Arteritis tętnicy skroniowej
Etiologia i przyczyny
Arteritis tętnicy skroniowej (GCA) to przewlekłe zapalenie naczyń średnich i dużych, głównie tętnic skroniowych, o podłożu autoimmunologicznym lub autozapalnym. Patogeneza obejmuje aktywację komórek dendrytycznych, rekrutację limfocytów CD4+ T (Th1 i Th17) oraz makrofagów, które wytwarzają cytokiny prozapalne, m.in. IL-6, oraz metaloproteinazę MMP-9 umożliwiającą migrację komórek zapalnych przez błonę podstawną. Genetyczne predyspozycje wiążą się z polimorfizmami w regionie MHC, zwłaszcza HLA-DRB1*04:04, HLA-DQA1*03:01, HLA-DQB1*03:02 oraz allelem FCGR2A-131RR, zwiększającym ryzyko rozwoju GCA sześciokrotnie. Wysoki poziom IL-6 koreluje z podwyższonym OB i CRP, a powikłania obejmują niedokrwienną neuropatię nerwu wzrokowego (AION) i niedrożność tętnic siatkówki (CRAO/BRAO), prowadzącą do trwałej utraty wzroku.
Etiologia arteritis tętnicy skroniowej (zapalenia tętnicy skroniowej)
Arteritis tętnicy skroniowej (olbrzymiokomórkowe zapalenie tętnic, GCA) to przewlekłe zapalenie naczyń krwionośnych dotyczące głównie średnich i dużych tętnic, szczególnie tętnic skroniowych, ale również innych naczyń zaopatrujących głowę, szyję i kończyny górne. Dokładna przyczyna tego schorzenia pozostaje nieznana, jednak istnieje kilka hipotez dotyczących jego etiopatogenezy.123
Podłoże autoimmunologiczne
Większość badaczy uważa, że arteritis tętnicy skroniowej ma podłoże autoimmunologiczne lub autozapalne. Oznacza to, że układ odpornościowy pacjenta nieprawidłowo atakuje własne naczynia krwionośne, co prowadzi do zapalenia i zwężenia tętnic.145 W procesie zapalnym komórki układu odpornościowego, głównie limfocyty T i makrofagi, naciekają ścianę naczynia, formując charakterystyczne zmiany ziarniniakowe z obecnością komórek olbrzymich.6
Kluczowe wydarzenia w patofizjologii GCA obejmują aktywację komórek dendrytycznych zlokalizowanych w połączeniu przydanki i błony środkowej naczynia, które inicjują odpowiedź immunologiczną poprzez prezentowanie antygenów i rekrutację limfocytów CD4+ T helper do ściany naczynia. Aktywowane limfocyty CD4+ T helper różnicują się na dwie odrębne linie komórkowe – Th1 i Th17, które produkują różne cytokiny prozapalne.7
Dostęp monocytów i limfocytów T do ściany naczyniowej jest kontrolowany przez metaloproteinazę macierzy (MMP)-9, kolagenazę typu IV, która jest produkowana w zmianach zapalnych GCA. Produkcja MMP-9 umożliwia limfocytom T przejście przez błonę podstawną zawierającą kolagen IV. Makrofagi zlokalizowane w przydance wytwarzają interleukinę-6 (IL-6), która dodatkowo wzmacnia kaskadę zapalną.8
Czynniki genetyczne
Na podstawie rodzinnego, etnicznego i geograficznego rozkładu zachorowań, arteritis tętnicy skroniowej wydaje się mieć predyspozycję genetyczną. Badania wykazały występowanie skupień rodzinnych i zgodność u bliźniąt jednojajowych.910
Zakrojone na szeroką skalę analizy genetyczne ujawniły silny związek między GCA a specyficznymi polimorfizmami w regionie głównego kompleksu zgodności tkankowej (MHC), takimi jak ludzki antygen leukocytarny (HLA)-DRB1*04:04, HLA-DQA1*03:01 i HLA-DQB1*03:02.1112
Osoby homozygotyczne dla HLA-DR4 i allelu FCGR2A-131RR mają sześciokrotnie większe ryzyko rozwoju arteritis tętnicy skroniowej. HLA-DR1, HLA-DR3 i HLA-DR5 mogą również być związane z wyższą częstością występowania choroby.13 Badania asocjacyjne całego genomu zidentyfikowały HLA-DRB1*04 jako najczęstszy gen wśród osób rasy kaukaskiej związany z wyższym ryzykiem arteritis tętnicy skroniowej, opornością na terapię glikokortykosteroidami i większą częstością powikłań, takich jak utrata wzroku.14
Odkryto również warianty w genach związanych z funkcją limfocytów T pomocniczych (Th) 1, Th17 i regulatorowych limfocytów T.1516 Wykazano także możliwy związek między polimorfizmem genu receptora Toll-like 4 a podatnością na GCA potwierdzone w biopsji.17
Czynniki infekcyjne
Dane wskazują, że choroba może być inicjowana przez ekspozycję na egzogenny antygen. Liczne wirusy i bakterie zostały zaproponowane jako potencjalne czynniki wywołujące, w tym:181920
- Wirus ospy wietrznej i półpaśca (varicella-zoster virus, VZV)2122
- Wirus opryszczki pospolitej (herpes simplex virus)23
- Wirus Epsteina-Barr24
- Parvowirus B192526
- Chlamydia pneumoniae2728
- Mycoplasma pneumoniae2930
Szczególną uwagę zwraca się na wirusa varicella-zoster (VZV), który ma tropizm do tętnic i może odgrywać rolę w wyzwalaniu olbrzymiokomórkowego zapalenia tętnic. Antygen VZV wykryto w 74% biopsji tętnicy skroniowej potwierdzających GCA, co sugeruje, że zakażenie VZV może wyzwalać kaskadę zapalną.3132
Badania epidemiologiczne, raporty i analizy wykorzystujące techniki wykrywania DNA potwierdziły obecność tych patogenów, jednak generalnie uważa się, że czynniki zakaźne są jedynie „niewinnym świadkiem” w patogenezie GCA.33 Mimo licznych podejrzeń, nie ustalono jednoznacznie związku przyczynowego między tymi czynnikami a GCA.34
Czynniki ryzyka
Wśród różnych czynników predysponujących do rozwoju arteritis tętnicy skroniowej najszerzej znane są:35
- Wiek – Zaawansowany wiek jest najważniejszym czynnikiem ryzyka rozwoju GCA. Choroba prawie nigdy nie występuje przed 50. rokiem życia, a jej częstość stale wzrasta po tym wieku, osiągając szczyt między 70. a 79. rokiem życia.363738
- Płeć – Badania epidemiologiczne wykazują przewagę zachorowań u kobiet, chociaż rola płci w patogenezie choroby pozostaje niejasna.394041
- Pochodzenie etniczne – Pochodzenie z Europy Północnej stanowi istotny czynnik ryzyka. Najwyższe wskaźniki zachorowalności odnotowuje się w krajach skandynawskich i wśród Amerykanów skandynawskiego pochodzenia.424344
- Polimialgia reumatyczna – GCA częściej występuje u osób z innym zaburzeniem zapalnym znanym jako polimialgia reumatyczna.454647
- Palenie tytoniu – Palenie zwiększa ryzyko GCA sześciokrotnie u kobiet.4849
Inne czynniki wyzwalające
Oprócz wymienionych czynników, istnieją doniesienia o innych potencjalnych czynnikach wyzwalających arteritis tętnicy skroniowej:
- Stres – Badania dotyczące związku między stresem a arteritis tętnicy skroniowej wskazują, że stres może przyczyniać się do rozwoju tej choroby. Przewlekły stres może zwiększać ryzyko wystąpienia zaostrzenia u osób, które już mają tę chorobę pod kontrolą.50
- Inhibitory punktów kontrolnych układu immunologicznego – Opisano przypadki GCA występujące po leczeniu inhibitorami punktów kontrolnych układu immunologicznego (ICI) stosowanymi w leczeniu nowotworów. Prezentacja kliniczna była głównie okulistyczna (przemijające podwójne widzenie, ślepota lub utrata wzroku).51
- Ciężkie infekcje i stosowanie wysokich dawek antybiotyków – Zaburzenie zostało powiązane z ciężkimi infekcjami i stosowaniem wysokich dawek antybiotyków.52
Mechanizm patofizjologiczny
Mechanizm patofizjologiczny arteritis tętnicy skroniowej jest wynikiem kaskady zapalnej, która jest wyzwalana przez nieustaloną jeszcze przyczynę, powodującą rekrutację przez komórki dendrytyczne w ścianie naczynia limfocytów T i makrofagów do tworzenia nacieków ziarniniakowych.53
Nadmierne uwalnianie cytokin związane z tym procesem może być odpowiedzialne za objawy ogólnoustrojowe często spotykane w tej chorobie. Prozapalna cytokina IL-6, odpowiedzialna za nasiloną ostrą fazę odpowiedzi immunologicznej, jest związana z wysokim poziomem wskaźnika sedymentacji erytrocytów (OB) i białka C-reaktywnego (CRP).54
Zakrzepica naczyń może prowadzić do niedokrwienia i martwicy tkanek. Trwała utrata wzroku w GCA wynika z przedniej niedokrwiennej neuropatii nerwu wzrokowego (AION), niedrożności tętnicy środkowej lub gałęziowej siatkówki (CRAO/BRAO), tylnej niedokrwiennej neuropatii nerwu wzrokowego (PION) lub, rzadziej, niedokrwienia mózgu.55
Niedokrwienne uszkodzenie w arteritycznym AION jest zazwyczaj konsekwencją niedrożności tętnicy rzęskowej tylnej, gałęzi tętnicy ocznej odchodzącej od tętnicy szyjnej wewnętrznej, stanowiącej główne unaczynienie tętnicze nerwu wzrokowego.56
Współczesne rozumienie etiologii arteritis tętnicy skroniowej
Arteritis tętnicy skroniowej to choroba o złożonej i wieloczynnikowej etiologii, której dokładna przyczyna pozostaje nieznana. Obecne dowody wskazują na ważną rolę czynników autoimmunologicznych, genetycznych i środowiskowych, które prawdopodobnie działają synergistycznie, prowadząc do rozwoju choroby.5758
Bieżące badania koncentrują się na lepszym zrozumieniu mechanizmów leżących u podstaw choroby, co może prowadzić do opracowania bardziej ukierunkowanych terapii. Szybkie rozpoznanie i leczenie pozostają kluczowe dla zapobiegania poważnym powikłaniom, takim jak utrata wzroku, które mogą być nieodwracalne.5960
Pomimo wielu postępów w zrozumieniu patofizjologii GCA, czynnik inicjujący tę chorobę zapalną naczyń pozostaje nieznany. Dalsza identyfikacja czynników genetycznych, środowiskowych i immunologicznych może pomóc w opracowaniu lepszych strategii diagnostycznych i terapeutycznych dla pacjentów z arteritis tętnicy skroniowej.6162
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Materiały źródłowe
- #1 Giant Cell Arteritis (Temporal Arteritis): Signs & Treatmenthttps://my.clevelandclinic.org/health/diseases/temporal-arteritis-giant-cell-arteritis
Temporal arteritis causes inflammation in your temporal arteries (the blood vessels near your temples). […] Researchers dont know the exact cause of giant cell arteritis, but many believe its an autoimmune or autoinflammatory disease. This means your bodys immune system attacks your healthy blood vessels. Because the condition mainly affects people as they age, some believe it could be linked to the aging process. They also believe genetics and environmental factors that stress your immune system may play a role.
- #2 Giant cell arteritis – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/giant-cell-arteritis/symptoms-causes/syc-20372758
Giant cell arteritis causes inflammation of certain arteries, especially those near the temples. […] What causes these arteries to become inflamed isn’t known, but it’s thought to involve abnormal attacks on artery walls by the immune system. Certain genes and environmental factors might increase your susceptibility to the condition.
- #3 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The etiology of temporal arteritis is multifactorial and is determined by both environmental and genetic factors. Data indicate that the disease is probably initiated by exposure to an exogenous antigen. Numerous viruses and bacteria have been proposed as potential precipitants, including parvovirus, parainfluenza virus, varicella-zoster virus, […] Chlamydia pneumoniae, and Mycoplasma pneumoniae. […] Both cellular and humoral immune systems contribute to the immunopathology of giant cell arteritis (GCA). Key events include the activation of vascular dendritic cells located in the adventitia-media junction, which trigger immune responses by presenting antigens and recruiting CD4+T helper cells to the vessel wall. Activated CD4+ T helper cells develop into two distinct T cell lineages Th1 and Th17 that produce various pro-inflammatory cytokines.
- #4 Temporal Arteritis: Symptoms, Causes, Treatmentshttps://www.webmd.com/heart-disease/arteritis-giant-cell
Giant cell arteritis, also called temporal arteritis, is a disease that causes your arteries — blood vessels that carry oxygen from your heart to the rest of your body — to become inflamed. […] Its an autoimmune disease. That means your immune system mistakenly attacks your body’s healthy tissues. In giant cell arteritis, immune cells react against blood vessels and make them inflamed. […] Doctors don’t know what triggers this, but you’re more likely to get it if you’re: Over 50, Female, Of European descent — especially if your family is from a country in Scandinavia (Norway, Sweden, Denmark, or Finland).
- #5 Patient’s Guide to Temporal Arteritis – Brigham and Women’s Hospitalhttps://www.brighamandwomens.org/neurology/neuro-ophthalmology/temporal-arteritis?TRILIBIS_EMULATOR_UA=…%3Fcmp%3Dhrgn%3Fcmp%3Dhrgn%2Cnsclpfpr%3Fcmp%3Dhrgn%3Fcmp%3Dhrgn
Temporal arteritis is a condition that causes inflammation of arteries the blood vessels that carry oxygen-rich blood from the heart. The exact cause of temporal arteritis is unknown, but the inflammation appears to be a result of the immune system overreacting and attacking the body’s own tissues. […] Inflammation of the arteries causes them to become narrowed and impairs their ability to supply oxygen-rich blood. The arteries that travel to the eye are especially vulnerable in patients with temporal arteritis. […] The reason it is so important to make an early diagnosis and start treatment as soon as possible is to try to stop the inflammation before it progresses to cause severe visual loss in both eyes.
- #6 Temporal arteritis: Symptoms, diagnosis, and causeshttps://www.medicalnewstoday.com/articles/312614
GCA affects the temporal arteries and it can develop in the thoracic artery, too. […] The exact cause of GCA is unknown, but it is thought to be an auto-immune condition, in which the bodys immune system attacks healthy cells in the arteries. This leads to inflammation. […] When the blood vessel lining becomes inflamed, giant cell lesions can form. […] These giant cells form when numerous immune cells fuse together. These immune cells are a type of white blood cell.
- #7 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The etiology of temporal arteritis is multifactorial and is determined by both environmental and genetic factors. Data indicate that the disease is probably initiated by exposure to an exogenous antigen. Numerous viruses and bacteria have been proposed as potential precipitants, including parvovirus, parainfluenza virus, varicella-zoster virus, […] Chlamydia pneumoniae, and Mycoplasma pneumoniae. […] Both cellular and humoral immune systems contribute to the immunopathology of giant cell arteritis (GCA). Key events include the activation of vascular dendritic cells located in the adventitia-media junction, which trigger immune responses by presenting antigens and recruiting CD4+T helper cells to the vessel wall. Activated CD4+ T helper cells develop into two distinct T cell lineages Th1 and Th17 that produce various pro-inflammatory cytokines.
- #8 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The access of monocytes and T cells to the vascular wall is controlled by matrix metalloproteinase (MMP)-9, a type IV collagenase that is produced in the vasculitic lesions of giant cell arteritis. MMP-9 production allows T cells to pass through collagen IV containing basement membrane. Adventitia-based macrophages produce interleukin-6 (IL-6), which further augments the inflammatory cascade. […] The exuberant release of cytokines associated with this process may be responsible for the constitutional symptoms frequently encountered with the disease. Proinflammatory cytokine IL-6, responsible for the exaggerated acute phase of the immune response, is implicated in high levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). […] On the basis of its familial, ethnic, and geographic distribution, temporal arteritis appears to have a genetic predisposition. Studies have shown familial clustering and monozygotic twin concordance. Most genetic factors center on the human leukocyte antigen (HLA) genes. It is likely that various HLA alleles predispose to temporal arteritis and mediate its severity.
- #9 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The access of monocytes and T cells to the vascular wall is controlled by matrix metalloproteinase (MMP)-9, a type IV collagenase that is produced in the vasculitic lesions of giant cell arteritis. MMP-9 production allows T cells to pass through collagen IV containing basement membrane. Adventitia-based macrophages produce interleukin-6 (IL-6), which further augments the inflammatory cascade. […] The exuberant release of cytokines associated with this process may be responsible for the constitutional symptoms frequently encountered with the disease. Proinflammatory cytokine IL-6, responsible for the exaggerated acute phase of the immune response, is implicated in high levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). […] On the basis of its familial, ethnic, and geographic distribution, temporal arteritis appears to have a genetic predisposition. Studies have shown familial clustering and monozygotic twin concordance. Most genetic factors center on the human leukocyte antigen (HLA) genes. It is likely that various HLA alleles predispose to temporal arteritis and mediate its severity.
- #10 Giant cell arteritis (temporal arteritis) Guide: Causes, Symptoms and Treatment Optionshttps://www.drugs.com/health-guide/giant-cell-arteritis-temporal-arteritis.html
Giant cell arteritis, also called temporal arteritis, is a disease in which the large arteries and their branches, including those that supply the eye, scalp, and face, become inflamed and narrowed. […] The cause of giant cell arteritis is unknown, although there has been speculation that in some people, the body’s immune system responds incorrectly to an infection, and begins to attack the lining of blood vessels as it would a foreign invader. […] There may be a genetic contribution as well, as suggested by occasional cases that affect more than one member of the same family. […] One possibility is that the immune system of certain individuals or family members may be genetically programmed to respond to an infection abnormally, a response that leads to giant cell arteritis.
- #11 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #12 Giant Cell Arteritis (Temporal Arteritis) – MD Searchlighthttps://mdsearchlight.com/health/giant-cell-arteritis-temporal-arteritis/
Giant Cell Arteritis (GCA) is a health condition that tends to affect older people, particularly those of Northern European ancestry. Its also more common in women, though why this is the case is not fully understood. The exact cause of this disease is still unknown, but scientists believe that it has links to certain genes and environmental influences. Large-scale genetic studies show a strong connection between the disease and certain genetic traits in the area of the major histocompatibility complex, a part of the immune system. These traits include the human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Researchers have also found variations in genes that are linked to different types of T helper (Th) cells; these are important cells in our immune system that help control our bodys immune response. These include Th1, Th17, and regulatory T-cell genes.
- #13 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
Individuals homozygous for HLA-DR4 and the FCGR2A-131RR allele have a sixfold greater risk for temporal arteritis. HLA-DR1, HLA-DR3, and HLA-DR5 may also be associated with a higher incidence of the disease. Genome-wide association studies have identified HLA-DRB1*04, as the most common gene among Caucasians associated with a higher risk for temporal arteritis, resistance to glucocorticoid therapy, and greater incidence of complications such as visual loss.
- #14 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
Individuals homozygous for HLA-DR4 and the FCGR2A-131RR allele have a sixfold greater risk for temporal arteritis. HLA-DR1, HLA-DR3, and HLA-DR5 may also be associated with a higher incidence of the disease. Genome-wide association studies have identified HLA-DRB1*04, as the most common gene among Caucasians associated with a higher risk for temporal arteritis, resistance to glucocorticoid therapy, and greater incidence of complications such as visual loss.
- #15 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #16 Giant Cell Arteritis (Temporal Arteritis) – MD Searchlighthttps://mdsearchlight.com/health/giant-cell-arteritis-temporal-arteritis/
Giant Cell Arteritis (GCA) is a health condition that tends to affect older people, particularly those of Northern European ancestry. Its also more common in women, though why this is the case is not fully understood. The exact cause of this disease is still unknown, but scientists believe that it has links to certain genes and environmental influences. Large-scale genetic studies show a strong connection between the disease and certain genetic traits in the area of the major histocompatibility complex, a part of the immune system. These traits include the human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Researchers have also found variations in genes that are linked to different types of T helper (Th) cells; these are important cells in our immune system that help control our bodys immune response. These include Th1, Th17, and regulatory T-cell genes.
- #17 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #18 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The etiology of temporal arteritis is multifactorial and is determined by both environmental and genetic factors. Data indicate that the disease is probably initiated by exposure to an exogenous antigen. Numerous viruses and bacteria have been proposed as potential precipitants, including parvovirus, parainfluenza virus, varicella-zoster virus, […] Chlamydia pneumoniae, and Mycoplasma pneumoniae. […] Both cellular and humoral immune systems contribute to the immunopathology of giant cell arteritis (GCA). Key events include the activation of vascular dendritic cells located in the adventitia-media junction, which trigger immune responses by presenting antigens and recruiting CD4+T helper cells to the vessel wall. Activated CD4+ T helper cells develop into two distinct T cell lineages Th1 and Th17 that produce various pro-inflammatory cytokines.
- #19 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #20 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #21 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #22 Giant cell arteritis – Wikipediahttps://en.wikipedia.org/wiki/Giant_cell_arteritis
The cause is unknown. […] The underlying mechanism involves inflammation of the small blood vessels that supply the walls of larger arteries. […] The varicella-zoster virus (VZV) antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade. […] The pathological mechanism is the result of an inflammatory cascade that is triggered by an as of yet undetermined cause resulting in dendritic cells in the vessel wall recruiting T cells and macrophages to form granulomatous infiltrates.
- #23 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #24 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #25 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #26 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #27 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #28 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #29 Temporal Arteritis: Symptoms, Treatments, and Causeshttps://www.healthline.com/health/temporal-arteritis
Temporal arteritis has no definitive cause, but researchers speculate that a viral or bacterial infection may be the trigger in many cases. […] Some of the suspected viruses and bacteria that may be triggers include: varicella-zoster virus (VZV), which causes chickenpox and shingles, herpes simplex virus, EpsteinBarr virus, parvovirus B19, chlamydia pneumoniae, mycoplasma pneumoniae. […] However, there is no evidence to definitively prove or disprove this. Temporal arteritis, once it occurs, appears to be autoimmune in nature. This means that the body’s own immune cells attack healthy tissue in the artery walls.
- #30 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #31 Temporal Artery Vascular Diseaseshttps://pmc.ncbi.nlm.nih.gov/articles/PMC8745856/
GCA remains of course the first cause of temporal arteritis. GCA is a granulomatous large vessel vasculitis involving large vessels, mainly the aorta and extracranial branches of the external carotid artery such as the TA. […] Some infections can also affect the temporal artery, primarily an infection caused by the varicella-zoster virus (VZV), which has an arterial tropism that may play a role in triggering giant cell arteritis. Drugs, mainly checkpoint inhibitors that are used to treat cancer, can also trigger giant cell arteritis. […] The pathophysiological mechanisms of GCA are becoming clearer but the triggering factor of this vasculitis has not been identified yet. It is likely that an agent, infectious or not, activates the Toll-like receptor of dendritic cells located in the adventitia and then leads to their activation and the recruitment of T cells and monocytes and finally to the formation of a granulomatous vasculitis with an intense vascular remodeling process. Several infectious agents have been associated with the occurrence of GCA but none has been actually confirmed. The most recent is the varicella-zoster virus, which is probably more consistent with another type of vasculopathy that we will discuss later in this review.
- #32 Giant cell arteritis – Wikipediahttps://en.wikipedia.org/wiki/Giant_cell_arteritis
The cause is unknown. […] The underlying mechanism involves inflammation of the small blood vessels that supply the walls of larger arteries. […] The varicella-zoster virus (VZV) antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade. […] The pathological mechanism is the result of an inflammatory cascade that is triggered by an as of yet undetermined cause resulting in dendritic cells in the vessel wall recruiting T cells and macrophages to form granulomatous infiltrates.
- #33 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
A possible association between Toll-like receptor 4 gene polymorphism and susceptibility to biopsy-proven GCA has been found. […] Epidemiological observations, reports, and studies using DNA detection techniques have implicated Chlamydia pneumoniae, Mycoplasma pneumoniae, parvovirus B19, and varicella zoster as the impetus for the destructive inflammation. […] Nevertheless, it is generally accepted that these infectious agents are only „innocent bystanders.” […] The immune system (both cellular and humoral) has been implicated in the pathogenesis of GCA. The granulomatous histopathology of GCA has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines.
- #34 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #35 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #36 Clinical manifestations of giant cell arteritis – UpToDatehttps://www.uptodate.com/contents/clinical-manifestations-of-giant-cell-arteritis
Giant cell arteritis (GCA, also known as Horton disease, cranial arteritis, and temporal arteritis) is categorized as a vasculitis of large- and medium-sized vessels because it can involve the aorta and great vessels. […] The greatest risk factor for developing GCA is aging. The disease almost never occurs before age 50 years, and its incidence rises steadily thereafter, peaking between the ages of 70 to 79. […] In addition to age, ethnicity is a major risk factor for GCA. The highest incidence figures are found in Scandinavian countries and among Americans of Scandinavian descent. […] Autopsy studies suggest that GCA is more frequent than reported in studies of clinically diagnosed cases. […] Familial aggregation of GCA is not unusual. […] To date, no definite ways of stratifying risk factors for permanent visual loss in GCA have been established. Age, hypertension, thrombocytosis, jaw claudication, and other features have been proposed as risk factors.
- #37 Temporal Arteritis: Symptoms, Causes, Treatmentshttps://www.webmd.com/heart-disease/arteritis-giant-cell
Giant cell arteritis, also called temporal arteritis, is a disease that causes your arteries — blood vessels that carry oxygen from your heart to the rest of your body — to become inflamed. […] Its an autoimmune disease. That means your immune system mistakenly attacks your body’s healthy tissues. In giant cell arteritis, immune cells react against blood vessels and make them inflamed. […] Doctors don’t know what triggers this, but you’re more likely to get it if you’re: Over 50, Female, Of European descent — especially if your family is from a country in Scandinavia (Norway, Sweden, Denmark, or Finland).
- #38 Temporal Arteritis – Symptoms, Causes, Treatmentshttps://resources.healthgrades.com/right-care/vascular-conditions/temporal-arteritis
Temporal arteritis is believed to be an autoimmune disorder in which the immune system mistakenly attacks normal cells of the large and medium arteries in the head. […] The cause of temporal arteritis is not known. However, the aging process probably plays a role in developing temporal arteritis, as most people with the disorder are older than age 50.
- #39 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #40 Temporal Arteritis: Symptoms, Causes, Treatmentshttps://www.webmd.com/heart-disease/arteritis-giant-cell
Giant cell arteritis, also called temporal arteritis, is a disease that causes your arteries — blood vessels that carry oxygen from your heart to the rest of your body — to become inflamed. […] Its an autoimmune disease. That means your immune system mistakenly attacks your body’s healthy tissues. In giant cell arteritis, immune cells react against blood vessels and make them inflamed. […] Doctors don’t know what triggers this, but you’re more likely to get it if you’re: Over 50, Female, Of European descent — especially if your family is from a country in Scandinavia (Norway, Sweden, Denmark, or Finland).
- #41 Giant Cell Arteritis Causes, Symptoms, and Treatmentshttps://www.upmc.com/services/heart-vascular/conditions/giant-cell-arteritis
Giant cell arteritis is a rare type of vasculitis, or inflammation in the blood vessels. […] While the cause of giant cell arteritis is unknown, doctors believe the following play a role in causing it: Inflammation, Possible infection, Age, Gender. […] Some risk factors of giant cell arteritis can include: Age – People over 50 are more likely to have this condition. Gender – Women are more likely than men to get giant cell arteritis.
- #42 Giant Cell Arteritis (Temporal Arteritis) – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK459376/
Although the exact etiology is unknown, researchers have associated the disease with several genetic and environmental factors. Large-scale genetic analyses reveal a strong association between GCA and specific polymorphisms in the major histocompatibility complex region, such as human leukocyte antigen (HLA)-DRB1*04:04, HLA-DQA1*03:01, and HLA-DQB1*03:02. […] Additional variants have also been identified in genes involving T helper (Th) 1, Th17, and regulatory T-cell function. […] Among the various predisposing risk factors, advancing age and Northern European ancestry are the most widely known. […] Epidemiological studies also demonstrate a predominance in females, although the role of gender in the pathogenesis of the disease remains unclear. […] Although numerous triggers, including various pathogens, have been suggested, researchers have not definitively established a causal link between these triggers and GCA.
- #43 Clinical manifestations of giant cell arteritis – UpToDatehttps://www.uptodate.com/contents/clinical-manifestations-of-giant-cell-arteritis
Giant cell arteritis (GCA, also known as Horton disease, cranial arteritis, and temporal arteritis) is categorized as a vasculitis of large- and medium-sized vessels because it can involve the aorta and great vessels. […] The greatest risk factor for developing GCA is aging. The disease almost never occurs before age 50 years, and its incidence rises steadily thereafter, peaking between the ages of 70 to 79. […] In addition to age, ethnicity is a major risk factor for GCA. The highest incidence figures are found in Scandinavian countries and among Americans of Scandinavian descent. […] Autopsy studies suggest that GCA is more frequent than reported in studies of clinically diagnosed cases. […] Familial aggregation of GCA is not unusual. […] To date, no definite ways of stratifying risk factors for permanent visual loss in GCA have been established. Age, hypertension, thrombocytosis, jaw claudication, and other features have been proposed as risk factors.
- #44 Temporal Arteritis: Symptoms, Causes, Treatmentshttps://www.webmd.com/heart-disease/arteritis-giant-cell
Giant cell arteritis, also called temporal arteritis, is a disease that causes your arteries — blood vessels that carry oxygen from your heart to the rest of your body — to become inflamed. […] Its an autoimmune disease. That means your immune system mistakenly attacks your body’s healthy tissues. In giant cell arteritis, immune cells react against blood vessels and make them inflamed. […] Doctors don’t know what triggers this, but you’re more likely to get it if you’re: Over 50, Female, Of European descent — especially if your family is from a country in Scandinavia (Norway, Sweden, Denmark, or Finland).
- #45 Giant cell arteritis: MedlinePlus Medical EncyclopediaLockhttps://medlineplus.gov/ency/article/000448.htm
Giant cell arteritis (GCA) is inflammation and damage to the blood vessels that supply blood to the head, neck, upper body and arms. It is also called temporal arteritis. […] The cause of the condition is unknown. It is believed to be due in part to a faulty immune response. The disorder has been linked to some infections and to certain genes. […] Giant cell arteritis is more common in people with another inflammatory disorder known as polymyalgia rheumatica.
- #46 Giant cell arteritis: When a headache might be something more | Aging | Eyes and Vision | Women’s Health | UT Southwestern Medical Centerhttps://utswmed.org/medblog/giant-cell-arteritis/
Giant cell arteritis (GCA) is a type of vasculitis, or inflammation of the blood vessels, usually affecting the arteries that supply blood to the head and scalp, including the area over the temples, which is why its sometimes called temporal arteritis. […] There is no known cause for GCA, but there are several factors that can increase your risk of getting it, including: […] People who have polymyalgia rheumatica (PMR) also are at increased risk of developing giant cell arteritis. […] GCA is a rare condition that can go unrecognized or be mistaken for another condition.
- #47 Giant cell arteritis – information and resources | RNIBhttps://www.rnib.org.uk/your-eyes/eye-conditions-az/giant-cell-arteritis/
The cause of GCA is unknown. Its not a common condition, and it rarely affects people under the age of 50 years old. It can affect people from 60 years of age, with the highest incidence seen in those over 70 years old. Women are more commonly affected by GCA than men. […] About half the people with GCA have another condition called polymyalgia rheumatica (PMR) where the blood vessels supplying some of the larger muscles in your body are inflamed. The muscles particularly affected by PMR are those in your shoulders, neck, hips and back. These muscles can be painful and stiff, particularly on waking. It is possible to have GCA without having PMR as well. It is thought they might be different conditions with the same underlying cause, and they are both treated with steroids.
- #48 Understanding Temporal Arteritis: Symptoms, Causes & Treatmentshttps://conloneyeinstitute.com/understanding-temporal-arteritis-symptoms-causes-treatments/
Temporal arteritis, also called temporal arteritis, or giant cell arteritis (GCA), is a systemic inflammatory vasculitis affecting medium to large arteries, primarily in elderly individuals. […] Although age, ethnicity, and geography have been identified as potential risk factors, the primary cause of GCA is believed to be an inadequate response to endothelial injury, which may involve vascular endothelial growth factors. […] Genetic factors, such as low body mass index, early menopause, and relative adrenal hypofunction, have been linked to GCA. Additionally, smoking increases the risk of GCA by a factor of six in women. Research suggests that GCA is an antigen-driven disease characterized by its granulomatous histopathology. Local T-cell and macrophage activation can be seen in and around the elastic tissue of arterial walls.
- #49 Temporal Arteritis: Causes, Symptoms, Treatment and Costhttps://www.lybrate.com/topic/temporal-arteritis
The specific aetiology of temporal arteritis is unclear, however various variables may be linked, including: […] Certain genetic factors may make a person more susceptible to developing temporal arteritis. […] Infection with certain viruses and bacteria may trigger an immune response that leads to temporal arteritis. […] The chance of having temporal arteritis rises with age and is most prevalent in those over the age of 50. […] Smoking has been linked to increased risk of developing temporal arteritis, presumably due to its effects on the immune system and inflammation pathways in the body.
- #50 Stress and Temporal Arteritis: The Relationship, Symptoms & Treatmentshttps://www.verywellmind.com/stress-and-temporal-arteritis-6834218
Chronic stress puts your body through significant physical and psychological changes. Many people often underestimate the ability of stress to trigger several physical and mental health conditions. One such condition is temporal arteritis or giant cell arteritis. […] Research into the connection between stress and temporal arteritis reveals that stress can contribute to the development of the condition. […] As mentioned, stress can contribute to the development of temporal arteritis. Stress can increase the risk of a flare-up occurring in people who already have the condition but have it under control. […] Theres an established connection between stress and the development of temporal arteritis. When left undiagnosed and untreated, the latter condition can result in complications such as blindness, aneurysm, and stroke. The condition can also be prevented. In cases where its stress-induced, managing your stress levels may go a long way in helping to prevent the condition from developing.
- #51 Temporal Artery Vascular Diseaseshttps://pmc.ncbi.nlm.nih.gov/articles/PMC8745856/
The involvement of this signaling pathway is highlighted by the description of a few cases of GCA occurring after treatment with immune checkpoint inhibitors (ICI) for cancer. The clinical presentation was mainly ophthalmologic (transient diplopia, amaurosis, or blindness). In most cases, TAB confirmed the diagnosis of GCA by showing typical granulomatous vasculitis lesions.
- #52 Temporal arteritis/giant cell arteritis – Autoimmune Associationhttps://autoimmune.org/disease-information/temporal-arteritisgiant-cell-arteritis/
Temporal arteritis commonly occurs in the arteries around the temples (temporal arteries). […] The cause of the condition is unknown. […] It is believed to be due in part to a faulty immune response. […] The disorder has been linked to severe infections and the use of high doses of antibiotics. […] The problem may develop with or following another inflammatory disorder known as polymyalgia rheumatica. […] The condition may run in families.
- #53 Giant cell arteritis – Wikipediahttps://en.wikipedia.org/wiki/Giant_cell_arteritis
The cause is unknown. […] The underlying mechanism involves inflammation of the small blood vessels that supply the walls of larger arteries. […] The varicella-zoster virus (VZV) antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade. […] The pathological mechanism is the result of an inflammatory cascade that is triggered by an as of yet undetermined cause resulting in dendritic cells in the vessel wall recruiting T cells and macrophages to form granulomatous infiltrates.
- #54 Temporal Arteritis Pathology: Definition, Epidemiology, Etiologyhttps://emedicine.medscape.com/article/1612591-overview
The access of monocytes and T cells to the vascular wall is controlled by matrix metalloproteinase (MMP)-9, a type IV collagenase that is produced in the vasculitic lesions of giant cell arteritis. MMP-9 production allows T cells to pass through collagen IV containing basement membrane. Adventitia-based macrophages produce interleukin-6 (IL-6), which further augments the inflammatory cascade. […] The exuberant release of cytokines associated with this process may be responsible for the constitutional symptoms frequently encountered with the disease. Proinflammatory cytokine IL-6, responsible for the exaggerated acute phase of the immune response, is implicated in high levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). […] On the basis of its familial, ethnic, and geographic distribution, temporal arteritis appears to have a genetic predisposition. Studies have shown familial clustering and monozygotic twin concordance. Most genetic factors center on the human leukocyte antigen (HLA) genes. It is likely that various HLA alleles predispose to temporal arteritis and mediate its severity.
- #55 Clinical manifestations of giant cell arteritis – UpToDatehttps://www.uptodate.com/contents/clinical-manifestations-of-giant-cell-arteritis
Permanent loss of vision in GCA results from arteritic anterior ischemic optic neuropathy (AION), central or branch retinal artery occlusion (CRAO/BRAO), posterior ischemic optic neuropathy (PION), or, rarely, cerebral ischemia. […] The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve. […] Most AION is nonarteritic and commonly secondary to atherosclerotic disease. […] Atherosclerosis, especially involving the carotid arteries, accounts for the bulk of cases of CRAO. […] GCA can affect the subclavian arteries distal to the take-off of the vertebral arteries and extend through the axillary arteries to the proximal brachial arteries.
- #56 Clinical manifestations of giant cell arteritis – UpToDatehttps://www.uptodate.com/contents/clinical-manifestations-of-giant-cell-arteritis
Permanent loss of vision in GCA results from arteritic anterior ischemic optic neuropathy (AION), central or branch retinal artery occlusion (CRAO/BRAO), posterior ischemic optic neuropathy (PION), or, rarely, cerebral ischemia. […] The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve. […] Most AION is nonarteritic and commonly secondary to atherosclerotic disease. […] Atherosclerosis, especially involving the carotid arteries, accounts for the bulk of cases of CRAO. […] GCA can affect the subclavian arteries distal to the take-off of the vertebral arteries and extend through the axillary arteries to the proximal brachial arteries.
- #57 Giant Cell Arteritis – Vasculitis Foundationhttps://vasculitisfoundation.org/education/vasculitis-types/giant-cell-arteritis/
Giant cell arteritis (GCA) is a form of vasculitis, a family of rare disorders characterized by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues. Also called temporal arteritis, GCA typically affects the arteries in the neck and scalp, especially the temples. It frequently affects the aorta and its large branches to the head, arms, and legs. GCA is the most common form of vasculitis in adults over the age of 50. […] The cause of GCA is not yet fully understood. Vasculitis is classified as an autoimmune disorder, a disease that occurs when the body’s natural defense system mistakenly attacks healthy tissue. Researchers believe a combination of factors may trigger the inflammatory process. Studies have linked genetic factors, infectious agents, and the environment to the development of GCA.
- #58 Temporal Arteritis: Key Facts You Need to Knowhttps://rheumatologyde.com/temporal-arteritis/
Temporal arteritis, also known as giant cell arteritis (GCA), is a chronic inflammatory disease that primarily affects the blood vessels, particularly the temporal artery, which runs along the sides of the head. […] Although the exact cause of temporal arteritis is unknown, researchers believe that a combination of genetic and environmental factors may contribute to its development. […] Temporal arteritis is an autoimmune condition where the immune system attacks blood vessel walls, particularly the temporal artery, leading to inflammation and potential complications. Its causes are unclear, though genetic and environmental factors may contribute, and ongoing research aims to better understand the underlying mechanisms.
- #59 Temporal Arteritis | Giant Cell Arteritis | MedlinePlushttps://medlineplus.gov/giantcellarteritis.html
Giant cell arteritis is a disorder that causes inflammation of your arteries, usually in the scalp, neck, and arms. It narrows the arteries, which keeps blood from flowing well. […] Both are more common in women than in men. They almost always affect people over the age of 50. […] Treatment is usually with corticosteroids. Early treatment is important; otherwise there is a risk of permanent vision loss or stroke. However, when properly treated, giant cell arteritis rarely comes back.
- #60 TEMPORAL ARTERITIS (Chapter 2) – Uncommon Causes of Strokehttps://www.cambridge.org/core/books/uncommon-causes-of-stroke/temporal-arteritis/6A52BB12289D0D689166BDA4D0F98926
Temporal (giant cell) arteritis is a systemic disease, involving various medium-sized and larger arteries, that occurs mostly in elderly patients. […] The mainstay of treatment is corticosteroids, although there is much debate about the optimal dose and use of steroid sparing immunosuppressives.
- #61 Giant Cell Arteritis (Temporal Arteritis): Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/332483-overview
Giant cell arteritis (GCA), or temporal arteritis, is a systemic inflammatory vasculitis of unknown etiology that occurs in older persons and can result in a wide variety of systemic, neurologic, and ophthalmologic complications. […] Age and female sex are established risk factors for GCA, a genetic component seems likely, and infection may have a role (see Etiology). […] The exact etiology of giant cell arteritis (GCA) remains unknown. Despite increased understanding of the inflammatory cascade responsible for the disease process, the initial event that triggers the cascade remains uncertain. Genetic, environmental, and autoimmune factors have been identified. […] Reports of familial aggregation, association with the HLA-DR4 haplotype, and an apparent higher frequency of these conditions in northern Europe and in persons in the United States with similar ethnic backgrounds suggest a genetic or hereditary predisposition.
- #62 Giant cell arteritis | EdRheumhttps://www.edrheum.org/giant-cell-arteritis/
GCA is one of the commonest types of vasculitis. It is an inflammatory disease, meaning the bodys immune system inappropriately attacks the health blood vessels. […] The exact cause of GCA is unknown, but a persons genes and factors in the environment play a part.