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We report a young girl who developed ingravescent intestinal symptoms as the first manifestation of cutaneous polyarteritis nodosa (PAN) while the typical skin nodules developed later during the disease course. Cutaneous PAN predominantly affects children and presents with crops of painful skin nodules in the medial aspect of the foot, often preceded by sore throat. Visceral manifestations including gut involvement are commonly associated with the classical form of PAN while they are rarely reported in the cutaneous form. In our patient the severity of the abdominal symptoms required a laparoscopy, which revealed diffuse erythematosus swelling of the intestine on the serosal side. The administration of penicillin and steroids was followed by a dramatic improvement in the disease course. Chronic anterior uveitis developed 4 months after the disease onset and responded to local treatment. At a 2-year follow-up the girl is in good condition under prophylaxis with benzathine-penicillin with no recurrence of the illness. Our case confirms that cutaneous PAN is often related to streptococcal infection, and suggests that ASO titers should be determined in children with vasculitides to ensure a timely diagnosis and treatment of the condition if present.

In order to assess the prevalence of hepatitis C virus (HCV) in polyarteritis nodosa (PN), 38 patients with systemic necrotizing angiitis were retrospectively tested for the presence of anti-HCV antibodies (Ab). Twenty-one patients were hepatitis B virus (HBV) positive, comprising group A, and 17 were HBV negative, comprising group B. Two patients from group A had anti-HCV Ab (2/21: 9.5%). One was treated unsuccessfully with corticosteroids, then with vidarabine and plasma exchanges; HBe/anti-HBe seroconversion was not observed and anti-HCV Ab disappeared 8 months after the onset of PN. The second patient was successfully treated with corticosteroids, then vidarabine and plasma exchanges; he recovered from PN, HBV seroconversion occurred, and the anti HCV Ab remained detectable. These results show that: 1) the prevalence of anti HCV Ab in PN related to HBV is nearly the same (9.5%) as the prevalence of HCV Ab observed in patients with chronic hepatitis related to HBV infection; 2) the course of these two viral infections can be different and the role of HCV as an etiologic factor in PN has not been established.

We have investigated hepatitis B virus (HBV) infection in systemic necrotizing vasculitis (SNV). Our approach included the detection of the viral surface antigen (HBsAg) with a radioimmunoassay employing monoclonal anti-HBs (m-RIA); in addition, HBV DNA was looked for in serum and peripheral mononuclear blood cells. Among 28 subjects with SNV, 12 were found to be positive for HBsAg with the conventional test (p-RIA) and 7 additional subjects had anti-HBc and/or anti-HBs. From the 16 HBsAg negative individuals, 9 had HBsAg epitopes identified in serum with the m-RIA test and 1 had a low amount of circulating viral DNA. In contrast, only 1 among 6 subjects with other systemic vasculitis showed a positive test for m-RIA and HBV DNA assays; this individual had acquired HIV infection through transfusions which were also probably the source of his HBV infection. HBV DNA sequences were identified in peripheral mononuclear blood cells of 9 from the 37 tested, including 2 individuals who were HBsAg positive only with m-RIA. Therefore, our study indicates a much higher rate of HBV infection in patients with polyarteritis nodosa than previously suspected.