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 mechanism(s) of an inappropriate secretion of insulin is poorly understood. We report a case of reactive hypoglycemia associated with an unusually exaggerated insulin secretion. The patient, a 32-year-old man, developed frequent episodes of postprandial hypoglycemia after interferon treatment was begun for chronic type C hepatitis. Oral glucose challenge test confirmed the patient's extremely high plasma IRI response, i.e., more than 1000 microU/ml, and that of plasma C-peptide 56.9 ng/ml at 90 min, followed by symptomatic hypoglycemia (plasma glucose 34 mg/dl) at 240 min. The plasma proinsulin level also was high, but the molar ratio of immuno reactive insulin (IRI)/plasma C-peptide and IRI/proinsulin was within the normal range. Antibodies to insulin or insulin-receptor were negative. Plasma IRI response was apparently greater when the glucose was given orally than when given intravenously. The response of plasma glucagon-like-peptide (GLP)-1 to oral glucose was quite high (from baseline of 45.5 to 303.2 pmol/L) and showed a close parallel with the change in the plasma IRI concentration. The greatly enhanced insulin secretion leading to reactive hypoglycemia in this patient may therefore be attributed to the increased secretion of GLP-1.
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PMID:Highly increased insulin secretion in a patient with postprandial hypoglycemia: role of glucagon-like peptide-1 (7-36) amide. 762 58

The high oncogenic efficiency of woodchuck hepatitis virus (WHV) has been correlated with the ability of this virus to provoke insertional activation of myc family genes. To assess the impact of viral integration on liver cell transformation, we have generated transgenic mice carrying the mutated c-myc gene and adjacent viral DNA from a woodchuck tumor, in original configuration. Virtually all mice from two different strains developed hepatocellular carcinoma with a mean latency period of 8-12 months. The c-myc transgene was expressed transiently in neonatal livers, and re-expressed at preneoplastic and neoplastic stages in adult livers. Woodchuck c-myc mRNA driven by the normal P1 and P2 promoters and WHV-specific transcripts encoding viral surface antigens were produced in a strictly co-regulated fashion during development and tumorigenesis, indicating a predominant regulatory influence of the viral enhancer. Furthermore, the activity of the viral enhancer in response to various biological stimuli was apparently modulated by glucose uptake and glucagon/insulin balance in differentiated hepatocytes. In this model, a viral integration event selected from a naturally occurring tumor proved to be determinant for induction of hepatocarcinogenesis, although enforced, liver-specific expression of c-myc was limited to a particular developmental stage.
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PMID:Liver-specific expression and high oncogenic efficiency of a c-myc transgene activated by woodchuck hepatitis virus insertion. 810 15

Acute alcohol ingestion can affect life expectancy and is directly responsible for 3,500 deaths per year. Acute lung diseases are mainly caused by pneumococci, Gram negative bacilli and anaerobic germs, and are often due to multiple microbes. In this case, evolution toward abscess can be feared. Septicaemia and enterobacterial peritonitis are frequently observed in cirrhotic patients. Ethanol, hypokaliemia and hypophosphoraemia also lead to rhabdomyolysis. Rhabdomyolysis can be complicated with acute renal failure and hyperkaliaemia. Alcoholic ketoacidosis and the hypoglycaemia favored by prolonged inadequate nutrition, are corrected by infusion of glucose solutions. Hyponatraemia can be complicated by convulsions and central pontine myelinolysis. Minor forms of alcoholic hepatitis remiss after stopping alcohol intoxication. The major forms can evolve toward fatal encephalopathy; treatment with corticosteroids improves the prognosis in severe hepatitis. The cardiac failure with lactic acidosis in shoshin beriberi rapidly evolves to collapsus; treatment is based on emergency administration of vitamin B1. Management of patients in acute alcohol episodes requires great vigilance. Careful clinical examination and biological tests should eliminate severe somatic complications before concluding to simple alcoholic intoxication.
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PMID:[Severe somatic complications of acute alcoholic intoxication]. 813 83

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

Hypoglycaemia is a known complication of fulminant hepatic failure. Massive destruction of liver tissue, along with hyperinsulinism and defective glucose storage in extrahepatic organs are some of the mechanisms contributing to the hypoglycaemia. We describe here a case of reversal of fulminant-hepatitis-associated hypoglycaemia at the anhepatic stage of liver transplantation. It is suggested that non-insulin hypoglycaemic factors secreted by the damaged liver may be responsible for this complication.
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PMID:Reversal of fulminant-hepatitis-associated hypoglycaemia at the anhepatic stage during liver transplantation. 871 32

In the present study, neurotransmitters related to the regulation of food intake were investigated in hypothalamus of LEC rats. The experiment was conducted using LEC and LEA (control) rats aged 4, 10 and 20 weeks. Cu concentration in hypothalamus of LEC rats aged 4 weeks was lower than that in the control, and similar to the control in 10 weeks of age. In contrast, Cu concentration of LEC rats aged 20 weeks was significantly higher (p < 0.01) than that in the control. The acetylcholine release from lateral hypothalamus of LEC rats aged 4 weeks was significantly higher (p < 0.05) than that in the control, but no significant difference of acetylcholine release was found between LEC and control rats aged 10 and 20 weeks. The metabolism of serotonin (5-HT) in hypothalamus of LEC rats was facilitated in 20 weeks of age. Furthermore, the 5-hydroxytryptophan, precursor of 5-HT in LEC rats aged 10 weeks was significantly higher (p < 0.05) than that in the control. No significant difference was found in norepinephrine (NE), dopamine (DA), 3, 4-dihydroxyphenyl acetic acid and homovanilic acid concentrations in each age of hypothalamus, except a significant decrease in NE concentration in LEC rats aged 10 weeks (p < 0.05). The daily and total food intake were suppressed in LEC rats from a young age. Furthermore, blood glucose, albumin and total cholesterol concentrations in LEC rats were lower than those in the control rats. The present study demonstrated that age dependent changes in Cu concentration and the metabolism of neurotransmitters related to the regulation of food intake occurred in hypothalamus of LEC rats. These results suggest that suppression of the food intake observed in LEC rats is not only due to hepatitis but also due to suppressive effects of feeding regulation center in central nervous system.
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PMID:Changes in brain neurotransmitters in hypothalamus related to feeding behavior in LEC rat. 875 32

Glucose intolerance is associated with chronic liver disease, particularly cirrhosis, and overt diabetes mellitus is two to four times more common than in the general population. Little attention has been paid to the relationship between the cause of cirrhosis and the development of glucose intolerance or whether cirrhosis is a prerequisite. We found glucose intolerance to be particularly common in patients with chronic hepatitis C, and in this retrospective study we attempt to confirm this possible association. To investigate this question we reviewed the files of 128 patients with chronic hepatitis C and 40 with chronic hepatitis B and active liver disease. Demographic, laboratory, imaging and pathology data were abstracted. The mean fasting blood glucose (+/-SD) in the hepatitis C and B groups was 160 +/- 83 and 103 +/- 18 mg/dl (P < 0.0001) with 2.5% and 39.1% respectively being overtly diabetic (P < 0.00001). However, the mean age of the hepatitis C group was much higher (45.6 +/- 12.5 vs. 60.1 +/- 12.3 years, P < 0.00001). The prevalence of diabetes was much higher among the hepatitis C patients than in the general population. Cirrhosis was not more frequent in biopsies from hepatitis C diabetic patients compared with non-diabetic or hepatitis B patients. Multivariate analysis showed that type of hepatitis and age were significant and independent predictors for developing diabetes. We conclude that there appears to be an association between diabetes mellitus and chronic hepatitis C that is not present in patients with chronic hepatitis B.
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PMID:Diabetes mellitus is associated with chronic hepatitis C but not chronic hepatitis B infection. 875 86

The therapeutic effect of most immunosuppressive agents is unspecific and therefore often limited by an increased risk of infection by viral, bacterial or fungal organisms as well as by an increased incidence of malignant neoplasms. This short review includes the most commonly used immunosuppressants such as corticosteroids, azathioprine, methotrexate, cyclophosphamide and cyclosporine. The most common risks of long-term corticosteroid treatment are Cushing-like changes, decreased glucose tolerance and the usually benign steroid diabetes. Also clinically important is osteoporosis, since it can be prevented by physical training, calcium supplementation and treatment with vitamin D if necessary. Although there is still no proof of a significantly increased risk of peptic ulcer during steroid therapy, patients may develop gastrointestinal hemorrhage and even perforation without producing pain while being treated with corticosteroids. Mineralocorticoid effects, such as salt and water retention, are seen only with hydrocortisone and prednisone, whereas with synthetic steroids such as dexamethasone, sodium retention is absent despite their strong antiphlogistic activity. The most important side effect of the cytotoxic agents azathioprine, methotrexate and cyclophosphamide is marrow suppression. Due to the high turnover of neutrophils, patients most frequently suffer neutropenia rather than thrombocytopenia or anemia. Neutropenia, as well as impaired humoral and cellular immune mechanisms, are responsible for increased susceptibility to bacterial, viral or parasitic diseases during immunosuppressive therapy. Hepatotoxicity has been reported among patients receiving azathioprine (cholestatic hepatitis) and methotrexate (elevated AST levels and, rarely, liver fibrosis or cirrhosis). Cyclophosphamide causes hemorrhagic cystitis in a substantial proportion of patients, as well as an increased incidence of urothelial neoplasms. Both these side effects may be prevented by Mesna. The most important side effects of cyclosporine are acute and chronic nephrotoxicity usually associated with significantly elevated plasma levels of the drug. It must be borne in mind that severe nephrotoxicity may occur in patients receiving cyclosporine and ketoconazole together, since the latter may inappropriately increase the plasma cyclosporine level.
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PMID:[Immunosuppression--a tightrope walk between iatrogenic harm and therapy]. 892 65

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1

The patients with chronic congestive heart failure and acute deterioration of heart failure (pulmonary oedema, significant reduction of blood pressure) have decrease liver's perfusion with signs of acute damage of liver's cells--ischemic hepatitis. Aspat, AIAT and LDH in blood rich very high level. The level of bilirubin, alkaline phosphatase and glucose increase slightly. Hepatotoxic viruses are never observed. The authors described a case of 34 years old man, who two years earlier had large myocardial infarction with aneurysm of heart and congestive heart failure. He was admitted to hospital in shock. The shock was caused probably by overdose of nitroglycerin. In ECG and Echo examinations he had no signs of acute myocardial infarction, but we observed serious damage of liver's cells with very high levels of AspAT, AIAT and LDH. Based on clinical and biochemical examinations we diagnosed ischemic hepatitis. The patient's clinical and biochemical tests were normalized after improvement of heart failure. Biopsy of liver was normal at that time. Prognosis in ischemic hepatitis depends on course of heart failure.
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PMID:[Ischemic hepatitis]. 952 68


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