E. Michael Sarrell, MD, Avigdor Mandelberg, MD, Herman Avner Cohen, MD and Ernesto Kahan, MD, MPH
Background: Primary care physicians' adherence to accepted asthma guidelines is necessary for the proper care of asthma patients.
Objectives: To investigate the compliance of primary care physicians with clinical guidelines for asthma treatment and their participation in related educational programs, and to evaluate the influence of their employment status.
Methods: A questionnaire was administered to a random sample of 1,000 primary care practitioners (pediatricians and family physicians) in Israel.
Results: The response rate was 64%. Of the physicians who participated, 473 (75%) had read and consulted the guidelines but only 192 (29%) had participated in an educational program on asthma management in the last 12 months. The younger the responding physician (fewer years in practice), the more likely his/her attendance in such a program (P<0.0001). After consulting the guidelines 189 physicians (40%) had modified their treatment strategies. Significantly more self-employed than salaried physicians had read the guidelines and participated in educational programs; physicians who were both self-employed and salaried fell somewhere between these groups. This trend was not influenced by years in practice.
Conclusions: All primary care physicians should update their knowledge more often. The publication of guidelines on asthma must be followed by their proper dissemination and utilization. Our study suggests that major efforts should be directed at the population of employed physicians.
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..
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.
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 31.3±0.76, SBP/DBP 124±2.1/85.4±1.8, MAP 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 (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 and plasma NE 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.
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BMI = body mass index
SBP/DBP = systolic blood pressure/diastolic blood pressure
MAP = mean arterial pressure
UNOx = urinary nitric oxide
RMR – resting metabolic rate
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