PubMed Health⌕ Search

Biomedical subjects

Moses S Elisaf

Publications and source records attributed to Moses S Elisaf.

At least 37 records · Page 2Linked to original sources

Evaluation of methods for the measurement of low-density lipoprotein cholesterol.

A high concentration of low-density lipoprotein cholesterol (LDL-C) in plasma is one of the strongest risk factors for atherosclerotic cardiovascular disease and mortality. The most common approach to determining LDL-C in the clinical laboratory is the Friedewald calculation. There is an increased interest to improve the accuracy of LDL-C estimated by this equation. The expert panel convened by National Cholesterol Education Program has recommended the development of accurate direct methods to measure LDL-C. Several homogeneous and fully automated methods have been introduced in recent years that show improved precision and accuracy over earlier methods, especially the Friedewald calculation. Each of the atherogenic particles in plasma--very-low, intermediate-, and low- density lipoprotein--as well as lipoprotein (a), contain one molecule of apolipoprotein B (apoB) and thus, plasma total concentration of apoB reflects the number of atherogenic particles. Several studies suggested that the measurement of apoB could improve the prediction of risk of coronary artery disease. Thus, in addition to the newly developed direct assays, alternative calculation procedures have been proposed that also take into consideration total serum apoB concentration for the estimation of LDL-C and the presence of small, dense LDL particles. The new generation of homogenous methods for the measurement of LDL-C and the use of serum apoB concentration for the estimation of LDL-C can contribute to the accurate LDL-C determination.

Blood Chemical Analysis↗

A review of the lipid-related effects of fluvastatin.

BACKGROUND: Statin therapy has been shown to significantly decrease vascular events and overall mortality in primary and secondary prevention trials. This review considers the pharmacology, nonlipid-lowering effects and clinical trial evidence of fluvastatin based on a survey of PubMed entries. FINDINGS: Recent clinical data show that treatment with fluvastatin is associated with a variety of benefits in different high-risk populations along with a good safety profile. Fluvastatin exerts non-lipid lowering-associated pleiotropic effects in both clinical and experimental studies. Furthermore, an extended-release formulation of fluvastatin with a favourable pharmacokinetic profile is available. CONCLUSION: Treatment with fluvastatin offers a convenient, safe and evidence-based approach to managing dyslipidaemias and preventing vascular events.

Coronary Artery Disease↗

Therapeutic management of hyperglycaemic hyperosmolar syndrome.

Hyperglycaemic hyperosmolar syndrome is a major acute complication of decompensated diabetes mellitus. It represents the second most common aetiology of diabetic coma and is associated with excess mortality. It is characterised by severe hyperglycaemia, hyperosmolality and dehydration in the absence of significant ketosis, afflicting principally middle-aged-to-elderly patients. Early clinical diagnosis and prompt treatment, consisting of fluid replacement, insulin therapy, restoration of electrolyte disturbances and management of concurrent illnesses may improve the outcome. This review provides an outline of the diagnostic approach of patients with manifestations of hyperglycaemic hyperosmolar syndrome and discusses the contemporary therapeutic recommendations.

Adult↗

Fenofibrate: metabolic and pleiotropic effects.

Disturbances of lipoprotein metabolism represent one of the most important risk factors for vascular events. However, dyslipidaemic patients often have a number of additional abnormalities (such as endothelial dysfunction, hypertension, low-grade inflammation, haemostatic abnormalities and hyperuricaemia) that may accelerate the atherosclerotic process. Thus, the ideal lipid-modifying drug, along with exerting beneficial effects on lipoprotein metabolism, should also improve these coexisting disturbances. Fibric acid derivatives (fibrates) are a class of lipid-modifying drugs mainly used in patients with elevated triglyceride levels. These drugs mainly exert their actions via the activation of specific nuclear receptors called peroxisome proliferator-activated receptors alpha (PPARalpha). In this review, we summarize the current evidence suggesting that fenofibrate, one of the most widely used fibric acid derivatives, along with its well established actions on lipids also exerts several other antiatherogenic actions. Based on recently published studies, fenofibrate is a useful option for patients with primary combined dyslipidaemias or secondary dyslipidaemias, such as those associated with diabetes mellitus, metabolic syndrome or HIV infection. Additionally, in cases of refractory dyslipidaemia, the combination of fenofibrate with statins is a therapeutic option.

Anti-Inflammatory Agents↗

Effect of apolipoprotein E polymorphism on serum uric acid levels in healthy subjects.

BACKGROUND: We have previously shown that apolipoprotein E (apo E-) polymorphism may affect serum creatinine concentration and predicted glomerular filtration rate in healthy individuals. On the other hand, there are limited data regarding the possible influence of apo E- polymorphism on serum uric acid (SUA) levels. METHODS: Two hundred ninety (148 male, 142 female) apparently healthy white individuals were studied. apo E- genotypes, serum lipid parameters including apolipoproteins, insulin resistance using the homeostasis model assessment (HOMA) as a marker, serum and urine creatinine levels, and serum and urine uric acid concentration were determined in all participants. RESULTS: The apo E-2 allele was associated with lower serum levels of total cholesterol, higher levels of triglycerides and apo E-, and increased serum creatinine concentration compared with the apo E-3 and apo E-4 alleles in our population. Furthermore, the apo E-2 allele was associated with higher SUA levels (321.3+/-101.1 micrmol/L [5.4+/-1.7 mg/dL]) compared with the apo E-3 allele (261.8+/-89.2 micromol/L [4.4+/-1.5 mg/dL]; p= .012) and the apo E-4 allele (243.9+/-65.4 micromol/L [4.1+/-1.1 mg/dL]; p= .010), whereas the apo E-2 allele was associated with a nonsignificantdecrease in the fractional renal excretion of uric acid (FEUA) compared with the apo E-3 and apo E-4 alleles (7.9+/-2.2% vs 8.7+/-4.2% vs 8.9+/-5.1%, respectively; p = .53). These observations remained statistically significant when the effect of apo E- polymorphism on SUA levels was adjusted for gender, age, systolic and diastolic blood pressure, body mass index, serum creatinine, and triglyceride and apo E- levels, as well as for HOMA index and FEUA. CONCLUSIONS: Our data provide evidence, for the first time, that the apo E-2 allele is independently associated with increased SUA levels in healthy individuals.

Aged↗

Serum potassium concentration in hyperglycemia of chronic dialysis.

We analyzed abnormalities in serum potassium ([K]) in 40 episodes of diabetic ketoacidosis (DKA)--6 episodes in peritoneal dialysis (PD) and 34 episodes in hemodialysis (HD)--and in 245 episodes of nonketotic hyperglycemia (NKH)--70 episodes in PD and 175 episodes in HD. Serum glucose ([Glu]) was 25 mmol/L or higher in all episodes. We compared the PD and HD hyperglycemic episodes separately for DKA and NKH. For DKA, [Glu] was 55.5 + 4.8 mmol/L in PD and 51.9 +/- 12.2 mmol/L in HD [p = nonsignificant (NS)], and [K] was 6.4 +/- 1.5 mmol/L in PD and 6.3 +/- 1.1 mmol/L in HD (p=NS). Also for DKA, [K] was 5.5 mmol/L or higher in 4 episodes (66.7%) in PD and in 26 episodes (76.5%) in HD (p=NS), and 6.0 mmol/L or higher in 3 episodes (50.0%) in PD and in 22 (episodes 64.7%) in HD (p=NS). For NKH, [Glu] was 39.4 +/- 14.7 mmol/L in PD and 37.8 +/- 12.4 mmol/L in HD (p=NS), and [K] was 4.3 +/- 0.9 mmol/L in PD and 5.1 +/- 0.8 mmol/L in HD (p < 0.001). Also for NKH, [K] was 5.5 mmol/L or higher in 7 episodes (10.0%) in PD and in 55 episodes (31.4%) in HD (p < 0.001), and 6.0 mmol/L or higher in 4 episodes (5.7%) in PD and in 31 episodes (17.7%) in HD (p = 0.023). Serum sodium, tonicity, urea, osmolality, creatinine, chloride and anion gap, and arterial blood pH and partial pressure of carbon dioxide did not differ between PD and HDfor either DKA or NKH episodes, but serum total carbon dioxide content was lower in PD than in HD DKA episodes (6.5 + 3.8 mmol/L vs. 9.5 + 2.8 mmol/L, p = 0.038), and higher in PD than in HD NKH episodes (22.5 + 6.0 mmol/L vs. 20.9 + 4.4 mmol/L, p = 0.004). Although PD and HD DKA episodes appear not to differ in [K], the mean [K] and the frequency of hyperkalemia are both lower in PD than in HD NKH episodes. Differences between PD and HD in acid-base balance and, probably, in other factors affecting [K] (such as mineralocorticoid metabolism and blood levels) may account for the differences in [K] between PD and HD NKH episodes.

Acid-Base Equilibrium↗

Cryoglobulinemic purpura in visceral leishmaniasis.

Visceral leishmaniasis may present with cytopenias along with the formation of many autoantibodies and, rarely, with the presence of mixed cryoglobulinemia, type II, resembling an autoimmune disease. The syndrome of mixed cryoglobulinemia is characterized by the triad of purpura, arthralgias, and asthenia, in conjunction with cryoglobulins in the serum. In this article mixed cryoglobulinemia, type II, was diagnosed in a negative for hepatitis B or C patient suffering from visceral leishmaniasis. Antimicrobial therapy against leishmania eliminated the cryoglobulin titer, as well as the clinical manifestations of cryoglobulinemia. The role of the immune system and the type of immune response for the formation of cryoglobulins are discussed.

Aged, 80 and over↗

Influence of apolipoprotein E polymorphisms on serum creatinine levels and predicted glomerular filtration rate in healthy subjects.

BACKGROUND: There are conflicting results regarding the effect of apolipoprotein (ApoE) polymorphisms on the progression of a variety of renal diseases. However, there are no data on the possible effect of the ApoE alleles on serum creatinine levels and predicted glomerular filtration rate (GFR) in healthy subjects. METHODS: 290 apparently healthy individuals were studied. ApoE genotyping was performed by the polymerase chain reaction; the Modification of Diet in Renal Disease equation (MDRD) predicted the GFR. RESULTS: ApoE2 was associated with lower levels of total cholesterol, low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol, as well as with higher levels of triglycerides in our population. Furthermore, the ApoE2 allele was associated with increased serum creatinine levels compared with both the E3 and E4 alleles (1.04+/-0.13 vs 0.92+/-0.13 vs 0.88+/- 0.11 mg/dl, respectively, P = 0.0077), while the MDRD-predicted GFR was decreased in ApoE2 carriers compared with both E3 and E4 carriers (80.3+/-10.2 vs 88.1+/-9.6 vs 89.3+/-9.7 ml/min/1.73 m(2), respectively, P = 0.031). These observations remained significant statistically even if the effect of ApoE polymorphisms on age- and body-mass index-adjusted serum creatinine and MDRD-predicted GFR was separately analysed in both men and women. Although, ApoE4 carriers tended to exhibit lower levels of serum creatinine and higher values of predicted GFR compared with the E3 carries, these differences did not reach statistical significance. CONCLUSIONS: ApoE2 allele seems to be associated with increased serum creatinine levels and decreased MDRD-predicted GFR in healthy subjects.

Adult↗

Effects of statin treatment on uric acid homeostasis in patients with primary hyperlipidemia.

BACKGROUND: Epidemiologic studies have shown that serum uric acid is a risk factor of coronary artery disease. In addition to fenofibrate, there is some evidence that atorvastatin may have a hypouricemic action, but the underlying mechanisms remain speculative. METHODS: This randomized trial was conducted to investigate the effects of atorvastatin and simvastatin on uric acid homeostasis in patients treated for primary hyperlipidemia. A total of 180 patients were enrolled; patients were randomly assigned to 40 mg/d of either atorvastatin or simvastatin. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment; random urine samples were simultaneously obtained for creatinine, sodium, and uric acid determinations. RESULTS: Baseline serum uric acid levels correlated positively with the body mass index, serum insulin, creatinine, and triglyceride levels and inversely with serum HDL cholesterol levels. Both statins caused a favorable effect on lipids and a significant decrease in fibrinogen and high-sensitivity CRP levels. However, only atorvastatin reduced serum uric acid levels (from 5.6 +/- 1.7 to 4.9 +/- 1.5 mg/dL, P <.0001) by augmenting its urinary fractional excretion (from 10.4% +/- 7.9% to 12.0% +/- 7.4%, P <.01). In a multivariate logistic regression analysis, the reduction of uric acid levels was independently associated with baseline serum uric acid concentration but not to other variables, including lipid parameters (OR, 1.65; 95% CI, 1.14 to 2.40; P =.008). CONCLUSIONS: Atorvastatin (but not simvastatin) significantly lowered serum uric acid levels. This result may be in favor of a preferable choice of atorvastatin for the treatment of hyperlipidemic patients presenting with hyperuricemia.

Atorvastatin↗

Evaluation of alternative calculation methods for determining low-density lipoprotein cholesterol in hemodialysis patients.

OBJECTIVES: To evaluate alternative equations for the estimation of low-density lipoprotein cholesterol (LDL-C) than the Friedewald equation in hemodialysis patients. DESIGN AND METHODS: The equations LDL-C = 0.41TC - 0.14TG + 0.66ApoB - 10.43 and LDL-C = 0.94TC - 0.94HDL-C - 0.19TG were evaluated in 86 patients and compared with the Friedewald equation and the ultracentrifugation procedure. RESULTS: The alternative equations yield significantly lower bias than the Friedewald equation and are less affected by increased triglycerides (TG) levels. CONCLUSION: The alternative equations for LDL-C yield slightly better results than the Friedewald equation especially in hypertriglyceridemia.

Adult↗

The influence of serum apolipoprotein E concentration and polymorphism on serum lipid parameters in hemodialysis patients.

BACKGROUND: Apolipoprotein E (ApoE) polymorphism has been shown to influence serum lipid parameters and ApoE levels in both healthy subjects and hemodialysis (HD) patients. Conversely, ApoE concentration significantly affects serum lipid levels in the general population, independently of ApoE polymorphism, by modulating lipoprotein production, lipolytic conversion, and receptor-mediated clearance. Therefore, studying the effect of ApoE polymorphism on serum lipid levels without taking into account ApoE levels could lead to confounding results. However, such a combined study has not been performed in HD patients to date. METHODS: Three hundred one patients without diabetes on long-term maintenance HD therapy and 200 matched healthy subjects were studied. Determination of levels of fasting serum ApoE and other lipid parameters, as well as common ApoE genotypes, was performed in all subjects. RESULTS: HD patients had a significantly lower prevalence of the epsilon4 allele and greater levels of ApoE compared with the control population. ApoE2 allele carriers had significantly lower levels of ApoB and serum total, low-density lipoprotein, and non-high-density lipoprotein cholesterol, as well as increased ApoE levels. When ApoE levels were included in analysis, ApoE levels themselves were proven to be important determinants of serum lipid levels, whereas the effect of ApoE polymorphism became more pronounced. The combination of these 2 factors explains a much greater percentage of the variation in the studied parameters than each factor alone. CONCLUSION: For the first time, our study provides data to support that ApoE concentration in combination with the ApoE polymorphism significantly influences serum lipid parameters in HD patients.

Aged↗

Hypouricemia in individuals admitted to an inpatient hospital-based facility.

BACKGROUND: Decreased serum uric acid levels resulting from renal urate wasting occasionally are reported in hospitalized patients because of isolated or generalized proximal tubular damage. There are limited recent findings with regard to the incidence and cause of hypouricemia in patients admitted to an internal medicine clinic. The aim of this study is to examine the prevalence of hypouricemia in individuals admitted to our inpatient hospital-based facility and identify underlying causes and pathogenetic mechanisms and any association of hypouricemia and uricosuria with other tubular defects. METHODS: A total of 7,250 serum urate measurements were available on patients' admission. Hypouricemia is defined as a serum urate level less than 2.5 mg/dL (149 micromo/L). In all hypouricemic cases, a detailed clinical and laboratory investigation was performed. RESULTS: Hypouricemia was found in 90 patients (1.24%). In all except one patient, hypouricemia was associated with inappropriate uricosuria (urate fractional excretion [FE] > 10%; range, 10.8% to 94%). There was an inverse correlation between serum uric acid level and its FE (r = -0.73; P < 0.0001). The most common causes of hypouricemia were obstructive jaundice of any cause (n = 18), solid or hematologic neoplasias (n = 17), diabetes mellitus (n = 12), drugs affecting urate homeostasis (n = 10), and intracranial diseases (n = 8). Seventeen patients with hypouricemia showed one or more other manifestations of proximal tubular damage, such as glucosuria, inappropriate phosphaturia leading to hypophosphatemia, and kaliuria resulting in hypokalemia. CONCLUSION: Hypouricemia caused by inappropriate uricosuria is not rare in patients admitted to an internal medicine clinic, is related to underlying diseases, and may be associated with other abnormalities of proximal tubular function.

Blood Glucose↗

Lipid-lowering drugs and serum liver enzymes: the effects of body weight and baseline enzyme levels.

The most important side effects of fibrate and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment are hepatic toxicity and myopathy. Obese individuals may have higher levels of serum transaminases than their lean counterparts. The main purpose of this study was to examine the effects of statins and fibrates on liver enzymes in obese patients and to compare them with their effects on patients with various body mass indexes (BMI). Two hundred and sixty-three hyperlipidemic patients of both sexes aged 31-74 years were studied for 24 weeks. One hundred and three patients received fluvastatin (40 mg/day), 62 atorvastatin (10-20 mg/day), 45 micronized fenofibrate (200 mg/day), 44 ciprofibrate (100 mg/day) and nine patients received gemfibrozil (900 mg/day). Laboratory determinations were performed at baseline, after 8 weeks of treatment and at the end of the follow-up period. At baseline, obese patients tended to exhibit elevated liver enzymes more frequently than their lean counterparts (12 of 105 vs. 5 of 67). At the end of the study period, 11 obese, seven overweight and six lean subjects exhibited elevated liver enzymes. Twelve patients who experienced a moderate elevation of serum liver enzymes at baseline had their liver enzyme profile normalized at the end of the study. Furthermore, in 12 patients who had normal serum liver enzyme levels at baseline, abnormal levels of at least one enzyme were observed after 24 weeks of treatment. Fibrates and statins are safe drugs for the treatment of hyperlipidemia in obese patients as well as in those with moderately increased liver enzymes.

Adult↗

Magnesium homeostasis in patients undergoing continuous ambulatory peritoneal dialysis: role of the dialysate magnesium concentration.

We carried out this retrospective study to examine the magnesium status of our chronic ambulatory peritoneal dialysis (CAPD) patients dialyzed with 0.75 mmol/L (group I) or 0.50 mmol/L (group II) magnesium peritoneal dialysis solution. A total of 34 anuric patients on CAPD (age:31-72 years; duration of CAPD:7-74 months) were studied. None of them received magnesium-containing phosphate binders or vitamin D. Biochemical parameters including magnesium, calcium, phosphate, parathormone, and albumin were measured in all patients. The corrected for hypoalbuminemia serum magnesium concentration in group I was significantly higher compared to that found in group II. However, there were no significant differences in the other measured parameters between the two groups of CAPD patients, though iPTH levels were somewhat increased in group II patients. Serum magnesium levels were weakly correlated with serum prealbumin levels in both groups of CAPD patients (r=0.16, P=0.08 and r=0.17, P=0.07). The incidence of hypermagnesemia was significantly higher in group I patients versus those in group II (13/19 68.4%] vs. 2/15 13.3%], P<0.01). On the other hand, no patient developed hypomagnesemia (corrected total magnesium <0.65 mmol/L), despite the trend toward decreased magnesium levels in group II patients. Our results point out that serum iPTH levels and nutritional parameters, such as prealbumin levels, should be taken into account in the choice of the magnesium concentration of the peritoneal dialysis fluid.

Adult↗

Lipoprotein (a) levels and apolipoprotein (a) isoform size in patients with subclinical hypothyroidism: effect of treatment with levothyroxine.

The increased risk for ischemic heart disease (IHD) associated with subclinical hypothyroidism (SH) has been partly attributed to dyslipidemia. There is limited information on the effect of SH on lipoprotein (a) [Lp(a)], which is considered a significant predictor of IHD. Serum Lp(a) levels are predominantly regulated by apolipoprotein [apo(a)] gene polymorphisms. The aim of our study was to evaluate the Lp(a) levels and apo(a) phenotypes in patients with SH compared to healthy controls as well as the influence of levothyroxine substitution therapy on Lp(a) values in relation to the apo(a) isoform size. Lp(a) levels were measured in 69 patients with SH before and after restoration of a euthyroid state and in 83 age- and gender-matched healthy controls. Apo(a) isoform size was determined by sodium dodecyl sulfate (SDS) agarose gel electrophoresis followed by immunoblotting and development via chemiluminescence. Patients with SH exhibited increased Lp(a) levels compared to controls (median value 10.6 mg/dL vs. 6.0 mg/dL, p = 0.003]), but this was not because of differences in the frequencies of apo(a) phenotypes. There was no association between thyrotropin (TSH) and Lp(a) levels in patients with SH. In subjects with either low (LMW; 25 patients and 28 controls) or high (HMW; 44 patients and 55 controls) molecular weight apo(a) isoforms, Lp(a) concentrations were higher in patients than in the control group (median values 26.9 mg/dL vs. 21.8 mg/dL, p = 0.02 for LMW, and 6.0 mg/dL versus 3.3 mg/dL, p < 0.001 for HMW). Levothyroxine treatment resulted in an overall reduction of Lp(a) levels (10.6 mg/dL baseline vs. 8.9 mg/dL posttreatment, p = 0.008]). This effect was mainly evident in patients with LMW apo(a) isoforms associated with high baseline Lp(a) concentrations (median values 26.9 mg/dL vs. 23.2 mg/dL pretreatment and posttreatment, respectively; p = 0.03). In conclusion, even though a causal effect of thyroid dysfunction on Lp(a) was not clearly demonstrated in patients with SH, levothyroxine treatment is beneficial, especially in patients with increased baseline Lp(a) levels and LMW apo(a) isoforms.

Adult↗