Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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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)

In the majority of patients with intestinal infarction, it is generally agreed that the occlusion of mesenteric arteries or vein is the primary etiologic factor; however, some showed no evidence of thrombosis, embolization or vasculitis as the causative factor. In many patients, this particular type of infarction is the terminal event of the episode. From October 1977 to December 1986, 24 patients with mesenteric infarction were investigated following cardiovascular surgery in our institute. Among them, 15 were diagnosed with organic vascular occlusion; however, the other 9 showed no evidence of thromboembolism or any other organic vascular occlusive lesion of mesenteric vessels and were diagnosed as non-occlusive mesenteric infarctions. All of these patients were in severe cardiac failure (LOS) postoperatively. There was no typical symptom, although abdominal fullness and diarrhea were the major and consistent findings. In blood chemical analysis, the enzymatic levels such as serum GOT, LDH and CPK were significantly elevated and discrepancy between serum GOT and serum GPT was observed. In this clinical situation, it was difficult to establish a correct diagnosis mainly because of the few signs and symptoms present relating to the mesenteric infarction. On the other hand, when the correct diagnosis was made, these patients were too critically ill to be treated conservatively. The outcome of these patients was grave and all of them died which showed 100% of mortality rate. The conservative management did not produce favorable progress, which accelerated LOS and prevented patients from recovering from cardiac failure. The aggressive surgical approach to this particular type of acute mesenteric ischemia might have offered an improved prognosis from these catastrophic events.
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PMID:[Non-occlusive mesenteric infarction following cardiovascular surgery]. 202 11

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.
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PMID:Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom? 252 Mar 58

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

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80

Among 2175 patients seen over the last three years in a non-specialized department of internal medicine with no intensive care unit, 100 had supranormal serum lactic dehydrogenase activities. These patients' case-reports have been analyzed. Nearly half the patients (47/100) had a malignant disease (cancer or hemopathy). Among the remaining patients, 19 had a hepatic disorder (alcohol hepatitis in 10, viral hepatitis in 8, and isoniazide hepatitis in 1), 7 had a heart disease (heart failure with hepatomegaly in 5, myocardial infarction in 2), and 27 had various other conditions (including hemolysis in 6 and polymyositis en 3). The value of serum LDH assay is obvious in situations other than acute conditions such as myocardial infarction of pulmonary embolism; these are better known and have not been studied here as their prevalence was low among the patients enlisted in our study. In comparison to other enzymes (alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), transaminases (GOT, GPT) that were also routinely assayed in our patients, abnormal serum LDH activities are much less common and their significance is quite different. An increase in serum and their significance is quite different. An increase in serum LDH activity indicates a serious condition, often with a fatal outcome. The "various other conditions" group includes patients with hemolysis, hepatitis and myositis; the other patients in this group either had severe infectious diseases or died suddenly in the first few days of their hospitalization before diagnosis had been established. Each etiologic group has been analyzed to asses the characteristics of patients with increased LDH activity according to each etiology. Analysis of coincident abnormalities of the other enzymes listed above shows marked differences between etiologic groups; diagnostic accuracy can thus be enhanced in certain conditions. Most patients with malignancies had poorly differentiated tumors, with metastases: 28 had an epithelial tumor, with hepatic and/or bone metastases in 23 cases, 5 had cancer of the liver, 10 had a malignant hemopathy (2 lymphomas, 5 myeloproliferative syndromes, 3 acute leukemias), and 4 had a sarcoma. Cancer of the lung is the most common malignancy (10 cases) and may be responsible for increased serum LDH activity even in patients without metastases. Serum LDH assay is of value for monitoring the course in patients with initially increased activities as it falls under effective therapy and rises during exacerbations.
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PMID:[Value and diagnostic significance of serum lactic dehydrogenase in internal medicine (author's transl)]. 628 24

T-1982 (cefbuperazone), a new injectable cephamycin antibiotic, was studied for its antibacterial activity, concentration in serum and urine, penetration into cerebrospinal fluid (CSF) as well as clinical application. The following results were obtained. 1. Antibacterial activity: The susceptibilities of clinically isolated K. pneumoniae, E. coli and E. cloacae to T-1982 were superior to those of CEZ CMZ, and ABPC. T-1982 seemed to be useful for various infections due to Gram-negative rods. 2. Concentration in serum and urine: Subjects were 10 children with congenital heart failure but no abnormal renal and liver functions. T-1982 was given intravenously to 3 groups at 200 mg/kg by one shot (4 cases), 20 mg/kg by 1 hour drip infusion (3 cases) and 10 mg/kg by 1 hour drip infusion (3 cases). The half-lives were 60, 78 and 85 minutes, respectively. 3. Penetration into cerebrospinal fluid: Three children with malignant tumor were injected 20 mg/kg intravenously. A small amount of T-1982 was penetrated into CSF. 4. Clinical efficacy: T-1982 was administered daily 40-116 mg/kg t.i.d. or q.i.d. for 2-14 days to 17 children comprising 1 bronchopneumonia, 1 bronchitis, 4 tonsillitis, 1 lymphadenitis, 1 sepsis, 1 pharyngitis, 1 impetigo, 1 acute sinusitis and 6 pyelonephritis. Clinical efficacy was excellent in 10, good in 2, fair and poor in 3, and the efficacy rate was 70.6%. Bacteriological effect was as follows; eradicated in 9 cases and unknown in 8 cases. As side effect, GOT and GPT elevations unrelated to the drug were observed in 2 cases. Other abnormal findings were not found. T-1982 seems to be safe antibiotic in the field of pediatrics.
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PMID:[Fundamental and clinical studies on T-1982 (cefbuperazone) in the field of pediatrics]. 634 37

Serum guanase activity was measured by a new method using direct colorimetric determination of ammonia in 25 patients with acute myocardial infarction, 21 dogs with experimental myocardial infarction and 6 CCl4-treated dogs, and compared with serum GOT and GPT activity. We found normal serum guanase activity in patients with acute myocardial infarction and in dogs with experimental myocardial infarction without liver damage, even when the serum GOT and GPT activities increased. On the other hand, serum guanase and transaminase activities were elevated significantly in the patients with acute myocardial infarction who had prominent symptoms of cardiac failure and congestion of the liver and CCl4-treated dogs. These findings suggested that the serum guanase activity was more specific than serum GOT and GPT activity as an indicator of liver damage and determination of serum guanase activity in the patients with acute myocardial infarction might be useful in assessing the presence of liver impairment.
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PMID:Clinical and experimental studies of the determination of serum guanase activity in acute myocardial infarction. 723 May 7

Acute idopathic pericarditis can be accompanied by myocarditis, and in all types of acute pericarditis there are electrocardiographic signs of myocardial lesions. In order to determine the severity of the myocardial disease in acute idiopathic pericarditis, a prospective study has been carried out in a group of 25 patients with this diagnosis. The clinical evaluation included phonomecardiographic measurements of the systolic intervals, Weissler index in 24 cases, and echocardiographic study of the left ventricle in eight cases. Besides that, the serum levels of the myocardial enzymes (GOT, GPT, CPK, and LDH and its isoenzymes) were determined in all cases. The results showed a gallop rhythm in 8 percent of the cases, supraventricular arrhythmias in 4 percent, dysfunction of the left ventricle by systolic intervals and/or echocardiography in 32 percent, and increase of the myocardial enzymes in 24 percent, which represents a global incidence of myocardial disease of 44 percent. However, only three patients presented clinical manifestations of myocardial disease, although the congestive cardiac failure was always secondary to cardiac tamponade and not to myocardial failure. The increase of myocardial enzymes can determine important problems of differential diagnosis with an acute myocardial infarction. The clinical course was favourable in all of the cases, including the ones which showed myocardial disease.
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PMID:[Myocardial disease in acute idiopathic pericarditis (author's transl)]. 736 77

To assess the longevity of the liver, arterialized, orthotopic liver grafts were performed using syngeneic male BN/BiRij rats. Young (5-month-old) livers were transplanted into 5-month-old recipients (group I, n = 27), and old (28-month-old) livers were transplanted into 5-month-old rats (group II, n = 28). Recipient survival after transplantation was similar in both groups. The average age of the livers at the time of death was 16.7 months in group I and 39.1 months in group II. Four of the livers in group II survived for more than 4 years (48.1 to 52.4 months). Early deaths (less than 1 year) after transplantation were most commonly caused by biliary obstruction and cholangitis in both groups. Late deaths (more than 1 year) after grafting were mainly from heart failure or tumors. None of the animals died of liver failure or liver disease. Weight gain in the rats, total serum protein levels, and alanine transaminase levels after transplantation did not differ significantly between the two groups. There was a trend for the histological features of aging of the liver-fibrosis, bile duct proliferation, and pigment deposition-to become more prevalent as the livers became very old (mean age, 46 months). Nevertheless, typical aging changes, as individual findings, were absent in nearly half of the oldest organs. The alterations in morphology had no apparent effect on the ability of the livers to sustain the lives of the recipients. The liver of the BN/BiRij rat was capable of surviving far beyond the maximum life span of BN/BiRij rats, and rats in general. It did not become diseased in the process.
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PMID:Assessment of the longevity of the liver using a rat transplant model. 902 57

Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58 +/- 8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Forty-one (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (> 4 mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6 +/- 0.6 vs 2.9 +/- 0.7 gm/dL, respectively; P < 0.05), a longer prothrombin time (13 +/- 6 vs 16 +/- 6 s, respectively; P < 0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P < 0.05) and more patients with ascites (8 vs 50%, respectively; P < 0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9 +/- 4.5 vs 17.1 +/- 4.1 mmHg, respectively; P < 0.01) and a lower systemic vascular resistance (SVR; 1144 +/- 332 vs 1010 +/- 318 dyn.s/cm5, respectively; P < 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5 were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.
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PMID:Gall-bladder wall thickening in patients with liver cirrhosis. 919 2


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