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 middle-aged diabetic woman after four weeks of chlorpropamide treatment developed cholestatic hepatitis with systemic manifestations of idiosyncratic reaction. After recovery, unintended rechallenge with the same drug induced a brisk exacerbation of the symptoms and signs that reversed completely following chlorpropamide withdrawal. Tolbutamide medication was subsequently well tolerated for several weeks, followed by another flare of cholestatic liver lesion and cutaneous eruption with eosinophilia (after each reaction the patient was treated with insulin). Eventually glibenclamide (glyburide) was instituted resulting in very satisfactory control of diabetes, with no untoward reaction.
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PMID:Favorable effects of glibenclamide in a patient exhibiting idiosyncratic hepatotoxic reactions to both chlorpropamide and tolbutamide. 644 88

Most immunologically-mediated diseases are inflammatory in nature, as assessed by cellular infiltrates at the lesion site. Recent immunohistological studies using monoclonal antibodies on tissue sections and synovial or cerebrospinal fluid reveal that B- and T-lymphocytes (predominantly T) participate in this reaction, together with monocytes and macrophages. The etiopathogenesis of inflammatory diseases of immunological origin can be discussed at two levels. (1) Lesions may be secondary to the cytopathic effect of antibodies, either by direct cytolysis or by opsonization, antigenic modulation, or blockage of functionally-relevant molecules. Immune complexes formed in the circulation or locally at the lesion site may intervene. Direct cellular mechanisms are probably involved, as suggested by evidence in hepatitis (indirect) and in juvenile insulin-dependent diabetes (direct). K-cells may act by antibody-dependent cytotoxicity, particularly in autoimmune diabetes and thyroiditis where lymphocyte-dependent antibodies are demonstrated. Unfortunately, the absence of adequate markers does not permit adequate detection of K-cells in inflammatory reaction sites. (2) Etiological factors are multiple in a given disease and even in a single patient. Deficiency of suppressor T-cells, assessed using monoclonal anti T-cell antibodies, represents a major predisposing factor, although suppressor cell deficit may be restricted to some antigens (EBV) in certain patients. The deficiency of interleukin-2 production in lupus and rheumatoid arthritis is intriguing but the mechanism and its relationship to disease etiology are unknown. Other immunological factors include intrinsic B-cell hyperactivity, anti-T-cell auto-antibodies, and complement deficiencies, whereas non-immunological factors such as viruses, drugs or sex hormones are important but ill-defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The immunological basis of inflammatory diseases. 648 71

6 girls, aged 4-16 years, with acanthosis nigricans and hirsutism were studied. Fasting and postglucose hyperinsulinism was present in the 5 older girls. In the youngest, a transitory diabetes with hyperinsulinism was induced by a cortisone therapy for hepatitis. Insulin resistance, suggested by the failure to significantly decrease blood glucose after insulin injection (0.1 U/kg), was demonstrated in three steps: (1) Patient plasma failed to bind 125I-insulin after a 5-day incubation followed by precipitation by antihuman globulin serum. (2) Specific 125I-insulin binding to rat liver membranes was identical in the presence of patient plasma and control plasma. (3) Specific 125I-insulin binding to the erythrocytes of the 6 patients (3.5-7.0%) was significantly lower (p less than 0.01) than in controls (4.5-19.5%). Moreover, the significant correlation present in controls between total binding and reticulocyte counts (r = 0.824, p less than 0.001) was absent in the patients. These data demonstrate further that, in the juvenile type of acanthosis nigricans, insulin resistance which may precede hyperinsulinism is not related to anti-insulin antibodies nor to antireceptor antibodies, but results from a primary defect of insulin receptors.
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PMID:Insulin-specific binding to erythrocytes in 6 girls with acanthosis nigricans. 648 30

Antipyrine-clearance calculated from a single 24 hrs blood sample following i. v. injection of 1 g was determined in insulin dependent diabetics (n = 20), patients with liver cirrhosis (n = 8), with fatty liver + hepatitis (n = 5) and alcoholics with normal liver morphology (n = 3). Antipyrine-clearance values in normal subjects amounted to 58,7 +/- 4,8 ml/min (means +/- s), in cirrhotics to 11,8 +/- 10,1 ml/min (p less than 0.01), in patients with fatty liver to 43,3 +/- 10,1 ml/min (p less than 0.01), and in alcoholics to 62,5 +/- 18,6 ml/min. In diabetics, diseased for many years, also a decrease in the clearance values was seen (41 +/- 17,5 ml/min; p less than 0.05). 15 out of them were below the 2 s range of normal subjects. Thus, the drug-metabolizing capacity in diabetics seems to be markedly reduced, and drug dosage might have to take account of this fact.
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PMID:[Antipyrine clearance as a measure of drug metabolism in patients with diabetes mellitus]. 650 25

The lipid composition of nerves, with and without xanthomatous alteration, and other tissues, was investigated post-mortem in a 36-year-old man with cholestatic hepatitis of unknown cause and insulin-dependent diabetes mellitus (IDDM). Cholesteryl esters were found to be markedly increased in both endoneurium and epi- and perineurium of hepatic nerves (showing xanthomatous change), but not in sciatic nerve (without this change). Cholesteryl ester concentrations were also increased, but to a lesser degree, in kidney tissue. The fatty acid composition of stored cholesteryl esters in hepatic nerve endoneurium revealed that oleic acid was the most favoured substrate for esterification. A widespread depletion of triacylglycerol was also demonstrated in hepatic and sciatic nerves and liver and skin tissues obtained from this patient. This abnormality did not appear to be due to an alcoholic or biliary cirrhosis, or to inanition. Whether the depletion of triacylglycerol is drug-related or represents an endogenous metabolic error remains unclear.
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PMID:Lipid abnormalities of xanthomatous nerves. 672 18

The effects of insulin and glucagon administration on serum amino acid levels were investigated in patients with severe liver disease, since simultaneous injection of pancreatic hormones has been recently introduced as a therapeutic approach. The changes in serum amino acid concentrations, as observed 3 h after ceasing a 3 h infusion of insulin and glucagon in 500 ml glucose solution, were an elevation of serum branched chain amino acid (BACA) levels and of the molar ratio of BCAA/aromatic amino acid (AAA) levels in patients with liver cirrhosis. Similar increases of serum BCAA levels during the infusion were also observed in patients with fulminant hepatitis. The results suggest that insulin-glucagon therapy for severe liver disease has no harmful side effects at least with respect to alterations in the serum aminogram.
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PMID:Effects of insulin and glucagon on serum amino acid concentrations in liver disease. 676 Jun 74

A 47-year-old patient with panlobular emphysema and insulin-dependent diabetes had an alpha-1-antitrypsin phenotype Pi ZZ deficiency. Liver function tests were abnormal, and postmortem examination of the liver demonstrated abnormal intrahepatocytic globules of A1AT (a typical finding when the allele Z is present), but also fibrosis with steatosis. The patient's sister, Pi ZZ, had neither diabetes nor bronchopneumopathy, and no anomalies in liver function. Needle puncture biopsy of the liver had not been conducted. The phenotype Pi ZZ is typically associated with panlobular emphysema in adults, and cholestatic hepatitis in children. From reports in the published literature, it appears that isolated hepatic lesions or those associated with emphysema are rare. The fortuitous association of diabetes and hepatic lesions in this typical case of pulmonary affection in an adult is discussed.
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PMID:[Pulmonary emphysema, hepatic lesions, and insulin-dependent diabetes in a patient with alpha-1-antitrypsin (Pi ZZ) deficiency (author's transl)]. 697 May 36

Early immunoreactive insulin and glucose alterations were studied in the pancreatoduodenal vein of dogs with experimental hepatitis after rapid glucose injection into the pancreatic artery. The blood was collected from the pancreatoduodenal vein every 10 s. In the early period of insulin release the stimulant effect of glucose on insulin secretion was less pronounced in animals with experimental hepatitis as compared with control.
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PMID:[Insulin secretion in dogs with experimental pancreatitis to the intrapancreatic administration of glucose]. 699 61

Twenty-one viral hepatitis patients underwent i.v. glucose tolerance tests during the acute phase of the illness. The results, expressed as the constant of glucose disappearance (Kg), were compared with those of 10 healthy control subjects. When the patients were grouped according to Kg-less than 0.9 or greater than 1.2 min-1-it was found that eight showed a delayed glucose disappearance together with a moderate hypoinsulinemic response (pattern 1). Another eight showed a normal glucose disappearance together with a hyperinsulinemic response (pattern 2). Five patients had intermediate Kg values. High levels of plasma free fatty acids (FFA) were a consistent finding in all patients, indicating that unrestrained lipolysis is an important feature of hepatitis. The extent of decrease in plasma FFA in response to the glucose load was markedly lower in all hepatitis patients than in the control subjects; the rate of decrease was most delayed in the pattern 1 patients. This suggested that the increased FFA availability is an expression of adipose tissue insulin resistance, which, in contrast to glucose disappearance, remains uncompensated by the relative hyperinsulinemia. It may contribute to the diminished peripheral glucose utilization, particularly in pattern 1 patients. We conclude that the different patterns of response in hepatitis may be discerned in one patient group by extending the diagnostic criteria of the glucose tolerance test. In addition to the differences in the magnitude of the peripheral insulin resistance, the main distinction between the two patterns lies in the capacity of the pancreas to adjust insulin secretion in order to maintain normal glucose homeostasis.
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PMID:Patterns of glucose intolerance and free fatty acid behavior in viral hepatitis. 700 83

On 35 patients with acute hepatitis had been carried out intravenous glucose-tolerance-tests (0,5 g glucose/kg). The assimilation coefficient of glucose and the level of insulin were determined during the acute phase of illness and the recovery phase. In 8 cases additionally C-peptide was determined to interpret the regulation of insulin-secretion and hepatic reduction. During the acute phase of illness the glucose-tolerance-test proofed 15 x clearly and 13 x limiting pathological. Except one patient all cases showed an improvement during recovery and 21 x a normalisation of glucose-tolerance. The serum-insulin-analysis gave 28 x lower figures during the acute phase compared to the healing-phase, whereas the determination of the C-peptide showed higher figures matching the enhanced glucose concentrations, which proves a normal regulation of insulin-secretion during the acute phase of disease in hepatitis. Because of the enhanced C-peptide/insulin-index our results support that in the early state of hepatitis the lower insulin figures are caused through a higher insulin clearance of the acute inflamed liver.
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PMID:[The behavior of glucose tolerance, serum insulin and C-peptide in acute viral hepatitis]. 702 Nov 26


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