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)

Case report on a 40 years old patient with pulmonary tuberculosis, in whom a treatment with Rifampicin plus Ethambutol has caused a transient hepatic and renal failure. By histology a chronic aggressive hepatitis and a destruction of renal tubular epithelium could be found. The etiologic role of Rifampicin is believed to be probable. Pathomechanism and differential diagnosis are discussed.
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PMID:[Liver and kidney damage in rifampicin and ethambutol treatment]. 648 86

beta-Galactosidase and associated activities (beta-glucosidase and beta-fucosidase) have been studied in rabbit and bovine liver and rabbit spleen. The physico-chemical (optimal pH, pI, MW) and kinetical (Km, Vmax, Ki) properties were determined for all the activities. Two enzyme forms were separated in rabbit spleen. beta-Galactosidase, beta-fucosidase and beta-glucosidase activities were catalyzed by the same enzyme in rabbit and bovine liver. The enzyme from bovine liver showed nonlinear double-reciprocal plots, suggesting a substrate-activation model, and the presence of more than one binding site in the enzyme. The enzyme activities of several glycosidases were determined in human sera fom control groups and from patients with diabetes mellitus, pancreatitis, hepatitis, cirrhosis, stomach and breast cancer, myocardial infarction and renal failure. The results show significantly different enzyme levels for several glycosidases in all the studied diseases. Experimentally-induced diabetes mellitus, alcoholism and nephrotoxicity in rats showed different glycosidase levels in several tissues, as compared with control groups.
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PMID:[Glycosidases of mammals: association of activities and changes of levels in some disorders]. 681 36

Patients with liver disease have increased morbidity and mortality following general anesthesia and surgery when compared with the general population. The increase in mortality appears to be directly related to the severity of hepatic parenchymal cell failure and to the magnitude and duration of the surgical procedure. The importance of preoperative detection of subclinical liver disease by use of a variety of blood tests has been emphasized. However, with the exception of hepatitis B and non-A non-B hepatitis, a precise diagnosis of the exact cause of liver disease is usually less important to the anesthesiologist than is a full characterization of the severity of hepatic dysfunction. Recognition and understanding of the central metabolic role played by the liver in maintaining carbohydrate, fat, and protein homeostasis can help in predicting and managing abnormalities which may complicate the preoperative, interoperative, and postoperative periods. Liver failure after anesthesia and surgery is treated by the same management principles used for liver failure with acute hepatitis. The incidence of postoperative renal failure may be increased in patients who have severe hyperbilirubinemia and its occurrence should be differentiated from the hepatorenal syndrome. It should be understood that complications of portal hypertension may develop in the absence of overt hepatic parenchymal cell failure and that liver failure may occur without gross evidence of portal hypertension. Either situation must be recognized and treated as far in advance of surgery as possible. In general, elective surgery in the patient with liver disease should be delayed until consequences of hepatic parenchymal cell dysfunction and portal hypertension are optimally corrected.
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PMID:Medical evaluation of the patient with liver disease prior to surgery. 701 90

Paraquat poisoning is very severe. When it is ingested, this herbicide may be responsible for causative lesions of the digestive tract, cytolytic hepatitis, renal tubular necrosis, circulatory failure, and/or pulmonary fibrosis. Since a very low dose (as little as one mouthful) is potentially lethal, it is important to understand why 11 of our 28 patients who entered our department for paraquat poisoning survived. The main prognostic factors appear to be the following: Route of administration. Of four patients who had inhaled paraquat aerosols and/or contaminated their skin with the herbicide, all survived. Ingested amount. Above 50 mg/kg, patients died of circulatory failure within 72 h; between 35 and 50 mg/kg, a progressive pulmonary fibrosis occurred. Delay between ingestion and the last meal. Paraquat is adsorbed and neutralized by foodstuffs. Caustic gastric lesions revealed by early endoscopic examination. The occurrence of an organic renal failure. The plasma paraquat concentrations within the first 24 h. Patients whose plasma concentrations do not exceed 2.0, 0.6, 0.3, 0.16, and 0.1 mg/L at 4, 6, 10, 16, and 24 h, respectively, are likely to survive. The different treatments that have been tested (fuller's earth, forced diarrhea, furosemide, hemodialysis, hemoperfusion, artificial ventilation with hypoxic breathing mixtures) did not modify the initial prognosis. The 11 survivals are only linked to the circumstances of the poisonings (route of administration, ingested amount, delay between ingestion and the last meal, etc.). The treatments did not modify the outcome.
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PMID:Prognosis and treatment of paraquat poisoning: a review of 28 cases. 717 91

Two cases are reported of combined renal and hepatic failure following exposure to halothane anesthesia. Both patients presented with postoperative fever and rapidly deteriorating liver and kidney function. Both required peritoneal dialysis. Both patients died, and in both cases this was the second exposure to halothane. The pathologic features of the 2 cases were similar in that the liver changes were typical of those seen with halothane hepatitis and the renal lesion was similar to that of methoxyflurane nephritis. This is, to our knowledge, the third report of renal failure occurring after halothane anesthesia. Possible mechanisms regarding its toxicity are discussed.
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PMID:Halothane-induced nephrotoxicity. 722 20

The hepato-renal syndrome is defined as potentially reversible functional renal failure associated with acute fulminant hepatitis or, more often, with advanced chronic liver failure. It is characterized by oliguria, azotemia, retention of sodium and water with formation of ascites, and hyponatremia. While urinary sodium concentration of less than 10 mEq/l reflects intact tubular sodium absorption, the kidney lacks the ability for adequate free-water generation. This condition must be separated from specific renal diseases which may arise during the course of intra-or extrahepatic diseases and which must be classified accordingly. Pathophysiological aspects of the hepa-to-renal syndrome include hemodynamic factors, such as changes in intrarenal blood flow distribution in the presence of elevated intrarenal and reduced peripheral vascular resistance. The functional relationship of vasoconstrictor, sodium retaining, and anti-diuretic hormones (e.g., renin-angiotensin, aldosterone, and vasopressin) to vasodilator, diuretic, and natriuretic hormonal factors (e.g., prostaglandins, kinins, and natriuretic hormone) may be altered as well. Finally, a pre- and intrahepatic spillover resulting in decreased endotoxin clearance must be considered. Due to the lack of understanding of their complex interactions, so far pharmacological and therapeutic approaches remained ineffective to correct at least some of these factors. Today, recovery from hepato-renal syndrome will, therefore, mainly depend on the course of the underlying liver disease.
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PMID:[Hepato-renal syndrome (author's transl)]. 727 84

Due to a combination of ingested ethanol and inhaled trichloroethylene (Tri) a 28 year old man developed toxic hepatitis and acute oliguric renal failure, both of which had a favorable evolution. Tri has been described as a cause of hepatic disfunction and acute renal failure due to acute tubular necrosis, although some of the cases described are controversial, because Tri was either contaminated by other dissolvents or could not be proven pure, with the exception of one case. In many there was ethanol ingestion. The Tri inhaled by our patient was found to contain less than 1% of carbon tetrachloride (C-Tchl). This would suggest the C-Tchl to be responsible for the clinical picture although the combination Tri/ethanol cannot be discarded as the causal agent, due to the small amount of contaminant present.
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PMID:[Toxic hepatitis and acute renal failure after inhalation of chloride solvents: report of one case (author's transl)]. 732 30

An alcoholic patient developed severe hepatitis and renal failure after ingesting the contents of a 300 ml. bottle of Nyquil for its ethanol content. This illness was presumably related to the 6 gm. of acetaminophen contained in this nonprescription preparation. Although hepatic damage with or without renal failure is usually described after a massive overdose of acetaminophen, the changes in drug metabolism induced by chronic ethanol consumption may increase the risk for acetaminophen toxicity. The large number of nonprescription acetaminophen-ethanol preparations available should be considered in evaluating an alcoholic patient seen with acute hepatic and renal dysfunction.
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PMID:Alcoholism, nonprescription drug and hepatotoxicity. The risk from unknown acetaminophen ingestion. 733 85

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

Hepatitis C virus (HCV) infection is one of the important causes of chronic and severe hepatitis in China. In an attempt to understand if there is any relationship between HCV infection and glomerulonephritis (GN), serum samples from 570 GN patients and 100 normal volunteers were screened for anti-HCV antibody (HCV-Ab) with ELISA method. Among the cases with positive HCV-Ab, serum HCV-RNA was tested with nested RT-PCR method. The incidence of serum HCV-Ab was 2 in 100 normal volunteers (2%) and 34 in 570 GN patients (6%). The incidence of positive serum HCV-RNA was 0 in normal volunteers whereas 21 in GN patients. The main clinical manifestation of GN patients with serum positive HCV-Ab was an unique proteinuria with/without nephrotic syndrome or renal failure, whereas the pathologic lesions in GN patients with serum positive HCV-Ab or HCV-RNA consisted of different disease entities. There was no close link between MPGN and active HCV infection. From the data observed, it seems that there is a coincidence between glomerular diseases and HCV infection rather than a matter of cause and consequence.
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PMID:[Is there hepatitis C virus associated glomerulonephritis?]. 753 65


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