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Biomedical subjects

Moses Elisaf

Publications and source records attributed to Moses Elisaf.

At least 73 records · Page 4Linked to original sources
PubMed2002

Benign migratory glossitis or geographic tongue: an enigmatic oral lesion.

Benign migratory glossitis, or geographic tongue, is usually an asymptomatic inflammatory disorder of unknown etiology that affects the epithelium of the tongue. Local loss of filiform papillae leads to ulcer-like lesions that rapidly change the color and size. Histopathologic findings parallel the clinical appearance, and may have a psoriasiform pattern. The disorder is characterized by exacerbations and remissions. In most cases, patients do not require treatment other than reassurance about the benign nature of the disorder.

Adult↗
PubMed2002

Atorvastatin preferentially reduces LDL-associated platelet-activating factor acetylhydrolase activity in dyslipidemias of type IIA and type IIB.

Human plasma platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A(2) that is primarily associated with low density lipoprotein (LDL). PAF-AH activity has also been found in high density lipoprotein (HDL), although it has recently been indicated that there is no PAF-AH protein in HDL. Plasma paraoxonase 1 (PON1) is an HDL-associated esterase, which also exhibits PAF-AH-like activity. The effect of atorvastatin (20 mg per day for 4 months) on PAF-AH and PON1 activities in patients with dyslipidemia of type IIA (n=55) or type IIB (n=21) was studied. In both patient groups, atorvastatin significantly reduced plasma PAF-AH activity because of the decrease in LDL plasma levels and the preferential decrease in PAF-AH activity on dense LDL subfractions (LDL-4 and LDL-5). Drug therapy did not affect HDL-associated PAF-AH activity or serum PON1 activities toward paraoxon and phenylacetate in either patient group. However, because of the reduction in LDL cholesterol levels, the ratios of HDL-associated PAF-AH and serum PON1 activities to LDL cholesterol levels were significantly increased after drug administration. The reduction of the LDL-associated PAF-AH activity and the elevation in the ratios of HDL-associated PAF-AH and PON1 activities to LDL plasma levels may represent a new dimension in the antiatherogenic effect of atorvastatin.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2002

Alarming atrioventricular block and mitral valve prolapse in the Kearns-Sayre syndrome.

Kearns-Sayre syndrome (KSS) is a multisystem mitochondrial disorder characterized by the invariant triad: onset before 20, progressive external ophthalmoplegia and pigmentary retinal degeneration, plus at least one of the following: complete (or not) heart block, cereberal dysfunction and CSF protein above 100 mg/dl. Autopsies from patients with KSS revealed widespread tissue distribution mtDNA deletions. These deletions result in significantly lower activities of the enzymes of the respiratory chain. The same deletion of mitochondrial DNA present in skeletal muscle is found in myocardial tissue. An 18-year-old girl diagnosed with the KSS was admitted to our hospital because of an upper respiratory tract infection and dysphagia. ECG showed cardiac conduction defects. The patient had no history of syncope. At her surface ECG there was a complete RBBB (QRS duration approximately 130 ms), a clockwise rotation with an axis of approximately 90 degrees and a slight QT prolongation (420 ms). Echocardiography showed prolapse with thickening and degeneration of both mitral valve leaflets but without mitral regurgitation. The patient was started on a diet rich in potassium and pharmaceutical therapy with magnesium oxide (240 mg of elemental Mg p.o. per day), 1 g of calcium carbonate t.i.d., vitamin D (calcitriol 0.25 microg p.o. per day) and coenzyme Q(10) 100 mg daily and discharged 6 days later with slightly improved biochemical profile but apparent clinical improvement. Urgent pacemaker implantation was decided but unfortunately the patient died due to acute cardiac arrest 10 days later.

Adolescent↗
PubMed2002

Hypokalaemia in alcoholic patients.

Hypokalaemia is commonly found among the electrolyte abnormalities observed in chronic alcoholics. However, the underlying mechanisms of the decreased potassium levels are not well known. We undertook the present study to analyse the possible pathogenetic mechanisms of hypokalaemia in a large group of alcoholic patients (n = 127) admitted to our hospital for causes related to alcohol abuse. Serum potassium levels were significantly lower in alcoholic patients compared to the control population (3.8 + 1.1 mmol/l vs. 4.6 + 0.9 mmol/l). In 12 of these patients inappropriate kaliuresis was observed due mainly to the coexistent hypomagnesaemia. Two of the remaining four patients had a history of diarrhoea, while the other two had alcohol withdrawal syndrome with considerable respiratory alkalosis. Patients with hypokalaemia had hypomagnesaemia and respiratory alkalosis more commonly compared to the normokalaemic ones. We conclude that hypokalaemia is a relatively common electrolyte abnormality observed in alcoholic patients owing to various pathophysiological mechanisms. Among them, inappropriate kaliuresis due to the co-existent hypomagnesaemia predominates.

Adult↗
PubMed2002

Are the effects of tamoxifen on the serum lipid profile modified by apolipoprotein E phenotypes?

BACKGROUND: Tamoxifen has favorable effects on the serum lipid profile. It has been suggested that the apolipoprotein (Apo) E phenotype can influence serum lipid parameters; the ApoE allele 4 (ApoE4) is associated with higher total and low-density lipoprotein (LDL) cholesterol levels. The ApoE phenotype also affects lipid responses to diets or treatment with statins. However, the effect of tamoxifen on the lipid profile in different ApoE phenotypes is unknown. PATIENTS AND METHODS: In the present study, we evaluated the effects of tamoxifen on the serum lipid profile in 11 ApoE4-positive postmenopausal women with breast cancer (phenotypes 3/4 and 4/4) compared with 33 ApoE4-negative women (phenotypes 3/2 and 3/3). Serum lipid parameters [high-density (HDL), LDL and total cholesterol, triglycerides, ApoAI, ApoB and lipoprotein (a)] were measured after an overnight fast before treatment and after 3 and 12 months. ApoE isoforms were determined by isoelectric focusing of delipidated very-low-density lipoproteins (VLDL). RESULTS: During the follow-up period, serum levels of total and LDL cholesterol and ApoB decreased significantly in both groups, but no significant differences were found. Concentrations of serum HDL cholesterol were not significantly different between both groups. However, serum ApoAI levels increased significantly in ApoE4-negative subjects (p = 0.00005), but no significant changes in ApoE4-positive women were observed. Serum triglyceride levels increased by 23.2% (p < 0.05) in ApoE4-positive patients, but they did not change significantly in ApoE4-negative patients. The LDL/HDL cholesterol ratio decreased similarly in the two groups, but the ApoAI/ApoB ratio, which may be a better predictor of cardiovascular events, significantly changed in the ApoE4-negative subjects. Finally, the median level of Lp(a) decreased by 43.4% in the ApoE4-negative patients, whereas it did not change significantly in the ApoE4-positive group. CONCLUSION: In postmenopausal Greek women with breast cancer, the levels of Lp(a) and triglycerides and the ApoAI/ApoB ratio respond more favorably to tamoxifen treatment in ApoE4-negative than in ApoE4-positive patients.

Aged↗
PubMed2002

Multiple metabolic abnormalities in a patient with the syndrome of inappropriate antidiuresis.

The syndrome of inappropriate ADH secretion (SIADH) is a common cause of hyponatremia. However, other metabolic abnormalities have infrequently been described in patients with the syndrome of inappropriate antidiuresis. Here, we describe a female patient with hyponatremia due to SIADH who presented with a cluster of metabolic abnormalities and specifically hypouricemia associated with uricosuria, hypokalemia caused by renal potassium wasting, hypomagnesemia with inappropriate magnesiuria, hypophosphatemia with renal phosphate wasting and inappropriate calciuria. These abnormalities could be partly due to the extracellular volume expansion and were corrected with the water restriction-induced increase in serum sodium levels.

Blood Volume↗
PubMed2002

Hypokalemia due to Fanconi syndrome in a patient with obstructive jaundice.

There are limited data regarding tubular dysfunction in patients with obstructive jaundice. Here, we present a patient aged 79 years with protracted obstructive jaundice due to choledocholithiasis who developed hypokalemia with inappropriate kaliuria as a part of a non-acidotic generalized proximal tubular dysfunction, which included renal phosphate, uric acid and glucose wasting.

Aged↗
PubMed2002

Effect of ciprofibrate on lipoproteins, fibrinogen, renal function, and hepatic enzymes.

AIM: The action of ciprofibrate in hypertriglyceridemic patients is well established. Not only is ciprofibrate able to alter the lipid profile, but it can also change the values of fibrinogen, C-reactive protein, creatinine, transaminases, gamma-glutamyl transpeptidase and serum alkaline phosphatase. However, previous studies focused on the effect of ciprofibrate in hypertriglyceridemic patients, leaving unanswered the question of whether ciprofibrate exerts the same effect on hyperlipidemic patients with normal triglyceride values. The aim of this study is to answer this question. METHODS: In this randomized clinical trial, 64 men and women with elevated cholesterol or triglyceride levels were included. Two subgroups were formed according to triglyceride levels: one (36 patients) with elevated triglyceride levels (> 200 mg/dL [2.26 mmol/L]) and another (28 patients) with normal triglyceride levels (< 200 mg/dL [2.26 mmol/l]). After a 6-week period of step 1 diet according to the National Cholesterol Education Program, ciprofibrate (100 mg once daily) was administered for 16 weeks. Primary efficacy points were the changes of lipid parameters (total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides, apoproteins A1, B, E and lipoprotein [a], high sensitivity C reactive protein, fibrinogen, glucose, insulin, aspartate transaminase, alanine transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase, urea and creatinine levels in a fasting blood sample before and after treatment with ciprofibrate. RESULTS: The subgroup with triglyceride < 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate total cholesterol and low-density lipoprotein cholesterol were reduced by 15% (P < 0.001), and 19% (P < 0.001), respectively, while high-density lipoprotein cholesterol increased by 9% (P = 0.02). Apoproteins B and E levels were reduced by 21% (P < 0.001) and 11% (P = 0.002), respectively. Subgroup with triglyceride > 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate, no significant change in LDL cholesterol levels was observed. Total cholesterol levels were reduced by 15% (P < 0.001) and high-density lipoprotein cholesterol levels were increased by 13% (P = 0.004). Apoprotein B and apoprotein E levels were reduced by 16% (P < 0.001) and 30% (P < 0.001), respectively. Apoprotein-A1 levels were increased by 5% (P = 0.024). In the whole group of patients, the fibrinogen levels fell by 7% (P = 0.043), and the serum creatinine level increased by 10% (P < 0.001). This rise in serum creatinine was more pronounced in patients with low triglyceride levels (15% vs 5%, P = 0.009). Ciprofibrate decreased C-reactive protein levels by 26% in 44 patients who had C-reactive protein measurements (P < 0.001). gamma-glutamyl transpeptidase activity was similarly decreased (by approximately 40%) in both groups of patients. Alkaline phosphatase activity decreased in both groups, a reduction which was greater in hypertriglyceridemics (20% vs 10%, P = 0.004). CONCLUSIONS: Ciprofibrate improved some of the vascular risk factors, such as total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apoproteins A1, B, and E, and fibrinogen levels in both hypertriglyceridemics and normotriglyceridemics. In addition, ciprofibrate raised the serum creatinine and improved the activity of the hepatic enzymes in the plasma in both patient subgroups.

Analysis of Variance↗
PubMed2002

The effects of the addition of micronised fenofibrate on uric acid metabolism in patients receiving indapamide.

OBJECTIVE: Hyperuricaemia is associated with indapamide administration. In contrast, micronised fenofibrate can significantly decrease serum uric acid levels. However, there are no data on the effect of combination therapy of indapamide with micronised fenofibrate on uric acid metabolism. METHODS: We studied 20 non-diabetic hypertensive patients with mixed dyslipidaemia in whom serum metabolic parameters, including uric acid levels in serum and urine, were measured before and after eight weeks of indapamide administration (2.5 mg once daily). This study was continued for a further eight weeks, when the indapamide was combined with micronised fenofibrate (200 mg once daily). RESULTS: Indapamide significantly decreased mean systolic and diastolic blood pressure (BP) from 153 +/- 9/97 +/- 8 mmHg to 138 +/- 8/93 +/- 4 mmHg (p< 0.05 for both comparisons). A significant increase in serum uric acid levels occurred after indapamide administration (from a mean value of 5.6 +/- 1.3 mg/dl (0.33 +/- 0.07 mmol/l) to 6.4 +/- 1.1 mg/dl (0.38 +/- 0.06 mmol/l), p < 0.01]. This effect was associated with a decrease in the fractional excretion of uric acid (from a mean value of 9.5 +/- 5% to 7 +/- 5.5%, p < 0.05). The addition of micronised fenofibrate significantly decreased plasma fibrinogen levels as well as total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B (ApoB) and triglycerides, and increased high-density lipoprotein cholesterol and ApoA, levels. Fenofibrate administration was followed by a significant decrease in serum uric acid levels to 4.7 +/- 1.2 mg/dl (0.28 +/- 0.07 mmol/l), p < 0.01, owing to a substantial increase in fractional urate excretion to 11 +/- 3%, p < 0.01. CONCLUSION: The addition of micronised fenofibrate can correct the hyperuricaemic effect of indapamide administration.

Adult↗
PubMed2002

Combined treatment with fibrates and small doses of atorvastatin in patients with mixed hyperlipidemia.

Combined statin and fibrate therapy is often imperative for the improvement of the serum lipid profile in patients with mixed hyperlipidemia. However, the potential risk of myopathy has limited the widespread use of such therapy. Preferably this treatment should involve low optimally tolerable doses of hypolipidemic drugs. Thus, we undertook a study to determine the safety and efficacy of combination therapy with fibrates and small doses of atorvastatin. Twenty-two patients with mixed hyperlipidemia were started on a fibrate regimen (micronised fenofibrate 200mg/day or ciprofibrate 100 mg/day). Because after 12 weeks of therapy the fibrate failed to normalise the serum lipid profile, small doses of atorvastatin (5 mg/day) were added for a further 12 weeks. The administration of the fibrates resulted in a significant decrease in total and LDL-cholesterol levels, as well as in triglycerides, and an increase in HDL-cholesterol levels. The addition of atorvastatin (5 mg/day) resulted in a further decrease in total and LDL-cholesterol levels. Consequently, the hypolipidemic therapy target was achieved in most of the patents. Combination therapy was well tolerated and no significant increases in serum liver and muscle enzymes were noticed. We conclude that the careful administration of small doses of atorvastatin in patients with mixed dyslipidemia receiving fibrates is associated with a significant amelioration of lipid abnormalities.

Adult↗
PubMed2002

The effect of fluvastatin on plasma fibrinogen levels.

There are conflicting data with regard to the effect of statins, including fluvastatin, on plasma fibrinogen levels. We undertook the present study to examine the influence of fluvastatin (40 mg/day) on plasma fibrinogen levels in hypercholesterolemic non-smoker patients with normal triglyceride levels (< 2.25 mmol/l) (n = 65). Fluvastatin administration was followed by a significant decrease of plasma fibrinogen levels by 8% (from 3.6 g/l to 3.33 g/l median value, p < 0.02). No correlation was found between the change in lipids and that in fibrinogen levels. Furthermore, there was no correlation between plasma fibrinogen levels and the change in fibrinogen concentration after fluvastatin administration. These results are in contrast with previously published data. However, the majority of the previous studies included patients with ischemic heart disease, unlike our study population. Furthermore, in some of these studies, which Included relatively small numbers of patients, there was a trend towards a decrease in plasma fibrinogen concentration after fluvastatin administration. We conclude that fluvastatin can significantly decrease plasma fibrinogen levels. However, more studies using fluvastatin and other drugs of this class are necessary to clarify this issue.

Anticholesteremic Agents↗
PubMed2002

Effects of fibrates on serum metabolic parameters.

Fibric acid derivatives are a class of hypolipidaemic drugs used in the treatment of patients with hypertriglyceridaemia, mixed hyperlipidaemia and diabetic dyslipidaemia. Fibrate therapy results in a significant decrease in serum triglycerides and an increase in high-density lipoprotein (HDL) cholesterol levels. The latest drugs of this class are also effective in lowering low-density (LDL) cholesterol levels and can change the distribution of LDL towards higher and larger particles. The effects of fibrates on lipid metabolism are mostly mediated through the activation of peroxisome proliferator-activated receptors (PPARalpha). A number of angiographic and clinical trials have confirmed that fibrates can slow the progression of atherosclerotic disease and decrease cardiovascular morbidity and mortality. Recently published data suggest that the ability of fibrates to prevent atherosclerosis is not related only to their hypolipidaemic effects but also to other 'pleiotropic effects', such as their anti-inflammatory, antioxidant and antithrombotic effects, as well as their ability to improve endothelial function. Interestingly, fibrates may favourably influence the thrombotic/fibrinolytic system. In fact, most of these drugs can significantly decrease plasma fibrinogen levels and inhibit tissue factor expression and activity in human monocytes and macrophages. Some studies have shown that fibrates can improve carbohydrate metabolism in patients with dyslipidaemia, including diabetic patients. Among fibrates only fenofibrate can significantly decrease serum uric acid levels by increasing renal urate excretion. Fibrates, with the possible exception of gemfibrozil, can significantly increase serum creatinine and homocysteine levels. Finally, a reduction in serum alkaline phosphatase and gamma glutamyltranspeptidase (gammaGT) activity is a well-documented effect of therapy with fibrates. The fibrates are generally well-tolerated drugs with few side-effects. The most important side-effect is myositis, which is observed in patients with impaired renal function or when statins are given concomitantly.

Anticholesteremic Agents↗
PubMed2002

HDL cholesterol levels in patients with molecularly defined familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is the most common genetic disorder leading to premature atherosclerosis. Typically, it is due to mutations in the LDL receptor gene resulting in elevated total and LDL cholesterol levels. The type of the LDL receptor gene mutations may affect the severity of hypercholesterolemia and consequently the incidence of coronary atherosclerosis. Furthermore, high-density lipoprotein (HDL) cholesterol levels have been recently shown to be an independent risk factor for coronary heart disease in this population. We examined the effect of the type of the LDL receptor gene mutations and of common gene polymorphisms possibly affecting HDL metabolism [cholesterol ester transfer protein (CETP), apolipoprotein A-IV (ApoA-IV), angiotensin converting enzyme (ACE), and apolipoprotein E (ApoE)] on HDL cholesterol levels in patients with molecularly defined heterozygous FH who were attending our lipid clinic (n=84). The nature of the LDL receptor gene mutation (81T>G, n=12; 858C>A, n=13; 1285G>A, n=12; 1646G>A, n=22; and 1775G>A, n=25) did not significantly influence HDL cholesterol levels. Unlike other gene polymorphisms, the apolipoprotein (apo) E gene polymorphism did significantly affect these levels. In fact, the presence of the E4 allele was associated with lower HDL cholesterol levels compared to patients not carrying this allele. We conclude that HDL cholesterol levels in heterozygous FH patients may be affected by the apoE gene polymorphism.

Adolescent↗
PubMed2002

Altered distribution of platelet-activating factor- acetylhydrolase activity between LDL and HDL as a function of the severity of hypercholesterolemia.

Platelet-activating factor-acetylhydrolase (PAF-AH) is a lipoprotein-associated phospholipase A2 capable of hydrolyzing platelet-activating factor (PAF) and oxidatively modified phospholipids. We studied the plasma- and lipoprotein-associated PAF-AH activity in patients with primary hypercholesterolemia. Thirty-eight unrelated patients with heterozygous familial hypercholesterolemia (HeteroFH), five patients with homozygous FH (HomoFH), and 33 patients with primary non-FH hypercholesterolemia (NonFH) participated in the study. In all patient groups the plasma PAF-AH activity was significantly elevated compared with 33 normolipidemic controls, the HomoFH having the highest and the NonFH patients showing the lowest enzyme activity. Gradient ultracentrifugation studies showed that this increase is not only due to the elevation in the plasma LDL but also to the increase in the PAF-AH activity associated with each LDL subfraction, being more profound in the small-dense LDL-5. Unlike LDL, no difference in the HDL-associated PAF-AH activity was observed among all groups. Consequently, an altered distribution of enzyme activity among apolipoprotein B (apoB)- and apolipoprotein A-I (apoA-I)-containing lipoproteins is observed in hypercholesterolemic patients, resulting in a significant decrease in the ratio of the HDL-associated PAF-AH to the total plasma enzyme activity compared with controls. This reduction is proportional to the increase of the plasma LDL-cholesterol (LDL-C) levels and consequently to the severity of the hypercholesterolemia. Thus, the ratio of HDL-associated PAF-AH-total plasma enzyme activity may be useful as a potential marker of atherogenicity in subjects with primary hypercholesterolemia.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗