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• W2129334226 abstract "A 39-year-old man presented with 3 months of intermittent pain in the lower abdomen, vomiting, diarrhea, weight loss of 15 kg, and fatigue. The blood count, liver enzyme level, lactate level, and microbiologic stool test results were normal. However, the erythrocyte sedimentation rate was increased to 55 mm (in the first hour) and the C-reactive protein level to 60 mg/L. Sigmoidoscopy showed a normal rectum but severe sigmoiditis with multiple ulcers resulting in a tight sigmoid stenosis (Figure A). The histology biopsy examination showed necrotic debris intermingled with granulocytes but no signs of chronic inflammation. This suggested an ischemic cause, which was confirmed when angiography of the inferior mesenteric artery showed narrowing and abrupt cutoffs of branches of the inferior mesenteric artery (not shown). Moreover, selective angiography of the superior mesenteric artery (Figure B) showed beading (alternating dilatation and narrowing of arteries, black arrows) and aneurysms of the intestinal branches (white arrowhead) and severe segmental luminal narrowing and occlusions (black arrowheads) of the right colic and ileocolic branches of the superior mesenteric artery. Although the radiologic findings were typical of polyarteritis nodosa, tests for antineutrophil cytoplasmic antibodies (pANCA, cANCA), antinuclear antibodies (ANA), and hepatitis B virus infection were negative. Cryoglobulinemia, clinical neuropathy, and renal impairment also were absent. However, positive hepatitis C virus (HCV) antibodies and a viral load of 4,470,000 IE/mL HCV (type 3a) were detected. Liver histology disclosed no signs of vasculitis. The patient was treated with 6 cycles of cyclophosphamide and prednisolone. Cytomegalovirus infection of the colon occurred and required ganciclovir therapy. Finally, the diarrhea stopped, the patient put on 11 kg of weight, and the abdominal pain eased. After completing immunosuppressive therapy, antiviral treatment was initiated with peginterferon alfa-2a and ribavirin. After 12 weeks of antiviral therapy, HCV was no longer detectable by polymerase chain reaction. A final ileocolonoscopy showed a normal sigmoid but short-segment stenotic scarring of the ascending colon. Cryoglobulinemic vasculitis is a well-known extrahepatic feature of chronic HCV infection.1Ferri C. Mascia M. Cryoglobulinemic vasculitis.Curr Opin Rheumatol. 2006; 18: 54-63PubMed Google Scholar In contrast, (isolated) ischemic enteritis caused by cryoglobulin-negative polyarteritis nodosa is a very rare initial presentation of chronic HCV infection.2Elias N. Sabo E. Naschitz J. et al.Colonic ulcers in a patient with hepatitis C virus-associated polyarteritis nodosa.J Clin Gastroenterol. 1998; 26: 212-215Crossref PubMed Scopus (9) Google Scholar, 3Lefrou L. Luthier F. Dubois J. et al.Acute ischemia of the small intestine due to periarteritis nodosa revealing hepatitis C viral cirrhosis.Gastroenterol Clin Biol. 2003; 27: 1048-1050PubMed Google Scholar A standard therapy has not been established yet for HCV-associated polyarteritis nodosa. The question arises as to which should be treated first or whether it is best to treat everything at once. We opted for initial immunosuppressive therapy followed by antiviral treatment. Fortunately, our patient now is doing well." @default.
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• W2129334226 date "2006-11-01" @default.
• W2129334226 modified "2023-10-01" @default.
• W2129334226 title "Ischemic Enteritis Caused by Hepatitis C Virus–Associated Polyarteritis Nodosa" @default.
• W2129334226 cites W1964502902 @default.
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• W2129334226 doi "https://doi.org/10.1016/j.cgh.2006.03.011" @default.
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