Biomedical subjects

P Galajda

Publications and source records attributed to P Galajda.

28 records · Page 2Linked to original sources

PubMed1997

[Plasminogen activator inhibitor (PAI-1) and markers of endothelial dysfunction in patients with diabetes mellitus].

The authors examined 25 patients with diabetes mellitus type 2 (NIDDM) without vascular complications, treated by sulphonyl urea preparations, 12 hyperinsulinaemic (HI) non-diabetic subjects and 11 normoinsulinaemic healthy subject s. Patients with NIDDM and HI non-diabetics had significantly elevated PAI-1 levels which correlated with the C-peptide level (r = 0.519, p < 0.001), triacylglycerols (TG) (r = 0.685, p < 0.001), BMI (r = 0.607, p < 0.001) and levels of endothelial markers such as von Willebrand s factor and thrombomodulin (TM). In the group of patients with NIDDM no relationship of PAI-1 and C-peptide was found and a significant correlation was found with TM levels (r = 0.609, p = 0.001) and TG levels (r = 0.476, p = 0.046). The results suggest that the endothelial department has an effect on the regulation of PAI-1 levels in patients with NIDDM.

Adult↗

PubMed1996

[Insulin resistance and pathogenesis of non-insulin-dependent diabetes mellitus (part II)].

A review of the existing views is given, focused on the role of insulin resistance (IR), impaired insulin secretion and reduced suppression of hepatic glucose output and in the pathogenesis of noninsulin dependent diabetes mellitus (NIDDM). Currently, there are two basic theories on the sequence of these defects. Most of the authors suggest that NIDDM is caused primarily by insulin resistance (IR) (which is also considered an earliest detectable defect) with subsequent inability of the pancreas sufficiently compensate for IR. However, some authors suggest that NIDDM results from the abnormal pancreatic beta-cell function (disturbed pulsatility and first-phase of stimulated insulin secretion). These authors consider IR a secondary defect. It seems, that both these theories are well founded. Actually NIDDM is not a single disorder but is rather a syndrome of diverse etiology and pathogenesis. In case of NIDDM with obesity the primary etiopathogenetic role can be rather ascribed to IR. while in non-obese NIDDM subjects the secretory defect is more probable as a primary cause.

Diabetes Mellitus, Type 2↗

PubMed1996

[Hemostasis in patients with diabetes mellitus. I. Markers of endothelial dysfunction].

In the submitted pilot study the authors examined 47 diabetic patients without vascular complications and 15 healthy blood donors. In an aged-matched sub-group the authors confirmed significantly elevated levels of Willebrand factor (vWF) in patients with non-insulin dependent diabetes mellitus (NIDDM), as compared with healthy blood donors, while the thrombomodulin (TM) levels did not differ significantly. The mutual correlation of parameters with calcium-dependent release (vWF, platelet factor PF4 and C-peptide) was confirmed in the group of patients with NIDDM with normal TM values and in the group of blood donors. These findings could be explained by the hypothesis that raised intracellular calcium levels, described already in early stages of diabetes could in diabetic patients participate also in the activation of haemostasis.

Diabetes Mellitus↗

PubMed1996

[Hemostasis in patients with diabetes mellitus. II. Tissue factor and the extrinsic blood coagulation inhibitor].

In the submitted pilot study we examined 37 patients suffering from diabetes mellitus without vascular complications and 15 healthy blood donors. The diabetic patients had not, as compared with the blood donors, significantly elevated values of the tissue factor (TF) and tissue factor pathway inhibitor (TFPI). The TFPI levels correlated with other markers of endothelial dysfunction, in particular thrombomodulin (r = 0.452, p < 0.01) and with triacylglycerol and cholesterol levels. They did not correlate with age, the C-peptide level and BMI.

Adult↗

PubMed1992

[Endogenous digitalis-like substance in relation to glycemia and insulinemia].

The digitalis-like substance (DLS), insulin resistance, and hyperglycemia are ascribed important roles in the pathogenesis of essential hypertension. The relationship between DLS and glycemia (insulinemia) was investigated in the present study. The levels of glycemia, insulinemia and DLS were measured during oral glucose load in a group of 18 subjects with various blood pressure values. Fasting levels of glycemia and insulinemia were in each subject within the physiological range and no correlation was found to exist between the fasting levels of DLS and glycemia (insulinemia). One hour after oral glucose load the increase of glycemia and insulinemia was significantly higher in the group of subjects with SBP > 140 and/or DBP > 90 mmHg than in normotensive subjects (p < 0.001). The increase in glycemia (insulinemia) was followed by a decrease of DLS. This contrary trend could be expressed as a significant inverse correlation between the change in plasma DLS and the change in glycemia (r = -0.660 p = 0.0039), and also between the change in plasma DLS and the change insulinemia (r = -0.687 p = 0.0023). These findings are assumed to suggest certain mechanisms involved in the pathophysiology of essential hypertension. (Tab. 3, Fig. 2, Ref. 20.)

Adult↗

PubMed1992

[Immunologic indicators in ascites].

The authors investigated specific and non-specific immunological parameters in malignant, cirrhotic, cardial and nephrogenic ascites. At the same time bacteriological and cytological examinations of ascites were made. In the submitted paper the authors compare, using statistical methods, immunological parameters of ascites in different patient groups and pay attention to their relationship with positive bacteriological and cytological findings in ascites. The authors recorded the largest number of positive bacteriological cultivation in cirrhotic and malignant ascites which correlates with lower values of some non-specific immunological parameters in ascites.

Antigen-Antibody Complex↗

PubMed1989