential Thrombocythemia: Definition, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/24031-essential-thrombocythemia
    Essential thrombocythemia is an acquired genetic disorder. […] Essential thrombocythemia is an acquired genetic condition, meaning it happens when certain genes mutate or change. […] Essential thrombocythemia is an acquired genetic disorder that happens when certain genes mutate. Researchers don’t know why these genes mutate, so you can’t prevent that from happening. […] When these genes mutate, they set off a chain reaction that puts stem cell production into overdrive, producing more platelets than your body can use.
  • #65 What is essential thrombocythaemia? | Cancer Research UK
    https://www.cancerresearchuk.org/about-cancer/essential-thrombocythaemia/what-is-et
    Essential thrombocythaemia (ET) is a rare blood cancer that causes a high number of blood cells called platelets to form. […] We dont know exactly what causes ET. Researchers have found that around 50 to 60 in 100 people (around 50 to 60%) with ET have a change in the JAK2 gene. The JAK2 gene makes a protein that controls how many blood cells are made by the stem cells. This gene change causes too much of this protein to be made and that causes the stem cells to make more platelets. People with ET might also have a genetic change in either the CALR or MPL gene. […] Genetic faults might happen because youve been exposed to hazardous chemicals over time but more research is needed. Often gene changes are because of a copying mistake when a cell is dividing. In most cases, these genetic faults happen during a persons lifetime. You are not born with them, so you cant pass them on to your children. […] In rarer cases, you might have a history of myeloproliferative neoplasms (MPNs) in your family. This might mean there is a faulty gene in your family that increases your risk of developing MPNs.
  • #66 Thrombocytosis: Essential Thrombocythemia and Reactive Causes – Clinical Tree
    https://clinicalpub.com/thrombocytosis-essential-thrombocythemia-and-reactive-causes/
    ET is considered a distinct entity, and its diagnosis is based on exclusion of reactive causes of elevated platelet counts or on demonstration of increased numbers of large, dysplastic-appearing megakaryocytes on bone marrow biopsy specimens and also on the presence of genetic biomarkers suggestive of clonal MPNs. […] The diagnosis of ET continues to rely in part on exclusion of the secondary causes of elevated platelet counts. […] The TPO-independent mechanism has also been invoked for the extreme thrombocytosis observed in some African Americans, who are homozygous positive for a missense mutation in the c-MPL gene that results in a K39N substitution. […] Dysregulation of the TPO c-MPL system in ET is suggested. […] The JAK2 V617F mutation on exon 14 is a gain-of-function mutation resulting in hypersensitivity or even independence of intracellular JAK-STAT pathway signaling to external stimulation of the MPL, EPO, and G-CSF receptors by circulating cytokines and growth factors. […] No consistent gene mutation or chromosomal defect or causal gene association for ET has been identified to date.
  • #67 What is essential thrombocythaemia? | Cancer Research UK
    https://www.cancerresearchuk.org/about-cancer/essential-thrombocythaemia/what-is-et
    Essential thrombocythaemia (ET) is a rare blood cancer that causes a high number of blood cells called platelets to form. […] We dont know exactly what causes ET. Researchers have found that around 50 to 60 in 100 people (around 50 to 60%) with ET have a change in the JAK2 gene. The JAK2 gene makes a protein that controls how many blood cells are made by the stem cells. This gene change causes too much of this protein to be made and that causes the stem cells to make more platelets. People with ET might also have a genetic change in either the CALR or MPL gene. […] Genetic faults might happen because youve been exposed to hazardous chemicals over time but more research is needed. Often gene changes are because of a copying mistake when a cell is dividing. In most cases, these genetic faults happen during a persons lifetime. You are not born with them, so you cant pass them on to your children. […] In rarer cases, you might have a history of myeloproliferative neoplasms (MPNs) in your family. This might mean there is a faulty gene in your family that increases your risk of developing MPNs.
  • #68 Thrombocytosis: Symptoms, Causes, and Treatment | Doctor
    https://patient.info/doctor/thrombocytosis
    This can be secondary to a number of conditions. It is an exaggerated physiological response to a primary problem, such as an infection. The trigger factor (eg, infection) results in the release of cytokines which mediate an increase in platelet production. It is often a transient phenomenon which disappears when the underlying cause is resolved. […] Mutations in the key regulators of thrombopoietin, the thrombopoietin receptor MPL and JAK2, are found in 50-60% of patients with essential thrombocythaemia or primary myelofibrosis and in 10-20% of hereditary thrombocytosis. When present in a heterozygous state the JAK2-V617F mutation preferentially stimulates megakaryopoiesis and in most cases manifests as essential thrombocythaemia. Homozygous JAK2-V617F reduces megakaryopoiesis in favour of increased erythropoiesis, resulting in polycythaemia vera and/or myelofibrosis.
  • #69 Thrombocytosis: Essential Thrombocythemia and Reactive Causes – Clinical Tree
    https://clinicalpub.com/thrombocytosis-essential-thrombocythemia-and-reactive-causes/
    ET is considered a distinct entity, and its diagnosis is based on exclusion of reactive causes of elevated platelet counts or on demonstration of increased numbers of large, dysplastic-appearing megakaryocytes on bone marrow biopsy specimens and also on the presence of genetic biomarkers suggestive of clonal MPNs. […] The diagnosis of ET continues to rely in part on exclusion of the secondary causes of elevated platelet counts. […] The TPO-independent mechanism has also been invoked for the extreme thrombocytosis observed in some African Americans, who are homozygous positive for a missense mutation in the c-MPL gene that results in a K39N substitution. […] Dysregulation of the TPO c-MPL system in ET is suggested. […] The JAK2 V617F mutation on exon 14 is a gain-of-function mutation resulting in hypersensitivity or even independence of intracellular JAK-STAT pathway signaling to external stimulation of the MPL, EPO, and G-CSF receptors by circulating cytokines and growth factors. […] No consistent gene mutation or chromosomal defect or causal gene association for ET has been identified to date.
  • #70 Essential thrombocythemia (ET) – MPN Research Foundation
    https://mpnresearchfoundation.org/essential-thrombocythemia-et/
    Essential thrombocythemia (ET) is a chronic myeloproliferative neoplasm (MPN) characterized by an increased number of platelets in the blood. […] No one knows what causes the onset of essential thrombocythemia (ET) or other myeloproliferative neoplasms (MPNs). […] However, researchers have discovered mutations that alter the activity of proteins that control signaling pathways (important regulators of cell growth and development) in many patients with ET. […] Risk factors associated with ET include: […] Approximately half of all ET patients have a mutation of the JAK2 gene in their blood-forming cells. […] Nearly a quarter (23.5%) of those diagnosed with MF and ET have a mutation called Calreticulin, or CALR. […] A small minority of people with ET may later develop acute leukemia (less than 10%) or postpolycythemic myelofibrosis (15%), both of which can be life threatening. […] Potential new treatments for ET are currently being developed and tested as a result of the discovery of the link between the JAK2 mutation and the incidence of ET.
  • #71 How I Work up the Patient with Thrombocytosis – The ASCO Post
    https://ascopost.com/issues/march-15-2012/how-i-work-up-the-patient-with-thrombocytosis/
    Causes of primary thrombocytosis include myeloproliferative neoplasms, myelodysplastic syndromes, myelodysplastic syndrome/myeloproliferative neoplasm overlap syndromes, and other myeloid malignancies. […] Essential thrombocythemia is currently defined as a persistent thrombocythemic state (platelet count 450 109/L) that is neither reactive nor associated with an otherwise defined myeloid malignancy (including polycythemia vera), primary myelofibrosis (including prefibrotic primary myelofibrosis), CML, and myelodysplastic syndromes. […] The first evidence of monoclonality in essential thrombocythemia was suggested in the early 1980s by clonality studies that utilized glucose-6-phosphate dehydrogenase (G6PD) isoenzyme analysis. These early observations were subsequently confirmed by X-linked DNA analysis. Unlike the situation for CML, the primary molecular abnormality in essential thrombocythemia has not been identified.
  • #72 How I Work up the Patient with Thrombocytosis – The ASCO Post
    https://ascopost.com/issues/march-15-2012/how-i-work-up-the-patient-with-thrombocytosis/
    Both structural and numerical abnormalities involving many individual chromosomes (including trisomies 9 and 8, and long-arm deletions of chromosomes 5, 7, 13, 17, and 20) have been associated with essential thrombocythemia. […] It is worth reiterating the value of mutation screening for JAK2V617F in distinguishing essential thrombocythemia from reactive thrombocytosis but not from other myeloproliferative neoplasms. In addition, rare cases of genetically defined essential thrombocythemia (eg, activating mutation of MPL) have been described and must be kept in mind while evaluating a patient with either a lifelong or family history of thrombocytosis.
  • #73 Thrombocytosis: Essential Thrombocythemia and Reactive Causes – Clinical Tree
    https://clinicalpub.com/thrombocytosis-essential-thrombocythemia-and-reactive-causes/
    Thrombocytosis may be pragmatically categorized as (1) nonclonal; (2) due to hereditary, reactive, or spurious causes; or (3) an autonomous clonal process in which the elevated platelet count is a manifestation of a primary myeloproliferative neoplasm (MPN). […] The category of spurious thrombocytosis usually represents laboratory artifact, often precipitated by a concurrent disease state. […] RT is caused by increased megakaryocyte production of platelets mediated by a physiologically normal megakaryocyte response to elevated circulating levels of thrombopoietic and inflammatory cytokines. […] In general, RT is a much more common cause of elevated platelet counts than ET or thrombocythemia due to the other MPNs. […] Familial thrombocytosis is a very rare condition in which extremely high platelet counts have been observed in multiple individuals in successive generations; it affects both sexes and is usually transmitted through an autosomal dominant inheritance mode.
  • #74 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    Congenital or idiopathic nephrotic syndrome […] Ovarian cancer – In particular, of germ cell origin […] Osteogenesis imperfecta. […] Essential (or primary) thrombocytosis (ET) may be suspected if any or a combination of the following features is present and if no obvious cause of secondary thrombocytosis exists: Enlarged liver and/or spleen […] History of thrombosis or bleeding […] Family history of thrombocytosis or myeloproliferative neoplasia (MPN; such as polycythemia vera [PV]) […] Persistent (3 mo) thrombocytosis. […] ET due to MPN is commonly associated with anemia and leukocytosis. […] Secondary thrombocytosis is usually mediated by the increased release of numerous cytokines in response to infections, inflammation, vasculitis, tissue trauma, and other factors. […] Thrombopoietin (THPO), the primary cytokine for platelet production and maturation, and interleukin (IL)-6 levels are usually initially elevated in response to the primary events mentioned earlier; they stimulate platelet production.
  • #75 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    The common factor among the various underlying causes of secondary thrombocytosis is the presence of inflammatory compounds, such as interleukin 6 (IL6), which enhance thrombopoietin secretion and subsequently increase megakaryocyte production. Secondary thrombocytosis etiologies are often categorized under the „5 I’s”—inflammation, ischemia, infection, infarction, and iron deficiency. […] Acute bacterial, viral, or chronic infectious conditions (eg, tuberculosis) can cause secondary thrombocytosis due to increased production of IL6—an inflammatory component that enhances thrombopoietin synthesis. […] The major functions of the spleen are immune activity and blood filtration. Up to 90% of splenectomized patients experience thrombocytosis postoperatively due to the loss of splenic sequestration.
  • #76
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    In both children and adults, thrombocytosis is usually defined as a platelet count of more than 450 109/L. As there are many primary and secondary causes, as well as false or spurious conditions mimicking thrombocytosis, establishing the cause requires considering clinical features and hematologic parameters. Pediatric primary thrombocytosis is very rare, but reactive thrombocytosis (RT) can be frequently observed in children with infections, iron deficiency, tissue damage, hemolysis, autoimmune diseases, malignancies, and other causes of an acute-phase response. The incidence of secondary forms due to infections is significantly higher in childhood than in adulthood, and infections are the main cause of pediatric RT, with reported incidence rates ranging from 37% to 78%. […] In pediatric patients with infections, RT is due to increased megakaryopoiesis and thrombopoiesis, which can be stimulated up to 10-fold. Under these conditions, platelet production is altered and may be regulated by various cytokines, such as interleukin (IL-)1 alpha, IL-8, IL-6, and tumor necrosis factor. IL-6 plays a major direct and indirect role by stimulating megakaryopoiesis or hepatic thrombopoietin (TPO) production. Many reports indicate that bacterial infections are more frequently associated with childhood RT than viral infections.
  • #77 Increased number of platelets call for review of thrombocytosis
    https://www.dvm360.com/view/increased-number-platelets-call-review-thrombocytosis
    Causes of canine thrombocytosis […] The fundamental causes responsible for thrombocytosis in dogs are: […] It may be a reaction to a disorder or disease in another part of the body. […] It may be a sign of an underlying disease in the bone marrow. […] Thrombocytosis as a reaction to another disorder in the dog’s body results from increased production of platelets in the bone marrow and increased release of stored platelets from the spleen. […] Infections may be accompanied by a reactive thrombocytosis, which is thought to be due to cytokines that are produced as part of the body’s normal defense against infection. […] The response of the bone marrow to acute or chronic blood loss is to produce not only more red blood cells but also more platelets – this occurs in response to cytokines.
  • #78 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    In severe infections, such as bacterial meningitis, one of the causes may be a rebound phenomenon after initial thrombocytopenia due to the rapid consumption of platelets. […] The most common infection associated with thrombocytosis is pneumonia. […] A retrospective study by Zheng et al found that out of 3156 children with respiratory tract infection, 817 (25.9%) had secondary thrombocytosis (500 X 109 platelets/L or higher). […] In some instances, such as chronic hemolytic anemia, the stimulus (hypoxia) to produce cytokines persists, causing long-term elevation of platelet counts. […] While thrombocytosis in association with iron-deficiency anemia is well documented, the mechanism remains unclear. […] A rare disorder of unknown etiology, idiopathic cyclic thrombocytopenia is characterized by female predominance, fluctuation of platelet count with rebound thrombocytosis (with peak 1 million/L), and a median age of onset of 35 years, although the youngest patient described was aged 1 year.
  • #79 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    A patient’s exercise regimen can influence platelet release, activation, and function. Studies have confirmed that acute exercise leads to a transient increase in platelet count, partially due to hemoconcentration and mobilization from the liver, lungs, and spleen. However, regular exercise training reduces platelet adhesion and aggregation, thereby exerting an antithrombotic effect.
  • #80 Thrombocytosis: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/13350-thrombocytosis
    Reactive thrombocytosis happens when your body reacts to various conditions by overproducing platelets. […] Causes of reactive thrombocytosis include: Anemia, Blood disorders, Cancer, Infections, Inflammatory conditions, Injury, Kidney failure, Some medications, Surgery (especially abdominal surgery), Removal of your spleen, Treatment of a vitamin B12 deficiency. […] There are many more causes of reactive thrombocytosis. […] High platelets arent life-threatening, but the complications that can result from the condition blood clots or severe bleeding can be. […] The most common causes of thrombocytosis are short-lived and dont put you at risk of serious blood clots. […] The risk is greater with essential thrombocytosis. […] Essential thrombocythemia (ET), or primary thrombocytosis, can cause serious bleeding or clotting complications. […] Taking medicine that keeps your platelet levels normal can help prevent this. […] After many years of having the disease, however, bone marrow fibrosis (scarring) can develop. […] A small percentage of people with essential thrombocythemia develop leukemia.
  • #81 Thrombocytosis in the ED – emDocs
    https://www.emdocs.net/thrombocytosis-in-the-ed/
    Both reactive thrombocytosis and clonal thrombocytosis may be associated with vasomotor symptoms. The key difference is that thrombotic and bleeding events are much more common in myeloproliferative thrombocytosis, whereas they are unusual in reactive thrombocytosis, regardless of platelet count. […] Thrombosis is the most concerning complication of clonal thrombocytosis. Classically, patients with essential thrombocythemia develop Budd-Chiari syndrome, or thrombotic occlusion of the hepatic vein and/or IVC. However, they may develop many types of vascular occlusion, including venous occlusion (e.g. DVT/PE) and arterial occlusion (e.g. CVA, MI, erythromelalgia). […] Serious bleeding in association with thrombocytosis should raise suspicion for DIC, coagulation factor deficiency, and acquired von Willebrand disease. Extreme thrombocytosis occurs in von Willebrand disease due to abnormal platelet adsorption of circulating vW factor. […] Reactive thrombocytosis may be secondary to trauma/surgery, splenectomy, infection or inflammation, blood loss, malignancy, medication use, etc. Reactive thrombocytosis tends to be transient, whereas clonal thrombocytosis is sustained.
  • #82 Thrombocytosis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/thrombocytosis/symptoms-causes/syc-20378315
    The cause of this disorder is unclear. It often appears to be connected to changes in certain genes. The bone marrow produces too many of the cells that form platelets, and these platelets often don’t work properly. This poses a much higher risk of clotting or bleeding complications than does reactive thrombocytosis.
  • #83 Primary & Secondary Thrombocytosis | Apollo Hospitals
    https://www.apollohospitals.com/health-library/primary-secondary-thrombocytosis/
    Thrombocytosis occurs when there are too many platelets in your bloodstream. […] Though the bone marrow is known to have certain gene mutations, the cause for primary thrombocytosis is unknown. […] Secondary or reactive thrombocytosis is caused by another underlying condition/infection. This can include acute bleeding, anaemia (iron deficiency), cancer, inflammation disorders such as rheumatoid arthritis, or surgery like splenectomy (spleen removal). […] Essential or primary thrombocythemia poses a much greater risk of clotting or bleeding complications. However, secondary thrombocytosis accounts for 80-90% of the cases.
  • #84 Thrombocytosis in the ED – emDocs
    https://www.emdocs.net/thrombocytosis-in-the-ed/
    Both reactive thrombocytosis and clonal thrombocytosis may be associated with vasomotor symptoms. The key difference is that thrombotic and bleeding events are much more common in myeloproliferative thrombocytosis, whereas they are unusual in reactive thrombocytosis, regardless of platelet count. […] Thrombosis is the most concerning complication of clonal thrombocytosis. Classically, patients with essential thrombocythemia develop Budd-Chiari syndrome, or thrombotic occlusion of the hepatic vein and/or IVC. However, they may develop many types of vascular occlusion, including venous occlusion (e.g. DVT/PE) and arterial occlusion (e.g. CVA, MI, erythromelalgia). […] Serious bleeding in association with thrombocytosis should raise suspicion for DIC, coagulation factor deficiency, and acquired von Willebrand disease. Extreme thrombocytosis occurs in von Willebrand disease due to abnormal platelet adsorption of circulating vW factor. […] Reactive thrombocytosis may be secondary to trauma/surgery, splenectomy, infection or inflammation, blood loss, malignancy, medication use, etc. Reactive thrombocytosis tends to be transient, whereas clonal thrombocytosis is sustained.
  • #85 Thrombocytosis in the ED – emDocs
    https://www.emdocs.net/thrombocytosis-in-the-ed/
    Both reactive thrombocytosis and clonal thrombocytosis may be associated with vasomotor symptoms. The key difference is that thrombotic and bleeding events are much more common in myeloproliferative thrombocytosis, whereas they are unusual in reactive thrombocytosis, regardless of platelet count. […] Thrombosis is the most concerning complication of clonal thrombocytosis. Classically, patients with essential thrombocythemia develop Budd-Chiari syndrome, or thrombotic occlusion of the hepatic vein and/or IVC. However, they may develop many types of vascular occlusion, including venous occlusion (e.g. DVT/PE) and arterial occlusion (e.g. CVA, MI, erythromelalgia). […] Serious bleeding in association with thrombocytosis should raise suspicion for DIC, coagulation factor deficiency, and acquired von Willebrand disease. Extreme thrombocytosis occurs in von Willebrand disease due to abnormal platelet adsorption of circulating vW factor. […] Reactive thrombocytosis may be secondary to trauma/surgery, splenectomy, infection or inflammation, blood loss, malignancy, medication use, etc. Reactive thrombocytosis tends to be transient, whereas clonal thrombocytosis is sustained.
  • #86 Thrombocytosis
    https://enotes.tripod.com/thrombocytosis.htm
    A Philadelphia chromosome (or its molecular equivalent) establishes CML as the diagnosis and excludes essential thrombocythemia. […] Approximately 50% of patients with essential thrombocytosis may be asymptomatic at presentation. […] It is believed that these symptoms, especially erythromelalgia, are the result of small vessel platelet-endothelium interaction with associated inflammation and transient thrombotic occlusion. […] The key guide to long-term management of essential thrombocythemia is the patient’s risk of thrombosis based on a history of prior thrombosis and age older than 60 years. […] Cytoreductive (platelet-lowering) therapy reduces the risk of thrombosis in high-risk patients, in whom the platelet count may need to be reduced to 400,000/L or lower.
  • #87 Thrombocytosis: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/13350-thrombocytosis
    Reactive thrombocytosis happens when your body reacts to various conditions by overproducing platelets. […] Causes of reactive thrombocytosis include: Anemia, Blood disorders, Cancer, Infections, Inflammatory conditions, Injury, Kidney failure, Some medications, Surgery (especially abdominal surgery), Removal of your spleen, Treatment of a vitamin B12 deficiency. […] There are many more causes of reactive thrombocytosis. […] High platelets arent life-threatening, but the complications that can result from the condition blood clots or severe bleeding can be. […] The most common causes of thrombocytosis are short-lived and dont put you at risk of serious blood clots. […] The risk is greater with essential thrombocytosis. […] Essential thrombocythemia (ET), or primary thrombocytosis, can cause serious bleeding or clotting complications. […] Taking medicine that keeps your platelet levels normal can help prevent this. […] After many years of having the disease, however, bone marrow fibrosis (scarring) can develop. […] A small percentage of people with essential thrombocythemia develop leukemia.
  • #88 Essential thrombocythemia (ET) – MPN Research Foundation
    https://mpnresearchfoundation.org/essential-thrombocythemia-et/
    Essential thrombocythemia (ET) is a chronic myeloproliferative neoplasm (MPN) characterized by an increased number of platelets in the blood. […] No one knows what causes the onset of essential thrombocythemia (ET) or other myeloproliferative neoplasms (MPNs). […] However, researchers have discovered mutations that alter the activity of proteins that control signaling pathways (important regulators of cell growth and development) in many patients with ET. […] Risk factors associated with ET include: […] Approximately half of all ET patients have a mutation of the JAK2 gene in their blood-forming cells. […] Nearly a quarter (23.5%) of those diagnosed with MF and ET have a mutation called Calreticulin, or CALR. […] A small minority of people with ET may later develop acute leukemia (less than 10%) or postpolycythemic myelofibrosis (15%), both of which can be life threatening. […] Potential new treatments for ET are currently being developed and tested as a result of the discovery of the link between the JAK2 mutation and the incidence of ET.
  • #89 Secondary Thrombocythemia – Blood Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/blood-disorders/myeloproliferative-disorders/secondary-thrombocythemia
    Secondary thrombocythemia is excess platelets in the bloodstream that develops as a result of another disorder and rarely leads to excessive blood clotting or bleeding. […] When thrombocythemia is caused by such an underlying disorder, the thrombocythemia is called secondary thrombocythemia (or reactive thrombocytosis) and is not classified as a myeloproliferative neoplasm. […] Causes of secondary thrombocythemia include bleeding, removal of the spleen, other surgical procedures, trauma, infections, rheumatoid arthritis, inflammatory bowel disease, and other inflammatory disorders, certain cancers, premature destruction of red blood cells (hemolysis), iron deficiency, and sarcoidosis. […] Although an increased number of platelets might be thought to cause excessive blood clotting, this rarely happens in secondary thrombocythemia unless people also have severe arterial disease.
  • #90 Understanding High Platelet Count: Causes, Symptoms, and Treatment Options – Dr. James O’Donovan
    https://www.doctorodonovan.com/videos/understanding-high-platelet-count-causes-symptoms-and-treatment-options
    The most common causes of high platelets are short-lived, and they don’t usually put you at risk of serious blood clots. The risk for this is greater with essential thrombocytosis. […] Your platelets might be elevated for various reasons, and many cases and causes of high platelets don’t require treatment.
  • #91
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Given the prevalence of RT in clinical practice (and therefore in underwriting), it is important to understand how it is diagnosed. Several factors point toward a reactive etiology rather than a primary cause. The presence of, for example, comorbid conditions such as an infection, a connective tissue disease, bleeding, splenectomy, trauma, or postoperative state would favor a diagnosis of RT, whereas the absence of these conditions would suggest PT. […] In adults, acute infection, tissue damage, chronic inflammatory disorders, and malignancy are the most common causes of RT, with one or more of these present in more than 75% of RT cases. […] The risk of thrombotic complications from RT is considered to be low, occurring in only 1.6% of patients in one large case series, with all thrombotic events identified as venous and occurring in patients with other risk factors, such as a postoperative state or with underlying malignancy.
  • #92
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Interestingly, RT in patients with iron deficiency anemia has been associated with a twofold thrombosis risk compared with patients with iron deficiency anemia alone. […] The presence of RT in infections and cancer may also be predictive of poor outcomes. […] This elevated mortality risk has been validated in other investigations on hospitalized patients, with one study showing a 30-day mortality risk 2.5 times higher in those with RT of 500,000/microL compared to those with normal platelet counts. […] Elevated platelets are associated with worse outcomes in individuals hospitalized with COVID-19.
  • #93
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Interestingly, RT in patients with iron deficiency anemia has been associated with a twofold thrombosis risk compared with patients with iron deficiency anemia alone. […] The presence of RT in infections and cancer may also be predictive of poor outcomes. […] This elevated mortality risk has been validated in other investigations on hospitalized patients, with one study showing a 30-day mortality risk 2.5 times higher in those with RT of 500,000/microL compared to those with normal platelet counts. […] Elevated platelets are associated with worse outcomes in individuals hospitalized with COVID-19.
  • #94
    https://journals.lww.com/pidj/fulltext/2012/01000/thrombocytosis_and_infections_in_childhood.22.aspx
    Moreover, some studies have shown that RT can also occur during antibiotic treatment for pediatric infections. It may appear as a laboratory side effect after treatment with carbapenems (ie, imipenem/cilastatin, meropenem) and cephalosporins (ie, ceftriaxone and ceftazidime) in the case of neonatal and childhood central nervous system or respiratory tract infection, and it has an incidence of nearly 10% in treated patients. The occurrence of childhood RT is age dependent: the highest incidence is found among neonates (particularly premature babies) and infants aged up to 24 months, which gradually decreases up to the age of 10 years. […] As thromboembolic events have not been reported in children with RT secondary to infections, treatment with platelet aggregation inhibitors is not required even when the platelet count is high (ie, 1000 109/L). It is important to remember that a conservative approach is recommended and treatment should be aimed at the underlying infection and not the platelet count.
  • #95 What’s Behind Thrombocytosis in Apparently Healthy Patients
    https://www.cliniciansbrief.com/article/thrombocytosis-diagnosis-cause-platelet-count
    Prolonged thrombocytosis can be seen with essential thrombocythemia, a chronic myeloproliferative disease (clonal disorder of megakaryocytes) that is rare in animals and characterized by marked thrombocytosis, normal WBC and RBC counts, and bone marrow megakaryocytic hyperplasia. […] Thrombocytosis can also occur with other myeloproliferative diseases, including polycythemia vera, myelofibrosis, chronic myeloid leukemia, and myelodysplastic syndrome. […] Reactive thrombocytosis typically resolves over time, after resolution of the inciting cause.
  • #96 Secondary Thrombocytosis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/206811-overview
    Platelets are acute-phase reactants; therefore, platelet counts increase in response to various stimuli, including systemic infections, inflammatory conditions, bleeding, and tumors. This phenomenon is called reactive or secondary thrombocytosis, and it is a benign form of thrombocytosis. […] The primary treatment of secondary thrombocytosis should address the underlying cause of the thrombocytosis. Once the causal agent is managed, platelets counts typically normalize. […] Etiologic conditions associated with secondary thrombocytosis (reactive thrombocytosis) include the following: Infection and inflammation, Trauma or surgery, Chronic inflammatory conditions, Hemorrhage, blood loss, or both, Iron-deficiency anemia, Rebound thrombocytosis, Asplenia (anatomic or functional), Hyposplenism or postsplenectomy, Malignancy, Electric shock, Enoxaparin, Idiopathic.
  • #97
    https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity
    Thrombocytosis, a condition defined as having a platelet count of more than 450,000 per microliter of blood (450 x 109/L), can be either physiologic in nature or due to primary or secondary causes. […] Secondary or reactive thrombocytosis (RT) is far more prevalent than primary or clonal thrombocytosis, and the presence of comorbid conditions in RT, a transient rise in platelets, and lack of genetic mutations favor a secondary etiology. […] Causes of thrombocytosis can be physiologic (exercise, parturition) and can also be primary/clonal (e.g., essential thrombocythemia, polycythemia vera, primary myelofibrosis, and other hematologic malignancies) as well as secondary/reactive (due to infectious and inflammatory diseases, neoplasms, anemia, trauma, surgery, asplenia, and iron deficiency).
  • #98 Thrombocytosis: Causes, Symptoms, Treatment, and More
    https://www.verywellhealth.com/thrombocytosis-overview-and-more-5187124
    Essential thrombocytosis (ET) is a dysfunction in the bone marrow that causes too many platelets to be made. The cause of ET is not entirely clear, but about 90% of cases have an acquired mutation in JAK2, CALR, or MPL. […] Reactive thrombocytosis is an elevation in platelet counts for a reason outside of the bone marrow. The platelets increase in reaction to something such as iron deficiency, infection, inflammation, cancer, or bleeding.
  • #99 High Platelet Count (Thrombocytosis): Symptoms, Causes and Treatment
    https://www.citizenshospitals.com/blogs/high-platelet-count-thrombocytosis-symptoms-causes-and-treatment
    Thrombocytosis may be primary, caused by a bone marrow disorder, or secondary, resulting from another medical condition. […] The primary cause of thrombocytosis is a bone marrow disorder known as essential thrombocythemia (ET). In ET, the bone marrow produces excess platelets due to mutations in specific genes, such as JAK2, CALR, or MPL. […] Secondary thrombocytosis is more common than the primary form and occurs as a reaction to an underlying condition. Some of the most prevalent causes include: […] Infections: Bacterial, viral, or fungal infections can stimulate the immune system, leading to increased platelet production. […] Inflammation: Conditions such as rheumatoid arthritis, inflammatory bowel disease (IBD), and lupus can trigger an inflammatory response, resulting in elevated platelet counts.
  • #100 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK560810/
    Secondary thrombocytosis, also known as reactive thrombocytosis, is characterized by an abnormally high platelet count due to underlying events, infections or diseases, or certain medications. Secondary thrombocytosis, which is more common than primary thrombocytosis, is typically identified through routine laboratory studies. In most cases, secondary thrombocytosis symptoms are due to an underlying disorder rather than the thrombocytosis itself. Rarely, extreme thrombocytosis may lead to thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism. […] Approximately 80% to 90% of individuals with thrombocytosis are known to have secondary thrombocytosis. Causes of secondary thrombocytosis include transient conditions like acute blood loss or infection, as well as sustained factors such as iron deficiency, asplenia, cancer, chronic inflammation, or infectious diseases. Reactive thrombocytosis is a laboratory anomaly that generally resolves once the underlying causative condition is addressed.
  • #101 High Platelets and Thrombocytosis: Symptoms, Causes, and More
    https://resources.healthgrades.com/right-care/blood-conditions/high-platelets
    Having high platelets means that the blood contains more platelets than is typically expected. […] High platelet levels can be a sign of an underlying condition. This means that an existing illness is causing the body to produce more platelets than necessary. […] When high platelets occur as a result of another condition, this is called thrombocytosis. […] Thrombocytosis, also known as secondary or reactive thrombocytosis, is when high platelets occurs as a symptom of another disease or condition. It can result from anemia, infection, or cancer. […] Thrombocytosis is the occurrence of high platelets as a symptom of another condition. […] A wide range of diseases and conditions can cause high platelets, including: anemia, such as from iron deficiency or hemolytic anemia; cancer, particularly lymphoma, gastrointestinal cancer, breast cancer, or ovarian cancer; chemotherapy; surgery; splenectomy, or surgical removal of the spleen; an adverse reaction to a medication or to exercise; an allergic reaction; an infection; stress and anxiety; inflammation and inflammatory diseases, such as Kawasaki disease; tissue damage; myelodysplasia, which refers to a group of conditions in which the blood cells develop or function atypically.
  • #102 Understanding High Platelet Count or Thrombocytosis
    https://www.verywellhealth.com/things-that-elevate-your-platelet-count-401336
    A high platelet count indicates too many of the small cells (platelets) that help form blood clots. This can cause dangerous clots and bleeding. Also called thrombocytosis or thrombocythemia, depending on the cause, a high platelet count is more than 450,000 platelets per microliter of blood. […] Reactive thrombocytosis is caused by an underlying condition like: Infection, Inflammation or inflammatory diseases, Iron deficiency, Bleeding, Cancer, Recent surgery, Splenectomy (removal of the spleen). […] Essential thrombocythemia describes platelet counts rising independently due to bone marrow dysfunction. […] The causes of RT are described in seven broad categories: Infections, Chronic Inflammatory Diseases, Allergic Conditions, Anemia, Asplenia, Medications, Cancer. […] Essential thrombocythemia (ET), also known as primary thrombocythemia, is a less common cause of high platelet counts. ET is a disease in and of itself and one that is thought to be influenced by a person’s genetics.
  • #103 Thrombocytosis Causes, a pediatric clinical case review and discussion 
    https://pediatriceducation.org/2012/12/10/what-causes-thrombocytosis/
    What Causes Thrombocytosis? […] The differential diagnosis of thrombocytosis includes: […] Extreme or hyperthrombocytosis is generally defined as 1 million platelets. […] Infection 31% […] Postsplenectomy or hyposplenism 19% […] Malignancy 14% […] Trauma 14% […] Inflammation (noninfectious) 9% […] Blood loss 6% […] Rebound thrombocytosis 3% […] Uncertain 4%
  • #104 Pediatric Thrombocytosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/959378-overview
    Congenital or idiopathic nephrotic syndrome […] Ovarian cancer – In particular, of germ cell origin […] Osteogenesis imperfecta. […] Essential (or primary) thrombocytosis (ET) may be suspected if any or a combination of the following features is present and if no obvious cause of secondary thrombocytosis exists: Enlarged liver and/or spleen […] History of thrombosis or bleeding […] Family history of thrombocytosis or myeloproliferative neoplasia (MPN; such as polycythemia vera [PV]) […] Persistent (3 mo) thrombocytosis. […] ET due to MPN is commonly associated with anemia and leukocytosis. […] Secondary thrombocytosis is usually mediated by the increased release of numerous cytokines in response to infections, inflammation, vasculitis, tissue trauma, and other factors. […] Thrombopoietin (THPO), the primary cytokine for platelet production and maturation, and interleukin (IL)-6 levels are usually initially elevated in response to the primary events mentioned earlier; they stimulate platelet production.
  • #105 Association between secondary thrombocytosis and viral respiratory tract infections in children | Scientific Reports
    https://www.nature.com/articles/srep22964
    The mechanism by which infection can promote thrombocytosis has not yet been fully elucidated. Reports in the literature show that ST is related to increased endogenous levels of several cytokines, such as thrombopoietin (TPO), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-1alpha (IL-1a) and tumor necrosis factor alpha (TNF-a). […] Therefore, increased platelet counts may be a clinical marker associated with the severity of RTI. Our logistic regression analysis showed that patients who had clinical manifestations of wheezing, bronchiolitis and a longer course of disease were more inclined to develop thrombocytosis. Additionally, HRV single infection was a risk factor associated with thrombocytosis. […] In summary, research regarding viral respiratory tract infections and thrombocytosis is lacking and we performed a large sample analysis that linked a specific viral agent to thrombocytosis in this clinical retrospective study. Childhood ST is related to respiratory tract infections, the occurrence rate is approximately 25.9% and the most common viruses are RSV and HRV, but infections with ADV or IFV seldom cause thrombocytosis. HRV single infection is a risk factor associated with thrombocytosis.
  • #106 Thrombocytosis: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/13350-thrombocytosis
    Reactive thrombocytosis happens when your body reacts to various conditions by overproducing platelets. […] Causes of reactive thrombocytosis include: Anemia, Blood disorders, Cancer, Infections, Inflammatory conditions, Injury, Kidney failure, Some medications, Surgery (especially abdominal surgery), Removal of your spleen, Treatment of a vitamin B12 deficiency. […] There are many more causes of reactive thrombocytosis. […] High platelets arent life-threatening, but the complications that can result from the condition blood clots or severe bleeding can be. […] The most common causes of thrombocytosis are short-lived and dont put you at risk of serious blood clots. […] The risk is greater with essential thrombocytosis. […] Essential thrombocythemia (ET), or primary thrombocytosis, can cause serious bleeding or clotting complications. […] Taking medicine that keeps your platelet levels normal can help prevent this. […] After many years of having the disease, however, bone marrow fibrosis (scarring) can develop. […] A small percentage of people with essential thrombocythemia develop leukemia.
  • #107 Reactive Thrombocytosis: Everything You Should Know
    https://www.healthline.com/health/reactive-thrombocytosis
    Reactive thrombocytosis is an unusually high platelet count. Also known as secondary thrombocytosis, it results from an underlying health condition, an injury, or a medication. […] Reactive thrombocytosis, which is also known as secondary thrombocytosis, is an unusually high platelet count due to an underlying health condition, an injury, or the use of a medication. […] Causes of reactive thrombocytosis may include: blood loss from an injury, an infection, iron deficiency anemia, not having a spleen (asplenia), cancer, chronic inflammatory conditions, certain medications. […] If your doctor determines that your platelet count is high, they may recommend additional testing to rule out health conditions like cancer.
  • #108 Thrombocytosis – Diagnosis and treatment – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/thrombocytosis/diagnosis-treatment/drc-20378319
    Treatment for this condition depends on the cause. […] If you have a chronic infection or an inflammatory disease, your platelet count likely will remain high until the condition is under control. […] If you’ve had your spleen removed, you might have lifelong thrombocytosis, but you’re unlikely to need treatment. […] You might need to take prescription medicine or have procedures to lower your platelet counts if you: Have a history of blood clots and bleeding. […] Your doctor might prescribe platelet-lowering drugs such as hydroxyurea (Droxia, Hydrea), anagrelide (Agrylin) or interferon alfa (Intron A). […] In emergencies, platelets can be filtered from your blood with a machine. This procedure is called plateletpheresis. The effects are only temporary.