Resistance to alpha interferon therapy in HCV chronic liver disease: role of hepatic fibrosis.

The response rate to interferon in HCV chronic liver disease is insufficient to date and the causes of this failure are not fully understood. Hepatic fibrosis hinders the blood-hepatocyte exchange of substances and we hypothesized that this process may also reduce the efficacy of interferon. Serum levels of connective tissue metabolites are related, to some extent, to the amount of extracellular matrix in the liver. Therefore, the usefulness was evaluated of serum tests of connective tissue metabolism compared to standard biochemical and histological parameters in predicting the probability of primary response to interferon. Sixty-eight patients with HCV chronic liver disease were treated with alpha-interferon for 1 year. At multivariate analysis time 0, the serum level of the P1 fragment of laminin was found to be the only factor independently associated with the response to treatment. As is well known, higher serum concentrations of the P1 fragment of laminin are associated with active basement membrane turnover and derangement of the hepatic structure. Therefore, this process seems to reduce the probability of response to interferon and, if confirmed, evaluation of serum the P1 fragment of laminin may be a useful test to predict the response to interferon and to define the therapeutic strategy, especially as far as the dose of interferon is concerned.

[Juvenile xanthogranuloma. Description of a case with liver involvement]. / Xantogranuloma giovanile. Descrizione di un caso con interessamento epatico.

Juvenile Xanthogranuloma. Report of a case with hepatic involvement. The Authors present a case of Juvenile Xanthogranuloma (JX) in a 3 months female child with cutaneous and hepatic nodules associated to dyspnea attributable to obstructive bronchopneumopathy. Histologically the lesions are xanthomatous with proliferation of fat-laden histiocytes. The hepatic involvement is characterized by hepatomegaly and yellow nodules on liver surface as seen at laparoscopy. On liver biopsy there is remarkable expansion of portal triad caused by aggregates of large foamy mono-polynuclear histiocytes with Touton giant cells. The cutaneous nodule biopsy shows histiocytic infiltrate in inter-adnexal dermal space with many giant cells holding great lipidic vacuoles. The patient's follow-up is characterized by slow and progressive clinical improvement with resolution of cutaneous, hepatic and pulmonary pathology. The Authors emphasize the differential diagnosis between this systemic form of JX and Langerhans cell Histiocytosis (Histiocytosis X) with multiorgan involvement. This diagnosis is necessary in order to establish therapy and prognosis.