Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Severe hepatotoxicity from phenobarbital occurred in an infant boy who had a complicated illness with chronic bilateral subdural hematomas and sepsis. Skin rash began after 2 weeks of treatment, and signs of hepatocellular failure developed 3 weeks after phenobarbital had been started. Signs of severe liver disease included elevated aminotransferases, conjugated hyperbilirubinemia, significant coagulopathy, hepatosplenomegaly and ascites. Other features of this adverse drug reaction were unremitting fever, leukocytosis with eosinophilia and atypical lymphocytosis, and proteinuria. Sepsis, viral hepatitis, and metabolic liver disease were excluded. The child was on no other medication and had been previously well. In-vitro rechallenge of the patient's lymphocytes with cytochrome P-450 generated metabolites of phenobarbital showed extensive cytotoxicity compared to control. These data support the hypothesis that a defect in drug detoxification was responsible for the child's susceptibility to this drug hepatotoxicity.
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PMID:Phenobarbital hepatotoxicity in an 8-month-old infant. 233 96

Seventy eight patients with diffuse hepatic lesions were selected for this study. They were classified after liver biopsy histopathologically into four groups. 45 patients with pure bilharzial hepatomegaly (group 1). 12 patients with mixed bilharzial hepatosplenomegaly with hepatitis (group 2). 16 patients with chronic active hepatitis and cirrhosis (group 3) and 5 patients with extrahepatic cholestasis (group 4). Ultrasonography of gall bladder was done for all patients. Group 3 patients showed the highest incidence of gall stones (29.4%) as compared to other groups (P less than 0.05).
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PMID:Pattern of gall bladder sonography in chronic liver diseases. 267 Nov 76

Cytomegalovirus (CMV) infection is relatively frequent and severe in immunosuppressed patients giving rise to diagnostic and therapeutic problems. We describe a series of 7 patients, six with acute lymphoblastic leukemia and one with aplastic anemia. All patients had CMV infection at the moment of maximum immunodepression. Two patients had undergone recent bone-marrow transplant. Six had been transfused in the two months prior to the onset of infection. Diagnosis was established through isolation of CMV from blood or serological methods. Symptoms ranged from prolonged fever to multi-organic involvement. Two cases had pulmonary involvement as well as fever, hepatitis and petechial rash. Two other cases presented with fever and hepatosplenomegaly and in the remaining, 3, fever was the only sign. Clinical course was favourable in all cases including the two with pneumonitis; of these two the first received acyclovir and anti-CMV Ig and the other received no specific therapy. One of the remaining cases was also given acyclovir and specific anti CMV Ig was administered to the 3 patients with isolated fever. In conclusion, CMV infection should be suspected in immunosuppressed patients with prolonged fever.
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PMID:[Cytomegalovirus disease in immunosuppressed patients]. 283 17

A 3 years old girl presented with clinical feature of an acute hepatitis-like illness, with jaundice, hepatosplenomegaly, high alanine aminotransferase activity (ALT) and high gamma-globulin values. We were able to demonstrate high titre of anti-liver-kidney microsome antibodies type 1 (LKMA1) in the serum of this patient using immunofluorescence, ELISA (Enzyme-linked immunoabsorbent assay) and Western blot (WB) analysis. This observation together with the liver morphology and after excluding other possible causes of hepatitis established the diagnosis of chronic active hepatitis associated with anti-LKM1 antibody. Immunosuppressive therapy was therefore started immediately.
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PMID:Chronic active hepatitis associated with anti-liver-kidney microsome antibody type 1. 325 76

Hepatic fibrin-ring granulomas and leishmania parasites were found in the liver biopsy specimens of 3 patients with prolonged fever and hepatosplenomegaly. It was recognition of the leishmanias in the liver biopsy specimen that prompted the diagnosis in all cases. There was no evidence of Q fever, Hodgkin's disease, cytomegalovirus hepatitis, or allopurinol treatment, which are the recognized causes of hepatic fibrin-ring granulomas. This report extends the range of etiologies of hepatic fibrin-ring granulomas. As a result, leishmaniasis should always be a consideration to the pathologist and the clinician in the differential diagnosis of fibrin-ring granulomas.
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PMID:Hepatic fibrin-ring granulomas in visceral leishmaniasis. 341 Feb 27

Subchronic and chronic toxicities of hexachlorobenzene (HCB) were studied in both sexes of Swiss mice, Syrian golden hamsters and Sprague-Dawley rats, at dietary dosages of 0, 100 and 200 ppm (mice), and 0, 200 and 400 ppm (hamsters and rats) for 90 days. At day 91, 25/50 animals in each of 18 groups were killed for histology studies. The rest were killed at 6-week intervals until the study was ended. Marked hepatosplenomegaly, enlarged thymuses and lymph nodes, or swollen and granular-looking renal cortices with depressions or nodulary areas were commonly observed. Dose- and sex-dependent progressive changes included toxic-degenerative hepatitis, chronic cirrhosis, hepatomas, bile-duct adenomas and a few hepatocarcinomas in older animals. A generalized lymphohaematopoietic response led to thymic, splenic and nodal lymphosarcomas, especially in female mice. Toxic-tubular nephritis with cortical infarcts developed into regenerative foci and renal adenomas in low incidences. Liver lesions were more prominent in females, while renal changes were most common in male rats. HCB was retested in both sexes of rats at oral doses of 0, 75 and 150 ppm for up to 2 years. At the start, each group contained 94 rats, and four randomly selected rats were killed at weeks 0, 1, 2, 3, 4, 8, 16, 32, 48 and 64 for microscopy. Progressive liver lesions started as hyperaemia and degenerations (4 weeks), and developed into toxic hepatitis, cirrhosis and formation of pre- and neoplastic foci (36 weeks), with hepatomas, bile-duct adenomas and hepatocellular carcinomas (64 weeks) in very high incidences in females and renal adenomas in male rats.
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PMID:Oncogenicity of hexachlorobenzene. 359 33

A 19-week-old English girl developed acute viral hepatitis, which became chronic with persistent hepatosplenomegaly and abnormal liver function tests. Liver biopsy at 1 year showed an active cirrhosis with multinucleated giant cells. The Australia (Au) antigen was detected repeatedly in the infant's serum by immunodiffusion and by electron microscopy at the time of the acute attack and during the development of cirrhosis. She had apparently acquired the hepatitis from her mother, who had had jaundice at the end of pregnancy and for one month thereafter, and who was subsequently shown to be a carrier of Au antigen. Particles with surface projections resembling paramyxoviruses were observed in two of the later specimens of the infant's serum.
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PMID:Cirrhosis associated with the Australia antigen in an infant who acquired hepatitis from her mother. 499 28

Peak activity over the spleen as a percentage of peak activity over the liver was measured in 265 (99m)Technetium sulphur colloid liver scintiscans. The value exceeded 70% in 50 cases. In 32 of these cirrhosis was present; the other 18 scans were from patients with a wide variety of conditions, including secondary deposits, hepatitis, and diseases involving the reticuloendothelial system. A measure of the total activity in the spleen was derived from the peak activity and the length of the spleen. In cirrhosis this was closely related to the finding of oesophageal varices thus showing the importance of a collateral circulation (which allows colloid to bypass the liver) in the increased uptake of colloid by the spleen. In eight patients with hepatosplenomegaly due to blood dyscrasia or disease involving the reticuloendothelial system, total activities in the liver and spleen were estimated from the anteroposterior colour dot scan, and both liver and spleen blood flow were measured by methods independent of reticuloendothelial cell function. The results showed that the main factor causing increased uptake of colloid by the spleen in these diseases was an increased blood flow in the spleen relative to that in the liver.
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PMID:Significance of increased "splenic uptake" on liver scintiscanning. 538 28

In a prospective study 43 consecutive children in hospital, aged between 6 months and 7 years and displaying at least one of the clinical signs of infectious mononucleosis (IM), were investigated for Epstein-Barr (EB) virus-specific IgM antibodies by an indirect immunofluorescence test. On this basis EB virus infection was considered confirmed in 8 patients, each of whom had IgM antibodies in the initial serum sample. In one additional patient, IgM antibodies were only detected in a second sample. The IgM antibodies disappeared with 3-11 weeks. Assessment of IgG antibodies had no diagnostic value in the acute phase of IM. Clinically the 3 youngest children, about 1 year of age, were diagnosed as having pneumonia or hepatitis, the 5 other consecutive patients as having IM. Hepatosplenomegaly was fairly frequently associated with IM, while sore throat, lymphadenopathy, and rash were often signs of other diseases. Only the oldest child had heterophil antibodies. Atypical lymphocytes (greater than 10%) were present in 4 of the 9 IM cases and were seen in children with other diseases as well. Our data stress the importance of measuring EB virus-specific IgM antibodies in order to diagnose IM in early childhood.
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PMID:Primary Epstein-Barr virus infection in early childhood. 625 87


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