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)

A 46-year-old woman, who had been treated with anti-arrhythmic drugs and digitalis for mitral stenosis and paroxysmal atrial fibrillation, suddenly developed severe abdominal pain and nausea. There was tenderness around right CVA. BUN and serum-creatinine were elevated, 57 mg/dl and 4.5 mg/dl respectively. She was in acute renal failure (ARF). WBC, GOT, GPT, LDH were also elevated. Abdominal ultrasonography showed normal-size right kidney (12 cm) and atrophic left kidney (8.5 cm). Selective right renal angiography revealed right renal arterial embolism, suggesting that ARF developed from right renal infarction complicated by left atrophic kidney. Renal scintigram using 99mTc-DTPA indicated non-function type left kidney. Because of the high risk of surgery, she received anticoagulant therapy. Fifteen days later, BUN and serum-creatinine returned to 14mg/dl, 2.2mg/dl, respectively.
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PMID:[A case of acute renal failure due to left contracted kidney, complicated by right renal infarction]. 147 26

In a 40-year-old patient unexplained recurrent attacks of epigastric colic with transient cholestatic icterus occurred over a 9-year period. When the patient was again hospitalised because of progressive pain-free icterus associated with mild pruritus (alkaline phosphatase 900 U/l, direct bilirubin 305 mumol/l, GOT 187 U/l, GPT 103 U/l) sonography revealed liver enlargement to 17 cm, extended intrahepatic bile ducts and an echodense area of about 1 cm size in the region of the bifurcation of the common hepatic duct. Fine-needle puncture did not yield clear cytological findings. Endoscopic retrograde cholangiopancreatography pointed to sclerosing cholangitis. This diagnosis was confirmed by liver punch biopsy. Since the patient did not agree to a liver transplantation, he was treated with 450 mg ursodeoxycholic acid twice daily, resulting in marked reduction of the liver parameters until severe cholangiosepsis and acute renal failure occurred about 4 months later. The septic condition and its complications could not be managed despite thorough intensive-care measures so that a liver transplant had to be performed after all. Histology of the explantate revealed a cholangiocarcinoma in the region of the bifurcation of the common hepatic duct. At first the patient's condition improved markedly but one and half months later the transplant was rejected and the patient died.
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PMID:[Primary sclerosing cholangitis]. 173 82

A 55-year-old man with addiction of alcohol was admitted to our hospital with hematoemesis. After admission, the rupture of esophageal varices was observed and it was treated with endoscopic injection sclerotherapy. On the 3rd hospital day, the patient showed alcohol withdrawal syndrome and therefore haloperidol was administered intramuscularly and intravenously. After a half day of this treatment, high fever, diaphoresis, hypotension, tachycardia, muscular rigidity and tremor developed. With the laboratory data including high serum levels of CK, LDH, GOT and GPT, neuroleptic malignant syndrome (NMS) was suspected. Regardless of intensive care, hepatic failure, DIC and acute renal failure promptly developed, and he died on the 11th hospital day. Neuroleptics may cause serious side effects, such as NMS, when the physical status of patients was deteriorated. Especially in exhausted patient such as our case, even the small dose of neuroleptics caused NMS within short term. Thus, it seemed to be important for clinicians to pay attention to choice of neuroleptics.
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PMID:[A case of neuroleptic malignant syndrome developed in liver cirrhosis patient addicted to alcohol]. 177 76

Biochemical evaluation of 60 patients with crush syndrome developing after the Armenian earthquake demonstrated informative value of some parameters: total blood protein, aspartate and alanine aminotransferase, myoglobin and middle-mass molecules. An aggravation of the disease accompanied acute renal failure and concomitant injuries. The above parameters proved valuable criteria in diagnosis of the clinical alterations.
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PMID:[Clinical-laboratory parallels in crush syndrome]. 178 87

We identified 39 patients with acute cocaine intoxication and rhabdomyolysis over an 8-year period. Twenty-three of the patients (59%) demonstrated biochemical evidence for hepatic dysfunction. Sixteen of these patients had severe liver injury as defined by an alanine aminotransferase (ALT) of greater than 400 U/l (group A). Seven had an ALT between 36-399 U/l (group B) and 16 showed no evidence of liver injury (group C). In contrast to those with normal ALT, the clinical course of the group A patients was more often accompanied by profound hypotension (44 vs. 0%, p less than 0.025), disseminated intravascular coagulation (50 vs. 0%, p less than 0.005), hyperpyrexia (75 vs. 25%, p less than 0.025) and acute renal failure (81 vs. 0%, p less than 0.001). Seven of the group A patients expired (44%). Histologic examination of liver tissue obtained from post-mortem samples demonstrated extensive centrilobular and midzonal necrosis in three cases and panlobular necrosis in two others. A mild lymphocytic infiltrate with bile duct proliferation was present in each specimen. We conclude that cocaine intoxication can be accompanied by liver dysfunction which is most likely multifactorial; the presence of severe dysfunction identifies a patient with potentially significant morbidity and mortality.
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PMID:Hepatic dysfunction accompanying acute cocaine intoxication. 194 Feb 59

An autopsy case of rhabdomyolysis following homicidal intoxication of paraphenylenediamine was reported and the toxicological mechanism of PPD against skeletal muscles was discussed. The case was a 44 years old, previously healthy male, drinking a beverage containing PPD, prepared for a homicidal use. Total intake of PPD was about 3 g (63 mg/kg). Principal clinical manifestation of the patient was muscle rigor with tenderness, initially developed in the lower extremities and subsequently extending to all over the skeletal muscles. Laboratory examinations disclosed high CPK (137,600), LDH (3895), GOT (3400) and GPT (545), and leukocytosis (26600), indicating massive skeletal muscle necrosis. ECG revealed mild depression of ST junction in the II and aVF leads. Urine showed dark brownish discoloration and diminished in volume subsequently. Scattered necrosis of muscular fibers was observed in a biopsy of the femoral muscles. The consciousness was rather clear during the course. The patient collapsed suddenly and soon died in the course of about 30 hours. Clinically, the cause of death was thought to be acute renal failure due to rhabdomyolysis. Afterwards PPD was detected in the urine obtained in the hospital. Autopsy confirmed the clinical diagnosis: Renal collecting ductules and distal tubules were occluded by dark brownish myoglobin casts and its epithelium massively necrotized; Skeletal muscles showed scatteredly coagulation necrosis and were partially associated with inflammatory cell infiltration.
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PMID:[Rhabdomyolysis due to paraphenylenediamine (hair dye)--report of an autopsy case]. 207 68

Nine G-6-PD subjects developed acute hemolysis and severe hyperbilirubinemia (up to 61.1 mg/dl) following viral hepatitis. All except one had fever at presentation. Neutrophilic leukocytosis was a common feature. Elevation of both alanine aminotransferase (SGPT) and extremely high level of aspartate aminotransferase (SGOT) were prominent. Three developed acute renal failure. All patients survived, one after peritoneal dialysis. Recognition of the clinical picture is essential to prevent serious complications and for successful management.
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PMID:Severe hyperbilirubinemia in glucose-6-phosphate dehydrogenase deficient patients during viral hepatitis. 228 Feb 2

Hepatic dysfunction was observed in 34 patients with nontraumatic rhabdomyolysis. The serum levels of lactic dehydrogenase were markedly elevated in all patients. The peak values occurred within 72 h of hospitalization. There was no significant difference among patients with (9,044 +/- 1,154 U/l) and without acute renal failure (ARF; 9,125 +/- 3,067 U/l). Similarly, marked elevation in both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were observed within 72 h after admission to the hospital. They were significantly higher in patients with ARF (ALT: 4,718 +/- 785 vs. 2,496 +/- 927 U/l, p less than 0.01; AST: 3,635 +/- 820 vs. 1,352 +/- 624 U/l, p less than 0.01). Hyperbilirubinemia was noted in 13 of 22 (60%) patients with ARF and in 5 of the 12 (41%) of those without ARF. Serum levels of bilirubin ranged from 2.6 to 14.3 mg/dl. Prothrombin time was prolonged in 4 of 12 (33%) without ARF and in 14 of 22 (63%) of patients with ARF. This abnormality lasted from 1 to 13 days. The magnitude and duration of hyperbilirubinemia and abnormal prothrombin time were similar in patients with and without ARF. Hepatic dysfunction appears to occur in about 25% of patients with rhabdomyolysis. The pathogenesis of these abnormalities is not well defined and may be multifactorial. Hyperpyrexia, hypotension and proteases released from injured muscle may each or all be contributory. These hepatic derangements are reversible.
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PMID:Reversible hepatic dysfunction associated with rhabdomyolysis. 234 80

A 24-year-old woman was admitted to our hospital with acute paracetamol poisoning, and severe hepatic injury. The peak blood level of GOT, GPT and LDH were 32,600 U, 119,200 U and 36,500 U respectively. Glucagon-insulin and glutathione were administered to save the liver function. On the third hospital day, hemodialysis was administered to treat acute renal failure. On the 16th hospital day, when the liver and renal functions recovered, severe pulmonary congestion occurred and right heart catheterization revealed high pulmonary pressure. Echocardiography showed left ventricular enlargement accompanied by a severe diffuse impairment of left ventricular wall motion. Multi-focal ventricular arrhythmia was frequent during this period. Hemodialysis and artificial respiration were carried out for the treatment of heart failure. Three months after admission, myocardial perfusion scintigram showed patchy reduction in the uptake of Tl-201 throughout the myocardium, and left ventriculography showed mild diffuse impairment of the LV wall motion (ejection fraction: 49%). In this case, acute heart failure appeared approximately 2 weeks after the severe hepatic injury. Apparently myocardial damage following paracetamol overdosage is caused not only by direct toxicity but by severe metabolic derangement.
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PMID:A case of myocardial damage following acute paracetamol poisoning. 252 40

Cardiac output (CO), renal blood flow (RBF) and hepatic blood flow (HBF) were measured by the microsphere method before (control) and at 4 and 10 h after the induction of acute renal failure by intramuscular injection of glycerol in water-drinking, long-term saline-drinking and long-term captopril (converting enzyme inhibitor)-drinking rats. At 4 h after glycerol injection, CO, RBF and HBF significantly decreased in all three groups. At 10 h after glycerol injection, CO, RBF and HBF recovered to 88% of the respective control levels in only the saline-drinking rats, whereas CO, RBF and HBF further decreased to 53, 38 and 58% of the control levels, respectively in the captopril-drinking rats. At this time, not only acute renal failure but also hepatic disorder developed in the water-drinking and captopril-drinking rats as indicated by elevations of serum creatinine, urea nitrogen, alanine aminotransferase and other blood chemistry levels. The development of acute renal failure was not suppressed by captopril, but by long-term saline load. Thus, we conclude that the decrease in CO is an important variable of the early decrease in renal and hepatic perfusion in glycerol-induced acute renal failure, and that the early recovery of HBF as well as RBF may play an important role in preventing the development of acute renal failure.
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PMID:Cardiac output, renal blood flow and hepatic blood flow in rats with glycerol-induced acute renal failure. 260 3


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