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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemistry, biochemistry, toxicity, and industrial use of monoethanolamine (MEA), diethanolamine (DEA), and triethanolamine (TEA) are reviewed. The dual function groups, amino and hydroxyl, make them useful in cutting fluids and as intermediates in the production of surfactants, soaps, salts, corrosion control inhibitors, and in pharmaceutical and miscellaneous applications. In 1995, the annual U.S. production capacity for ethanolamines was 447,727 metric tons. The principal route of exposure is through skin, with some exposure occurring by inhalation of vapor and aerosols. MEA, DEA, and TEA in water penetrate rat skin at the rate of 2.9 x 10(-3), 4.36 x 10(-3) and 18 x 10(-3) cm/hr, respectively. MEA, DEA, and TEA are water-soluble ammonia derivatives, with pHs of 9-11 in water and pHa values of 9.3, 8.8, and 7.7, respectively. They are irritating to the skin, eyes, and respiratory tract, with MEA being the worst irritant, followed by DEA and TEA. The acute oral LD50s are 2.74 g/kg for MEA, 1.82 g/kg for DEA, and 2.34 g/kg for TEA (of bw), with most deaths occurring within 4 d of administration. MEA is present in nature as a nitrogenous base in phospholipids. These lipids, composed of glycerol, two fatty acid esters, phosphoric acid, and MEA, are the building blocks of biomembranes in animals. MEA is methylated to form choline, another important nitrogenous base in phospholipids and an essential vitamin. The rat dietary choline requirement is 10 mg kg-1 d-1; 30-d oral administration of MEA (160-2670 mg kg-1 d-1) to rats produced "altered" liver and kidney weights in animals ingesting 640 mg kg-1 d-1 or greater. Death occurred at dosages of 1280 mg kg-1 d-1. No treatment-related effects were noted in dogs administered as much as 22 mg kg-1 d-1 for 2 yr. DEA is not metabolized or readily eliminated from the liver or kidneys. At high tissue concentrations, DEA substitutes for MEA in phospholipids and is methylated to form phospholipids composed of N-methyl and N, N-dimethyl DEA. Dietary intake of DEA by rats for 13 wk at levels greater than 90 mg kg-1 d-1 resulted in degenerative changes in renal tubular epithelial cells and fatty degeneration of the liver. Similar effects were noted in drinking water studies. The findings are believed to be due to alterations in the structure and function of biomembranes brought about by the incorporation of DEA and methylated DEA in headgroups. TEA is not metabolized in the liver or incorporated into phospholipids. TEA, however, is readily eliminated in urine. Repeated oral administration to rats (7 d/wk, 24 wk) at dose levels up to and including 1600 mg kg-1 d-1 produced histopathological changes restricted to kidney and liver. Lesions in the liver consisted of cloudy swelling and occasional fatty changes, while cloudy swelling of the convoluted tubules and loop of Henle were observed in kidneys. Chronic administration (2 yr) of TEA in drinking water (0, 1%, or 2% w/v; 525 and 1100 mg kg-1 d-1 in males and 910 and 1970 mg kg-1 d-1 in females) depressed body and kidney weights in F-344 rats. Histopathological findings consisted of an "acceleration of so-called chronic nephropathy" commonly found in the kidneys of aging F-344 rats. In B6C3F1 mice, chronic administration of TEA in drinking water (0, 1%, or 2%) produced no significant change in terminal body weights between treated and control animals or gross pathological changes. TEA was not considered to be carcinogenic. Systemic effects in rats chronically administered TEA dermally (0, 32, 64, or 125 mg kg-1 d-1 in males; 0, 63, 125, or 250 mg kg-1 d-1 in females) 5 d/wk for 2 yr were primarily limited to hyperplasia of renal tubular epithelium and small microscopic adenomas. In a companion mouse dermal study, the most significant change was associated with nonneoplastic changes in livers of male mice consistent with chronic bacterial hepatitis.
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PMID:Toxicology of mono-, di-, and triethanolamine. 895 58

Fibrosing cholestatic hepatitis is a histological variant of hepatitis B virus infection with a high rate of mortality. We describe a patient who acquired acute hepatitis B virus infection 8 months after renal transplantation. Clinical features of rapidly progressive liver failure, indicated by prolonged prothrombin time (57 seconds) and increased bilirubin (40.4 mg/dL) and ammonia (129 mumol/L) concentrations, were accompanied by an extremely high serum HBV DNA level (2.153 x 10(6) pg/mL). Liver biopsy specimen showed fibrosing cholestatic hepatitis with widespread balloon degeneration of hepatocytes, focal hepatocyte loss, bile stasis, periportal fibrosis, mild lymphocytic infiltration, and strongly positive immunohistochemical staining for hepatitis B surface antigen (HBsAg) and hepatitis B core antigen. Lamivudine therapy suppressed HBV DNA to < 10 pg/mL within 4 weeks, which was followed by gradual recovery of liver function from a state of hepatic precoma. Twenty-four months after the onset of hepatitis, the patient had normal prothrombin time and bilirubin, transaminase, and albumin levels. She remained HBsAg positive and hepatitis B e antigen negative. Renal allograft function was stable, with a creatinine level of 1.52 mg/dL. HBV DNA remained suppressed after 22 months of lamivudine therapy. Our experience shows that fibrosing cholestatic hepatitis and liver failure caused by HBV infection can be successfully treated with lamivudine.
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PMID:Treatment of fibrosing cholestatic hepatitis with lamivudine. 964 74

The effect of segmental transcatheter arterial chemoembolization (TAE) on serum amino acid levels and liver function were studied in 23 patients with HCC associated with hepatitis virus C (22 patients) or alcoholism (1 patient), with compensated liver cirrhosis (Child A 18 patients, Child B 5 patients). Serum levels of branched-chain amino acids (BCAA), tyrosine, branched-chain amino acids to tyrosine ratio (BTR), ammonia, total bilirubin and albumin, and prothrombin times were measured before and after TAE (24 h, 7 and 14 days). The BTR was increased significantly 24 h after TAE (p<0.001) and gradually decreased to pre-TAE levels. Serum tyrosine levels decreased at 24 h after TAE (p<0.005) and later increased. Serum BCAA levels increased slightly at 7days after TAE and were decreased at 14 days after TAE. This results indicated that the increased BTR was due primarily to the decreased tyrosine level at 24 h after TAE. Serum ammonia levels gradually decreased after TAE and the prothrombin time and serum levels of total bilirubin and albumin were not significantly changed. In this study, segmental TAE had little influence on liver function, and the BTR unexpectedly increased at 24 h after TAE. These results suggest that segmental TAE has minimal side effects and may have a beneficial effect on amino acid metabolism.
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PMID:Effect of segmental transcatheter arterial chemoembolization on branched chain amino acids and tyrosine ratio in patients with hepatocellular carcinoma. 1102 1

The administration of eplir (a phospholipid-containing hepatoprotector), as well as of the enterosorbents polyphepan and EST-1 (an agent obtained from dry peat extract), to rats with tetrachloromethane-induced hepatitis protect the liver parenchyma against dystrophy, necrosis, and inflammation, reduce hyperfermentemia, decrease the blood bilirubin, ammonia, phenols, and malonaldehyde, and increase the urea content in blood serum, while not fully restoring all these biochemical parameters on the normal level. The treatment of rats with toxic hepatitis by a combination of eplir and enterosorbents is accompanied by a synergistic increase in the therapeutic efficacy of each component, leading to normalization of the biochemical parameters reflecting the functional slate of liver.
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PMID:[Enteric sorbents potentiate hepatoprotective effect of eplir in experimental toxic hepatitis]. 1154 4

Acute liver disease was diagnosed in three pregnant patients: two 30-year-old women had a 'haemolysis, elevated liver enzymes, low platelets' (HELLP) syndrome and acute fatty liver of pregnancy, respectively, and a 20-year-old woman had acute liver failure due to acute hepatitis B. The first two patients had a caesarean section, the third one delivered her child, which died spontaneously shortly after birth at a gestational age of 23 weeks. She was then treated by liver transplantation. All three patients left the hospital in good condition. Liver diseases in pregnancy may be pregnancy-related, e.g. the HELLP syndrome and acute fatty liver of pregnancy, but they may also be coincidental phenomena, e.g. viral hepatitis. The HELLP syndrome is often associated with pre-eclampsia, and presents with epigastric pain and thrombocytopenia with haemolysis. Acute fatty liver disease and acute liver failure due to hepatitis present with liver insufficiency characterised by anorexia, nausea, coagulopathy, hypoglycaemia and elevated serum ammonia levels. Management depends on the diagnosis and the gestational age; pregnancy complicated by acute fatty liver disease should be terminated while pregnancy complicated by the HELLP syndrome early in pregnancy may be maintained to improve the outcome of the foetus. In acute liver failure due to viral hepatitis, termination of pregnancy alone does not affect the disease.
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PMID:[The pregnant patient with acute liver disease]. 1253 8

As reported in the literature, the mortality rates for patients with Acute Hepatic Failure (AHF) approaches 80% in cases in which liver transplantation is not possible. Post-transplant mortality mostly depends on the severity of the neurological condition at the time of the operation (20% in I-II degree coma patients and 44% in III degree coma patients). The primary indications for liver transplantation in AHF are Fulminant Hepatitis (FH)(93%), Subfulminant Hepatitis (5%) and other indications (2%). Other causes of AHF are Primary Non-Function (PNF) and Delayed Function (DF), which occur in 7-10%. Therefore it becomes necessary to monitor the patients with a Liver Support Device to be able to improve the clinical condition of the patients before liver transplantation (LT). In our experience we used the Molecular Adsorbent Recirculating System (MARS) (MARS Monitor; Teraklin AG, Rostock Germany), which enables the selective removal of albumin-bound substances accumulating in liver failure by the use of albumin-enriched dialysate. The system is used as a bridging device to orthotopic liver transplantation (OLT) of patients with FHF. We studied 34 patients, including 16 males and 18 females: 9 were affected by Primary-Non-Function (PNF), nine by Fulminant Hepatitis (FH), six by Delayed-Non-Function (DNF), and ten by Acute on Chronic Hepatic Failure (AOCHF). The average age of the patients was 41.8 years and the average number of applications was 6.4; the median length of application was about eight hours. The parameters that we monitored, before and after each treatment, were neurological status (EEG, cerebral CT, Glasgow Coma Score), haemodynamic parameters, acid base equilibrium, and blood gas analysis. We also monitored hepatic and renal function. In addition, the clinical conditions of the patients were monitored using kidney and liver ultrasound/ultrasonography (US). Inclusion criteria were bilirubin > 15 mg/dL, ammonia > 160 micro g/dL and a Glasgow Coma Score between 6 and 11. The reduction of bilirubin and ammonia were very significant (P < 0.01), whereas the changes of International Normalized Ratio (INR) were not significant. Also the modifications of albumin, total protein, sodium, potassium and calcium were not significant. In conclusion, four out of nine patients with PNF are alive without a second transplantation and were discharged after about 48 days; four out of nine underwent OLT, while one out of nine died; five out of six patients with DF are alive without a second transplantation, and they were discharged after an average time of 55.5 days, one out of six died; six out of nine patients with fulminant hepatitis underwent OLT and four of these are alive, while two died due to sepsis; three patients are alive without OLT. Four patients with AOCHF underwent OLT and are alive, three patients are alive and on a waiting list, two died while on a waiting list and one patient who experienced reactivation of HBV infection during chemotherapy for non-Hodgkin's lymphoma is alive. In spite of the limited number of cases of our study, we believe that MARS can be applied with high tolerance for a very long period of time. In addition, its repeatability allows it to be used in patients with DNF and FH as a bridge to transplant. In patients with DNF, it is used while waiting for complete recovery of the transplanted organ.
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PMID:MARS (Molecular Adsorbent Recirculating System): experience in 34 cases of acute liver failure. 1222 Mar 3

The visual evoked potential (VEP) record in response to a pattern stimulus is a non invasive and reliable method of detecting central and peripheral nerve system abnormalities. VEP recording have been used in animals with fulminant hepatic failure, and also in-patients with hepatic encephalopathy and acute severe hepatitis. Our aims were: a. to evaluate the potency of PVEP in assessing hepatic encephalopathy. b. to find the rate of pathologic PVEP in patients with advanced liver cirrhosis. VEP was recorded in 14 chronic liver cirrhotic patients (6 alcoholic, 6 HCV-related, 2 cryptogenic) and 14 controls. Patients with any neurologic abnormalities were excluded from the study. All patients were subjected to the Mental State Score (MSS) test, and venous blood ammonia was measured on the same day of VEP recording. In 10/14 (71%) patients some VEP recording abnormality was detected. In the cirrhotic patients, P100 latency was significantly longer (P < 0.05) than in controls. Low amplitude was observed in 8 patients compared to controls. Marked increase of N75 (3 patients) and marked increase of N145 (2 patients) were observed. Mean blood ammonia and MSS score were normal in all patients. No correlation was found between both MSS score and blood ammonia levels and the P100 delay. Five out of 10 patients with pathologic VEP developed hepatic encephalpathy during a follow-up of one year, compared to one out of 4 patients with no pathology on VEP recording. VEP recording may be a valuable tool in assessing patients with early hepatic encephalopathy and in predicting encephalopathy.
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PMID:Early detection of hepatic encephalopathy by recording visual evoked potential (VEP). 1253 59

Hepatotoxicity is a serious complication in patients taking HAART. Coinfection with hepatitis viruses increases the risk of liver toxicity while taking antiretroviral therapy. Baseline transaminases should be checked before beginning antiretorviral therapy and all patients should be screened for pre-existing liver disease, most notably hepatitis B and C infections. Regular monitoring of transaminases is mandatory when commencing antiretroviral therapy. In patients with normal liver function, transaminases may be checked monthly after commencing HAART for the first 3 months. If stable this can be broadened to 3 month intervals. In patients with pre-existing liver disease monitoring should be performed more frequently (every 2 weeks) when initiating therapy. Once stable liver enzymes should be checked monthly. The less hepatotoxic drugs such as lamivudine and abacavir should be preferred in patients at high risk for hepatotoxicity. Risks include co-infection with hepatitis B and C viruses, a previous record of hepatotoxicity, cirrhosis, obesity and female gender. Minor enzyme elevations (< 5-fold upper normal limit) are generally safe to tolerate and usually resolve. Patients must be closely observed with regular liver function tests and a hypersensitivity type drug reaction should be excluded. The onset of clinical symptoms, elevated serum lactate or evidence of severe hepatic dysfunction (coagulopathy or elevation of ammonia levels) are suggestive of severe toxicity and HAART should be withheld. Treatment of suspected HAART related hepatotoxicity should first involve withdrawal of therapy. Hypersensitivity reactions may be treated with corticosteroids. Nucleoside-induced mitochondrial damage may improve with riboflavin or thiamine therapy.
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PMID:Hepatotoxicity of antiretroviral therapy. 1287 6

The relation between ammonia intoxication and liver disease is not clear. Ammonia appears to be relatively non-toxic to normal individuals, whereas some patients with liver disease appear to be exquisitely sensitive to dietary protein, ammonia-releasing substances, and ammonium salts. In an attempt to elucidate this relationship the intravenous LD(50) of ammonium chloride was determined in both normal mice and in those with liver disease produced by a variety of means. Parenchymal damage was created by acute and chronic carbon tetrachloride intoxication, a low-protein, lipotrope-deficient diet, and mouse hepatitis virus. Mice in which the portal vein had been partially ligated and those infected with Schistosoma mansoni developed portal-systemic collateral circulation. Groups of these mice were placed on high-protein diets and ammonia drinking water for periods as long as two months. A combination of both parenchymal damage and collateral circulation was induced in mice either by bile duct ligation or by a combination of schistosomiasis and acute carbon tetrachloride intoxication. When the above groups of mice with liver disease were compared with normal control mice in the same weight range, the LD(50) of ammonium chloride showed no striking change.
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PMID:Liver disease and ammonia intoxication. 1399 82

In experiments on 182 white male rats hepatitis was modelled by percutaneous injection of 0.1 ml/500 g of tetrachloromethane (TCM) dissolved in olive oil. TCM was injected every other day for 65 days. After development of hepatitis (in 65 days) synthesis of glutamine and urea, partial oxygen pressure in the liver were studied. It is shown that modelling of chronic hepatitis leads to impairment of glutamine and urea synthesis, reduction of tissue blood flow and oxygen partial pressure. It is suggested that the reason of these changes is inhibition activity of glutamate dehydrogenase, arginase and short-term depression activity of phosphate-dependent glutaminase. The changes in the enzymatic activity lead to lowering tissue level of glutamine, urea, accumulation of ammonia ions. These changes persist for 14 days after the last injection of tetrachloromethane.
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PMID:[The ammonia neutralization function of the liver in chronic active hepatitis]. 1505 75


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