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עמוד בית
Fri, 22.11.24

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January 2007
October 2006
E. Kaluski, Z. Gabara, N. Uriel, O. Milo, M. Leitman, J. Weisfogel, V. Danicek, Z. Vered and G. Cotter
 Background: External counter-pulsation is a safe and effective method of alleviating angina pectoris, but the mechanism of benefit is not understood.

Objectives: To evaluate the safety and efficacy of external counter-pulsation therapy in heart failure patients.

Methods: Fifteen symptomatic heart failure patients (subsequent to optimal medical and device therapy) underwent 35 hourly sessions of ECPT[1] over a 7 week period. Before and after each ECPT session we performed pro-B-type natriuretic peptide and brachial artery function studies, administered a quality of life questionnaire, and assessed exercise tolerance and functional class.

Results: Baseline left ventricular ejection fraction was 28.1 ± 5.8%. ECPT was safe and well tolerated and resulted in a reduction in pro-BNP[2] levels (from 2245 ± 2149 pcg/ml to 1558 ± 1206 pcg/ml, P = 0.022). Exercise duration (Naughton protocol) improved (from 720 ± 389 to 893 ± 436 seconds, P = 0.0001), along with functional class (2.63 ± 0.6 vs. 1.93 ± 0.7, P = 0.023) and quality of life scores (54 ± 22 vs. 67 ± 23, P = 0.001). Nitroglycerine-mediated brachial vasodilatation increased (11.5 ± 7.3% vs. 15.6 ± 5.2%, P =0.049), as did brachial flow-mediated dilation (8.35 ± 6.0% vs. 11.37 ± 4.9%, P = 0.09).

Conclusions: ECPT is safe for symptomatic heart failure patients and is associated with functional and neurohormonal improvement. Larger long-term randomized studies with a control arm are needed to confirm these initial encouraging observations.


 





[1] ECPT = external counter-pulsation therapy

[2] BNP = B-type natriuretic peptide


V.H. Eisenberg, D. Raveh, Y. Meislish, B. Rudensky, Y. Ezra, A. Samueloff, A.I. Eidelman and M.S. Schimmel
 Background: Previous assessments of maternal group B Streptococcus carrier rates in women delivering at Shaare Zedek Medical Center ranged between 3.5 and 11% with neonatal sepsis rates of 0.2–0.9/1000 live births. Because of low colonization and disease rates, routine prenatal cultures of GBS[1] were not recommended, and intrapartum prophylaxis was mainly based on maternal risk factors.

Objectives: To determine whether this policy is still applicable. 

Methods: We performed prospective sampling and follow-up of women admitted for labor and delivery between February 2002 and July 2002. Vaginal and rectal cultures were obtained before the first pelvic examination. GBS isolation was performed using selective broth medium, and identified by latex agglutination and serotyping. Demographic data were collected by means of a standardized questionnaire. Data on the newborns were collected throughout 2002.

Results: Of the 629 sampled women, 86 had a positive culture and a carrier rate of 13.7%. A borderline significantly higher carriage rate was observed among mothers of North American origin (21% vs. 13.1%, P = 0.048), and a higher attack rate in their infants (3.8/1000 compared with 0.5/1000 live births in our general maternal population, P = 0.002). Eight newborns had early-onset neonatal GBS sepsis (a rate of 0.8/1000 live births), but none of them benefited from intrapartum antibiotic prophylaxis.

Conclusions: An increased neonatal disease rate was observed in a population with a higher colonization rate than previously seen. In lieu of the higher carrier rates, we now recommend routine prenatal screening for GBS in our perinatal population.


 





[1] GBS = group B Streptococcus


September 2006
Y. Haron, O. Hussein, L. Epstein, D. Eilat, B. Harash and S. Linn

Background: The Muslim Circassians in Israel represent a unique ethnic community, distinct from Jews and Arabs. This endogamous group has a limited genetic variability that allows studying risk factors associated with type 2 diabetes.

Objectives: To estimate the prevalence of type 2 diabetes among Israeli Circassians and its correlation to obesity and genetic susceptibility.

Methods: Israeli Circassian women (n=450) and men (n=289) older than 35 were included in the study. They were classified as having or not having diabetes, and their risk factors, including hypertension, body mass index, family history of diabetes, and laboratory tests, were examined retrospectively.

Results: The age-adjusted prevalence of diabetes among the 739 participants was 12% (men 14.6%, women 10.7%). It was higher among those with BMI[1] > 30 than in those with lower BMI and a family history of diabetes without high BMI. But the risk of diabetes with BMI > 30 plus a family history was three times higher than when these factors were missing (odds ratio 2.96, 95% confidence interval 1.30–6.6). Multivariate analysis, however, found familial history of diabetes to be the strongest risk factor, independent of obesity (OR[2] 2.47, 95% CI[3] 1.45–4.20).

Conclusions: The results yielded by this homogeneous Circassian population, sharing the same environmental influences and having an endogamous pattern of marriage, suggest a role of genetic risk factors for diabetes. Israeli Circassians are suitable for additional genetic studies that may lead to the identification of susceptibility genes for type 2 diabetes.






[1] BMI = body mass index



[2] OR = odds ratio



[3] CI = confidence interval


June 2006
M.A. Abdul-Ghani, G. Nawaf, G. Fawaz, B. Itzhak, O. Minuchin and P. Vardi
 Background: Microvascular complications of diabetes contribute significantly to the disease morbidity. The metabolic syndrome is very common among subjects with diabetes and is a very important risk factor for macrovascular complications. However, its contribution to the microvascular complication has not been assessed.

Objectives: To assess the risk of microvascular complications associated with the metabolic syndrome in diabetes subjects.

Methods: The study group comprised 415 diabetic subjects attending a primary care clinic. The prevalence of microvascular complications was compared between 270 diabetic subjects with metabolic syndrome (NCEP-III criteria) and 145 diabetic patients without.

Results: We found that as a group, diabetic subjects with metabolic syndrome had significantly higher frequency of microvascular-related complications than diabetic subjects without the syndrome (46.6% and 26.8% respectively, P = 0.0005). These include microalbuminuria (41.5% vs. 23.9%, P = 0.013), neuropathy (10.4% vs. 7.5%, P = 0.38), retinopathy (9.6% vs. 4.1%, P = 0.046) and leg ulcers (7.9% vs. 2.8%, P = 0.044). After adjustment for age, gender, glycemic control, disease duration, lipid profile and blood pressure, metabolic syndrome was associated with a significantly higher risk of microvascular complications: odds ratio (95% confidence interval) for nephropathy 2.27 (1.53–3.34), neuropathy 1.77 (0.79–4.0), retinopathy 3.42 (1.2–9.87), and leg ulcers 3.57 (1.08–11.95).

Conclusions: In addition to hyperglycemia and disease duration, the metabolic syndrome is a significant risk factor for the development of microvascular complications in diabetic subjects.

A. Glick, Y. Michowitz, G. Keren and J. George
 Background: Cardiac resynchronization therapy is a modality with proven morbidity and mortality benefit in advanced systolic heart failure. Nevertheless, not all patients respond favorably to CRT[1]. Natriuretic peptides and inflammatory markers are elevated in congestive heart failure and reflect disease severity.

Objectives: To test whether an early change in neurohormonal and inflammatory markers after implantation can predict the clinical response to CRT.

Methods: The study group included 32 patients with advanced symptomatic systolic heart failure and a prolonged QRS complex and who were assigned to undergo CRT. Baseline plasma levels of B-type natriuretic peptide and high sensitivity C-reactive protein were determined in the peripheral venous blood and coronary sinus. Post-implantation levels were determined 2 weeks post-procedure in the PVB[2]. Baseline levels and their change in 2 weeks were correlated with all-cause mortality and hospitalization for congestive heart failure.

Results: At baseline, coronary sinus levels of BNP[3] but not hsCRP[4] were significanly elevated compared to the PVB. Compared to baseline levels, BNP and hsCRP decreased significantly within 2 weeks after the implantation (BNP mean difference 229.1 ± 102.5 pg/ml, 95% confidence interval 24.2–434, P < 0.0001; hsCRP mean difference 5.2 ± 2.4 mg/dl, 95% CI[5] 0.3–10.1, P = 0.001). During a mean follow-up of 17.7 ± 8.2 months 6 patients died (18.7%) and 12 (37.5%) were hospitalized due to exacerbation of CHF[6]. Baseline New York Heart Association and CS[7] BNP levels predicted CHF-related hospitalizations. HsCRP levels or their change over 2 weeks did not predict all-cause mortality or hospitalizations.

Conclusions: BNP levels in the CS and peripheral venous blood during biventricular implantation and 2 weeks afterwards predict cilinical response and may guide patient management.


 





[1] CRT = cardiac resynchronization therapy

[2] PVB = peripheral venous blood

[3] BNP = B-type natriuretic peptide

[4] hs-CRP = high sensitivity C-reactive protein

[5] CI = confidence interval

[6] CHF = congestive heart failure

[7] CS = coronary sinus


February 2006
J.U. Holle, D. Capraru, E. Csernok, W.L. Gross and P. Lamprecht

Tumor necrosis factor-associated fever syndrome is an autosomal dominant disorder caused by mutations of the TNFRSF 1A gene encoding the 55 kD TNF receptor (p55 TNF-RI).

January 2006
C. Yosefy, R. Beeri and L. Reisin.

A 61 year old woman with chronic untreated hypertension presented for routine examination without any complaints.

June 2005
M.A. Abdul-Ghani, J. Kher, N. Abbas and T. Najami
 Background: Type 2 diabetes is usually associated with obesity, and both conditions are frequently detected in the Arab population in Israel. Recent studies have demonstrated that diabetes can be prevented by a change in lifestyle.

Objective: To assess the prevalence of diabetes in an Arab community, the contribution of obesity to diabetes development, and the therapeutic potential of a preventive program.

Methods: Data were obtained from the medical files of diagnosed diabetes patients attending a primary care clinic in an Arab village in northern Israel.

Results: Type 2 diabetes was diagnosed in 323 patients of whom 63% were women. The prevalence of diabetes below age 65 years was significantly higher among women than men. Diabetic women were younger than men at diagnosis (48.27 vs. 59.52 respectively) and were found to have higher body mass index (34.35 vs. 30.04 respectively) at diagnosis. The age at diagnosis of diabetes was strongly correlated with BMI[1] (r = 0.97, P < 0.0001).

Conclusions: Women of Arab origin are at higher risk of developing type 2 diabetes compared to men. Obesity in women seems to be associated with higher diabetes risk as well as earlier appearance of the disease. Therefore, they will have the disease for longer and, consequently, a higher risk for complications.


 





[1] BMI = body mass index


Z. Laron, H. Lewy, I. Wilderman, A. Casu, J. Willis, M.J. Redondo, I. Libman, N. White and M. Craig
 Background: Type 1 childhood-onset diabetes mellitus has a multifactorial origin involving an interplay between genetic and environmental factors. We have previously shown that many children who subsequently develop T1DM[1] have a different seasonality of birth than the total live births of the same population, supporting the hypothesis that perinatal viral infection during the yearly epidemics are a major trigger for the autoimmune process of T1DM.

Objectives: To compare the seasonality of children with T1DM in different populations around the world for which data were available.

Methods: We analyzed large cohorts of T1DM patients with a clinical disease onset before age 14 or 18 years.

Results: We found a seasonality pattern only in ethnically homogenous populations (such as Ashkenazi Jews, Israeli Arabs, individuals in Sardinia and Canterbury, New Zealand, and Afro-Americans) but not in heterogeneous populations (such as in Sydney, Pittsburgh and Denver).

Conclusions: Our findings attempt to explain the controversial data in the literature by showing that ethnically heterogeneous populations with a mixture of patients with various genetic backgrounds and environmental exposures mask the different seasonality pattern of month of birth that many children with diabetes present when compared to the general population.


 





[1] T1DM = type 1 childhood-onset diabetes mellitus


May 2004
S. Efrat

Type 1 diabetes mellitus is caused by an autoimmune destruction of pancreatic islet beta cells, leading to insulin deficiency. Beta-cell replacement is considered the optimal treatment for type 1 diabetes, however it is severely limited by the shortage of human organ donors. An effective cell replacement strategy depends on the development of an abundant supply of beta cells and their protection from recurring immune destruction. Stem/progenitor cells, which can be expanded in tissue culture and induced to differentiate into multiple cell types, represent an attractive source for generation of cells with beta-cell properties: insulin biosynthesis, storage, and regulated secretion in response to physiologic signals. Embryonic stem cells have been shown to spontaneously differentiate into insulin-producing cells at a low frequency, and this capacity could be further enhanced by tissue culture conditions, soluble agents, and expression of dominant transcription factor genes. Progenitor cells from fetal and adult tissues, such as liver and bone marrow, have also been shown capable of differentiation towards the beta-cell phenotype in vivo, or following expression of dominant transcription factors in vitro. These approaches offer novel ways for generation of cells for transplantation into patients with type 1 diabetes.

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