Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 1-week-old Jersey bull calf with a history of diarrhea, weakness, and lethargy was submitted for necropsy. Principal macroscopic findings were enteritis and multifocal necrotizing hepatitis. Histologically and ultrastructurally, organisms with characteristics of Bacillus piliformis were associated with the foci of necrosis in the liver.
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PMID:Bacillus piliformis infection (Tyzzer's disease) in a calf. 365 16

Idiopathic perforation of the bile duct is rare in children. Sixty-seven cases were reported in the English literature to 1980. It is, nevertheless, the second commonest surgical cause of jaundice in the neonate. The etiology is unknown though distal obstruction and weakness in the bile duct wall have been postulated. Limited surgical treatment with external drainage is the preferred therapy. In isolated cases internal drainage procedures or repeated aspiration have been successful. The diagnosis should be suspected in the presence of jaundice and ascites with or without abdominal pain and signs of peritoneal irritation. We describe a 3-month-old girl presenting with anemia, vomiting, jaundice, and ascites. This was initially diagnosed as hepatitis but bilious fluid was found on paracentesis. Computerized tomography with cholangiography and 99 MTC Diisopropyl IDA cholescintigraphy confirmed the diagnosis. The latter seems to be more accurate than I-131 Rose Bengal. The perforation was at the junction of the hepatic and cystic ducts. It was treated successfully by external drainage and a cholecystostomy. Direct attempts to close the perforation, or more complicated surgical procedures, are unnecessary while nonoperative treatment carries a high mortality. At follow-up after 1 year the IV cholangiogram and liver-function tests are normal. Cholecystostomy provided good drainage of the biliary ducts as well as easy access for follow-up cholangiography.
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PMID:Idiopathic perforation of the biliary tract in infancy. 664 92

Ulcerative hemorrhagic enteritis of swans induced by Sphaeridiotrema globulus is enzootic at Lake Musconetcong in northern New Jersey. It accounted for a calculated 250 deaths of wild mute swans (Cygnus olor) between 1970 and 1980. The swans died primarily in the winter and early spring. Sites of infection included the jejunum and ileum. Trematodes singly or in groups ulcerated the intestines. Severe hemorrhage from damaged submucosal capillaries provided a blood meal for the parasites and probably precipitated the anemia observed. The intensity of fatal infections ranged from 20 to 870 parasites. A mononuclear periportal hepatitis and secondary nodules in the spleen were commonly observed. Affected swans exhibited muscular weakness and appeared to have died from hypovolemic shock or some complication associated with it.
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PMID:Trematode (Sphaeridiotrema globulus)-induced ulcerative hemorrhagic enteritis in wild mute swans (Cygnus olor). 697 99

Modern serologic methods permit the classification of the particular course a virus hepatitis takes into individual types of pathogenesis. This is the case with hepatitis A in which only cholestatic courses have been proved for sure. Cholestatic courses are observed in 5-10% of all cases of acute hepatitis A, with variations from country to country. The duration of the disease is considerably longer than in non-cholestatic hepatitis A. It is between 80 and 130 or even more days! The diagnostic difficulty consists in the clear delimination to other diseases, particularly to intrahepatic cholestasis by drugs or to posthepatic stenosis. Sonography and ERCP are useful technological methods in this situation. Specific therapeutical measures are not available due to the lack of knowledge of the pathogenesis of this type of acute virus infection. The prognosis of cholestatic hepatitis A is good. Short-term glucocorticoid therapy is recommended by some authors in long-term cases, which are associated with pruritus, general weakness, loss of weight and distinct icterus. The course of the disease is obviously not changed by this therapy, but the sometimes agonizing symptomatology is relieved.
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PMID:[Clinical significance of cholestatic viral hepatitis]. 748 21

A patient with chronic inflammatory demyelinating polyneuropathy (CIDP) associated with type B and type C hepatitis virus infection is reported. A 54-year-old female who had a blood transfusion at the age of 31 years was diagnosed as a carrier of hepatitis B virus at the age of 43. Liver dysfunction was first noted in 1987 and gradually grew worse year by year. Beginning in early June 1992, the patients general fatigue became worse, her serum GOT and GPT levels became elevated, and she complained of a tingling sensation in her arms and legs. Neurological examination revealed moderate sensory disturbance of the glove-and-stocking type in all of her extremities. Deep tendon reflexes were all diminished. Hepatitis C antibody was detected in the serum at this time. On June 12, 1993, progression of her sensory disturbance was found to be associated with generalized muscle weakness. Cerebrospinal fluid studies showed increased protein without pleocytosis. Motor nerve conduction studies revealed marked prolongation of terminal latencies, reduction of conduction velocities, and abnormal temporal dispersion of the motor potentials. No sensory potentials could be evoked at any of the sites stimulated. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation. A diagnosis of CIDP was made. Treatment with corticosteroids was started, but there was little improvement in neurological function. The liver dysfunction progressed further and ultimately the patient died of hepatic failure. An autopsy demonstrated liver cirrhosis, but no malignant tumors were evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic inflammatory demyelinating polyneuropathy associated with chronic liver disease due to type B and type C hepatitis virus]. 766 15

We present here thirteen patients (5 men and 8 women, aged 31 to 73, mean 55 years) with spastic paraparesis who showed clinical features similar to those of HTLV-1 associated myelopathy without HTLV-1 antibody, but with positive antibody to hepatitis B virus (HBV). All of these patients showed slowly progressive difficulty in walking. Five patients had previous histories of blood transfusion, of these one with history of B hepatitis. Neurologically, muscle weakness, spasticity and exaggerated deep tendon reflexes in the lower extremities were common to all the patients. Seven patients showed Babinski's reflex. Disturbance of micturition was noted in 3 patients. None showed organic changes of the spine on magnetic resonance image (MRI). None was serologically positive for syphilis and had cryoglobulin and hypergammaglobulinemia. Elevated levels of the liver enzymes were noted in two patients. All patients were positive for hepatitis B surface antibody (HBs-Ab) (EIA) but negative for hepatitis B surface antigen (HBs-Ag) (EIA). Five patients were seropositive for hepatitis C virus (HCV) (PHA). In 3 of them, reverse transcriptase polymerase chain reaction was performed but failed to detect HCV-RNA. All patients underwent spinal tap, and showed normal cell count and protein concentration in their cerebrospinal fluid (CSF). Atypical cells were not observed in all the patients. The CSFs from three patients were tested for HBs-Ag and HBs-Ab. HBs-Ag was negative in all three patients, but HBs-Ab was positive in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hepatitis B virus antibody positive spastic paraparesis]. 795 26

Two cases of naturally occurring fatal disease in eagles (a booted eagle and a buzzard) are reported. Both eagles showed anorexia, weight loss, weakness, and inability to fly. Microscopically, stained liver sections showed wide non-zonal coagulation necrosis and eosinophilic intranuclear inclusion bodies in hepatocytes adjacent to the edges of necrotic regions. Ultrastructural studies of hepatocytes revealed multiple enveloped viral particles in the cytoplasm, focal paracrystalline arrays of virions within the nuclei, and some budding particles bound by a membrane, located in an evagination of nuclear membrane. The size and morphology of all of these particles were consistent with herpesvirus. To our knowledge, this is the first report of naturally occurring field cases of herpesvirus hepatitis in eagles (Accipitridae).
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PMID:Herpesvirus hepatitis in two eagles in Spain. 800 94

We immunologically examined the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with HB hepatitis. A 41-year-old male clerk has been suffered from muscle weakness, tingling and numbness in the distal portion of all limbs. All symptoms were compatible with the typical patterns of chronic inflammatory demyelinating polyradiculoneuropathy. We examined the patient's serum and biopsied sural nerve, using histochemical and immunological techniques. We detected the band that reacted with anti-HBs antibody in the sural nerve in western blotting. The result indicated that HBs antigen was expressed on the peripheral nerves in the patient. There were no anti-peripheral nerve antibodies neither in the sural nerve or serum. There was no increase of immune complex in the serum. No deposition of immunoglobulins and complements were detected in the sural nerve. Immunoadsorption therapy had no effect on this patient, but administration of prednisolone improved his symptoms drastically. These findings suggest that a cytotoxic T cell may had played a more important role than humoral factors in this patient's nerve injury. Though the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy remains unclear, our findings seem to be very interesting in that they go some way toward clarifying the pathogenesis of this disease.
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PMID:[A pathogenic study of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with hepatitis B infection]. 803 Dec 54

Over a period of 2 months an 88-year-old man developed progressively more severe breathing-related pain under the right shoulder blade, loss of appetite, general weakness, depressive mood, sub-febrile temperature and nocturnal sweating. Various inflammation parameters were raised (sedimentation rate 43 mm in the first hour; C-reactive protein 26 mg/dl; white cell count 12,500/microliters). There also were pleural effusion and signs of mild nonspecific hepatitis. Antibiotics were administered because bacterial pneumonia was suspected. But the patient's condition deteriorated and he developed nightly periods of disorientation. There was no evidence for any advanced malignancy. Immunological tests pointed towards older-onset systemic lupus erythematosus: titre for antinuclear antibodies markedly raised to 1:20 480; anti-DNA titre moderately raised to 1:125 IU/ml. The patient's general condition and the pleuritic pain improved within 2 days under treatment with prednisone (50 mg daily); the depression, disorientation and fever receded within a week. The anti-DNA titre fell to 47 IU/ml after 8 weeks. He was able to resume his usual social activities and was kept on a maintenance prednisone dose of 5.0 mg daily.
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PMID:[Lupus erythematosus in old age]. 820 42

A 74-year-old woman developed weakness, lack of appetite and abdominal swelling 7 months after starting treatment with carbimazole (10 mg/d for 10 weeks) and, subsequently, radioiodine for hyperthyroidism. Physical examination revealed generalized oedema and ascites. Computed tomography showed a liver of normal size but infiltrated by nodules up to 4 cm in diameter. Erythrocyte sedimentation rate was raised and there were abnormal concentrations of haemoglobin, total proteins, liver enzymes and creatinine, as well as decreased platelet and white cell counts. Thyroid function was normal. Viral and autoimmune diseases were largely excluded. Liver biopsy showed a severe, highly active hepatitis with parenchymal necroses, large-drop fatty infiltration and intralobular granuloma-like inflammatory reactions, as well as lympho-histiocytic inflammation of the portal areas. The most likely cause was the carbimazole treatment. In addition to symptomatic treatment she received prednisone (1 mg/kg), because an allergic diathesis could not be excluded. But she died of hepatic failure 6 weeks after admission.
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PMID:[Necrotizing hepatitis with a fatal outcome after carbimazole therapy]. 822 96


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