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)

Adenoviral infections were diagnosed in three neonatal lambs that died spontaneously, and no other etiologic agents were identified. Clinical signs were anorexia, weakness, abdominal distention, and sudden death. Microscopic lesions consisted of multifocal necrotizing hepatitis, multifocal subacute interstitial nephritis, and loss of enterocytes from intestinal villi. Adenovirus inclusions were identified by light microscopy in the kidneys only. Adenoviral antigen, however, was identified in the liver, kidney, and intestine of the lambs by immunohistochemical techniques. An ovine adenovirus serotype 7, not previously isolated from sheep in the United States, was characterized from these lambs.
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PMID:Ovine adenovirus serotype 7-associated mortality in lambs in the United States. 1173 97

We report two patients with chronic hepatitis C, both nonresponders to a previous course of interferon (IFN), who developed or suffered an exacerbation of sarcoidosis while under treatment with IFN-alpha2a, ribavirin and amantadine. Patient 1: symptoms appeared after week 4 and treatment was withdrawn at month 9 due to severe weight loss, marked dyspnea, muscular weakness, dryness of mouth and facial paralysis. Stage III pulmonary sarcoidosis and polyneuropathy were confirmed. The patient had become steroid dependent and nine months after cessation of the treatment dyspnea and muscular weakness still persisted. She achieved a complete sustained response of hepatitis C. Patient 2: presented with a previous diagnosis of granulomatous hepatitis with chronic active hepatitis C and chronic dermatitis. The treatment exacerbated a cutaneous sarcoidosis. Furthermore, hiliar adenopathies consistent with stage I sarcoidosis became evident. Sarcoidosis responded to corticosteroids, but elevated transaminases and hepatitis C viraemia resisted. Hence, the combination of amantadine with ribavirin and IFN can develop or exacerbate subclinical sarcoidosis. A synergistic effect of these three drugs is suggested.
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PMID:Sarcoidosis in two patients with chronic hepatitis C treated with interferon, ribavirin and amantadine. 1185 6

We report a 28-year-old woman with a history of chronic immune-mediated hepatitis, in whom the simultaneous manifestation of dermatomyositis and myasthenia gravis resulted in severe neck extensor weakness and subacute respiratory insufficiency, followed by proximal muscle weakness and external ophthalmoplegia. Radiological signs of a thymoma were absent. The distinguishing clinical, electrophysiological, and biopsy findings are discussed. We suggest that an underlying immunoregulatory disorder was present, explaining the occurrence of three rare immune-mediated diseases in one patient.
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PMID:Concomitant dermatomyositis and myasthenia gravis presenting with respiratory insufficiency. 1187 Jul 2

A 4-month-old Maltese puppy and a 7.5-year-old Collie were diagnosed with septicemia associated with Citrobacter freundii. The puppy died soon, after developing weakness and mucohemorragic diarrhea. The Collie had immune-mediated hemolytic anemia and thrombocytopenia and was treated with immunosuppressive drugs before being euthanized. Gross examination of the puppy revealed mucohemorrhagic intestinal contents. Focal necrotic hepatitis, fibrinous peritonitis, interstitial pneumonia, and hemorrhagic gastrointestinal contents were observed in the older dog. Histologically, there was a diffuse, moderate, histiocytic meningitis in the puppy and a focal fibrinonecrotic hepatitis in the adult dog. Lesions in both dogs contained numerous gram-negative rods. Citrobacter freudii is a potential cause of monomicrobic bacteraemia-septicemia in puppies or immunocompromized adult dogs. The gastrointestinal tract is probably the main site of entry.
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PMID:Citrobacter freundii septicemia in two dogs. 1273 57

A 56 year old man was admitted cause he had increasing symptoms as weakness, lethargy, disorientation. The total eosinophil count was 3000/mm3, the serum sodium concentration was 120 mmol per litre. In spite of severe hyponatriemia, urinary sodium excretion was not suppressed and serum osmolality (240 mOsm/Kg was lower than urine osmolality (488 mOsm/Kg). SIADH and Idiopathic Hypereosinophilic Syndrome was diagnosed because we found systemic failure signs due to hypereosinophilia (hepatitis, gastritis, pulmonary hypertension, and encefalopathy). Cortisonic treatment was started with symptoms improving, natriemia, eosynophil count and hepatitis signs normalization. After treatment stopping, reappeared asymptomatic hypereosinophilia, than we choosed Idrossiurea but, non-standing hypereosinophilia disappeared, appeared signs of preexisting adrenal insufficiency, emphasized by stopping cortisone therapy. A RMN showed an hypofiseal adenoma. Many cases of SIADH and Hypereosinophilia hiding adrenocortical insufficiency are reported with severe and unusual hypereosinophilia.
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PMID:[Association of hyponatremia and eosinophilia: correlated idiopathic hypereosinophilic syndrome and SIADH or adrenal insufficiency with secondary eosinophilia]. 1285 64

A 68-year old Japanese male with alcohol related rhabdomyolysis, hepatitis, and hematological disorders is presented. Biochemical data showed markedly elevated levels of serum hepatobiliary enzymes, lactate dehydrogenase and myoglobin, and decreased levels of serum sodium and phosphate. The serum creatine kinase level was approximately 40 times higher than the normal upper limit with 97% of MM fraction. Clinical manifestations of rhabdomyolysis, such as myalgia, muscle weakness and acute renal failure, were not recognized. Hematological examinations revealed mild neutropenia, lymphopenia, monocytopenia and thrombocytopenia but no anemia or macrocytosis. Initial treatment of an intravenous infusion of saline (30 mL/Kg body weight) and subsequent low sodium diet was successfully completed without severe complications. All the abnormal laboratory data were normalized within three weeks of his hospitalization. We suggest that hyponatremia and hypophosphatemia may be involved in the development of rhabdomyolysis, hepatitis and hematological disorders.
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PMID:Rhabdomyolysis, hepatitis and multiple hematological disorders associated with alcohol abuse: a case report. 1293 2

CoQ transfers electrons from complexes I and II of the mitochondrial respiratory chain to complex III. There are very few reports on human CoQ deficiency. The clinical presentation is usually characterized by: epilepsy, muscle weakness, ataxia, cerebellar atrophy, migraine, myogloblinuria and developmental delay. We describe a patient who presented with neonatal liver and pancreatic insufficiency, tyrosinemia and hyperammonemia and later developed sensorineural hearing loss and Leigh syndrome. Liver biopsy revealed markedly reduced complex I+III and II+III. Addition of CoQ to the liver homogenate restored the activities, suggesting CoQ depletion. Histological staining showed prominent bridging; septal fibrosis and widening of portal spaces with prominent mixed inflammatory infiltrate, associated with interface hepatitis, bile duct proliferation with numerous bile plugs. Electron microscopy revealed a large number of mitochondria, which were altered in shape and size, widened and disordered intercristal spaces. This may be the first case of Leigh syndrome with liver and pancreas insufficiency, possibly caused by CoQ responsive oxphos deficiency.
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PMID:Neonatal liver failure and Leigh syndrome possibly due to CoQ-responsive OXPHOS deficiency. 1294 44

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

The July 2003 Case of the Month (COM). A 62-year-old female patient experienced progressive muscular weakness over the last ten years, involving shoulder and pelvic girdle muscles, paraspinal and facial muscles. A biopsy was taken from the left deltoid muscle where hepatitis vaccination had taken place 4 weeks previously. The specimen revealed macrophagic myofasciitis due to the injection of aluminium-bound vaccines. The finding can be reproduced experimentally by injecting vaccines in rats. The pathomechanism is supposed to involve immune stimulation due to long term persistence of the adjuvant. Macrophagic myofasciitis has been suggested to occasionally cause myopathy but is supposed to be unrelated to the underlying myopathy in our patient.
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PMID:July 2003: 62-year-old female with progressive muscular weakness. 1499 43

Disseminated visceral coccidiosis (DVC) caused by Eimeria spp. was recognized as a disease entity in captive sandhill cranes (Grus canadensis) and whooping cranes (Grus americana) in the late 1970s. While most avian species of Eimeria inhabit the intestinal tract of its host, the crane eimerians, Eimeria reichenowi and Eimeria gruis, invade and multiply systemically and complete their development in both digestive and respiratory tracts. In DVC, cranes, especially chicks, may succumb to acute infections resulting in hepatitis, bronchopneumonia, myocarditis, splenitis, and enteritis. Cranes may also develop chronic, subclinical infections characterized by granulomatous nodules in various organs and tissues. This paper reviews the pathology and pathogenicity of natural and experimental DVC in sandhill and whooping cranes. Naturally infected birds appeared clinically normal, but progressive weakness, emaciation, greenish diarrhea, and recumbency before death were observed in birds administered doses > or = 10 x 10(3) sporulated oocysts per os. At necropsy, naturally infected birds had nodules in the mucosa of the oral cavity and the esophagus, and in thoracic and abdominal viscera. Experimentally infected birds necropsied less than 7 days after infection (a.i.) had no gross lesions. Birds examined later had hepatosplenomegaly, liver mottling, lung congestion and consolidation with frothy fluid in airways, and turgid intestinal tracts with hyperemic mucosa. From 28 days a.i., grossly visible granulomatous nodules were seen in the esophagus, heart, liver, cloaca, and eyelids. By light microscopy, the basic host response was a granulomatous inflammation with non-suppurative vasculitis affecting many organs and tissues. With time, multifocal aggregates of mononuclear cells, many laden with asexual coccidial stages, increased in size and number. Widespread merogony resulted in morbidity and death, particularly in birds administered 20 x 10(3) sporulated oocysts. Ultrastructural examination revealed developing asexual coccidian stages in the cytoplasm of large lymphocytes or monocytes within a parasitophorous vacuole, often indenting the nucleus. Oocysts and gametocytes were found in the intestines by 12 days a.i., and in the esophagus, trachea, bronchi, and lung by 14 days a.i., indicating that crane eimerians can complete their life cycle at these sites. Thus, DVC in cranes could be a useful animal model for the study of eimerian extra-intestinal stages and the evaluation of potential systemic anticoccidial drugs.
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PMID:Pathology and pathogenesis of disseminated visceral coccidiosis in cranes. 1522 53


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