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)

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
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PMID:Outbreake of Marburg virus disease in Johannesburg. 81 15

The cause of hyperamylasemia associated with chronic liver disease is unclear. In an attempt to identify the tissue of origin of hyperamylasemia in 3 patients with chornic active hepatitis their serum was isoelectrically focused. The isoamylase patterns obtained were compared to those of pancreatic and salivary amylase. The apparent salivary gland origin of the excessive blood amylase in the patients studied was substantiated by radiological demonstration of parotid sialoectasia in one patient and histological evidence of sialoadenitis in another. Further evidence was the coincident isoelectric points of the predominant isoamylase in the sera of the liver disease patients and of patients with parotid inflammatory disease. Hyperamylasemia associated with chronic liver disease may be of salivary gland origin and as such forms part of the spectrum of extrahepatic manifestations of chronic active hepatitis.
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PMID:A cause of hyperamylasemia associated with chronic liver disease. 83 1

On routine hospital admission, 23,714 patients received a 28-test serum metabolic profile. The 33 most common diseases (4,132 patients) of liver, pancreas, and gallbladder (LPG) had unique chemical templates averaging 15 significant serum deviations. Each LPG disease differed from all others by elevations of both leucine-aminopeptidase (LAP) and alkaline phosphatase (AP) levels. LAP level was low or normal and serum glutamic oxaloacetic transaminase (SGOT) and AP levels were elevated in 43 non-LPG diseases. Patients with acute and chronic pancreatitis had elevated amylase levels. The four nonmalignant diseases of the gallbladder were associated with normal levels of amylase and lactic dehydrogenase (LDH); except for silent cholelithiasis, each showed elevated total bilirubin (BIL) levels. Patients with solitary or scattered lesions of the liver had normal bilirubin levels (2,115 patients), and those with diffuse interstitial or parencymal disease had elevated BIL levels. Cancer patients had elevated LDH and alpha1 globulin (A1G) levels, but low albumin levels. The importance of comprehensive liver profiles in the treatment of psychoses is emphasized by significant liver damage in a number of these patients. A1G was normal and LDH was elevated in patients having mononucleosis, hepatitis, lupus erythematosus, alcoholism, and alcoholic cirrhosis.
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PMID:Serum chemistry templates of disease in liver, pancreas, and gallbladder. 116 26

Whether and to what extent the pancreas is involved in acute viral hepatitis is still unclear. In order to address this issue we evaluated serum and urinary amylase and isoamylase levels in 92 patients with acute viral hepatitis of different etiology and in 60 healthy volunteers. Furthermore, pancreatic structure and volume were evaluated by ultrasound scanning. Significant increase in serum and urinary pancreatic isoamylases was found in 12 and 35% of patients, respectively, in the early stage of the disease. Increase in serum pancreatic isoamylases was found only in patients suffering from B and non-A, non-B hepatitis. Ultrasonographic evaluation did not show any change in pancreatic structure and volume. In conclusion, this study suggests that mild pancreatic damage may occur during viral hepatitis.
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PMID:Mild pancreatic damage in acute viral hepatitis. 247 80

A patient with systemic lupus erythematosus presenting abdominal pain, nausea, vomiting and severe mucocutaneous vasculitis had significant elevation of serum amylase and hepatic enzymes levels during a flare-up of the disease. Clinical and laboratory alterations disappeared after therapeutic increase of corticosteroids given to the patient a fact that suggested etiologic correlation between systemic lupus erythematosus, hepatitis and pancreatitis.
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PMID:[Pancreatitis and hepatitis associated with systemic lupus erythematosus]. 248 88

One hundred consecutive patients were prospectively studied to assess the clinical and biochemical features of symptomatic choledocholithiasis. Biochemical tests were performed during the three days following the onset of symptoms. Pain was the most frequent symptom of choledocholithiasis, observed in 75% of the patients, but rarely occurred alone (12%). Clinical symptoms were not different according to age. High serum gamma glutamyl transpeptidase and alkaline phosphatase were the most frequent biochemical abnormalities in patients with symptomatic choledocholithiasis: they were increased in 94 and 91% of cases, respectively. Only one patient had no biochemical abnormality. Serum transaminases could reach very high levels just as in hepatitis. Biochemical data did not differ regardless of whether the common bile duct was enlarged or not. Biochemical abnormalities had been studied over the first 10 days of spontaneous evolution in 25 patients while choledocholithiasis persisted: serum bilirubin and transaminases significantly decreased while serum gamma glutamyl transpeptidase, alkaline phosphatase, and amylase remained unchanged. These results indicate that, in patients with suggestive symptoms, choledocholithiasis is unlikely in the absence of biochemical abnormalities in the first three days following the onset of symptoms.
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PMID:Prospective study of clinical and biochemical features of symptomatic choledocholithiasis. 287 Aug 85

Fourteen cases of alpha-1-antitrypsin deficiency are presented. All of them had a PIZZ phenotype except two in which a PIMZ phenotype was found. It must be pointed out that histological findings show a great variability among the different patients most of which did not have intracellular PAS-positive amylase inclusions in liver biopsy specimens. Clinical course did not correlate with either the age of onset of the disease or the phenotype found, thus indicating that other additional factors are involved in determining prognosis. We insist on the importance of a careful study of all neonatal hepatitis syndromes in order to rule out a alpha-1-antitrypsin deficiency.
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PMID:[Hepatic lesions caused by alpha 1-antitrypsin deficiency in childhood. Review of 14 cases]. 348 28

Brachytherapy by embolization with radiotherapeutic microspheres following intraarterial infusion of a radiosensitizer represents an attempt to combine several selective modalities into a more potent, focused attack on regionally confined tumors. In pursuit of this goal, we examined the ability of foxhounds with surgically implanted hepatic arterial (HA) delivery systems to tolerate a clinically relevant dosage of HA yttrium-90 (Y-90) by microsphere administration either alone or preceded by a 28-day constant HA infusion of either 5-bromo-2'-deoxyuridine (BUDR) or a control solution. Five dogs received BUDR (10 mg/kg/day) and five a control buffer infusion for 28 days immediately prior to the administration of Y-90-coated 15 micron resin microspheres (equivalent of 5000 rads to the entire liver) to each dog on day 31. In all animals, blood counts, bilirubin, amylase, appetite, weight, and behavior remained unchanged. Dogs receiving the microspheres after buffer infusion alone exhibited no hepatic enzyme alanine aminotransferase or alkaline phosphatase elevation. Alanine aminotransferase and alkaline phosphatase levels both rose during the third week of BUDR infusion, and while subsequent microsphere administration further increased enzyme levels, these levels had largely normalized by necropsy on day 82. At necropsy, the type and degree of hepatic toxicity among the animals receiving radioactive microspheres was comparable to that previously described in patients receiving external beam hepatic irradiation at conventional doses (2000-3000 rads). Also noted was a radiation-induced cholecystitis (due in large part to the gallbladder's total reliance on the hepatic artery for blood supply). One resin microsphere dog exhibited a small quantity of microspheres in the lungs causing focal radiation-induced granulomas suggesting the need to assess shunting of microspheres through the liver in clinical studies. Thus, HA Y-90 microspheres with BUDR can produce acceptable, nonlethal, and tolerable toxicities in this dog model suggesting that clinical studies of this combination are not likely to be contraindicated by synergistic toxicity. Although HA BUDR did not contribute significantly to the toxicity of the Y-90 microspheres, HA BUDR by itself administered uninterrupted for 4 weeks may, like HA FUDR (clinically), cause chemical hepatitis/cholangitis. The unexpected fragmentation of the resin spheres (albeit without myelosuppression) has led us to begin studies with a recently developed nondisruptible glass microsphere (ThereSphere) in which the Y-90 is part of the glass matrix and cannot leach.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of hepatic arterial yttrium-90 microsphere administration alone and combined with regional bromodeoxyuridine infusion in dogs. 358 Oct 69

The authors report two cases of hepatitis and a case of pancreatitis associated with indalpine. In one case of hepatitis, onset was acute and the clinical presentation was suggestive of cholecystitis; in the other case, hepatitis was discovered by biological tests. In the two cases, hepatitis was mainly cytolytic. Outcome was favorable upon interruption of drug administration. Onset of pancreatitis was inconspicuous, with progressively increasing pain. The pancreatic lesions were diffuse and massive. After interruption of administration, outcome was eventually favorable. Elevated amylasemia was also noted in the two cases of hepatitis. It is suggested that transaminase and amylase activities should be monitored during indalpine therapy.
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PMID:[Hepatitis and pancreatitis due to indalpine]. 400 81

Australia antigen [Au(1)], a particle associated with viral hepatitis, was isolated from the plasma of a patient with chronic anicteric hepatitis and leukemia who had received radioactive phosphorus. We have found that the immunoreactivity and appearance of Au(1) in the electron microscope were not altered by treatment with enzymes including trypsin, pronase, lipase, phospholipase C, ribonuclease, deoxyribonuclease, amylase, and neuraminidase. In contrast, other serum constituents were degraded by these enzymes. Therefore, treatment of the patient's plasma with many enzymes was exploited as an initial step for the isolation of Au(1). Subsequently, Au(1) was purified from the enzyme-treated (32)P-labeled plasma by gel filtration through Sephadex G-200 and centrifugation through sucrose and in cesium chloride gradients. There were no detectable human serum components in the purest fractions, as tested by immunoelectrophoresis and immunodiffusion. The density of the purified Au(1) was 1.21 in CsCl. The particle measured about 200 A in diameter, was predominantly spherical in shape and appeared to be composed of subunits. Nucleic acids were not detected by spectrophotometric, radiochemical, and chemical analyses. Immunoreactivity of purified Au(1) was destroyed by heating for 1 hr at 85 degrees C but was stable at 56 degrees C. Treatment with Carnoy's solution (3 parts ethanol:1 part glacial acetic acid) followed by pronase disrupted the particles as seen with the electron microscope. These findings, combined with other published information on Australia antigen and viral hepatitis, suggest that the bulk of Australia antigen in the blood of this patient is an incomplete virus or virus capsid.
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PMID:Australia antigen (a hepatitis-associated antigen): purification and physical properties. 424 40


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