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Query: EC:2.6.1.2 (
alanine aminotransferase
)
26,722
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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
In rabbits with chronic renal insufficiency the
prothrombin
index was increased by 25% and the
alanine aminotransferase
activity decreased by 20%; the results of other routine tests of hepatic function were not affected. The galactose elimination capacity was decreased by 12%, whereas the body clearance of antipyrine was unchanged. No change in hepatocytic structure was found.
...
PMID:Liver function during chronic renal failure in rabbits. 650 10
The plasma values for factors (F)VII, FVIII:C, FVIIIR:Ag, FIX, FX, and FXI and the thrombin clotting time (TCT) were determined for 28 dogs with naturally occurring hepatic disease. The major morphologic type of hepatic disease present in a given dog, as determined by hepatic biopsy and histopathologic examination, was degeneration (12 dogs), inflammation (9 dogs), cirrhosis (3 dogs), or neoplasia (4 dogs). A specific morphologic diagnosis also was made for each dog in the study. Plasma coagulation factor values and screening tests were consistently abnormal in greater than 50% of the dogs with each type of hepatic disease as follows: degeneration--decreased FXI; inflammation--increased FVIIIR:Ag; cirrhosis--shortened TCT, decreased FIX, FX, and FXI, and increased FVIIIR:Ag; and neoplasia--shortened TCT, decreased FVIII:C, and increased FVIIIR:Ag. The plasma coagulation factor values were compared with serum
alanine aminotransferase
(
ALT
) and alkaline phosphatase (ALP) activities, fibrinogen-fibrin degradation product (FDP) concentration, and the
prothrombin
time (PT) and activated partial thromboplastin time (APTT) to determine the sensitivity and specificity of each test in detection of hepatic disease. Of all dogs with hepatic disease, 93% had at least 1 abnormal coagulation test value. The PT and APTT were abnormal in 50% and 75%, respectively, of these same dogs. Increased serum
ALT
and ALP activities were present in 61% and 50%, respectively, and FDP concentrations were increased in 14% of dogs with hepatic disease.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Plasma coagulation factor abnormalities in dogs with naturally occurring hepatic disease. 666 Jun 23
A single oral dose of the lyophilized deathcap fungus Amanita phalloides (85 mg/kg body wt) caused gastrointestinal signs of diarrhea, retching, and vomiting in beagles after a latent period of 16 hr. The pathologic lesions; the increases in serum transaminase (GOT,
GPT
), alkaline phosphatase, and bilirubin, as well as the fall in
prothrombin
time all indicated that liver damage was maximal at about 48 hr after poisoning. Four of twelve dogs given A. phalloides died with signs of hepatic coma within 35 to 54 hr with the biochemical values in the survivors reverting to normal by the ninth day. Silibinin administration (50 mg/kg) 5 and 24 hr after intoxication suppressed the serum changes and the fall in
prothrombin
time. The degree of hemorrhagic necrosis in the liver was markedly reduced, and none of the silibinin-treated dogs died.
...
PMID:Protection by silibinin against Amanita phalloides intoxication in beagles. 671 56
Choice of anaesthetic did not affect packed cell volume, urea or total protein concentration,
alanine aminotransferase
activity or
prothrombin
time. Slightly higher plasma glucose values were obtained after carbon dioxide. All values were well within the laboratory reference ranges.
...
PMID:Comparison between ether and carbon dioxide anaesthesia for removal of small blood samples from rats. 677 47
The authoress presents results of examinations of 228 vinyl chloride exposed workers. Considerable exposure is revealed by 5 cases of acroosteolysis and 45 cases of vascular disturbances in peripheral segments of extremities. The statistical analysis of numerical values of
GPT
, GOT, GGTP, AP, serum Che, bilirubin,
prothrombin
and proteinogram did not show any significant differences between the vinyl chloride exposed group and 70 controls. Of 50 persons in whom additionally BSP test and liver scintigram were performed and half-life of activity decrease was determined after intravenous administration of Bengal rose 131-J, 26 cases of moderate megalohepatia (scintigram) and 9 cases with positive BSP test were found. The half-life of 131-J elimination from blood lasted about 10-26 minutes and did not correlate with BSP test. The authoress draws attention to the lack of reliable and generally accessible methods of early diagnosis of hepatopathy in vinyl chloride exposed workers.
...
PMID:[Difficulties of early diagnosis of liver damage in persons exposed to vinyl chloride]. 731 21
The metabolism and acute hepatotoxicity of styrene oxide were studied after ip administration of a high dose of 375 mg/kg to adult male rats. Liver glutathione was significantly depleted at 2 h, but became normal at 6 h. The activity of serum glutamic-oxaloacetic transaminase was increased during the entire period (24 h) of study, while the activities of alkaline phosphatase and serum
glutamic-pyruvic transaminase
were elevated at 2 and 24 h, respectively, after administration of the dose. Decreased body weights and increased liver weights were observed at 24 h. Both
prothrombin
time and urinary urobilinogen concentration were temporarily increased. While urinary mandelic and phenylglyoxylic acids were increased during the entire time period, urinary (but no fecal) nonprotein sulfhydryl contents were increased at 2 and 6 h. The results of biochemical tests of liver function suggest a mild liver pattern in rats treated acutely with styrene oxide.
...
PMID:Metabolism and acute hepatotoxicity of styrene oxide in rats. 732 98
Thirty four children with tuberculous meningitis were treated with rifampicin (mean, 17 mg/kg/day) and isoniazid (mean, 18 mg/kg/day). Fifteen (44%) showed rise in transaminase GOT and
GPT
values and four cases (11.7%) developed jaundice, hepatomegaly and low
prothrombin
levels. Rifampicin was removed in only nine of these 15 cases with signs of liver disfunction, but complete normalization of liver function and disappearance of symptoms occurred in all cases even when the treatment was not interrupted. Children are more sensitive to hepatic injury during rifampicin and isoniazid combination therapy than adults. Our results indicate very good prognosis for this hepatopathy and suggest that rifampicin need not be withdrawn in the benign situations. Removal of the rifampicin treatment may delay recovery of serious cases of tuberculous meningitis.
...
PMID:[Hepatotoxicity of rifampicin and isoniazid in the treatment of tuberculous meningitis (author's transl)]. 733 8
Reference intervals for
prothrombin
time (PT) and activated partial thromboplastin time (APPT) of undiluted and serial dilutions of citrated platelet-poor plasma were determined for 30 healthy dogs. The PT and APTT were similarly determined for 32 dogs with naturally occurring hepatic disease. Hepatic disease was confirmed by histopathologic examination of hepatic biopsy materials and comprised degeneration (13 dogs), inflammation (11 dogs), cirrhosis (4 dogs), and neoplasia (4 dogs). Coagulation test values were compared with serum
alanine aminotransferase
, alkaline phosphatase, and gamma-glutamyl transpeptidase activities and Bromsulphalein retention for sensitivity in detecting hepatic disease in the dog. Coagulation test results were at variance with reference values in 66% of the 32 dogs with hepatic disease; serum
alanine aminotransferase
, alkaline phosphatase, and gamma-glutamyl transpeptidase were increased in 59%, 72%, and 75%, respectively and Bromsulphalein retention was increased in 22% of the 32 dogs. Thus, the PT and APTT were sensitive indicators of hepatic disease. However, the PT and APTT lacked specificity for any given hepatic disease. The sensitivity of the coagulation tests for detecting hepatic disease was enhanced by using dilutions of citrated platelet-poor plasma. Only 15% of dogs with hepatic disease showed variances from reference values in the coagulation tests done with undiluted plasma, but 66% showed variances in the tests with dilutions of plasma. Coagulation tests were also done in 13 dogs with normal hepatic function amd morphology, but with various extrahepatic diseases: chronic renal disease (5 dogs), dirofilariasis (4 dogs), encephalitis (1 dog), cutaneous disease (2 dogs), and femoral fracture (1 dog). Twelve of the 13 dogs had coagulation test values within the reference intervals.
...
PMID:Alterations of prothrombin time and activated partial thromboplastin time in dogs with hepatic disease. 734 May 74
Frozen section examination was performed on 385 donor livers before transplantation. Exclusion criteria were applied to the donor livers examined to exclude potentially dysfunctional livers. The exclusion criteria included the following: severe macrovesicular steatosis, ischemic necrosis, prominent chronic portal inflammation, prominent periductular fibrosis, granulomatous inflammation, bridging fibrosis, and malignancy. Twenty-seven of the 385 donor livers examined were excluded before transplantation. The following histologic features were present in the excluded livers: severe steatosis (22), ischemic necrosis (2), portal inflammation (1), and periductular fibrosis (2). Steatosis was present in 51 of the 385 (13.25%) organs examined, including 22 of the donor organs excluded before transplantation. Twenty-nine livers with mild to moderate steatosis were implanted into size and blood type-matched recipients. Indicators of allograft function (
prothrombin
time and bilirubin) and damage (aspartate aminotransferase and
alanine aminotransferase
) were measured daily for the first 10 days after transplant. There was no statistically significant difference between the group of nonfat livers and donor livers containing mild steatosis. Statistically significant higher posttransplant serum
alanine aminotransferase
and
prothrombin
time levels were present in the patients with livers implanted with mild versus moderate steatosis. The 1-year survival rate for patients receiving fatty versus nonfatty donor livers was not statistically different (Kaplan-Meier, P = 0.592). No significant differences were found in the clinical and laboratory characteristics of donors whose organs were implanted compared with the clinical and laboratory characteristics of donors whose organs were excluded. The primary nonfunction rate after applying the exclusion criteria was 1.4%, which is a significant decrease compared with our primary nonfunction rate of 8.5% before using frozen section examination. Frozen section examination is useful in excluding donor organs which may become dysfunctional after transplantation.
...
PMID:Frozen section evaluation of donor livers before transplantation. 750 53
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