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Migdal Ha‘Emeq, Israel

Saliba W.,ek Medical Center
Harefuah | Year: 2012

Anemia is common in diabetes. The role of hepcidin in diabetic anemia is unknown. To assess the relationship between serum hepcidin and anemia in diabetic patients without renal failure. We prospectively studied 86 consecutive type II diabetic patients--39 with anemia (cases) and 47 without anemia (controls). Patients with renal failure, iron and vitamin B12 deficiency and chronic inflammatory diseases were excluded. Univariate analyses showed that patients with anemia were older and had longer duration of diabetes compared to patients without anemia (P < 0.051). The median hepcidin level was 15 ng/mL (2-140 ng/ml) in patients with anemia compared to 14 ng/mL (2-128 ng/ml) in patients without anemia (P = 0.386]) Serum erythropoietin and creatinine levels were higher in patients with anemia compared to patients without anemia (P < 0.05). Patients with anemia had tower HbA1c levels (P = 0.035), and greater usage of anti-diabetic drugs; metformin 73% versus 46.8% (P = 0.016), and sulfonylurea 47.2% versus 19.1% (P = 0.006). After adjusting for age, the two groups still differed in duration of diabetes (P = 0.043), erythropoietin (P = 0.007) creatinine (P < 0.001), and usage of metformin, sulfonylurea and insulin (P < 0.05). Subjects with diabetic anemia have Longer diabetes duration than subjects with diabetes without anemia. Based on the results of this small study, hepcidin was not associated with diabetic anemia. Source


Saliba W.,Technion - Israel Institute of Technology | Saliba W.,ek Medical Center | Barnett-Griness O.,Technion - Israel Institute of Technology | Rennert G.,Technion - Israel Institute of Technology
European Journal of Internal Medicine | Year: 2013

Background Few studies examined the relationship between obesity and urinary tract infection (UTI), showing inconsistent results. This study aims to examine the association between obesity and UTI, and to assess whether this association is independent of diabetes mellitus and 25(OH)D level. Methods Using the computerized database of the largest healthcare provider in Israel, we identified a cohort of subjects ≥ 18 years old with available BMI and serum 25(OH)D level measurements between January 2009 and December 2009. The cohort was followed for the first UTI diagnosis from January 2010 through June 2011. Cox proportional hazard model was used to test the relationship between obesity and UTI. Results During follow-up, 25,145/110,736 (22.7%) females, and 4032/42,703 (9.4%) males had UTI. The crude HR for UTI in those with BMI ≥ 50 compared to BMI < 25 was 2.54 (95% CI, 1.50-4.30) in males and 1.39 (1.14-1.69) in females. After adjusting for age, 25(OH)D level, and history of diabetes mellitus, the HR for UTI in those with BMI ≥ 50 compared to BMI < 25 was 2.38 (1.40-4.03) in males and 1.25 (1.03-1.52) in females. The HR for those in the lowest quartile of serum 25(OH)D compared to the highest quartile was 1.23 (1.13-1.35) in males and 0.98 (0.95-1.02) in females. The HR for subjects with diabetes was 1.23 (1.16-1.32) in males, and 1.25 (1.20-1.28) in females. Conclusions Obesity is independently associated with UTI particularly in males. Low serum 25(OH)D levels are associated with increased risk of UTI in males. © 2012 European Federation of Internal Medicine. Source


Saliba W.,Technion - Israel Institute of Technology | Saliba W.,ek Medical Center | Barnett-Griness O.,Technion - Israel Institute of Technology | Rennert G.,Technion - Israel Institute of Technology
Osteoporosis International | Year: 2013

Summary: This study examines the relationship between obesity and the increase in serum 25(OH)D levels in response to vitamin D supplementation among adults with baseline serum 25(OH)D levels <50 nmol/L. This study revealed that the increase in serum 25(OH)D in response to vitamin D supplementation was higher in lean subjects as compared to obese subjects. Introduction: Serum 25(OH)D is lower among obese than non-obese. This study examines the relationship between obesity and the increase in serum 25(OH)D in response to vitamin D supplementation in a large sample of adults with baseline serum 25(OH)D <50 nmol/L, relatively long average treatment duration and large average daily cholecalciferol. Methods: The computerized database of the Clalit Health Services, which the largest nonprofit health maintenance organization in Israel, was retrospectively searched for all subjects aged ≥20 years who performed serum 25(OH)D test in 2011. Subjects with more than one test at different occasions in 2011 were identified and were included if the result of the first test was <50 nmol/L, and were treated with cholecalciferol between the first and the last test in 2011 (n = 16,540 subjects). Results: The mean increase in serum 25(OH)D level after treatment was 28.7 (95 % confidence interval (CI), 28.0-29.4) nmol/L, 23.6 (23.0-24.2) nmol/L, and 20.1 (19.6-20.6) nmol/L in subject with BMI of <25, 25-29.9, and ≥30 kg/m2, respectively (P < 0.001). The results were similar after adjustment for the potential confounders. Similarly, the proportion of subjects who achieved serum 25(OH)D ≥ 50 nmol/L after treatment was inversely associated with BMI; 65.1, 58.3, and 49.1 % for BMI of <25, 25-29.9, and ≥ 30 kg/m2, respectively. Compared to BMI of ≥30 kg/m2, the adjusted odds ratio for achieving levels of ≥50 nmol/L were 2.12 (95 % CI, 1.94-2.31) and 1.42 (1.31-1.54) for BMI of <25 kg/m2, and BMI of 25-29.9 kg/m2, respectively. Conclusions: BMI is inversely associated with the increase in serum 25(OH)D levels in response to vitamin D supplementation. © 2012 International Osteoporosis Foundation and National Osteoporosis Foundation. Source


Markel A.,ek Medical Center
Israel Medical Association Journal | Year: 2011

Hypercholesterolemia is one of the main factors in the development of atherosclerotic cardiovascular disease. The advent of statins led to huge progress in the treatment of hypercholesterolemia, yet the proportion of patients with prohibitive lipid values and the high incidence of cardiovascular events despite treatment are still very high. Niacin, one of the older drugs used to treat hyperlipidemia, was shown to reduce low-density lipoprotein-cholesterol (LDL-C) and triglycerides and to markedly increase high density lipoprotein-cholesterol (HDL-C) levels. This drug came into disuse owing to frequent side effects, mainly flushing, but in recent years a reemergence of its application has occurred, and multiple clinical trials have shown its effectiveness in the treatment of hyperlipidemia and in the reduction of cardiovascular events. New formulations such as extended-release niacin (ERN) have been developed with the purpose of reducing side effects. Lately, a new compound, laropiprant, which selectively antagonizes the prostaglandin 2 (PGD2) receptor responsible for flushing, has been developed. Laropiprant, when combined with ERN, significantly reduces the incidence of flushing. New and ongoing trials will definitively prove in the long term whether this drug combination significantly reduces the severity of flushing and the incidence of cardiovascular events. Source


DiMauro S.,Columbia University | Spiegel R.,ek Medical Center
Acta Myologica | Year: 2011

In this selective review, we consider a number of unsolved questions regarding the glycogen storage diseases (GSD). Thus, the pathogenesis of Pompe disease (GSD II) is not simply explained by excessive intralysosomal glycogen storage and may relate to a more general dysfunction of autophagy. It is not clear why debrancher deficiency (GSD HI) causes fixed myopathy rather than exercise intolerance, unless this is due to the frequent accompanying neuropathy. The infantile neuromuscular presentation of branching enzyme deficiency (GSD IV) is underdiagnosed and is finally getting the attention it deserves. On the other hand, the late-onset variant of GSD IV (adult polyglucosan body disease APBD) is one of several polyglucosan disorders (including Lafore disease) due to different etiologies. We still do not understand the clinical heterogeneity of McArdle disease (GSD V) or the molecular basis of the rare fatal infantile form. Similarly, the multisystemic infantile presentation of phosphofructokinase deficiency (GSD VII) is a conundrum. We observed an interesting association between phosphoglycerate kinase deficiency (GSD IX) and juvenile Parkinsonism, which is probably causal rather than casual. Also unexplained is the frequent and apparently specific association of phosphoglycerate mutase deficiency (GSD X) and tubular aggregates. By paying more attention to problems than to progress, we aimed to look to the future rather than to the past. Source

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