Background: Outcome of infantile intrahepatic cholestasis is highly variable. Aim to investigate various factors affecting outcome of infantile cholestasis. Methods: Retrospective study was conducted through data collection of 70 infant's files who presented with intrahepatic cholestasis. They were divided into two groups according to the fate of jaundice at the end of the first year follow up. Group I: cases with persistent jaundice and group II: cases that were jaundice free by the end of the year. A comparison was done at presentation, 3 and 12 months between the two groups. Results: Group I had a higher mortality and morbidity. Both groups were significantly different regards etiology, onset of jaundice, presentation to medical care, prevalence of consanguinity and pruritus. After 3 month, group I showed significant bigger and firm liver, higher ALT, AST, S.bilirubin. At 1 year, differences in weight, splenic size and S.albumin were found. Conclusion: The predictive parameters of a high risk group of intrahepatic cholestasis at presentation included etiology, age of onset, positive consanguinity and itching, where at 3rd month of follow-up included big firm liver, persistently pale stool, high ALT and AST and at one year included splenomegaly and lower albumin.
H epatic venous outflow obstruction is uncommonly reported in children (1). Although it is a rare disease in populations with a high standard of living, it is a leading cause for liver-related hospital admission in others with a lower standard of living (2). Hepatic venous outflow obstruction may run an acute, chronic, or fulminant course. Although commonly manifested by abdominal pain, ascites, and hepatosplenomegaly, cases have been reported in which there was a complete absence of symptoms, this being strongly associated with large hepatic vein collaterals (3). The syndrome is caused by a wide variety of conditions, including congenital or acquired inferior vena caval webs, thrombotic, inflammatory, or neoplastic disorders (4).Churg-Strauss syndrome (CSS) is characterized by eosinophilia and systemic vasculitis and occurs in patients affected by asthma and allergic rhinitis (5). In 1990, the American College of Rheumatology developed diagnostic criteria for the syndrome, namely moderate to severe asthma, peripheral blood eosinophilia (>10%), mono-or polyneuropathy, nonfixed pulmonary infiltrates, paranasal sinus abnormality, and histological proof of vasculitis with extravascular eosinophilia. The presence of at least 4 of these criteria is required for diagnosis (6). Epidemiological association of CSS with the use of antileukotrienes suggested the possibility that, in some instances, CSS may be a drug-induced illness (7).
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