Results obtained in three successive investigations involving various groups of population are presented. In a first study gamma-glutamyltransferase (gammaGT) activity was found to exceed the upper limit of the normal in 70% of the 36 subjects from a rural community in Northern Transylvania who were known by the local physician as being addicted to alcohol since at least five years. In a subsequent study gammaGT activity was determined in 86 patients seeking psychiatric help for a drinking problem. Only 55% of these patients were presenting increased gammaGT values and this finding could be explained by the fact that some of the psychiatric patients were admitted to the clinic for pathological bouts of dipsomania and not because of longstanding chronic intake of alcohol. When studied in connexion with the behaviour of serum triglyceride and alanineaminotransferase (GPT) levels, gammaGT activity was found to be particularly high in hypertriglyceridemic alcoholics and in those presenting a moderate increase of serum transaminases. Population studies emphasized that gammaGT activity exceeded the upper normal limit in 49.2% of the men and in 21.6% of the women working for more than five years in the industry of alcoholic beverages, while an increased activity of this enzyme was detected only in 19% of the men and in 1.7% of the women in a random population.

Adult↗

PubMedDate not supplied

Value of gamma-glutamyltransferase in the diagnosis of liver metastases.

Gamma-glutamyltransferase (gamma-GT) was found to exceed the upper normal limit in 31 of the 32 patients with liver metastases verified during surgery or at autopsy, while the level of this enzyme was normal in 25 of the 28 patients with proven neoplasma but without evidence of metastatic involvement of the liver. Particularly high values of gamma-GT activity were noted in 9 patients in whom liver metastases were accompanied by clinical jaundice. A similar behaviour was noted for alkaline phosphatase but changes affecting this enzyme were less obvious. Thus, for a mean increase of gamma-GT to levels up to seven times the upper normal limit, the level of alkaline phosphatase increased only three times. A decrease of serum pseudocholinesterase occurred in most patients with neoplasma, the process being more evident when liver metastases were present. It is concluded that an increase of gamma-GT in a patient with neoplasma could be considered as a marker of hepatic metastases, if chronic alcoholism or hepatobiliary disease can be excluded.

Clinical Enzyme Tests↗

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Serum lipids and gamma-glutamyltransferase in acute pancreatitis.

Serum cholesterol and triacylglycerol levels as well as gamma-glutamyltransferase and alkaline phosphatase activities were investigated in 40 patients with acute pancreatitis (AcP) and in 46 selected normolipidemic control subjects. Obvious hypertriglyceridemia (HTG) (serum triacylglycerol greater than 3.5 mmol/L) was noted in 11 patients. Preexistent type IV/V hyperlipoproteinemia had been documented in three of these patients years before the attack of acute pancreatitis. A wide individual variation in the decrease rate of the excessively raised triacylglycerol levels as well as the occurrence of intermediate lipoprotein patterns were noted in the days following the acute event in 7 patients who could be serially investigated. Serum gamma-glutamyltransferase activity was increased mainly in patients with associated biliary disease and in patients who admitted being chronic consumers of alcohol. Release of this enzyme from injured pancreatic tissue cannot however be excluded in cases with severe autolytic and necrotic phenomena.

Acute Disease↗

PubMedDate not supplied

[A case of malignant hyperthermia].

Explore the source record for details and available documents.

Adult↗

PubMedDate not supplied

Fibrinolysis in diabetes mellitus. Role of overweight and hypertriglyceridemia.

The variations of dilute blood clot lysis time (DBCLT) in 103 diabetic patients were investigated in terms of insulin dependency, body weight, serum lipids and presence of diabetic vascular diseases. The results showed that DBCLT was significantly longer in the 34 overweight diabetic patients (437 +/- 68 min) than in the 69 diabetics at or below the ideal body weight (240 +/- 28 min) or in the 76 normalipidemic normal weight control subjects (253 +/- 12 min). DBCLT was also longer in the hypertrigliceridemic diabetic patients than in the normolipidemic ones. The mean lysis time was similar in diabetic patients with and without retinopathy. However, a higher level of fibrinolytic inhibitors was found in patients with diabetic small vessel disease. In vitro inhibition of plasma factor XIII by p-chlormercuribenzoate (PCMB) caused an acceleration of DBCLT and the differences between lysis time in the overweight diabetics and in the controls were attenuated. These results suggested that deficient thrombolysis is rather due to overweight and to disturbances of lipid metabolism than to diabets and/or its vascular complications and that enhanced fibrin crosslinking is at least partially responsible for delayed clot lysis.

Adolescent↗

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Antithrombin III in patients with prosthetic cardiac valves.

When compared to 40 control subjects and to 13 patients with mitral stenosis (8 of them commissurotomized) antithrombin III (AT III) activity, assessed by a clotting technique, was found to be slightly but significantly depressed in the 18 patients with prosthetic valves in mitral position. Decrease of AT III level occurred mainly in patients with metallic Björk-Shiley prostheses in whom mitral valve replacement had been performed more than 12 months before the investigation. Particularly low AT III activities were noted in the three patients who developed thromboembolic complications with lethal evolution. Impaired AT III activity in a patient with prosthetic cardiac valves might be considered as a marker of ongoing in vivo activation of coagulation. Such a finding should be a warning and an indication for intensifying the antithrombotic therapy.

Adult↗

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Antithrombin III deficiency in a Romanian family. Pathogenic role of concomitantly increased plasma level of clotting factors VII and X.

Antithrombin III deficiency in a Romanian family is presented. The propositus, a 27 year-old man, had a history of recurrent venous thrombosis and was found to present a plasma antithrombin III level of only 50% of the normal values. His mother and two of his five children had low antithrombin III levels but no episodes of venous thrombosis. In opposition to his family members, the propositus presented overweight, slight hypertriglyceridemia and displayed a high level of clotting factors VII and X. The findings suggest that development of thromboembolic disease in a subject with familial antithrombin III deficiency is enhanced by additional factors, for example by an increased plasma level of vitamin K-dependent clotting factors.

Adult↗

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Behaviour of uricemia in hyperlipoproteinemic subjects.

When compared to values obtained in 40 normalweight normolipemic healthy control subjects, serum uric acid levels were found to be significantly increased in 68 subjects with type II-b and especially in 68 subjects with type IV hyperlipoproteinemia. A much lesser increase of uricemia occurred in 22 patients with type II-a. A significant positive correlation between uricemia and serum triglyceride level could be demonstrated but no such correlation was found with serum cholesterol. Overweight and hypertensive hyperlipemic subjects were presenting higher levels of serum uric acid than normalweight normotensive ones. On the other hand, clinical atherosclerosis and diabetes mellitus had no additive effects upon uricemia in hyperlipoproteinemic patients. It is suggested that hyperinsulinism and accelerated turnover of lipoproteins, often encountered in obese and hypertriglyceridemic subjects, might lead to an enhanced synthesis of purines and subsequently increased production of uric acid.

Adult↗

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Plasma von Willebrand factor and antithrombin III in patients submitted to open heart surgery.

Cardiovascular surgery for valve replacement led to a significant (p < 0.001) increase of plasma von Willebrand factor antigen level from 227% +/- 30.9 (x +/- SEM) recorded before surgery, to 397% +/- 40.7 at the end of the surgical procedure and the levels of this endothelia-derived glycoprotein remained high (427% +/- 38.9) 48 hours later. On the other hand plasma antithrombin III activity decreased from 85.4% +/- 8 before surgery, to 67.0% +/- 6 at the end of the surgical intervention and rose to 81.3% +/- 7, two days later. Lethal outcome occurred in a patient with initial low antithrombin III level (62%). These observations stress the importance of a thorough investigation of hemostatic variables in patients submitted to cardiovascular surgery.

Adult↗

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Plasma protein C and antithrombin III in patients with acute leukemia.

When compared to values recorded in the 32 healthy control subjects, plasma protein C activity was found to be significantly decreased in the 29 patients with acute leukemia and especially in those considered to be in a critical condition. On the other hand, plasma antithrombin III activity did not significantly differ from the values noted in control subjects. The concomitantly occurring high plasma fibrinogen levels and low serum cholinesterase activity were highly suggestive for a switch of hepatic protein synthesis towards the production of acute phase proteins. It is therefore considered that in the absence of a consumption coagulopathy, changes affecting plasma protein C and antithrombin III should be related to a modified pattern of hepatic protein synthesis.

Acute Disease↗

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Antithrombin III deficiency.

Data on clinical features and laboratory diagnosis of familial antithrombin deficiency, a rather heterogeneous group of disorders, are illustrated by observations on two Romanian kindreds afflicted by recurrent thrombotic episodes. In a first family, both plasma antithrombin III antigen and activity were reduced to 50% of normal, a condition characteristic for a heterozygous type I (quantitative) familial antithrombin III deficiency. In a second kindred, the two brothers who had experienced thrombotic events since they were teenagers, displayed exceedingly low AT III heparin cofactor activity (13% and 16% of the normal, respectively) while values around 50% of the normal were recorded in their parents who had not experienced thrombotic episodes. Since plasma antithrombin III antigen and total progressive antithrombin III activity were within normal limits in all the investigated members of this family it was considered that the two brothers were homozygotes or compound heterozygotes and the parents were heterozygotes for a qualitative-antithrombin III deficiency caused by an abnormality of the heparin binding site.

Adolescent↗

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Plasma protein S-antigen (PS:Ag) in selected disease states.

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.

Adult↗

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Plasminogen activator inhibitor (PAI) in obese men and obese women.

When compared to plasma PAI activity noted in selected control normal-weight normolipidemic women (9.36 AU/ml +/- 1.2) and men (13.6 AU/ml +/- 1.96), this inhibitor of fibrinolysis was found to be significantly (p < 0.001) higher in gender-matched obese patients. Obese men younger than 45 years, however, displayed a plasma PAI activity (32.5 AU/ml +/- 5.45) significantly higher (p < 0.01) than that recorded in age-matched obese women (17.8 AU/ml +/- 2.25). No significant difference concerning PAI activity was noted between women older than 45 years (26.4 AU/ml +/- 3.66) and age-matched men (23.8 AU/ml +/- 3.29). High plasma PAI activity was accompanied by an increased resistance of plasma clots to exogenous t-PA induced fibrinolysis. Since PAI depleted plasma clots however displayed a weak resistance to t-PA induced fibrinolysis, it was concluded that plasma PAI may be the main, but not the only factor, responsible for the prolonged plasma clot lysis time in obese subjects.

Adult↗