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עמוד בית
Thu, 18.07.24

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June 2002
Nurit Rosenberg, PhD, Ariella Zivelin, PhD, Angela Chetrit, PhD, Rima Dardik, PhD, Nurit Kornbrot, MSc, Dov Freimark, MD and Aida Inbal, MD

Background: Platelet adhesion and aggregation are mediated by specific platelet membrane glycoproteins GPIa/IIa, GPIba, and GPIIb/IIIa, and are essential steps in thrombus formation and development of acute myocardial infarction.

Objective: To evaluate the risks exerted by each of the following polymorphisms: HPA-1a/b in GPIIIa; 807C/T in GPIa; and HPA-2a/b, VNTR and Kozak C/T in GPIba in young males with AMI[1]..

Methods: We conducted a case-control study of 100 young males with first AMI before the age of 53 and 119 healthy controls of similar age. All subjects were tested for the above polymorphisms.

Results: The allele frequencies of each of the platelet polymorphism were not significantly different between the young men with AMI and the controls. Smoking alone was associated with a 9.97-fold risk, and the presence of at least one metabolic risk factor resulted in a 2.57-fold risk of AMI.

Conclusion: These results indicate that platelet glycoproteins polymorphisms are not an independent risk factor for AMI.






[1] AMI = acute myocardial infarction


Eliezer Golan, MD, Bruria Tal, PhD, Yossef Dror, PhD, Ze’ev Korzets, MBBS, Yaffa Vered, PhD, Eliyahu Weiss, MSc and Jacques Bernheim, MD

Background: Multiple factors are involved in the pathogenesis of hypertension in the obese individual.

Objective: To evaluate the role of a decrease in sympathetically mediated thermogenesis and the effect of the correlation between the plasma leptin and daily urinary nitric oxide levels on obesity-related hypertension.

Methods: We evaluated three groups: 25 obese hypertensive patients (age 45.7±1.37 years, body mass index 34.2±1.35 kg/m2, systolic/diastolic blood pressure 155±2.9/105±1.3, mean arterial pressure 122±1.50 mmHg); 21 obese normotensive patients (age 39.6±1.72, BMI[1] 31.3±0.76, SBP/DBP[2] 124±2.1/85.4±1.8, MAP[3] 98.2±1.80); and 17 lean normotensive subjects (age 38.1±2.16, BMI 22.1±0.28, SBP/DBP 117±1.7/76.8±1.5, MAP 90.1±1.50). We determined basal resting metabolic rates, plasma insulin (radioimmunoassay), norepinephrine (high performance liquid chromatography) in all subjects. Thereafter, 14 obese hypertensives underwent a weight reduction diet. At weeks 6 (n=14) and 14 (n=10) of the diet the above determinations were repeated. Plasma leptin (enzyme-linked immunosorbent assay) and UNOx[4] (spectrophotometry) were assayed in 17 obese hypertensives and 17 obese normotensives, and in 19 obese hypertensives versus 11 obese normotensives, respectively.

Results: Obese hypertensive patients had significantly higher basal RMR[5] and plasma NE[6] levels. Insulin levels were lower in the lean group, with no difference between the hypertensive and normotensive obese groups. At weeks 6 and 14, BMI was significantly lower, as were insulin and NE levels. RMR decreased to values of normotensive subjects. MAP normalized but remained significantly higher than that of obese normotensives. Leptin blood levels and the leptin/UNOx ratio were significantly higher in the obese hypertensive compared to the obese normotensive patients. Both these parameters were strongly correlated to BMI, MAP5, RMR, and plasma NE and insulin .Obese hypertensive patients excreted less urinary NO metabolites. A strong correlation was found between MAP and the leptin/UNOx ratio.  

Conclusions: A reduction of sympathetically mediated thermogenesis, as reflected by RMR, results in normalization of obesity-related hypertension. In contrast, insulin does not seem to play a major role in the pathogenesis of hypertension associated with obesity. Increased leptin levels in conjunction with decreased NO production in the presence of enhanced sympathetic activity may contribute to blood pressure elevation in the obese.

_____________________

[1] BMI = body mass index

[2] SBP/DBP = systolic blood pressure/diastolic blood pressure

[3] MAP = mean arterial pressure

[4] UNOx = urinary nitric oxide

[5] RMR – resting metabolic rate

[6] NE = norepinephrine

Gideon D. Charach, MD, Itamar Groskopf, MD, Dan Turner, MD, Michael Y. Barilan, MD, Chen Kugel, MD and Moshe S. Weintraub, MD
Lela Migirov, MD, Ana Eyal MD, and Jona Kronenberg, MD
May 2002
Alik Kornecki, MD, Riva Tauman, MD, Ronit Lubetzky, MD and Yakov Sivan, MD

Background: The role of continuous renal replacement therapy in patients with acute renal failure is well recognized. CRRT[1] has also become an important modality of treatment in various acute situations without renal failure.

Objectives: To describe our experience with CRRT in acutely ill infants and children without renal failure.

Methods: We analyzed all infants and children who underwent CRRT during the years 1998-2000 in the pediatric intensive care unit and we focus our report on those who were treated for non-renal indications.

Results: Fourteen children underwent 16 sessions of CRRT. The indications for CRRT were non-renal in 7 patients (age range 8 days to 16 years, median = 6.5). Three children were comatose from maple syrup urine disease, three were in intractable circulatory failure secondary to septic shock or systemic inflammatory response, and one had sepsis with persistent lactic acidosis and hypernatremia. Three children underwent continuous hemodiafiltration and four had continuous hemofiltration. The mean length of the procedure was 35 ± 24 hours. All patients responded to treatment within a short period (2–4 hours). No significant complications were observed. Two patients experienced mild hypothermia (34°C), one had transient hypotension and one had an occlusion of the cannula requiring replacement.

Conclusion: Our findings suggest that CRRT is a safe and simple procedure with a potential major therapeutic value for treating acute non-renal diseases in the intensive care setting.






[1] CRRT = continuous renal replacement therapy


Kobi Peleg, PhD, Haim Reuveni, MD and Michael Stein, MD
Gahl Greenberg, MD, Myra Shapiro-Feinberg, MD and Rivka Zissin, MD
April 2002
Jonathan Cohen, FCP (SA), Karina Chernov, RN, Ora Ben-Shimon, RN and Pierre Singer, MD
Anat Kesler, MD, Ronit Galili-Mosberg, MD and Natan Gadoth, MD
Pnina Romem, MmedSc, RN, Haya Reizer, BN, RN, Yitzhak Romem, MD and Shifra Shvarts, PhD

Southern Sinai, a mountainous desolated arid area, is inhabited by Bedouin nomad tribes composed of Arabic-speaking Moslems. Until the Six Day War between Egypt and Israel in 1967, healthcare services in the region were based on traditional medicine performed by the Darvish, a local healer. Over the course of Israeli rule (1967-1982) an elaborate healthcare service was established and maintained, providing modern, up to date, comprehensive medical services that were available to all free of charge.

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