Materiały źródłowe

• #1 Secondary Thrombocytosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560810/

  Thrombocytosis, or thrombocythemia, occurs when the platelet count exceeds 450,000/L of blood. This condition can be classified into primary and secondary thrombocytosis. Secondary thrombocytosis, also known as reactive thrombocytosis, is characterized by an abnormally high platelet count in the absence of chronic myeloproliferative disease due to underlying conditions, infections or diseases, inflammation, hemorrhage, or certain medications. […] Secondary thrombocytosis, which is more common than primary thrombocytosis, is typically identified through routine laboratory testing, as most patients are asymptomatic. In most cases, reactive thrombocytosis symptoms are due to the underlying disorder rather than the elevated platelet count itself. Rarely, extreme secondary thrombocytosis may lead to thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism. Although secondary thrombocytosis is generally benign, the underlying causes (such as malignancies, connective tissue disorders, and chronic infections) can increase the risk of adverse outcomes.

• #2 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. In contrast, clonal thrombocytosis (primary or essential thrombocytosis) is an unregulated abnormality of platelet production due to a clonal expansion of bone marrow progenitor cells. […] The pathophysiology of secondary thrombocytosis may vary, depending on the cause of thrombocytosis. Elevated platelet counts can be due to megakaryocyte proliferation, decreased platelet sequestration, or increased cytokine production (which stimulates platelet production). […] Overproduction of proinflammatory cytokines, such as interleukin (IL)-1, IL-6, and IL-11, occurs in chronic inflammatory, infective, and malignant states. Elevated levels of IL-1, IL-6, C-reactive protein (CRP), granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) lead to megakaryocyte growth and increased production of platelets.

• #3 Thrombocytosis in the ED – emDocs

  https://www.emdocs.net/thrombocytosis-in-the-ed/

  Thrombocytosis is defined as platelet count exceeding 450,000/microL. Typically in the ED, new thrombocytosis will be an asymptomatic lab finding. […] Approximately 80% of cases of thrombocytosis are reactive, even in cases of extreme thrombocytosis (i.e. platelet count >1,000,000/microL). Therefore, platelet count is not helpful in distinguishing reactive vs. clonal thrombocytosis. […] 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. […] It is unclear what pathophysiologic mechanism is responsible for this difference in incidence of thrombotic and bleeding complications.

• #4 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. […] Inflammation augments the release of IL6, which, in turn, stimulates proplatelet production by megakaryocytes and enhances hepatic thrombopoietin production. These mechanisms contribute to thrombocytosis, which can lead to thrombosis. Thrombocytosis may be driven by overproduction of thrombopoietin, IL6, other cytokines, or catecholamines in inflammatory, infectious, or neoplastic conditions or secondary to stress. […] In iron deficiency anemia, elevated platelet counts result from increased megakaryocyte proliferation, while in asplenia, decreased platelet sequestration is the primary cause of thrombocytosis.

• #5 What Is Thrombocytosis? | Carda Health

  https://www.cardahealth.com/post/what-is-thrombocytosis

  Chronic inflammatory conditions like rheumatoid arthritis or inflammatory bowel disease can stimulate the production of platelets. Chronic inflammation triggers the release of cytokines, which in turn promotes platelet production. […] Iron deficiency in the body can induce thrombocytosis as a compensatory mechanism. When the body lacks iron, it produces more platelets to help maintain blood clotting function. […] Certain types of cancer and blood disorders, such as leukemia or lymphoma, can disrupt normal blood cell production in the bone marrow. The malignant cells crowd out healthy cells, leading to abnormal platelet production and thrombocytosis. […] The spleen plays a crucial role in regulating platelet levels in the bloodstream. Surgical removal of the spleen, known as splenectomy, can result in an increased platelet count. […] Once thrombocytosis is diagnosed, appropriate treatment and management strategies can be implemented to address the condition and minimize the risk of complications.

• #6 Indian Pediatrics – Editorial

  https://www.indianpediatrics.net/aug2008/aug-669-677.htm

  Secondary or reactive thrombocytosis in childhood results from increased thrombopoiesis, as a reactive process due to an underlying infection, chronic inflammation, injury, malignancy, and surgical or functional splenectomy. […] In most children with reactive thrombocytosis, platelet counts are modestly elevated up to 700,000/L. […] Reactive thrombocytosis is also common in urinary tract infections. […] From the non-infectious causes of secondary thrombocytosis, iron deficiency is a common one, since it is the single most common nutritional deficiency worldwide. […] Autoimmune diseases, such as juvenile rheumatoid arthritis (JRA), small and large vessel vasculitides including polyarteritis nodosa, and Wegeners granulomatosis, KD, Henoch-Schoenlein purpura, and inflammatory bowel diseases account for 10% of cases of reactive thrombocytosis in children.

• #7 Indian Pediatrics – Editorial

  https://www.indianpediatrics.net/aug2008/aug-669-677.htm

  Malignancies, particularly solid tumors of the liver, such as hepatoblastoma and hepatocellular carcinoma are uncommon causes of reactive thrombocytosis in childhood. […] Reactive thrombocytosis can also be related to treatment with several drugs. […] Reactive thrombocytosis in children does not require treatment with platelet aggregation inhibitors, such as aspirin, even if the platelet count is greater than 1,000,000/L, unless additional well-defined thrombophilic risk factors exist. […] ET is a diagnosis of exclusion. […] In order to make the correct diagnosis, the diagnostic criteria proposed by the Polycythemia Vera Group are applied. […] ET is extremely rare in childhood with an incidence of 1 per million children, i.e., 60 times lower than in adults. […] The disease is due to a clonal defect in hematopoietic or megakaryopoietic progenitors that typically display decreased c-mpl expression. […] Hence, ET like polycythemia vera is a pre-malignant condition. […] In conclusion, thrombocytosis even when marked, is typically a benign, reactive phenomenon in children that does not require treatment.

• #8 Isotretinoin-Induced Thrombocytosis | Ataseven | Journal of Hematology

  https://thejh.org/index.php/jh/article/view/162/114

  We report a case of thrombocytosis possibly associated with isotretinoin. […] The exact mechanism by which isotretinoin caused thrombocytosis in this patient is not clearly understood. […] Thrombocytosis develops in three pathophysiological mechanisms; these are reactive or secondary thrombocytosis, familial thrombocytosis and clonal thrombocytosis, which is associated with essential thrombocytopenia and myeloproliferative diseases. […] However, the mechanisms are not clearly understood in the thrombocytosis associated with the medications including isotretinoin. […] It is hypothesized that IL-6 is involved in platelet elevation in patients who are receiving isotretinoin. […] However, the mechanism, which leads to an increased platelet count during isotretinoin use, is yet to be discovered.

• #9

  https://journals.lww.com/annalsplasticsurgery/abstract/1996/05000/thrombocytosis_after_major_lower_extremity_trauma_.10.aspx

  Increased rates of flap failure have been associated with reconstruction performed between 3 days and 6 weeks after injury, as well as in patients with thrombocytosis. […] We have found that serum platelet levels rise significantly after lower extremity injury. […] It is our theory that a circulating mediator or cytokine is released in response to injury, inducing the thrombocytosis. […] Interleukin-6 may, therefore, play a role in the mechanism of thrombocytosis. […] We suggest that because patients with complex bony injuries of the leg experience platelet elevations that peak approximately 2 weeks after injury, microvascular free flap reconstructions should be considered high risk during this time period.

• #10 Pathophysiology, classification, and complications of common asymptomatic thrombocytosis in newborn infants

  https://www.e-cep.org/journal/view.php?number=20125555473

  Thrombocytosis is known to increase the risk of hemorrhagic and thromboembolic complications in adults for which antiplatelet or cytoreductive treatment is required. Thrombocytosis frequently occurs in newborns and young infants younger than 2 years, with an estimated incidence of 3%13%, although the exact prevalence is unknown. Thrombocytosis in newborn infants is considered a reactive process in most cases, and it is rarely associated with complications. […] Reasons for frequent reactive thrombocytosis in newborn infants include higher levels of thrombopoietin (TPO) and more sensitive megakaryocyte precursor cells to TPO. […] Thrombocytosis is more frequently observed in preterm infants than in term infants during the first few postnatal weeks to months. In one study, thrombocytosis was found in 38% of low birth weight preterm infants. Thrombocytosis was observed in 32.6% of preterm infants with a gestational age 32 weeks who had not received recombinant human EPO. Higher TPO concentrations and more sensitive megakaryocyte precursor cells in preterm versus term infants are the speculated cause. […] Thrombocytosis in newborn infants, a reactive process following infection, acute/chronic inflammation, or anemia, is benign and resolves spontaneously, and unlike in adults, rarely associated with hemorrhagic or thromboembolic complications.

• #11 Essential Thrombocytosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK539709/

  Essential thrombocytosis is characterized by thrombocytosis and megakaryocytic hyperplasia of the bone marrow. […] The primary cause of essential thrombocythemia (ETT) is the overproduction of hematopoietic cells due to the mutations of the JAK2, CALR, or MPL genes. […] The driver genes JAK2, CALR, and MPL have specific functions which, when mutated, cause myeloproliferative effects. […] The point mutation causes a change in the amino acid from valine to phenylalanine at codon 617, hence, the abbreviation JAK2V617F. […] JAK 2 is a non-receptor tyrosine kinase found in the cytoplasm playing a pivotal role in hematopoiesis. […] CALR mutation occurs due to insertions or deletions causing a shift in the amino acid reading frame, which leads to the formation of a novel C terminus. […] MPL gene, on the other hand, is reported to be mutated via point mutation, and about 3% to 15% of essential thrombocytosis patients are affected by this mutation.

• #12 Essential Thrombocythemia (ET) – Myeloid Neoplasms – Hematology – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.15.7.

  Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by markedly elevated platelet counts and increased megakaryocyte proliferation in bone marrow. […] Most patients are found to harbor the JAK2 V617F mutation or other clonal genetic markers (MPL or CALR mutations). […] To establish the diagnosis of ET, all the following criteria must be fulfilled: […] Presence of the JAK2 V617F mutation or other clonal genetic markers; if these are absent, exclude reactive thrombocytosis. […] The choice of treatment depends on the presence of risk factors for thrombotic complications: age 60 years, mutational status, and prior thrombosis (arterial or venous).

• #13 Essential Thrombocytosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/206697-overview

  Essential thrombocytosis (primary thrombocythemia) is a nonreactive, chronic myeloproliferative disorder in which sustained megakaryocyte proliferation leads to an increase in the number of circulating platelets. Mutations in JAK2, CALR, or MPL are found in approximately 80-90% of patients with essential thrombocytosis. […] The cause of this increase in platelet production remains unclear, but possibilities include the following: Autonomous production, Increased sensitivities to cytokines (eg, interleukin-3 [IL-3]), Decreased effect of platelet-inhibiting factors (eg, transforming growth factor [TGF] beta), Defects in the accessory cell microenvironment. […] The majority of patients with essential thrombocytosis have mutations in one of three genes: Janus kinase 2 (JAK2), calreticulin (CALR), or myeloproliferative leukemia virus oncogene (MPL). These mutations result in the upregulation of the JAK-STAT pathway.

• #14 Essential thrombocythemia – Wikipedia

  https://en.wikipedia.org/wiki/Essential_thrombocythemia

  In ET, megakaryocytes are more sensitive to growth factors. […] Platelets derived from the abnormal megakaryocytes are activated, which, along with the elevated platelet count, contributes to the likelihood of forming blood clots. […] A mutation in the JAK2 kinase (V617F) is present in 4050% of cases and is diagnostic if present. […] In 2013, two groups detected calreticulin mutations in a majority of JAK2-negative/MPL-negative patients with essential thrombocythemia and primary myelofibrosis, which makes CALR mutations the second most common in myeloproliferative neoplasms. […] There are three known genetic mutations that cause ET. […] The most common genetic mutation is a JAK2 mutation. […] The JAK2 gene signals a protein that promotes the growth of cells. […] The most common JAK2 mutation is V617F which is the replacement of a valine amino acid with phenylalanine amino acid at the 617 position, hence the name V617F.

• #15 Essential Thrombocytosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/206697-overview

  JAK2 mutations possibly turn the thrombopoietin receptor on permanently, leading to overproduction of megakaryocytes. JAK2 mutation is seen in approximately 50-60% of patients. […] Somatic mutations in CALR are detected in peripheral blood in the approximately 25% of essential thrombocythemia cases. […] MPL mutations have been associated with only about 3-5% of essential thrombocytosis cases. […] The mechanism by which thrombocythemia produces hemorrhage or thrombosis is not well defined. Several defects have been described, including a decrease in aggregation, hyperaggregation, and intracellular concentration of various chemicals. […] Some reports show patients with an acquired deficiency of antithrombin III, protein C, and protein S.

• #16

  https://haematologica.org/article/view/4835

  The effect of thrombopoietin on megakaryocytopoiesis is mediated through its receptor, c-Mpl (CD110), which is found on both megakaryocytes and platelets, although at low levels on these latter. […] Somatic mutations of JAK2 or MPL lead to more efficient translation of the thrombopoietin signal and platelet production. […] Interestingly, an activating germline mutation of MPL has been found in families with essential thrombocythemia. This mutation [MPL (S505N)] has also been found as an acquired somatic mutation in patients with essential thrombocythemia or primary myelofibrosis. […] In other families with a similar condition, however, the molecular mechanism is a gain-of-function mutation in the thrombopoietin gene (THPO) that leads to increased thrombopoietin production. […] All mutations remove the inhibitory uORF and lead to increased translation of the THPO mRNA, causing overproduction of thrombopoietin and platelets. This represents a remarkable example of a novel molecular mechanism of disease that we defined translational pathophysiology. […] The activating splice mutation in intron 3 of the thrombopoietin gene is not found in patients with non-familial essential thrombocythemia.

• #17 Pathophysiology, classification, and complications of common asymptomatic thrombocytosis in newborn infants

  https://www.e-cep.org/journal/view.php?number=20125555473

  We frequently encounter newborn infants with thrombocytosis in the neonatal intensive care unit. However, neonatal thrombocytosis is not yet fully understood. Thrombocytosis is more frequently identified in newborns and young infants, notably more often in those younger than 2 years than in older children or adults. The production of megakaryocytes (megakaryopoiesis) and platelets (thrombopoiesis) is mainly regulated by thrombopoietin (TPO). Increased TPO levels during infection or inflammation can stimulate megakaryopoiesis, resulting in thrombopoiesis. A high TPO concentration and low TPO receptor expression on platelets leading to elevated plasma-free TPO, increased sensitivity of megakaryocyte precursor cells to TPO, a decreased red blood cell count, and immaturity of platelet regulation are speculated to induce thrombocytosis in preterm infants. Thrombocytosis in newborn infants is considered a reactive process (secondary thrombocytosis) following infection, acute/chronic inflammation, or anemia. Thrombocytosis in newborn infants is benign, resolves spontaneously, and, unlike in adults, is rarely associated with hemorrhagic and thromboembolic complications.

• #18 Indian Pediatrics – Editorial

  https://www.indianpediatrics.net/aug2008/aug-669-677.htm

  Much rarer in childhood is primary thrombocytosis, which is divided into familial and essential. […] The purpose of the present review is to discuss the physiology of megakaryopoiesis and the causes and management of TS in children. […] Thrombopoietin (Tpo) is the key regulator of platelet production in humans, and is primarily expressed in the liver, and to a lesser extend the kidneys, bone marrow and other organs. […] Longitudinal Tpo measurements in infants and children with acute infections, surgical trauma and other conditions show that the elevation of circulating Tpo concentration precedes TS. […] Besides Tpo, other cytokines or hematopoietic growth factors, such as stem cell factor, granulocyte-macrophage colony stimulating factor, IL-6, IL-8 and IL-11 play a major role in certain steps of megakaryopoiesis and thrombopoiesis.

• #19 Essential thrombocytosis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Essential_thrombocytosis_pathophysiology

  Essential thrombocytosis arises from hematopoietic stem cells which give rise to megakaryocytes which give rise to platelets (thrombocytes), that are normally involved in blood clotting. Development of essential thrombocytosis is the result of a genetic mutation in the janus kinase 2 (JAK2) gene in 50% of the patients. Other genes that may be involved in the pathogenesis of essential thrombocytosis are CALR, MPL, and THPO genes. […] Essential thrombocytosis arises from pluripotent hematopoietic stem cells of megakaryocytic lineage that give rise to platelets. […] Essential thrombocytosis is caused by point mutations in janus kinase 2 (JAK2) gene in 50% of the patients. […] Thrombopoietin destruction is also critical to the development of essential thrombocytosis. […] Despite the high platelet count, essential thrombocytosis paradoxically manifests with an increase in free circulating concentration of thrombopoietin as the abnormal platelets have defective thrombopoietin receptors which impair proper binding of thrombopoietin.

• #20 Thrombocytosis and thromboembolic complications | Treliński | Hematology in Clinical Practice

  https://journals.viamedica.pl/hematology_in_clinical_practice/article/view/34013

  Thrombocytosis is usually due to infection, inflammation or other causes connected with increased production of thrombopoietin. […] Thrombocytosis can also be caused by myeloproliferative neoplasms like essential thrombocythemia (ET) or polycythemia vera (PV), involving a defect of hematopoietic stem cells. […] Pathogenesis of thrombotic complications which comprise the main source of mortality in ET and PV is very complex. Dysfunction of platelets, increased activation of leukocytes, hyperviscosity of blood, pathological activation of coagulation system and endothelium are among most recognized causes. […] The role of JAK2V617F mutation in thrombosis development is under active research.

• #21 Essential Thrombocytosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK539709/

  The basic mechanism is thought to involve the absorption of large von Willebrand multimers by the platelet’s membranes. […] The goal of the treatment of essential thrombocytosis is to prevent vascular complications such as thrombotic and hemorrhagic events; this is because thrombosis and hemorrhage are the leading causes of morbidity and mortality. […] The International Prognostic Score for Essential Thrombocytosis (IPSET) defines age greater than or equal to 60 years, leukocyte counts greater than or equal to 11,000 /uL, cardiovascular risk factors (eg. diabetes, tobacco use, hypertension), the JAK2V617F mutation, and a history of prior thromboses as risk factors for overall survival (OS) thereby dividing ETT into 3 treatment groups. […] For cytoreductive therapy, Hydroxyurea is a common choice, with anagrelide and interferon (especially the pegylated forms) secondarily so.

• #22 Thrombocytosis in the ED – emDocs

  https://www.emdocs.net/thrombocytosis-in-the-ed/

  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. […] Vasomotor symptoms include headache, visual symptoms, lightheadedness, chest pain, acral dysesthesia, erythromelalgia (occlusion of small blood vessels, manifested by discomfort and burning sensations in the fingers or toes). These are the most common symptoms of clonal thrombocytosis.

• #23

  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. […] Clinical manifestations of RT can range from no symptoms (most common) to acute thrombosis (rare), and elevated platelet counts may also be a predictor of underlying disease and of mortality. […] Therefore, it is essential for an underwriter to identify RT, as RT is not always a benign entity, which means outcomes can vary. […] Reactive thrombocytosis (RT), also known as secondary thrombocytosis, is a proliferation of platelets caused by a response to growth factors released from an inflammatory or malignant condition, whereas primary thrombocytosis (PT) is caused by an underlying myeloproliferative or myelodysplastic neoplasm.

• #24

  https://www.rgare.com/knowledge-center/article/reactive-thrombocytosis-a-benign-entity

  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.

• #25

  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. […] 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. […] RT is typically a clinically silent and transient condition. […] 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. […] Interestingly, RT in patients with iron deficiency anemia has been associated with a twofold thrombosis risk compared with patients with iron deficiency anemia alone.

• #26 What Is Thrombocytosis? | Carda Health

  https://www.cardahealth.com/post/what-is-thrombocytosis

  Thrombocythemia occurs when the bone marrow produces an excessive number of platelets without any apparent underlying cause. […] Thrombocythemia is often associated with gene mutations, such as JAK2, CALR, or MPL, which disrupt the normal regulation of platelet production and lead to an elevated platelet count. […] Thrombocytosis, also referred to as secondary thrombocytosis, is also diagnosed when the platelet count surpasses the normal upper limit of 450,000 per microliter of blood. The difference is that this type of thrombocytosis occurs as a reactive response to an underlying condition or trigger. […] Unlike primary thrombocythemia, thrombocytosis is not a medical condition itself but rather a consequence of an underlying condition. Therefore, the treatment of secondary thrombocytosis involves addressing the underlying cause.

• #27

  https://link.springer.com/article/10.1007/s00277-008-0531-7

  Essential thrombocythaemia (ET) is an acquired myeloproliferative disorder (MPD), characterised by persistent peripheral thrombocytosis and a tendency for thrombosis and haemorrhage. […] Several lines of evidence suggest that ET is a heterogeneous disease entity, though the existence of distinct subgroups is difficult to validate. […] Hydroxycarbamide, also known as hydroxyurea, is a non-specific, cytotoxic, myelosuppressive agent that is used to treat all MPDs, including ET. Its mechanism of action involves inhibition of ribonucleotide diphosphate reductase activity, thus blocking the cell cycle at the G1/S phase and resulting in cell death. […] Anagrelide is a cytoreductive agent, with a selective effect on the megakaryocyte cell lineage. It reduces platelet production by inhibiting megakaryocyte colony development, thus reducing megakaryocyte size, ploidy and maturation.

• #28

  https://link.springer.com/article/10.1007/s00277-008-0531-7

  The mechanism of action of interferon- is thought to relate to its anti-proliferative effects on megakaryocytes, with reduction in platelet half-life also a contributing factor. […] The objective of ET treatment is to reduce the risk of thromboembolic and haemorrhagic complications associated with the disorder.

• #29 Mechanism of Action (MOA) | Nplate® (romiplostim)

  https://www.nplatehcp.com/itp-and-nplate/mechanism-of-action

  Nplate Increases Platelet Production at a Rate That Outpaces Platelet Destruction1,2 […] Nplate Binds and Activates the Thrombopoietin (TPO) Receptor, a Mechanism Analogous to Endogenous TPO (eTPO)1 […] Nplate, a TPO mimetic, increases platelet production and can outpace platelet destruction in ITP.1,2 […] Thrombotic/thromboembolic complications may result from increases in platelet counts with Nplate use. […] To minimize the risk for thrombotic/thromboembolic complications, do not use Nplate in an attempt to normalize platelet counts.

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