Introduction
Abdominal vasculitis, also known as mesenteric vasculitis, represents a complex group of conditions characterized by inflammation of the blood vessels supplying the gastrointestinal tract. As a critical area of concern, particularly in systemic vasculitic disorders, its diagnosis can be intricate and often delayed. Without prompt identification and intervention, abdominal vasculitis can lead to significant morbidity and mortality due to intestinal ischemia and subsequent complications. This article provides a comprehensive overview of abdominal vasculitis, detailing its clinical presentations, diagnostic approaches, and management strategies. It aims to enhance the understanding of this condition for specialists and healthcare professionals, emphasizing the crucial role of an interprofessional team in optimizing patient outcomes.
Etiology of Abdominal Vasculitis
Vasculitis classifications are often based on the size of the affected vessels; however, in abdominal vasculitis, overlap in vessel involvement is common. Various forms of vasculitis can manifest with mesenteric involvement, impacting arteries, capillaries, and veins of the gastrointestinal system. Table 1, originally provided in the source article, offers a detailed classification of vasculitides and their potential for mesenteric involvement. Understanding the underlying etiology is crucial for accurate Abdominal Vasculitis Diagnosis and targeted treatment.
Epidemiology of Mesenteric Vasculitis
Epidemiological data specifically focusing on mesenteric vasculitis is limited. However, information is available regarding the broader spectrum of vasculitis types and systemic diseases that can lead to mesenteric involvement.
Polyarteritis nodosa (PAN), a key cause of mesenteric vasculitis, predominantly affects adults aged 35 to 60, with a male-to-female ratio of 1.5:1. It’s important to distinguish between idiopathic PAN and Hepatitis B Virus (HBV)-associated PAN, as they are considered distinct clinical entities. The incidence of HBV-related PAN has declined in regions with effective HBV vaccination and treatment programs. A genetically determined form, Deficiency of ADA2 (DADA2) PAN, resulting from ADA2 gene mutations, is also recognized.
ANCA-associated vasculitis, another significant category, also shows male predominance (1.5:1) and typically manifests around 65 to 74 years of age. Immunoglobulin-A (IgA) vasculitis is the most prevalent form in children, particularly between 4 and 6 years old, with a slight male and Asian population predominance. Takayasu arteritis, while global, may be more common in Asia and predominantly affects women (over 80%), with onset between 10 and 40 years. Behcet’s disease is more frequently observed in Mediterranean and East Asian populations, affecting individuals aged 20 to 40, with no gender bias. Kawasaki disease mainly affects young children, especially of East Asian descent. Systemic lupus erythematosus (SLE) is more common in females, with a female-to-male ratio ranging from 3:1 in children to 12:1 in middle-aged adults, with most diagnoses between 16 and 55 years. Rheumatoid arthritis, more common in women and older adults, is typically diagnosed after age 50. These epidemiological factors provide context when considering abdominal vasculitis diagnosis in various patient demographics.
History and Physical Examination in Abdominal Vasculitis Diagnosis
In patients presenting with abdominal symptoms, abdominal vasculitis should be considered, especially if history, examination, or imaging raise suspicion. Symptoms often stem from intestinal ischemia, potentially leading to infarction. Ischemic colitis due to mesenteric vasculitis can mimic atherosclerotic ischemic colitis. Common symptoms include abdominal pain, tenderness, and rectal bleeding, along with nausea, vomiting, and diarrhea.
Acute mesenteric ischemia from thrombus occlusion often presents with sudden, severe pain disproportionate to physical findings and lower gastrointestinal bleeding. Chronic mesenteric ischemia, causing reduced intestinal blood flow, may manifest as post-prandial abdominal pain (abdominal angina) and weight loss. Hemodynamic instability and altered mental status can occur with severe complications like intestinal gangrene or perforation. A thorough history and physical examination are crucial first steps in abdominal vasculitis diagnosis.
Evaluation and Diagnostic Modalities for Abdominal Vasculitis
Initial laboratory assessments should include a basic metabolic panel, complete blood count, liver function tests, and urinalysis. Inflammatory markers like ESR and CRP, though non-specific, can be helpful. Specific tests such as viral hepatitis serology, serum cryoglobulins, ANCA, ANA, and rheumatoid factor are necessary for selected patients to refine abdominal vasculitis diagnosis. Serum lactic acid levels should be checked in suspected bowel ischemia. Genetic testing and functional ADA2 estimation are recommended for suspected DADA2.
Computerized tomography (CT) of the abdomen with intravenous contrast is the primary imaging modality for suspected mesenteric ischemia from vasculitis. For patients unable to undergo contrast CT, magnetic resonance angiography is a viable alternative. Endoscopy should be approached cautiously due to perforation risks in gastrointestinal vasculitis patients. Colonoscopic findings might be non-specific but useful in excluding other diagnoses. Acute ischemia may show pale, edematous, necrotic mucosa with normal segments interspersed, while severe cases may present with hemorrhages and ulcerations. Chronic cases can exhibit mucosal atrophy and strictures. Histopathology usually reveals mucosal damage and varying degrees of fibrosis, aiding in abdominal vasculitis diagnosis confirmation.
Treatment and Management Strategies for Abdominal Vasculitis
Treatment for abdominal vasculitis involves two main components: managing the underlying vasculitic process and addressing the gastrointestinal pathology specifically. Medical management of systemic vasculitis typically includes glucocorticoids and immunosuppressive therapies like cyclophosphamide, azathioprine, and mycophenolate mofetil. Biological agents, including rituximab and TNF alpha inhibitors, may be beneficial based on the underlying etiology.
Surgical intervention is crucial in patients with intestinal ischemia when complications like infarction or perforation are suspected. Segmental bowel resection can be life-saving. For chronic bowel ischemia, timely intervention is essential to prevent complications. Triple-phase CT angiography can detect stenosis and occlusion in mesenteric circulation. Symptomatic stenosis can be treated with percutaneous transluminal angioplasty (PTA) with or without stenting for revascularization. In younger patients, surgical bypass might be a more durable long-term solution compared to less invasive interventions. The specific treatment approach is tailored to the underlying cause of abdominal vasculitis.
Specific Vasculitis Types and Mesenteric Involvement
Polyarteritis Nodosa (PAN)
PAN is a necrotizing vasculitis affecting medium and small-sized visceral arteries. HBV infection is linked to about one-third of PAN cases, while others are idiopathic. Gastrointestinal symptoms are common, with abdominal pain being the most frequent complaint. Postprandial pain indicates transmural vasculitis involving mesenteric vasculature and bowel ischemia. Mucosal and submucosal artery inflammation can cause ischemia or perforation in the gallbladder, appendix, or colon. Splenic and hepatic infarcts and Budd-Chiari syndrome have also been reported.
In patients with gastrointestinal symptoms, imaging evidence of bowel wall thickening, visceral infarction, or rupture should raise suspicion for PAN in abdominal vasculitis diagnosis. CT angiography and catheter angiography can reveal aneurysms and stenotic segments, creating a “beaded” appearance. Screening for HBV, HCV, and HIV is essential. For suspected DADA2, genetic testing and functional ADA2 estimation are recommended. Immunosuppression is the primary treatment, often involving glucocorticoid pulse doses with cyclophosphamide. HBV-associated PAN treatment prioritizes antiviral therapy, along with plasmapheresis and corticosteroids. Anti-TNF agents are preferred for DADA2.
ANCA-Associated Vasculitis
ANCA-associated vasculitis includes granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA). GPA involves granulomatous inflammation of the respiratory tract and glomerulonephritis. MPA also affects the respiratory tract and causes crescentic glomerulonephritis. EGPA features asthma, rhinosinusitis, and eosinophilia. Gastrointestinal involvement is less common and usually occurs in advanced stages, ranging from mild abdominal pain to severe complications like bleeding or perforation.
Serological testing for ANCA is vital in suspected cases. GPA and MPA are often ANCA-positive, with anti-proteinase-3 antibodies in GPA and anti-myeloperoxidase in MPA. EGPA may be ANCA-negative in about half of cases. Mesenteric involvement indicates severe disease and typically requires cyclophosphamide and glucocorticoids for induction, followed by immunosuppression. Rituximab is also an option for mesenteric ischemia in GPA and MPA.
Immunoglobulin-A Vasculitis (Henoch-Schonlein Purpura)
IgA vasculitis, or Henoch-Schonlein purpura (HSP), is a small-vessel vasculitis common in children. Classical presentation includes palpable purpura, hematuria, and arthralgia. Gastrointestinal manifestations occur in about half of patients, often after the rash, with colicky abdominal pain as the main symptom. Intestinal wall edema, bleeding, and ischemia are underlying pathologies. Gastrointestinal hemorrhage can occur, and in children, bowel ischemia can lead to intussusception. It’s often preceded by upper respiratory infections.
Diagnosis is primarily clinical. Elevated serum IgA levels are not specific. Skin histopathology shows leukocytoclastic vasculitis with IgA deposition. CT abdomen is recommended for children with severe abdominal pain to rule out intussusception or obstruction. Glucocorticoids can provide symptomatic relief for abdominal pain, but their impact on disease course is unclear. The role of other immunosuppressants and rituximab is not well-established.
Single Organ Vasculitis of the Gastrointestinal Tract
Localized gastrointestinal vasculitis is often diagnosed incidentally via imaging or histopathology after surgery. It can affect the esophagus, stomach, intestines, appendix, or gallbladder. Intestinal involvement typically presents with abdominal pain, nausea, vomiting, and weight loss. Treatment and prognosis depend on the organ affected. Laparoscopic resection is effective for gallbladder or appendix vasculitis. Bowel resection may be necessary for intestinal involvement, with outcomes varying based on disease extent and severity.
Takayasu Arteritis
Takayasu arteritis is a granulomatous vasculitis affecting the aorta and its branches. Mesenteric circulation involvement is not uncommon, though many patients are asymptomatic due to collateral circulation. Glucocorticoids are the primary therapy, sometimes with additional immunosuppression. Mesenteric ischemia can occur from critical occlusion of the celiac or superior mesenteric artery, benefiting from percutaneous stenting.
Behcet’s Disease
Behcet’s disease is an idiopathic vasculitic syndrome with recurrent ocular and genital ulcerations. Gastrointestinal symptoms, due to mucosal ulceration in the terminal ileum, cecum, and ascending colon, include abdominal pain, diarrhea, and bloody stools, resembling inflammatory bowel disease. High clinical suspicion is necessary for abdominal vasculitis diagnosis. Glucocorticoids, azathioprine, and infliximab have been used effectively for mesenteric involvement.
Systemic Lupus Erythematosus (SLE)
Gastrointestinal vasculitis in SLE usually accompanies vasculitis in other organs. Lupus mesenteric vasculitis (LMV) occurs in up to 10% of SLE patients, particularly with active disease. Immune complex deposition and antiphospholipid antibodies contribute to mesenteric circulation occlusion, leading to intestinal ischemia. Abdominal pain is the most common symptom. LMV severity ranges from intestinal edema to gangrene and perforation.
Patients with SLE and abdominal symptoms require imaging. CT findings in LMV include bowel wall thickening, dilated loops, target sign, mesenteric circulation occlusion, and ascites. Prompt immunosuppressive treatment with high-dose intravenous steroids is crucial, with cyclophosphamide for refractory cases. Surgical exploration is needed for peritonitis signs. LMV prognosis varies, with mortality rates up to 50% reported.
Rheumatoid Arthritis
Vasculitis in rheumatoid arthritis is rare and typically occurs in long-standing, severe cases. Gastrointestinal vasculitis is very infrequent. Arteriolar involvement can cause ulcers, while medium-sized artery vasculitis can lead to bowel ischemia. Treatment focuses on the underlying rheumatoid arthritis with glucocorticoids, immunosuppressants, and biologics.
Mesenteric vasculitis has also been reported in other systemic vasculitides such as giant cell arteritis, relapsing polychondritis, Kawasaki disease, and cryoglobulinemic vasculitis.
Differential Diagnosis of Abdominal Vasculitis
A thorough history and physical examination are critical in abdominal vasculitis diagnosis. Differential diagnoses include atherosclerotic mesenteric ischemia, infections, malignancies, adverse medication effects, and other vessel occlusive processes. In patients with known vasculitis, ruling out other causes is essential before focusing on the underlying vasculitic disorder. Diagnosis is more challenging in those without a pre-existing vasculitis diagnosis. Symptoms suggesting other organ system involvement or bowel ischemia in patients without atherosclerosis risk factors should prompt investigations for mesenteric vasculitis.
Prognosis of Abdominal Vasculitis
Prognosis largely depends on the severity and extent of mesenteric involvement at presentation. The underlying disorder and involvement of other organ systems are also crucial. Mesenteric involvement often occurs late in the disease course. Untreated abdominal vasculitis has a poor prognosis. Early recognition and treatment are vital to improve morbidity and mortality outcomes.
Complications of Mesenteric Vasculitis
Mesenteric vessel vasculitis can lead to varying degrees of intestinal ischemia, potentially causing infarction. Superior mesenteric artery thrombosis is a common underlying cause. Serious complications include gastrointestinal bleeding, stricture-related obstruction, and intussusception from submucosal edema. Mesenteric circulation thrombus occlusion can result in acute mesenteric ischemia. Severe complications include bowel infarction, perforation, peritonitis, and sepsis from bacterial translocation. Ischemic hepatitis from vasculitis is often asymptomatic, manifesting as abnormal liver function tests.
Deterrence and Patient Education for Abdominal Vasculitis
Given the rarity, chronic nature, and variable manifestations of mesenteric vasculitis and vasculitis in general, patient and family education is crucial. Healthcare providers should offer direct counseling, educational materials, and support groups. Detailed discussions about the importance and potential side effects of medications are necessary to ensure patient compliance and safety.
Enhancing Healthcare Team Outcomes in Abdominal Vasculitis Management
Managing abdominal vasculitis requires an interprofessional approach. A patient-centered team, including primary care physicians, rheumatologists, gastroenterologists, and nurses, is essential for monitoring, therapy titration, and early complication recognition. Pharmacists play a vital role in coordinating medication dosing, interactions, and patient education. Long-term follow-up is necessary due to the chronic nature of vasculitis. Monitoring for infections and malignancies is also crucial, especially when initiating biological treatments.
Pharmacists should review medication records to identify potential drug-induced vasculitis and report findings to physicians. They also assist with medication reconciliation and dose verification. Nurses counsel patients, administer medications, monitor treatment progress, and watch for adverse drug reactions, communicating observations to the team. This interprofessional approach is essential for optimal therapy and improved outcomes in abdominal vasculitis management. Early diagnosis and management are critical to prevent dire consequences. Maintaining a high index of suspicion in patients with abdominal symptoms and other signs of vasculitis is crucial. Advances in medical treatment, endovascular interventions, and surgical options have significantly improved the prognosis for patients with mesenteric vasculitis.
Alt text: Table classifying different types of vasculitis including large vessel, medium vessel, small vessel, and variable vessel vasculitis, indicating their potential for mesenteric involvement. This table is critical for understanding the diverse etiologies of abdominal vasculitis.
Review Questions
(Note: Review questions are available in the original article and can be incorporated here for educational purposes if needed.)
References
1.Koster MJ, Warrington KJ. Vasculitis of the mesenteric circulation. Best Pract Res Clin Gastroenterol. 2017 Feb;31(1):85-96. [PubMed: 28395792]
2.Jennette JC, Falk RJ, Bacon PA, Basu N, Cid MC, Ferrario F, Flores-Suarez LF, Gross WL, Guillevin L, Hagen EC, Hoffman GS, Jayne DR, Kallenberg CG, Lamprecht P, Langford CA, Luqmani RA, Mahr AD, Matteson EL, Merkel PA, Ozen S, Pusey CD, Rasmussen N, Rees AJ, Scott DG, Specks U, Stone JH, Takahashi K, Watts RA. 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides. Arthritis Rheum. 2013 Jan;65(1):1-11. [PubMed: 23045170]
3.Watts RA, Robson J. Introduction, epidemiology and classification of vasculitis. Best Pract Res Clin Rheumatol. 2018 Feb;32(1):3-20. [PubMed: 30526896]
4.Watts RA, Scott DG. Epidemiology of the vasculitides. Curr Opin Rheumatol. 2003 Jan;15(1):11-6. [PubMed: 12496504]
5.Watts RA, Lane S, Scott DG. What is known about the epidemiology of the vasculitides? Best Pract Res Clin Rheumatol. 2005 Apr;19(2):191-207. [PubMed: 15857791]
6.Sharma A, Sharma K. Hepatotropic viral infection associated systemic vasculitides-hepatitis B virus associated polyarteritis nodosa and hepatitis C virus associated cryoglobulinemic vasculitis. J Clin Exp Hepatol. 2013 Sep;3(3):204-12. [PMC free article: PMC4216827] [PubMed: 25755502]
7.Zhou Q, Yang D, Ombrello AK, Zavialov AV, Toro C, Zavialov AV, Stone DL, Chae JJ, Rosenzweig SD, Bishop K, Barron KS, Kuehn HS, Hoffmann P, Negro A, Tsai WL, Cowen EW, Pei W, Milner JD, Silvin C, Heller T, Chin DT, Patronas NJ, Barber JS, Lee CC, Wood GM, Ling A, Kelly SJ, Kleiner DE, Mullikin JC, Ganson NJ, Kong HH, Hambleton S, Candotti F, Quezado MM, Calvo KR, Alao H, Barham BK, Jones A, Meschia JF, Worrall BB, Kasner SE, Rich SS, Goldbach-Mansky R, Abinun M, Chalom E, Gotte AC, Punaro M, Pascual V, Verbsky JW, Torgerson TR, Singer NG, Gershon TR, Ozen S, Karadag O, Fleisher TA, Remmers EF, Burgess SM, Moir SL, Gadina M, Sood R, Hershfield MS, Boehm M, Kastner DL, Aksentijevich I. Early-onset stroke and vasculopathy associated with mutations in ADA2. N Engl J Med. 2014 Mar 06;370(10):911-20. [PMC free article: PMC4193683] [PubMed: 24552284]
8.Navon Elkan P, Pierce SB, Segel R, Walsh T, Barash J, Padeh S, Zlotogorski A, Berkun Y, Press JJ, Mukamel M, Voth I, Hashkes PJ, Harel L, Hoffer V, Ling E, Yalcinkaya F, Kasapcopur O, Lee MK, Klevit RE, Renbaum P, Weinberg-Shukron A, Sener EF, Schormair B, Zeligson S, Marek-Yagel D, Strom TM, Shohat M, Singer A, Rubinow A, Pras E, Winkelmann J, Tekin M, Anikster Y, King MC, Levy-Lahad E. Mutant adenosine deaminase 2 in a polyarteritis nodosa vasculopathy. N Engl J Med. 2014 Mar 06;370(10):921-31. [PubMed: 24552285]
9.Camilleri M, Pusey CD, Chadwick VS, Rees AJ. Gastrointestinal manifestations of systemic vasculitis. Q J Med. 1983 Spring;52(206):141-9. [PubMed: 6604292]
10.Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004 May 24;164(10):1054-62. [PubMed: 15159262]
11.Ebert EC, Hagspiel KD, Nagar M, Schlesinger N. Gastrointestinal involvement in polyarteritis nodosa. Clin Gastroenterol Hepatol. 2008 Sep;6(9):960-6. [PubMed: 18585977]
12.Gnanapandithan K, Feuerstadt P. Review Article: Mesenteric Ischemia. Curr Gastroenterol Rep. 2020 Mar 17;22(4):17. [PubMed: 32185509]
13.Human A, Pagnoux C. Diagnosis and management of ADA2 deficient polyarteritis nodosa. Int J Rheum Dis. 2019 Jan;22 Suppl 1:69-77. [PubMed: 29624883]
14.Ha HK, Lee SH, Rha SE, Kim JH, Byun JY, Lim HK, Chung JW, Kim JG, Kim PN, Lee MG, Auh YH. Radiologic features of vasculitis involving the gastrointestinal tract. Radiographics. 2000 May-Jun;20(3):779-94. [PubMed: 10835128]
15.Angle JF, Nida BA, Matsumoto AH. Managing mesenteric vasculitis. Tech Vasc Interv Radiol. 2015 Mar;18(1):38-42. [PubMed: 25814202]
16.Rits Y, Oderich GS, Bower TC, Miller DV, Cooper L, Ricotta JJ, Kalra M, Gloviczki P. Interventions for mesenteric vasculitis. J Vasc Surg. 2010 Feb;51(2):392-400.e2. [PubMed: 20141962]
17.Pagnoux C, Seror R, Henegar C, Mahr A, Cohen P, Le Guern V, Bienvenu B, Mouthon L, Guillevin L., French Vasculitis Study Group. Clinical features and outcomes in 348 patients with polyarteritis nodosa: a systematic retrospective study of patients diagnosed between 1963 and 2005 and entered into the French Vasculitis Study Group Database. Arthritis Rheum. 2010 Feb;62(2):616-26. [PubMed: 20112401]
18.Stanson AW, Friese JL, Johnson CM, McKusick MA, Breen JF, Sabater EA, Andrews JC. Polyarteritis nodosa: spectrum of angiographic findings. Radiographics. 2001 Jan-Feb;21(1):151-9. [PubMed: 11158650]
19.Steele C, Bohra S, Broe P, Murray FE. Acute upper gastrointestinal haemorrhage and colitis: an unusual presentation of Wegener’s granulomatosis. Eur J Gastroenterol Hepatol. 2001 Aug;13(8):993-5. [PubMed: 11507371]
20.Stone JH, Merkel PA, Spiera R, Seo P, Langford CA, Hoffman GS, Kallenberg CG, St Clair EW, Turkiewicz A, Tchao NK, Webber L, Ding L, Sejismundo LP, Mieras K, Weitzenkamp D, Ikle D, Seyfert-Margolis V, Mueller M, Brunetta P, Allen NB, Fervenza FC, Geetha D, Keogh KA, Kissin EY, Monach PA, Peikert T, Stegeman C, Ytterberg SR, Specks U., RAVE-ITN Research Group. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med. 2010 Jul 15;363(3):221-32. [PMC free article: PMC3137658] [PubMed: 20647199]
21.Salvarani C, Calamia KT, Crowson CS, Miller DV, Broadwell AW, Hunder GG, Matteson EL, Warrington KJ. Localized vasculitis of the gastrointestinal tract: a case series. Rheumatology (Oxford). 2010 Jul;49(7):1326-35. [PubMed: 20360040]
22.Setty HS, Rao M, Srinivas KH, Srinivas BC, Usha MK, Jayaranganath M, Patil SS, Manjunath CN. Clinical, angiographic profile and percutaneous endovascular management of Takayasu’s arteritis – A single centre experience. Int J Cardiol. 2016 Oct 01;220:924-8. [PubMed: 27420344]
23.Hisamatsu T, Ueno F, Matsumoto T, Kobayashi K, Koganei K, Kunisaki R, Hirai F, Nagahori M, Matsushita M, Kobayashi K, Kishimoto M, Takeno M, Tanaka M, Inoue N, Hibi T. The 2nd edition of consensus statements for the diagnosis and management of intestinal Behçet’s disease: indication of anti-TNFα monoclonal antibodies. J Gastroenterol. 2014 Jan;49(1):156-62. [PMC free article: PMC3895195] [PubMed: 23955155]
24.Tian XP, Zhang X. Gastrointestinal involvement in systemic lupus erythematosus: insight into pathogenesis, diagnosis and treatment. World J Gastroenterol. 2010 Jun 28;16(24):2971-7. [PMC free article: PMC2890936] [PubMed: 20572299]
25.Yuan S, Ye Y, Chen D, Qiu Q, Zhan Z, Lian F, Li H, Liang L, Xu H, Yang X. Lupus mesenteric vasculitis: clinical features and associated factors for the recurrence and prognosis of disease. Semin Arthritis Rheum. 2014 Jun;43(6):759-66. [PubMed: 24332116]
26.Ko SF, Lee TY, Cheng TT, Ng SH, Lai HM, Cheng YF, Tsai CC. CT findings at lupus mesenteric vasculitis. Acta Radiol. 1997 Jan;38(1):115-20. [PubMed: 9059413]
27.Puéchal X, Gottenberg JE, Berthelot JM, Gossec L, Meyer O, Morel J, Wendling D, de Bandt M, Houvenagel E, Jamard B, Lequerré T, Morel G, Richette P, Sellam J, Guillevin L, Mariette X., Investigators of the AutoImmunity Rituximab Registry. Rituximab therapy for systemic vasculitis associated with rheumatoid arthritis: Results from the AutoImmunity and Rituximab Registry. Arthritis Care Res (Hoboken). 2012 Mar;64(3):331-9. [PubMed: 22076726]
28.Scola CJ, Li C, Upchurch KS. Mesenteric involvement in giant cell arteritis. An underrecognized complication? Analysis of a case series with clinicoanatomic correlation. Medicine (Baltimore). 2008 Jan;87(1):45-51. [PubMed: 18204370]
29.Sharma A, Gnanapandithan K, Sharma K, Sharma S. Relapsing polychondritis: a review. Clin Rheumatol. 2013 Nov;32(11):1575-83. [PubMed: 23887438]
30.Colomba C, La Placa S, Saporito L, Corsello G, Ciccia F, Medaglia A, Romanin B, Serra N, Di Carlo P, Cascio A. Intestinal Involvement in Kawasaki Disease. J Pediatr. 2018 Nov;202:186-193. [PubMed: 30029859]
Disclosure: Karthik Gnanapandithan declares no relevant financial relationships with ineligible companies.
Disclosure: Aman Sharma declares no relevant financial relationships with ineligible companies.