1/17. Hepatic capillariasis in children: report of 3 cases in brazil.capillaria hepatica is a helminth that may cause an extremely rare condition of parasitic hepatitis. Only 29 cases have been published, 2 of them in brazil. We report here 3 cases of children in brazil with massive hepatic capillariasis who presented the characteristic triad of this type of infection, i.e., persistent fever, hepatomegaly, and eosinophilia. The diagnosis was made by liver biopsy. All children responded well after treatment with thiabendazole (case 1), albendazole (case 3), and albendazole in combination with a corticoid (case 2). Case 1 has been followed-up for 24 years, an event not previously reported in the literature.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/17. alpha1-Antitrypsin deficiency and liver disease in children.This report describes the clinical, biochemical, and hepatic morphologic findings in ten children with severe serum alpha1-antitrypsin deficiency. Genetic protease inhibitor (Pi) phenotyping, using acid-starch gel and crossed antigen-antibody electrophoresis, demonstrated Pi phenotype ZZ in all our cases. In eight patients, manifestations of liver disease appeared during the first year of life. The case reports show that alpha1-antitrypsin deficiency should be suspected in any child with neonatal hepatitis, unexplained hepatomegaly or splenomegaly, or cirrhosis. In our report, one infant is normal at age 6 months, and one infant had progressive hepatic damage that culminated in liver failure and death at age 6 months. The variable clinical course and prognosis for infants with severe alpha1-antitrypsin deficiency is well illustrated by these two infants.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
3/17. Pseudo-budd-chiari syndrome: decompensated alcoholic liver disease mimicking hepatic venous outflow obstruction.Three patients with rapid onset decompensated liver disease who were referred to our hospital with presumed budd-chiari syndrome are described. This diagnosis was based on marked hepatomegaly, caudate lobe hypertrophy and failure to visualize hepatic veins by Doppler-ultrasound examination. Detailed history, biochemistry, and histology were, however, highly suggestive of alcoholic liver cirrhosis with steatohepatitis-induced hepatomegaly. On angiographic examination narrowed but patent hepatic veins were demonstrated in 2 patients. A third patient died before further work-up could be performed; autopsy showed patent hepatic veins. These cases show that the radiological diagnosis of budd-chiari syndrome due to hepatic vein obstruction can be false positive and that suspected hepatic vein occlusion on Doppler-ultrasound should be confirmed by angiographic studies and on liver histology.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
4/17. Non-A, non-B hepatitis: a new syndrome in uraemic patients.One hundred patients on chronic haemodialysis were studied prospectively over one year for evidence of hepatitis and of infection with hepatitis a or B virus. Five patients developed transient elevations of SGPT, accompanied by a consistent pattern of clinical manifestations, including low-grade fever, anorexia, nausea, hepatomegaly, and hypotension during dialysis. None of these patients had a positive test for A or B virus infection. Non-A non-B hepatitis appears to cause a specific syndrome in uraemic patients, and its transmission in a dialysis unit seems unrelated to blood transfusions.- - - - - - - - - - ranking = 7keywords = hepatitis (Clic here for more details about this article) |
5/17. Three cases of severe acute hepatitis after parenteral administration of amiodarone: the active ingredient is not the only agent responsible for hepatotoxicity.amiodarone is one of the most effective antiarrhythmic drugs available and is widely prescribed despite several potentially life-threatening side-effects. Hepatotoxicity is the most frequent one during long-term oral therapy: occasionally acute hepatitis necessitates the suspension of treatment but monitoring of a transient increase in serum aminotransferases is usually sufficient; the clinical-morphological pictures of liver cirrhosis have also been reported. Fulminant hepatitis soon after a parenteral load of the drug is far less well described in the literature. Most published cases were reversible after the suspension of treatment. A negative challenge after oral amiodarone exposure suggested that polysorbate 80, a solvent added to the intravenous infusion and already implied in the pathogenesis of a similar syndrome observed in infants, is a more likely cause of this complication. The occurrence of acute hepatitis complicating parenteral amiodarone treatment does not preclude subsequent oral use of the drug: an evidence-based therapeutic behavior now definitively consolidated. Because of the rarity of this diagnosis, we report 3 cases of short-term hepatotoxicity secondary to amiodarone treatment for supraventricular tachyarrhythmias: in 2 male patients with dilated cardiomyopathy and in a female with liver disease. The diagnosis was presumptive and based on a thorough drug history, the temporal relationship, the time-course of liver dysfunction, the exclusion of other causes and on the rapid improvement observed after parenteral amiodarone withdrawal in 2 cases; in no case could we find any other explanation for the liver damage. Since amiodarone is sometimes still an irreplaceable antiarrhythmic drug, we raise the question of whether careful and continuous vigilance should be mandatory in patients receiving the drug or whether it is possible to introduce a pharmaceutical preparation not containing the vehicle that induces acute liver toxicity.- - - - - - - - - - ranking = 7keywords = hepatitis (Clic here for more details about this article) |
6/17. New observations in a child with angiofollicular lymph node hyperplasia (Castleman's disease) originated from the mesenteric root.Localized plasma cell type Castleman's disease (CD) is an unusual pathologic entity. It is frequently associated with clinical and laboratory characteristics and rarely occurs in children. Total surgical excision results in cure in all aspects. To make early diagnosis of mesenteric CD is not easy, especially for children. An 11-year-old Taiwanese boy was recently evaluated for anemia and delayed growth. His clinical findings included a syndrome of severe hypochromic microcytic anemia, neutropenia, thrombocytosis, hypoferremia, hypergammaglobulinemia, and growth failure. Radiological examinations (abdominal ultrasound, small intestinal series, and computerized tomography) identified hepatosplenomegaly, nephromegaly, and huge masses in the middle abdomen with precaval, celiac, and paraaortic lymph nodal enlargement. However, detailed physical examination failed to detect a mass. At laparotomy a double-fist-sized confluent mass was found arising from the mesenteric root. Most masses were discrete and were excised individually. The pathologic diagnosis was plasma-cell type angiofollicular lymph node hyperplasia (Castleman's disease). Seven weeks after surgery, he had an episode of acute hepatitis b. Postoperatively, he exhibited a dramatic growth spurt; the hemoglobin, red blood cell indices, serum iron, and immunoglobulins returned to normal in 2 months. neutropenia, which has not been previously related to mesenteric CD, was an unexpected finding in our case; however, it resolved spontaneously 3 months after the surgery, suggesting its causal relationship with the tumor.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
7/17. Nonalcoholic steatohepatitis associated with psoriasis vulgaris.A 24-year-old man was admitted to our hospital because of liver dysfunction. He had been diagnosed as having psoriasis vulgaris at 18 years of age. physical examination demonstrated obesity, general erythema, and hepatomegaly. Laboratory data revealed elevated serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and glucose. A histological examination of the liver revealed macrovesicular fatty change and infiltration of inflammatory cells, including lymphocytes and polymorphonuclear cells, within the liver lobules. Pericentral fibrosis and pericellular fibrosis were also recognized. He was diagnosed as having nonalcoholic steatohepatitis (NASH), based on the fact that he had no habit of drinking alcohol, as well as psoriasis vulgaris and diabetes mellitus. We herein report a very rare case of NASH associated with psoriasis vulgaris.- - - - - - - - - - ranking = 5keywords = hepatitis (Clic here for more details about this article) |
8/17. Eosinophilic fasciitis presenting with a reactive hepatitis.We report a patient with eosinophilic fasciitis, reactive hepatitis and splenomegaly. Administration of prednisone resulted in normalization of liver enzymes and spleen-size and an improvement of his clinical condition. These uncommon manifestations are only part of the broadening clinical spectrum, which is discussed briefly.- - - - - - - - - - ranking = 5keywords = hepatitis (Clic here for more details about this article) |
9/17. Unusual clinical presentation of malignant histiocytosis in a 70-year-old woman.A 70-year-old woman was admitted for evaluation of hepatosplenomegaly, fever and elevated serum LDH levels. A biopsy specimen of the liver revealed histiocytic proliferation at the portal triad, and a mild degree of hepatitis. A bone marrow biopsy specimen showed proliferation of histiocytes with minimal immaturity and atypism, and haemophagocytosis by the proliferated histiocytes. fever, hepatosplenomegaly and elevation of LDH levels all disappeared spontaneously, and presumptive diagnosis of benign reticulosis with haemophagocytosis was made. One year later, fever, hepatosplenomegaly and elevation of LDH levels redeveloped, and the liver and bone marrow biopsy specimen showed proliferation of unequivocally malignant histiocytes. The patient died as a result of disseminated intravascular coagulation with shock 20 d later. We concluded that, in this case, malignant histiocytosis first presented as benign haemophagocytic reticulosis and, 1 year later, there was a typical malignant presentation.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
10/17. Patterns of hepatic injury induced by methyldopa.Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.- - - - - - - - - - ranking = 5keywords = hepatitis (Clic here for more details about this article) |
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