Vasculitis

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Vasculitis
Other namesVasculitides [1]
HSP Vasculitis.jpg
Petechia and purpura on the lower limb due to infection-associated vasculitis.
Pronunciation
Specialty Rheumatology, Immunology
Symptoms Weight loss, fever, myalgia, purpura, abdominal pain
Complications Gangrene, Myocardial infarction

Vasculitis is a group of disorders that destroy blood vessels by inflammation. [2] Both arteries and veins are affected. Lymphangitis (inflammation of lymphatic vessels) is sometimes considered a type of vasculitis. [3] Vasculitis is primarily caused by leukocyte migration and resultant damage. Although both occur in vasculitis, inflammation of veins (phlebitis) or arteries (arteritis) on their own are separate entities.

Contents

Signs and symptoms

The clinical presentation of the various vasculitides on the skin and internal organs is mostly determined by the diameter or size of the vessels mainly affected. [4] Non-specific symptoms are common and include fever, headache, fatigue, myalgia, weight loss, and arthralgia. [5] [6]

All forms of vasculitis, even large vessel vasculitides, may cause skin manifestations. The most common skin manifestations include purpura, nodules, livedo reticularis, skin ulcers, and purpuric urticaria. [7]

TypeNameMain symptoms
Primary large vessel vasculitis [8] Takayasu arteritis Diminished or absent pulses, vascular bruits, hypertension, Takayasu retinopathy, and aortic regurgitation. [9]
Giant cell arteritis Headache, scalp tenderness, jaw claudication, and blindness. [10]
Primary medium vessel vasculitis [8] Polyarteritis nodosa Mononeuritis multiplex, nodules, purpura, livedo, and hypertension. [11]
Kawasaki disease Fever, conjunctivitis, exanthema, palmoplantar erythema, cervical lymphadenopathy, and mucosal enanthema. [12] [13]
Primary small vessel antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis [8] Microscopic polyangiitis Focal segmental rapidly progressive glomerulonephritis, proteinuria, hemoptysis, palpable purpura, abdominal pain, and peripheral neuropathy. [14]
Granulomatosis with polyangiitis Crusting rhinorrhea, sinusitis, chronic otitis media, nasal obstruction, shortness of breath, and chronic cough. [15] [16]
Eosinophilic granulomatosis with polyangiitis Asthma, allergic rhinitis, sinusitis, nasal polyps, peripheral neuropathy, pulmonary infiltrates, and abdominal pain. [17] [18]
Primary immune complex small vessel vasculitis [8] Anti-glomerular basement membrane disease Glomerulonephritis, lung hemorrhage, hematuria, hemoptysis, cough, and dyspnea. [19]
Cryoglobulinemic vasculitis Palpable purpura, Raynaud's phenomenon, joint pain, and peripheral neuropathy. [20]
IgA vasculitis Palpable purpura, arthralgia, abdominal pain, nephritis, and haematuria. [21]
Hypocomplementemic urticarial vasculitis Hives, arthralgia, membranoproliferative glomerulonephritis, and chronic obstructive pulmonary disease. [22]
Primary variable vessel vasculitis [8] Behcet’s disease Oral ulcers, genital ulcers, papulopustular lesions, uveitis, superficial venous thrombosis and deep vein thrombosis. [23]
Cogan’s syndrome Interstitial keratitis, ocular redness, vertigo, and tinnitus. [24]
Single-organ vasculitis [25] [8] Cutaneous small-vessel vasculitis Palpable purpura, necrosis, ulceration, bullae, and nodules. [26]
Cutaneous arteritisNodules, livedo reticularis, ulcers, and gangrene. [27]
Primary central nervous system vasculitisHeadache, cognitive impairment, stroke, encephalopathy, and seizures. [28]
Retinal vasculitis Visual impairments, floaters, and macular edema. [29]
Secondary vasculitis [8] Lupus vasculitis Palpable purpura, petechiae, papulonodular lesions, urticaria lesions, and mononeuritis multiplex. [30]
Rheumatoid vasculitis Purpura, focal digital lesions, ulcers, digital necrosis, pyoderma, distal sensory or motor neuropathy, and mononeuritis multiplex. [31]

Causes

There are several different etiologies for vasculitides. Although infections usually involve vessels as a component of more extensive tissue damage, they can also directly or indirectly cause vasculitic syndromes through immune-mediated secondary events. Simple vascular thrombosis usually only affects the luminal process, but through the process of thrombus organization, it can also occasionally cause a more chronic vasculitic syndrome. The autoimmune etiologies, a particular family of diseases characterized by dysregulated immune responses that produce particular pathophysiologic signs and symptoms, are more prevalent. [32]

Classification

Primary systemic, secondary, and single-organ vasculitis are distinguished using the highest classification level in the 2012 Chapel Hill Consensus Conference nomenclature. [33]

Primary systemic vasculitis

Primary systemic vasculitis is categorized by the size of the vessels mainly involved. Primary systemic vasculitis includes large-vessel vasculitis, medium-vessel vasculitis, small-vessel vasculitis, and variable-vessel vasculitis. [33]

Large vessel vasculitis

The 2012 Chapel Hill Consensus Conference defines large vessel vasculitis (LVV) as a type of vasculitis that can affect any size artery, but it usually affects the aorta and its major branches more frequently than other vasculitides. [33] Takayasu arteritis (TA) and giant cell arteritis (GCA) are the two main forms of LVV. [8]

Medium vessel vasculitis

Medium vessel vasculitis (MVV) is a type of vasculitis that mostly affects the medium arteries, which are the major arteries that supply the viscera and their branches. Any size artery could be impacted, though. [33] The two primary types are polyarteritis nodosa (PAN) and Kawasaki disease (KD). [8]

Small vessel vasculitis

Small vessel vasculitis (SVV) is separated into immune complex SVV and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). [33]

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a necrotizing vasculitis linked to MPO-ANCA or PR3-ANCA that primarily affects small vessels and has few or no immune deposits. AAV is further classified as eosinophilic granulomatosis with polyangiitis (EGPA), granulomatosis with polyangiitis (GPA), and microscopic polyangiitis (MPA). [33]

Immune complex small vessel vasculitis (SVV) is vasculitis that primarily affects small vessels and has moderate to significant immunoglobulin and complement component deposits on the vessel wall. [33] Normocomplementemic urticarial vasculitis (HUV) (anti-C1q vasculitis), cryoglobulinemic vasculitis (CV), IgA vasculitis (Henoch-Schönlein) (IgAV), and anti-glomerular basement membrane (anti-GBM) disease are the categories of immune complex SVV. [8]

Variable vessel vasculitis

Variable vessel vasculitis (VVV) is a kind of vasculitis that may impact vessels of all sizes (small, medium, and large) and any type (arteries, veins, and capillaries), with no particular type of vessel being predominantly affected. [33] This category includes Behcet's disease (BD) and Cogan's syndrome (CS). [8]

Secondary vasculitis

The subset of illnesses known as secondary vasculitis are those believed to be brought on by an underlying ailment or exposure. Systemic illnesses (such as rheumatoid arthritis), cancer, drug exposure, and infection are the primary causes of vasculitis; however, there are still few factors that have a conclusively shown pathogenic relationship to the condition. [34] Vasculitis frequently coexists with infections, and several infections, including hepatitis B and C, HIV, infective endocarditis, and tuberculosis, are significant secondary causes of vasculitis. [35] Except for rheumatoid vasculitis, the majority of secondary vasculitis forms are exceedingly rare. [36]

Single-organ vasculitis

Single-organ vasculitis, formerly known as "localized," "limited," "isolated," or "nonsystemic" vasculitis, refers to vasculitis that is limited to one organ or organ system. Examples of this type of vasculitis include gastrointestinal, cutaneous, and peripheral nerve vasculitis. [34]

Diagnosis

Micrograph showing a vasculitis (eosinophilic granulomatosis with polyangiitis). H&E stain. Churg-Strauss syndrome - very high mag.jpg
Micrograph showing a vasculitis (eosinophilic granulomatosis with polyangiitis). H&E stain.
Severe vasculitis of the major vessels, displayed on FDG-PET/CT Vasculitis FDG PET-CT.png
Severe vasculitis of the major vessels, displayed on FDG-PET/CT
  • Some types of vasculitis display leukocytoclasis, which is vascular damage caused by nuclear debris from infiltrating neutrophils. [37] It typically presents as palpable purpura. [37] Conditions with leucocytoclasis mainly include hypersensitivity vasculitis (also called leukocytoclastic vasculitis) and cutaneous small-vessel vasculitis (also called cutaneous leukocytoclastic angiitis).
Laboratory Investigation of Vasculitic Syndromes [40]
DiseaseSerologic testAntigenAssociated laboratory features
Systemic lupus erythematosusANA including antibodies to dsDNA and ENA [including SM, Ro (SSA), La (SSB), and RNP]Nuclear antigensLeukopenia, thrombocytopenia, Coombs' test, complement activation: low serum concentrations of C3 and C4, positive immunofluorescence using Crithidia luciliae as substrate, antiphospholipid antibodies (i.e. anticardiolipin, lupus anticoagulant, false-positive VDRL)
Goodpasture's diseaseAnti-glomerular basement membrane antibodyEpitope on noncollagen domain of type IV collagen
Small vessel vasculitis
Microscopic polyangiitisPerinuclear antineutrophil cytoplasmic antibodyMyeloperoxidaseElevated CRP
Granulomatosis with polyangiitisCytoplasmic antineutrophil cytoplasmic antibodyProteinase 3 (PR3)Elevated CRP
Eosinophilic granulomatosis with polyangiitisperinuclear antineutrophil cytoplasmic antibody in some casesMyeloperoxidaseElevated CRP and eosinophilia
IgA vasculitis (Henoch-Schönlein purpura)None
CryoglobulinemiaCryoglobulins, rheumatoid factor, complement components, hepatitis C
Medium vessel vasculitis
Classical polyarteritis nodosaNoneElevated CRP and eosinophilia
Kawasaki's DiseaseNoneElevated CRP and ESR

In this table: ANA = antinuclear antibodies, CRP = C-reactive protein, ESR = erythrocyte sedimentation rate, dsDNA = double-stranded DNA, ENA = extractable nuclear antigens, RNP = ribonucleoproteins; VDRL = Venereal Disease Research Laboratory

Treatment

Treatments are generally directed toward stopping the inflammation and suppressing the immune system. Typically, corticosteroids such as prednisone are used. Additionally, other immune suppression medications, such as cyclophosphamide, are considered. In case of an infection, antimicrobial agents including cephalexin may be prescribed. Affected organs (such as the heart or lungs) may require specific medical treatment intended to improve their function during the active phase of the disease.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Giant cell arteritis</span> Inflammatory disease of large blood vessels

Giant cell arteritis (GCA), also called temporal arteritis, is an inflammatory autoimmune disease of large blood vessels. Symptoms may include headache, pain over the temples, flu-like symptoms, double vision, and difficulty opening the mouth. Complications can include blockage of the artery to the eye with resulting blindness, as well as aortic dissection, and aortic aneurysm. GCA is frequently associated with polymyalgia rheumatica.

<span class="mw-page-title-main">Granuloma</span> Aggregation of immune cells in response to chronic inflammation

A granuloma is an aggregation of macrophages that forms in response to chronic inflammation. This occurs when the immune system attempts to isolate foreign substances that it is otherwise unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as foreign objects, keratin, and suture fragments.

<span class="mw-page-title-main">Granulomatosis with polyangiitis</span> Autoimmune disease with chronic blood vessel inflammation

Granulomatosis with polyangiitis (GPA), formerly known as Wegener's granulomatosis (WG), after the German physician Friedrich Wegener, is a rare long-term systemic disorder that involves the formation of granulomas and inflammation of blood vessels (vasculitis). It is an autoimmune disease and a form of vasculitis that affects small- and medium-size vessels in many organs but most commonly affects the upper respiratory tract, lungs and kidneys. The signs and symptoms of GPA are highly varied and reflect which organs are supplied by the affected blood vessels. Typical signs and symptoms include nosebleeds, stuffy nose and crustiness of nasal secretions, and inflammation of the uveal layer of the eye. Damage to the heart, lungs and kidneys can be fatal.

<span class="mw-page-title-main">Eosinophilic granulomatosis with polyangiitis</span> Medical condition

Eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as allergic granulomatosis, is an extremely rare autoimmune condition that causes inflammation of small and medium-sized blood vessels (vasculitis) in persons with a history of airway allergic hypersensitivity (atopy).

<span class="mw-page-title-main">Kawasaki disease</span> Disease found in young children

Kawasaki disease is a syndrome of unknown cause that results in a fever and mainly affects children under 5 years of age. It is a form of vasculitis, in which medium-sized blood vessels become inflamed throughout the body. The fever typically lasts for more than five days and is not affected by usual medications. Other common symptoms include large lymph nodes in the neck, a rash in the genital area, lips, palms, or soles of the feet, and red eyes. Within three weeks of the onset, the skin from the hands and feet may peel, after which recovery typically occurs. The disease is the leading cause of acquired heart disease in children in developed countries, which include the formation of coronary artery aneurysms and myocarditis.

<span class="mw-page-title-main">Polyarteritis nodosa</span> Systemic necrotizing inflammation of medium-sized muscular arteries

Polyarteritis nodosa (PAN) is a systemic necrotizing inflammation of blood vessels (vasculitis) affecting medium-sized muscular arteries, typically involving the arteries of the kidneys and other internal organs but generally sparing the lungs' circulation. Small aneurysms are strung like the beads of a rosary, therefore making this "rosary sign" an important diagnostic feature of the vasculitis. PAN is sometimes associated with infection by the hepatitis B or hepatitis C virus. The condition may be present in infants.

<span class="mw-page-title-main">Fibrinoid necrosis</span> Deposition of fibrin within blood vessel walls

Fibrinoid necrosis is a pathological lesion that affects blood vessels, and is characterized by the occurrence of endothelial damage, followed by leakage of plasma proteins, including fibrinogen, from the vessel lumen; these proteins infiltrate and deposit within the vessel walls, where fibrin polymerization subsequently ensues.

<span class="mw-page-title-main">Takayasu's arteritis</span> Medical condition

Takayasu's arteritis (TA), also known as aortic arch syndrome, nonspecific aortoarteritis, and pulseless disease, is a form of large vessel granulomatous vasculitis with massive intimal fibrosis and vascular narrowing, most commonly affecting young or middle-aged women of Asian descent, though anyone can be affected. It mainly affects the aorta and its branches, as well as the pulmonary arteries. Females are about 8–9 times more likely to be affected than males.

<span class="mw-page-title-main">Myeloperoxidase</span> Mammalian protein found in Homo sapiens

Myeloperoxidase (MPO) is a peroxidase enzyme that in humans is encoded by the MPO gene on chromosome 17. MPO is most abundantly expressed in neutrophils, and produces hypohalous acids to carry out their antimicrobial activity, including hypochlorous acid, the sodium salt of which is the chemical in bleach. It is a lysosomal protein stored in azurophilic granules of the neutrophil and released into the extracellular space during degranulation. Neutrophil myeloperoxidase has a heme pigment, which causes its green color in secretions rich in neutrophils, such as mucus and sputum. The green color contributed to its outdated name verdoperoxidase.

<span class="mw-page-title-main">Anti-neutrophil cytoplasmic antibody</span> Group of autoantibodies

Anti-neutrophil cytoplasmic antibodies (ANCAs) are a group of autoantibodies, mainly of the IgG type, against antigens in the cytoplasm of neutrophils and monocytes. They are detected as a blood test in a number of autoimmune disorders, but are particularly associated with systemic vasculitis, so called ANCA-associated vasculitides (AAV).

Microscopic polyangiitis is an autoimmune disease characterized by a systemic, pauci-immune, necrotizing, small-vessel vasculitis without clinical or pathological evidence of granulomatous inflammation.

<span class="mw-page-title-main">Rapidly progressive glomerulonephritis</span> Medical condition

Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney function, with glomerular crescent formation seen in at least 50% or 75% of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute kidney failure and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents.

An overlap syndrome is a medical condition which shares features of at least two more widely recognised disorders. Examples of overlap syndromes can be found in many medical specialties such as overlapping connective tissue disorders in rheumatology, and overlapping genetic disorders in cardiology.

Pauci-immune vasculitis is a form of vasculitis that is associated with minimal evidence of hypersensitivity upon immunofluorescent staining for IgG. Often, this is discovered in the setting of the kidney.

<span class="mw-page-title-main">Systemic vasculitis</span> Medical condition

Necrotizing vasculitis, also called systemic necrotizing vasculitis, is a general term for the inflammation of veins and arteries that develops into necrosis and narrows the vessels.

<span class="mw-page-title-main">Cutaneous small-vessel vasculitis</span> Inflammation of small blood vessels, accompanied by skin bumps

Cutaneous small-vessel vasculitis (CSVV) is inflammation of small blood vessels, usually accompanied by small lumps beneath the skin. The condition is also known as hypersensitivity vasculitis, cutaneous leukocytoclastic vasculitis, hypersensitivity angiitis, cutaneous leukocytoclastic angiitis, cutaneous necrotizing vasculitis and cutaneous necrotizing venulitis,

<span class="mw-page-title-main">Retinal vasculitis</span> Medical condition

Retinal vasculitis is inflammation of the vascular branches of the retinal artery, caused either by primary ocular disease processes, or as a specific presentation of any systemic form of vasculitis such as Behçet's disease, sarcoidosis, multiple sclerosis, or any form of systemic necrotizing vasculitis such as temporal arteritis, polyarteritis nodosa, and granulomatosis with polyangiitis, or due to lupus erythematosus, or rheumatoid arthritis. Eales disease, pars planitis, birdshot retinochoroidopathy, and Fuchs heterochromic iridocyclitis (FHI) can also cause retinal vasculitis. Infectious pathogens such as Mycobacterium tuberculosis, visceral larva migrans can also cause retinal vasculitis. Drug-induced vasculitis may involve retina as well, as seen in methamphetamine induced vasculitis.

Ronald Jonathan Falk is the Nan and Hugh Cullman Eminent Professor and Chair of the Department of Medicine at the University of North Carolina-Chapel Hill (UNC). He is a clinical nephrologist and internationally recognized expert in anti-neutrophil cytoplasmic autoantibody (ANCA)-induced vasculitis and autoimmune kidney disease. His career as a translational physician-scientist spans more than three decades. His clinical practice and translational research focus on characterizing the cell, tissue and physiologic changes in the development of specific autoimmune kidney diseases and developing new approaches for studying autoimmunity, inflammation and basic neutrophil/monocyte biology. He was Chief of the UNC Division of Nephrology and Hypertension from 1993-2015. He co-founded the UNC Kidney Center in 2005 and continues as Co-Director. Falk is a Past-President of the American Society of Nephrology (ASN). Since 2015, he has served as Chair of the Department of Medicine at UNC.

<span class="mw-page-title-main">Lupus vasculitis</span> Medical condition

Lupus vasculitis is one of the secondary vasculitides that occurs in approximately 50% of patients with systemic lupus erythematosus (SLE).

Vasculitic neuropathy is a peripheral neuropathic disease. In a vasculitic neuropathy there is damage to the vessels that supply blood to the nerves. It can be as part of a systemic problem or can exist as a single-organ issue only affecting the peripheral nervous system (PNS). It is diagnosed with the use of electrophysiological testing, blood tests, nerve biopsy and clinical examination. It is a serious medical condition that can cause prolonged morbidity and disability and generally requires treatment. Treatment depends on the type but it is mostly with corticosteroids or immunomodulating therapies.

References

  1. ↑ "Vasculitis — Definition". Merriam-Webster Online Dictionary. Archived from the original on 1 July 2016. Retrieved 8 January 2009.
  2. ↑ "Glossary of dermatopathological terms. DermNet NZ". Archived from the original on 20 December 2008. Retrieved 8 January 2009.
  3. ↑ "Vasculitis" at Dorland's Medical Dictionary
  4. ↑ Sunderkötter, Cord (2022). "Vasculitis and Vasculopathies". Braun-Falco´s Dermatology. Berlin, Heidelberg: Springer Berlin Heidelberg. pp. 1125–1169. doi:10.1007/978-3-662-63709-8_64. ISBN   978-3-662-63708-1.
  5. ↑ Luqmani, Raashid; Robson, Joanna; Suppiah, Ravi (August 2018). "272: Vasculitis". In Davey, Patrick; Sprigings, David (eds.). Diagnosis and Treatment in Internal Medicine. Oxford University Press. pp. 927–931. ISBN   978-0-19-956874-1 . Retrieved 8 August 2024.
  6. ↑ Jayne, David (2009). "The diagnosis of vasculitis". Best Practice & Research Clinical Rheumatology. 23 (3): 445–453. doi:10.1016/j.berh.2009.03.001. PMID   19508950.
  7. ↑ Shavit, Eran; Alavi, Afsaneh; Sibbald, R. Gary (2018). "Vasculitis—What Do We Have to Know? A Review of Literature". The International Journal of Lower Extremity Wounds. 17 (4): 218–226. doi:10.1177/1534734618804982. ISSN   1534-7346. PMID   30501545.
  8. 1 2 3 4 5 6 7 8 9 10 11 Jennette, J. Charles (27 September 2013). "Overview of the 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides". Clinical and Experimental Nephrology. 17 (5). Springer Science and Business Media LLC: 603–606. doi:10.1007/s10157-013-0869-6. ISSN   1342-1751. PMC   4029362 . PMID   24072416.
  9. ↑ Johnston, S L; Lock, R J; Gompels, M M (14 March 2024). "Takayasu arteritis: a review". Journal of Clinical Pathology. 55 (7). BMJ Publishing Group: 481–486. doi:10.1136/jcp.55.7.481. PMC   1769710 . PMID   12101189.
  10. ↑ Hoffman, Gary S. (1 November 2016). "Giant Cell Arteritis". Annals of Internal Medicine. 165 (9): ITC65 –ITC80. doi:10.7326/AITC201611010. ISSN   0003-4819. PMID   27802475.
  11. ↑ Forbess, Lindsy; Bannykh, Serguei (2015). "Polyarteritis Nodosa". Rheumatic Disease Clinics of North America. 41 (1): 33–46. doi:10.1016/j.rdc.2014.09.005. PMID   25399938.
  12. ↑ Son, M. B. F.; Newburger, J. W. (1 April 2013). "Kawasaki Disease". Pediatrics in Review. 34 (4): 151–162. doi:10.1542/pir.34-4-151. ISSN   0191-9601. PMID   23547061.
  13. ↑ Hedrich, Christian M.; Schnabel, Anja; Hospach, Toni (10 July 2018). "Kawasaki Disease". Frontiers in Pediatrics. 6: 198. doi: 10.3389/fped.2018.00198 . ISSN   2296-2360. PMC   6048561 . PMID   30042935.
  14. ↑ Chung, Sharon A.; Seo, Philip (2010). "Microscopic Polyangiitis". Rheumatic Disease Clinics of North America. 36 (3): 545–558. doi:10.1016/j.rdc.2010.04.003. PMC   2917831 . PMID   20688249.
  15. ↑ Comarmond, Cloé; Cacoub, Patrice (2014). "Granulomatosis with polyangiitis (Wegener): Clinical aspects and treatment". Autoimmunity Reviews. 13 (11): 1121–1125. doi:10.1016/j.autrev.2014.08.017. PMID   25149391.
  16. ↑ Grygiel-Górniak, Bogna; Limphaibool, Nattakarn; Perkowska, Katarzyna; Puszczewicz, Mariusz (3 October 2018). "Clinical manifestations of granulomatosis with polyangiitis: key considerations and major features". Postgraduate Medicine. 130 (7): 581–596. doi:10.1080/00325481.2018.1503920. ISSN   0032-5481. PMID   30071173.
  17. ↑ Vaglio, A.; Buzio, C.; Zwerina, J. (2013). "Eosinophilic granulomatosis with polyangiitis (Churg–Strauss): state of the art". Allergy. 68 (3): 261–273. doi:10.1111/all.12088. ISSN   0105-4538. PMID   23330816.
  18. ↑ White, Jpe; Dubey, S. (2023). "Eosinophilic granulomatosis with polyangiitis: A review". Autoimmunity Reviews. 22 (1): 103219. doi: 10.1016/j.autrev.2022.103219 . PMID   36283646.
  19. ↑ Bharati, Joyita; Jhaveri, Kenar D.; Salama, Alan D.; Oni, Louise (2024). "Anti–Glomerular Basement Membrane Disease: Recent Updates". Advances in Kidney Disease and Health. 31 (3): 206–215. doi: 10.1053/j.akdh.2024.04.007 . PMID   39004460.
  20. ↑ Silva, Filipa; Pinto, Claudemira; Barbosa, Arsénio; Borges, Tiago; Dias, Carlos; Almeida, Jorge (2019). "New insights in cryoglobulinemic vasculitis". Journal of Autoimmunity. 105: 102313. doi:10.1016/j.jaut.2019.102313. PMID   31383568.
  21. ↑ Pillebout, Evangéline; Sunderkötter, Cord (2021). "IgA vasculitis". Seminars in Immunopathology. 43 (5): 729–738. doi:10.1007/s00281-021-00874-9. ISSN   1863-2297. PMID   34170395.
  22. ↑ Gu, Stephanie L.; Jorizzo, Joseph L. (2021). "Urticarial vasculitis". International Journal of Women's Dermatology. 7 (3): 290–297. doi:10.1016/j.ijwd.2021.01.021. PMC   8243153 . PMID   34222586.
  23. ↑ Bettiol, Alessandra; Prisco, Domenico; Emmi, Giacomo (1 May 2020). "Behçet: the syndrome". Rheumatology. 59 (Supplement_3): iii101 –iii107. doi:10.1093/rheumatology/kez626. ISSN   1462-0324. PMID   32348523.
  24. ↑ Iliescu, Daniela Adriana; Timaru, Cristina Mihaela; Batras, Mehdi; Simone, Algerino De; Stefan, Cornel (14 March 2024). "COGAN'S SYNDROME". Romanian Journal of Ophthalmology. 59 (1). Romanian Society of Ophthalmology: 6–13. PMC   5729811 . PMID   27373108.
  25. ↑ Martins-Martinho, Joana; Dourado, Eduardo; Khmelinskii, Nikita; Espinosa, Pablo; Ponte, Cristina (2021). "Localized Forms of Vasculitis". Current Rheumatology Reports. 23 (7): 49. doi:10.1007/s11926-021-01012-y. ISSN   1523-3774. PMC   8247627 . PMID   34196889.
  26. ↑ Russell, James P.; Gibson, Lawrence E. (2006). "Primary cutaneous small vessel vasculitis: approach to diagnosis and treatment". International Journal of Dermatology. 45 (1): 3–13. doi:10.1111/j.1365-4632.2005.02898.x. ISSN   0011-9059. PMID   16426368.
  27. ↑ Furukawa, Fukumi (2012). "Cutaneous Polyarteritis Nodosa: An Update". Annals of Vascular Diseases. 5 (3). Editorial Committee of Annals of Vascular Diseases: 282–288. doi:10.3400/avd.ra.12.00061. PMC   3595843 . PMID   23555526.
  28. ↑ Junek, Mats; Perera, Kanjana S; Kiczek, Matthew; Hajj-Ali, Rula A (26 August 2023). "Current and future advances in practice: a practical approach to the diagnosis and management of primary central nervous system vasculitis". Rheumatology Advances in Practice. 7 (3): rkad080. doi:10.1093/rap/rkad080. ISSN   2514-1775. PMC   10712448 . PMID   38091383.
  29. ↑ Abu El-Asrar, Ahmed M.; Herbort, Carl P.; Tabbara, Khalid F. (2005). "Retinal Vasculitis". Ocular Immunology and Inflammation. 13 (6): 415–433. doi:10.1080/09273940591003828. ISSN   0927-3948. PMID   16321886.
  30. ↑ Leone, Patrizia; Prete, Marcella; Malerba, Eleonora; Bray, Antonella; Susca, Nicola; Ingravallo, Giuseppe; Racanelli, Vito (5 November 2021). "Lupus Vasculitis: An Overview". Biomedicines. 9 (11). MDPI AG: 1626. doi: 10.3390/biomedicines9111626 . hdl: 11572/386878 . ISSN   2227-9059. PMC   8615745 . PMID   34829857.
  31. ↑ Bartels, Christie M.; Bridges, Alan J. (15 September 2010). "Rheumatoid Vasculitis: Vanishing Menace or Target for New Treatments?". Current Rheumatology Reports. 12 (6). Springer Science and Business Media LLC: 414–419. doi:10.1007/s11926-010-0130-1. ISSN   1523-3774. PMC   2950222 . PMID   20842467.
  32. ↑ Seidman, M.A. (2014). "Vasculitis". Pathobiology of Human Disease. Elsevier. pp. 2995–3005. doi:10.1016/b978-0-12-386456-7.05506-4. ISBN   978-0-12-386457-4.
  33. 1 2 3 4 5 6 7 8 Jennette, J. C.; Falk, R. J.; Bacon, P. A.; Basu, N.; Cid, M. C.; Ferrario, F.; Flores-Suarez, L. F.; Gross, W. L.; Guillevin, L.; Hagen, E. C.; Hoffman, G. S.; Jayne, D. R.; Kallenberg, C. G. M.; Lamprecht, P.; Langford, C. A.; Luqmani, R. A.; Mahr, A. D.; Matteson, E. L.; Merkel, P. A.; Ozen, S.; Pusey, C. D.; Rasmussen, N.; Rees, A. J.; Scott, D. G. I.; Specks, U.; Stone, J. H.; Takahashi, K.; Watts, R. A. (27 December 2012). "2012 Revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides". Arthritis & Rheumatism. 65 (1). Wiley: 1–11. doi: 10.1002/art.37715 . ISSN   0004-3591. PMID   23045170.
  34. 1 2 Mahr, Alfred; de Menthon, Mathilde (2015). "Classification and classification criteria for vasculitis". Current Opinion in Rheumatology. 27 (1). Ovid Technologies (Wolters Kluwer Health): 1–9. doi:10.1097/bor.0000000000000134. ISSN   1040-8711. PMID   25415531. S2CID   24318541.
  35. ↑ Suresh, E (1 August 2006). "Diagnostic approach to patients with suspected vasculitis". Postgraduate Medical Journal. 82 (970). Oxford University Press (OUP): 483–488. doi:10.1136/pgmj.2005.042648. ISSN   0032-5473. PMC   2585712 . PMID   16891436.
  36. ↑ Luqmani, Raashid Ahmed; Pathare, Sanjay; Kwok-fai, Tony Lee (2005). "How to diagnose and treat secondary forms of vasculitis". Best Practice & Research Clinical Rheumatology. 19 (2). Elsevier BV: 321–336. doi:10.1016/j.berh.2004.11.002. ISSN   1521-6942. PMID   15857799.
  37. 1 2 Eastham, A Brooke W (12 July 2021). "Leukocytoclastic Vasculitis: Practice Essentials, Pathophysiology, Etiology". Medscape Reference. Archived from the original on 19 October 2019. Retrieved 8 November 2019. Updated: 25 October 2018
  38. ↑ "Giant-Cell Arteritis and Polymyalgia Rheumatica". New England Journal of Medicine. 371 (17): 1652–1653. 23 October 2014. doi:10.1056/NEJMc1409206. ISSN   0028-4793.
  39. ↑ Dellavedova, L.; Carletto, M.; Faggioli, P.; Sciascera, A.; Del Sole, A.; Mazzone, A.; Maffioli, L. S. (2016). "The prognostic value of baseline 18F-FDG PET/CT in steroid-naïve large-vessel vasculitis: introduction of volume-based parameters". European Journal of Nuclear Medicine and Molecular Imaging. 43 (2): 340–348. doi:10.1007/s00259-015-3148-9. ISSN   1619-7070. PMID   26250689.
  40. ↑ Burtis, Carl A.; Ashwood, Edward R.; Bruns, David E. (2012). Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. St. Louis, Mo: Saunders. p. 1568. ISBN   978-1-4160-6164-9.
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