Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diversion of portal blood in congenital portosystemic shunts (CPSS) results in liver atrophy and passage of toxins into the systemic circulation causing hepatic encephalopathy. In some dogs, there is indirect evidence for hepatic insufficiency, but histologic findings are equivocal. This study determined whether hepatocyte integrity in PSS is comprised at a subcellular level using analytical subcellular fractionation of liver biopsies. Six dogs with CPSS had hypoproteinemia (6/6), increased serum alkaline phosphatase (6/6) and alanine aminotransferase (4/6) activity, hypocholesterolemia (6/6), and decreased blood urea (2/6). Liver biopsy specimens had increased activities (mU/mg protein) of alkaline phosphatase (17.9 +/- 10.1; controls 5.1 +/- 5.3: P less than 0.01), but not of other plasma membrane enzymes. There were increased activities of endoplasmic reticular (neutral alpha-glucosidase: 1.67 +/- 0.7; controls 0.86 +/- 0.2: P less than 0.01) and lysosomal enzymes (N-acetyl-beta-glucosaminidase: 12.6 +/- 2.3; controls 6.24 +/- 2.7: P less than 0.01; alpha-mannosidase: 0.85 +/- 0.5; controls 0.39 +/- 0.3: P less than 0.05). Subcellular fractionation on reorientating sucrose density gradients showed a high-density peak of alkaline phosphatase suggestive of a specific increase in the biliary canalicular component of enzyme activity. Neutral alpha-glucosidase was shifted to denser fractions, indicative of an increase in the proportion of rough-to-smooth endoplasmic reticulum and consistent with enhanced synthesis of membranous enzymes. There was also evidence for increased fragility of intracellular organelles, particularly lysosomes. In contrast, histology showed either no abnormalities or minor degenerative changes compatible with hepatic underperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hepatic organelle pathology in dogs with congenital portosystemic shunts. 161 98

It has been generally accepted that congestive heart failure does not lead to fulminant hepatic failure, unless it is associated with cardiac shock or low cardiac output. Only three cases have been reported, in which liver congestion is followed by fulminant hepatic failure without a history of shock or low cardiac output. Here we present a case of a 48-year-old man with dilated cardiomyopathy and pulmonary infarction, who developed fulminant hepatic failure from congestion. When he was admitted for the control of diabetes mellitus, hepatomegaly of 3-finger breadth and marked cardiomegaly without pulmonary congestion was noted. Diabetes was controlled using insulin. But 3 weeks after admission, he sometimes complained of back dullness because of pulmonary infarction. His heart gradually increased in size, and Jugular venous dilatation and pretibial pitting edema also worsened. Jaundice was noted and serum GOT and GPT increased. A large liver of 6-finger breath below the right costal margin was able to be felt. But within one week, the size of the liver markedly decreased and the signs of hepatic failure such as jaundice, hepatic encephalopathy and numerous petechiae appeared. Blood pressure was maintained and no hypotension or cardiac shock was noted. The patient died of fulminant hepatic failure on the 20th days after onset of the hepatic failure. The autopsy revealed liver atrophy with severe central lobular necrosis, and thrombus in the right main pulmonary artery which caused severe pulmonary infarction. The mechanism of fulminant hepatic failure not accompanied with low cardiac output is discussed.
 ...
PMID:[A case of fulminant hepatic failure secondary to congestive heart failure]. 187 44

Twenty patients with paracetamol(acetaminophen)-induced acute liver damage of varying severity were studied longitudinally with assessment of clinical state, standard liver function tests and radiometric hyaluronate (HYA) assay (Pharmacia). In patients (n = 6) who developed coma, HYA rose rapidly with clinical deterioration to reach a median value of 27,510 micrograms/l, 7 days post-ingestion, which was significantly higher (p less than 0.005) than in patients (n = 7) who exhibited only marked derangement of liver function tests without evidence of encephalopathy, HYA median value of 3240 micrograms/l. These peak values showed no correlation to the peak values of serum alanine aminotransferase (ALT). A third group of patients (n = 7) who were treated with N-acetyl cysteine, did not exhibit any evidence of liver failure and showed no significant rise in levels of HYA or ALT. The data demonstrate that HYA is a rapidly changing marker of liver derangement which appears to follow the clinical course of the patient. The increase to extremely high levels in patients with hepatic encephalopathy, suggests that there is a reversible defect in the hepatic endothelial cell HYA receptor, possibly due to endothelial cell damage or release of toxins from the necrotic liver.
 ...
PMID:Serum hyaluronate as a marker of hepatic derangement in acute liver damage. 191 80

Ten patients with severe chronic type B hepatitis confirmed by liver biopsy were treated with prednisolone for eight weeks and followed up for more than one year. The patients were comprised of 6 males and 4 females, ages 17 to 45 (mean 32) yrs. Serum alanine aminotransferase (ALT) was elevated more than one month before the treatment in all (mean: 379 U/L, range: 87 to 772 U/L). Initial serological tests showed hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) in all and hepatitis B virus DNA (HBV-DNA) in 7/10 (70%). Liver biopsy showed severe chronic active hepatitis with confluent necrosis or acinar hepatitis in all. Prednisolone, 60 mg/day, was administered initially and the dose was tapered every 2 weeks over the 8 weeks period. Two to six months after cessation of treatment, 5 of 10 patients showed a disappearance of HBeAg and serum HBV-DNA and return of serum ALT level to normal (responders). The initial serum ALT level in responders was slightly higher than that of non-responders (mean: 404 vs. 355 U/L), but there was no statistical significance. Among 5 responders, serum HBV-DNA was detected in three patients initially and was transiently detected in one patient during treatment. In non-responders, HBeAg persisted during and after the treatment and serum HBV-DNA persisted in three, but serum ALT was decreased in all. One patient who did not show any clinical or serological improvement, died of jaundice, ascites and hepatic encephalopathy 4 months later.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of short-term prednisolone therapy in patients with severe chronic type B hepatitis. 248 9

The causes and clinical signs of hepatobiliary involvement in disease are many and varied and often are not referable directly to this organ system. Laboratory investigation frequently is necessary to rule hepatic disease in or out, to assess the functional impact on the liver, and to decide whether hepatic disease is the patient's primary problem or a complication of something else. The selection and interpretation of laboratory tests to resolve these problems is based on an understanding of relevant functional anatomy and pathophysiology. The mainstay of such assessment is hepatic enzymology, which can detect active disease in both hepatocytes and the biliary system. The hepatocellular pattern of disease is characterized by increases in leakage enzymes such as SDH, GLDH, and ALT and the cholestatic pattern by increases in induced enzymes (ALP and GGT). In general, enzymology does not allow the intensity or functional effect of hepatobiliary disease to be assessed, and quite severe hepatopathies may have only minimal enzyme abnormalities. For this reason, the primary biochemical data base for ruling hepatobiliary disease in or out always should involve some screening tests of hepatic function, such as albumin, protein, bilirubin, glucose, or urea determinations; as well as urinalysis to search for bilirubinuria and urobilinogenuria in hyperbilirubinemic patients and for ammonium biurate crystals when hyperammonemia or hepatic encephalopathy is suspected. Because the liver synthesizes most clotting factors, evaluation of blood coagulation is indicated when surgery is contemplated on patients with liver disease or when bleeding is present. Paired pre- and post-prandial determinations of serum bile acids are the preferred method for assessment of hepatobiliary function in dogs and cats. However, the BSP clearance test continues to be useful in the functional assessment of the liver as long as the dye remains available to veterinarians. Clearance of BSP is delayed in hepatocellular, cholestatic, and portosystemic disease as well as by severe extrahepatic circulatory disturbances, In general, this functional test is less sensitive than serum bile acids or the ammonia tolerance test in the recognition of hepatic encephalopathy caused by portosystemic anomalies. The objectives of biochemical screening of the liver are to establish the type (hepatocellular, biliary, or mixed), duration (acute, chronic), and stage (aggressive, convalescent) of hepatobiliary disease and to assess functional status.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Biochemical evaluation of the hepatobiliary system in dogs and cats. 267 13

An outbreak of liver disease which killed more than 30 dogs at Alice Springs was associated with feeding meat from horses, some of which had developed Indigofera linnaei poisoning (Birdsville horse disease). Affected livers were small, nodular and yellow. There was associated jaundice, ascites, elevation of alanine aminotransferase levels in serum, a tendency to bleed, and signs of hepatic encephalopathy. Histologically, livers showed periacinar necrosis, collapse and haemorrhage, with severe swelling, vacuolation and cholestasis in remaining hepatocytes. Indospicine, a toxic amino acid found in the genus Indigofera, was detected in samples of suspect horsemeat. Experimental feeding of horsemeat containing 16 mg indospicine/kg for 32 days produced periacinar necrosis and hepatocellular swelling in 2 dogs, although neither died nor showed clinical illness. In another experiment, intakes of as little as 0.13 mg indospicine/kg bodyweight/day for 70 days produced periacinar liver lesions, and indospicine concentrations in serum, muscle and liver rose during this period to 3.9, 7.9 and 17.5 mg/kg, respectively. It was concluded that meat from horses grazing I. linnaei can be hepatotoxic for dogs, and that this toxicity may be related to its indospicine content.
 ...
PMID:Hepatotoxicity to dogs of horse meat contaminated with indospicine. 321 66

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
 ...
PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

We conducted a clinical trial to study the effects of a 10-week course of prednisone therapy and its withdrawal on serum aminotransferase levels and on hepatitis B virus (HBV) markers in patients with hepatitis B surface antigen (HBsAg) positive chronic active hepatitis (CAH-B). Eighteen patients with CAH-B were treated with prednisone, while another 18 patients matched for age, sex, race and sexual preference were followed simultaneously without treatment for the same duration. Nine of 18 prednisone-treated patients became transiently DNA polymerase positive. All nine patients developed a transient rise in serum alanine aminotransferase (ALT) levels of greater than 300 U/L above baseline values, which was associated with a drop in HBsAg levels from a mean of 186 micrograms/ml prior to therapy to 92 micrograms/ml at 6 months following treatment. Six of these patients developed fatigue, anorexia and dark urine, and four also developed either ascites or hemorrhage from esophageal varices, which was accompanied by hepatic encephalopathy. All six of these patients had histologic evidence of CAH with cirrhosis. In comparison, none of the control, untreated patients with CAH-B had any change in either HBV markers or serum ALT levels. Therefore, even a short course of prednisone in patients with CAH-B with cirrhosis is detrimental and its use should be discouraged.
 ...
PMID:Effects of short-term, high-dose prednisone treatment of patients with HBsAg-positive chronic active hepatitis. 388 51

The characteristics of 86 patients with acute non-A, non-B hepatitis were compared to 23 patients with acute hepatitis A and 76 with acute hepatitis B by medical record reviews of patients seen at 5 hospitals in Baltimore, Maryland, as part of case-control study of viral hepatitis. Results of serum aminotransferase levels, bilirubin, albumin, and prothrombin times alone could not distinguish the type of viral hepatitis because of extensive overlap. The alanine aminotransferase range for non-A, non-B hepatitis was 56 to 1819 IU/liters, for hepatitis A 250 to 1995 IU/liters, and for hepatitis B 203 to 2120 IU/liters. The ranges of aspartate aminotransferase and bilirubin for the types of hepatitis also overlapped. Fewer patients with non-A, non-B hepatitis or hepatitis A had a prolonged prothrombin time compared to patients with hepatitis B. Hepatic encephalopathy was seen only in two patients with hepatitis B. Forty-two percent of non-A, non-B hepatitis patients followed for 6 months or longer continued to have elevated alanine aminotransferase levels. Chronic alanine aminotransferase elevation was independent of the source of infection: transfusion, parenteral drug use, or all other sources. Prolonged follow-up is necessary to evaluate chronicity in patients with non-A, non-B hepatitis.
 ...
PMID:Community-acquired non-A, non-B hepatitis: clinical characteristics and chronicity. 642 May 13

Arterial ketone body ratio (AKBR) was continuously measured in 39 cases with hepatic encephalopathy (HE) in order to evaluate the immediate energy charge of the liver and predict the occurrence of HE and its prognosis. The results demonstrated that AKBR in patients before the onset of HE was significantly lower than that in healthy subjects (P < 0.005). AKBR was less than 0.65 when HE occurred. Patients were classified into three groups according to the value of AKBR. Patients in group A had AKBR above 0.7, patients in group B had a transient drop of AKBR to 0.4, and patients in group C had consistently low AKBR value of less than 0.4. The death rates in these three groups were 0, 33.3% (5/15) and 100% (14/14) respectively; the difference was quite significant (P < 0.001). Hepatic functional tests such as alanine transaminase, serum bilirubin, prothrombin time and albumin did not show such difference. Our findings suggest that AKBR can predict hepatic energy charge accurately. Patients whose AKBR value was consistently below 0.4 would have a poor prognosis.
 ...
PMID:[Arterial ketone body ratio as an indicator of energy charge in patients with hepatic encephalopathy]. 776 37


1 2 3 4 5 6 7 8 9 Next >>