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Biomedical subjects

M Elisaf

Publications and source records attributed to M Elisaf.

At least 37 records · Page 2Linked to original sources
PubMed2001

Reversible tubular dysfunction that mimicked Fanconi's syndrome in a patient with anorexia nervosa.

Patients with anorexia nervosa exhibit acid-base and electrolyte disturbances. Hypophosphatemia is commonly found in these patients during nutritional recovery. However, marked, possibly, life-threatening hypophosphatemia associated with proximal tubular dysfunction has not been previously described. We report a case of anorexia nervosa complicated by a nonacidotic proximal tubulopathy, which was manifested by renal glycosuria, as well as inappropriate phosphaturia and uricosuria resulting in hypophosphatemia and hypouricemia.

Adult↗
PubMed2001

Characterization and geographic distribution of the low density lipoprotein receptor (LDLR) gene mutations in northwestern Greece.

Familial Hypercholesterolaemia (FH) is a clinical syndrome characterised by elevated serum total cholesterol levels due to an increase in low density lipoprotein (LDL) cholesterol, by tendon xanthomata and clinical manifestations of ischaemic heart disease in early life. Typically, it results from mutations in the low-density lipoprotein receptor (LDLR) gene. So far, over 600 mutations have been reported for the LDLR gene and account for FH. The nature of LDLR gene mutations is different in various ethnicities and has also regional distribution within each ethnicity. Eleven mutations have already been described in the Greek population. This report describes seven LDLR gene mutations accounting for FH in Northwestern Greece (81T>G, 517T>C, 858C>A, 1285G>A, 1352T>C, 1646G>A and 1775G>A) and their geographic distribution. We have recently described one of these mutations (1352T>C) as a novel point mutation in a Greek family originating from Northwestern Greece. Furthermore, two previously identified mutations (81T>C, 1775G>A) were also detected in the Greek FH patients for the first time. The 1775G>A mutation was responsible for all the homozygous patients in our area, indicating a founder effect. These data will favor the development of tailed information and screening programs in Northwestern Greece for the primary prevention of cardiovascular disease in FH patients.

Adolescent↗
PubMed2001

Evaluation of five methods for determining low-density lipoprotein cholesterol (LDL-C) in hemodialysis patients(1).

OBJECTIVES: Current recommendations for the management of dyslipidemia are largely based on the concentration of LDL-C. Most clinical laboratories estimate the concentration of LDL-C by the recommended routine method, the equation of Friedewald, in specimens from fasting subjects and with TG concentrations < 4.52 mmol/L. Because of the limitations of the Friedewald calculation, direct methods for an accurate quantification of LDL-C are needed. DESIGN AND METHODS: In the present study we evaluated the accuracy of the following 5 different procedures for LDL-C in 98 patients on hemodialysis: the Friedewald equation, where LDL-C is calculated from HDL-C, measured either by the precipitation procedure with dextran sulfate-Mg(2+) (Method 1), or by a direct HDL-C assay (Method 2), the Direct LDL assay (Method 3), the homogeneous N-geneous LDL assay (Method 4) and the calculated LDL-C values deriving from the ApoB based equation: 0.41TC - 0.32TG + 1.70ApoB - 0.27, (Clin Chem 1997;43:808-815) (Method 5). RESULTS: All five LDL-C methods were found to be in good agreement with ultracentrifugation/dextran sulfate-Mg(2+) precipitation with the coefficients of correlation of the assays to ranging between 0.93-0.95. However, significant differences in the mean values and biases vs. the reference method were observed. The Friedewald equation and the Direct assay were less affected by high LDL-C levels, and they presented higher sensitivity and higher negative predictive value. The N-geneous assay and the ApoB derived calculation were less affected by high triglyceride levels, and they presented higher specificity and higher positive predictive value. At the diagnostic LDL-C level of 3.37 mmol/L, both Friedewald calculations correctly classified 82/92 patients; Direct assay 86/98; N-geneous assay 88/98; and ApoB derived calculation 88/98. At the diagnostic LDL-C level of 2.98 mmol/L, Friedewald calculations (Method 1 and Method 2) correctly classified 82/92 and 81/92 patients, respectively; Direct assay (LDL-3) 87/98; N-geneous assay (LDL-4) 91/98; and ApoB derived calculation (LDL-5) 91/98. CONCLUSIONS: Among hemodialysis patients, who commonly present "average" LDL-C concentrations and high TG levels, the N-geneous assay and the apoB derived calculation seem to yield more acceptable results for the estimation of LDL-C.

Apolipoproteins B↗
PubMed2001

Metabolic abnormalities in patients with primary open-angle glaucoma.

PURPOSE: Although there are few data on the underlying mechanisms of primary open-angle glaucoma (POAG), it has been suggested that metabolic diseases may play a role in the evolution of the disease. We carried out the present study to investigate the involvement of metabolic disturbances in POAG pathogenesis. MATERIAL/METHODS: Serum metabolic parameters were evaluated in 49 POAG patients without a known history of diabetes mellitus and 72 age and sex matched individuals without glaucoma (control group). RESULTS: Among the metabolic parameters examined, only fasting serum glucose and uric acid levels were found significantly higher in patients with glaucoma compared to the control population (117+/-17 mg/dl vs 105+/-11 mg/dl, p=0.05 and 6.2+/-1.9 mg/dl vs 5+/-1.2 mg/dl, p=0.006, respectively). Additionally, a considerably greater proportion of patients had disturbances of the carbohydrate metabolism and hyperuricemia. CONCLUSION: We conclude that disturbances of carbohydrate and uric acid metabolism could play a role in glaucoma damage and pathogenesis.

Aged↗
PubMed2001

Platelet-associated and secreted PAF-acetylhydrolase activity in patients with stable angina: sequential changes of the enzyme activity after angioplasty.

BACKGROUND: Platelet-activating factor (PAF), the lipid mediator of inflammation and potent platelet agonist, can be hydrolysed and inactivated by PAF-acetylhydrolase (PAF-AH). We investigated the PAF-AH activity in relation to PAF formation in platelets from patients with stable angina undergoing elective percutaneous transluminal coronary angioplasty (PTCA). DESIGN: Twenty-seven patients with stable angina, undergoing PTCA, and 30 age- and sex-matched controls were studied. The platelet-associated and secreted PAF-AH activity was measured, before PTCA, as well as at 4 h, 48 h and 6 months afterwards. PAF formation by thrombin-stimulated platelets and the platelet aggregation responses to PAF and ADP were also determined. RESULTS: The PAF-AH activity secreted by thrombin-stimulated platelets before PTCA (in pmol/10(9) cells/h) was significantly higher compared to controls (892 +/- 222 vs. 624 +/- 144, P < 0.001). The enzyme activity was not altered at 4 h after PTCA, but was significantly increased at 48 h (1284 +/- 312, P < 0.005) to return to the levels observed in the control group 6 months afterwards. Detectable levels of PAF in thrombin-stimulated platelets were found only at 6 months after PTCA. Furthermore, the cell-associated enzyme activity in resting platelets before PTCA was significantly lower compared with controls. Unlike in controls, the platelet-associated enzyme activity in the patient group was not increased after stimulation with thrombin and it was associated by a platelet hyperaggregability to PAF. Both the intact cell-associated activity and the platelet hyper-reactivity to PAF were restored at 6 months after PTCA. CONCLUSIONS: Alterations in the platelet PAF-AH activity, which affect the PAF formation in thrombin-stimulated platelets and are associated by an increased aggregatory response to PAF, are observed in patients with stable angina and are completely restored after PTCA.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2001

Impressive lipid changes following hypolipidaemic drug administration can unveil subclinical hyperthyroidism.

It is well known that thyroid hormones modulate lipoprotein metabolism. Thus, the presence of clinical or subclinical hyperthyroidism may influence lipid parameters of dyslipidaemic patients and the efficacy of hypolipidaemic therapy. Here we present a patient with mixed hyperlipidaemia whose impressive improvement of his lipid profile following ciprofibrate administration pointed towards the diagnosis of asymptomatic underlying subclinical hyperthyroidism.

Cholesterol, HDL↗
PubMed2001

Glibenclamide improves postprandial hypertriglyceridaemia in type 2 diabetic patients by reducing chylomicrons but not the very low-density lipoprotein subfraction levels.

AIM: There are scarce data dealing with the degree of postprandial lipaemia after sulphonylurea administration. The aim of this study was to examine the effect of acute glibenclamide administration on postprandial lipaemia in Type 2 diabetic patients. METHODS: Eight randomly selected Type 2 diabetic individuals, aged 43-65 years (mean, 54 years), who had never received any anti-diabetic drug, were included in the study. Each patient was given a 485 kcal mixed meal (45% fat, 40% carbohydrate and 15% protein) twice on separate days after an overnight fast: once with placebo and once with 5 mg glibenclamide, per os, in a random order. The two tests were performed with an interval of 7 days. Venous blood samples were drawn just before and 2 h, 4 h and 6 h after meal consumption. Total triglyceride levels in plasma, in chylomicrons (CM), in CM-deficient plasma, in very low-density lipoprotein (VLDL) subfractions (VLDL-1, VLDL-2) and in intermediate-density lipoprotein (IDL) were determined. Free fatty acid (FFA) and total cholesterol levels in plasma, as well as high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol levels in CM-deficient plasma, were also measured. Finally, serum glucose, insulin and C-peptide concentrations were measured in each sample. RESULTS: As expected there was a significant decrease in postprandial glycaemia after glibenclamide administration compared to placebo (mean area under the curve values: AUC = 53.3 +/- 18.2 and 69.1 +/- 21.6 mm/h, P = 0.00009). In addition, the mean AUC values of insulin and C-peptide were significantly greater after drug administration. The AUC values of total plasma triglyceride and of CM triglyceride following glibenclamide administration were significantly lower compared to placebo, while the AUC values of postprandial triglyceride in CM-deficient plasma and of postprandial triglyceride in VLDL-1, VLDL-2 and IDL were not different after drug administration compared to placebo. Finally, no significant differences were noted in the AUC values of total cholesterol, LDL cholesterol, HDL cholesterol and plasma FFA levels after glibenclamide administration. CONCLUSIONS: These results demonstrate that glibenclamide administration improves postprandial hypertriglyceridaemia acutely by reducing postprandial triglycerides of intestinal origin.

Adult↗
PubMed2001

Partially reversible renal tubular damage in patients with obstructive jaundice.

Decreased serum uric acid levels resulting from renal urate wasting have been occasionally encountered in jaundiced patients. However, in these cases, there are no data concerning the underlying renal tubular defects. In the present study, we investigated the renal tubular function in 35 patients with obstructive jaundice of various severity and causes (11 with lithiasis, 17 with carcinoma, and 7 with intrahepatic cholestasis). A detailed study of the renal tubular function was performed. Beyond the conventional methods, (1)H-NMR spectroscopy of urine was used to evaluate noninvasively renal damage by the characteristic perturbation in the excretion pattern of low-molecular weight endogenous metabolites. On admission, patients with obstructive jaundice had significantly lower serum uric acid and phosphate levels and higher bile acid concentrations compared with 40 age- and sex-matched controls. Serum uric acid levels presented a negative correlation with the total and direct bilirubin as well as the fractional excretion of uric acid. Furthermore, a great number of the patients studied developed one or more proximal tubular dysfunction manifestations beyond uricosuria, such as renal glucosuria, phosphaturia, and increased excretion of alpha(1)-microglobulin. (1)H-NMR spectroscopy of the urine showed decreased levels of citrate and hippurate and increased levels of 3-hydroxybutyrate and acetate. In 12 patients partial or complete remission of jaundice was followed by an improvement of the proximal renal tubular damage. In conclusion, obstructive jaundice can cause a partially reversible generalized proximal tubular dysfunction.

Adult↗
PubMed2001

Acute pancreatitis-induced hypomagnesemia.

We describe the case of an alcoholic patient admitted to our hospital with alcohol-induced acute pancreatitis who developed severe hypomagnesemia (serum magnesium 0.36 mmol/l) during hospitalization. The underlying pathogenetic mechanisms of hypomagnesemia are discussed.

Acute Disease↗