Israel Medical Association Journal

Background: Food intake has an immediate effect on the cardiovascular system. However, the effect of a large meal as an immediate trigger for the acute coronary syndrome has not been assessed.

Objectives: To assess the relative risk for an ACS[1] within a few hours after the ingestion of a heavy meal.

Methods: In a case-crossover study 209 patients were interviewed a median of 2 days after an ACS. Ingestion of a large meal in the few hours immediately before the onset of ACS was compared with the comparable few hours the day before and with the usual frequency of large meals over the past year. Large meals were assessed by a 5 level scale.

Results: The relative risk of an acute coronary event during the first hour after a heavy meal ingestion was RR[2] = 7 (95% confidence interval 0.75–65.8) when the day before the ACS served as the control data and RR = 4 (95% CI[3] 1.9–8.6) when the usual frequency of heavy meals ingestion during the previous year served as the control data. 

Conclusions: The ingestion of heavy meals can trigger the onset of an ACS. Education of the population to avoid heavy meals, especially in people at high risk for coronary heart disease, should be included in the prevention of ACS. Research on specific nutrients that may act as potential triggers for ACS should be considered.

Obstructive sleep apnea syndrome is a major public health hazard affecting 2–4% of the adult population; only 10% of these patients are recognized by healthcare providers. In the last decade the number of referrals for polysomnography increased threefold in Israel, compared to 12-fold worldwide, and is expected to increase even more in the coming years. This constant demand for PSG[1] studies is beyond the current capacity of sleep laboratories, thus preventing diagnosis for most patients with suspected OSAS[2]. In the current review, we examine problems facing decision-makers on how to treat the increasing flood of patients presenting with symptoms suggestive of sleep-disordered breathing. We evaluate the cost-effectiveness of current technologies for OSA diagnosis, i.e., laboratory versus at-home technologies. We conclude that no current alternative exists to the use of PSG for OSA diagnosis. When at-home technologies are suggested for OSAS diagnosis, data should be provided on factors influencing its cost-effectiveness, e.g., accuracy rates of diagnosis, relative cost of human resources, and case-mix of patients tested. Since PSG remains the gold standard for diagnosis of OSAS, in Israel resources should be allocated to increasing the volume of beds for PSG studies in order to increase access to diagnosis and treatment, which in turn provides better quality of life, saves scarce resources of the healthcare system, prevents unnecessary accidents and increases workers’ productivity.

Background: Laron Syndrome, first described in Israel, is a form of dwarfism similar to isolated growth hormone deficiency caused by molecular defects in the GH[1] receptor gene.

Objective: To characterize the molecular defects of the GH-R[2] in Laron syndrome patients followed in our clinic.

Methods: Of the 63 patients in the cohort, we investigated 31 patients and 32 relatives belonging to several ethnic origins. Molecular analysis of the GH-R gene was performed using the single strand conformation polymorphism and DNA sequencing techniques.

Results: Eleven molecular defects including a novel mutation were found. Twenty-two patients carried mutations in the extracellular domain, one in the transmembrane domain, and 3 siblings with typical Laron syndrome presented a normal GH-R. Of interest are, on one hand, different mutations within the same ethnic groups: W-15X and 5, 6 exon deletion in Jewish-Iraqis, and E180 splice and 5, 6 exon deletion in Jewish-Moroccans; and on the other hand, identical findings in patients from distinct regions: the 785-1 G to T mutation in an Israeli-Druze and a Peruvian patient. A polymorphism in exon 6, Gly168Gly, was found in 15 probands. One typical Laron patient from Greece was heterozygous for R43X in exon 4 and heterozygous for Gly168Gly. In addition, a novel mutation in exon 5: substitution of T to G replacing tyrosine 86 for aspartic acid (Y86D) is described.

Conclusions: This study demonstrates: a) an increased focal incidence of Laron syndrome in different ethnic groups from our area with a high incidence of consanguinity; and b) a relationship between molecular defects of the GH-R, ethnic group and geographic area.

Background: Prone sleeping has been recognized as a risk factor for sudden infant death syndrome. Ten years ago, non-prone sleeping was recommended in many countries around the world including Israel. The rate of infants sleeping prone and the rate of parents' adherence with the recommendations have not been studied.

Objectives: To study infants' sleep position and parents’ adherence to recommendations, and to identify risk factors for prone sleeping following the campaign to prevent prone sleeping in the Israeli population.

Methods: We conducted a longitudinal telephone survey with the parents of 608 randomly selected 2 month old infants, repeated at 4 and 6 months.

Results: Non-prone sleeping decreased from 75% to 67% and 63% at 2, 4 and 6 months respectively. There was a significant relationship between prone positioning and the use of a home apnea monitor at 2 months (P = 0.038, odds ratio 1.37, 95% confidence interval 0.94–2.15). Other risk factors for prone sleeping were the level of religious practice, with ultra-Orthodox Jews having the highest prevalence (2 months: OR[1] 2.78, 95% CI[2] 1.75–4.55) and higher parity – especially in families with more than five children (P = 0.041).

Conclusions: The prone sleeping position is relatively high in Israel. Groups at high risk were closely associated with the level of religiousness and parity. Efforts to promote supine sleeping should be directed towards identifiable groups.