Hepatitis A virus (HAV) infection in children is described as a mild condition, mostly asymptomatic. It is still a　major public health problem in developing countries [1]. Atypical manifestations are very rare. We report a case of an 8-years-old girl who presented with acute hepatitis due to HAV infection complicated by cryoglobulinemic vasculitis.

She persisted to have jaundice and pruritus. By eight weeks, she had an acute onset of epistaxis, arthritis of large joins (knees), and vasculitic rash (of legs, forearms, and the back), evolving for 2 days. The child was conscious with no neurological symptoms. She had normal body temperature and blood sugar. We found no other clinical abnormalities. Dipstick test was positive to proteins (2+) and blood (3+). Laboratory analysis showed cholestasis and hepatic cytolysis with no liver failure (prothrombin time = 84.4%, SGPT = 178 IU/l, SGOT=141 IU/L, total bilirubin = 66.1 mg/l, GGT = 101 IU/l, ALP=110 IU/l). Ultrasonography showed hepatosplenomegaly with acalculous gallbladder and thickened wall. The first hour, CRP=38.25 mg/L, she had normochromic normocytic anemia (hemoglobin, 10.1 g/dL), lymphocytosis (7220/mm3), mild proteinuria (180 mg/24h), and features of inflammation (ESR=80 mm). HAV serological test identified negative IgM antibodies and positive IgG antibodies. Due to the atypical manifestations, we biopsied the vasculitic rash and found a leukocytoclastic vasculitis. Negative serodiagnosis of Epotein Base virus, hepatitis B, C and E virus, Cytomegalovirus HIV eliminated another viral cause of this condition. While, repeated blood cultures to look for a bacterial or fungal infection remained sterile. There were no additional clinical or biological abnormalities suggesting an autoimmune cause for the vasculitis (e.g. systemic lupus erythematous, systemic juvenile arthritis, or systemic vasculitis as Wegener granulomatosis and polyarthritis nodosa). In this context, anti-nuclear antibodies, anti-DNA antibodies, rheumatoid factor, and anti-nuclear anti"cytoplasmic antibodies were negative. Biological tests to look for Wilson disease and auto-immune hepatitis were normal. Cryoglobulin assay was positive to IgM, IgA, and IgG (mixed cryoglobulinemia type II). Management consisted of starting oral steroids (prednisone) at 1 mg/kg/day. Ten days later, we noted total regression of cutaneous, and osteoarticular symptoms. The regression of clinical and biological cholestasis was achieved by three months, and prednisone tapering started. Steroids were withdrawn by the sixth month. The child remains asymptomatic, with a normal liver function.