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Background:Entry of nutrients into the small intestine activates neuro-hormonal signals that regulate food intake through induction of satiation.Objective:To evaluate whether caloric intake can be decreased by pharmacologically accelerating gastric emptying (GE) of nutrients into the small intestine.Methods:Subjects were tested in 2 days, at baseline (day1) and after randomly receiving, in a double-blind manner, a 1 h infusion of erythromycin (3 mg Kg−1, to accelerate GE) or placebo (day 2). Ad libitum caloric intake and postprandial gastrointestinal symptoms were evaluated using a validated nutrient drink test, simultaneously measuring gastric by scintigraphy. Plasma levels of satiation factors were also measured to evaluate their role in the modification of caloric intake and postprandial symptoms. Acceleration of GE was assessed as the difference in percentage emptied between day 2 and day 1 (DGE). The effects of DGE on caloric intake and symptoms were evaluated using multiple (lineal) regression.Results:Among 30 overweight/obese subjects (24F and 6 M), 15 received erythromycin and 15 placebo. The overall median age was 36 years (IQR: 30-42) and body mass index was 30 Kg m−2 (IQR: 27-36). Subjects receiving erythromycin on day 2 presented accelerated GE as compared with placebo (P=0.0002). DGE at 15 min after initiating eating had a significant effect on prospective caloric intake (P=0.004). From the best-fitted regression model (R 2=81%, P<0.0001), a 10% increase in GE at 15 min induced on an average a 135±43.5 Kcal decrease in caloric intake. Postprandial increase in cholecystokinin (CCK) (P=0.03) and insulin (P=0.02) was associated with decreased caloric intake. Acceleration of GE at 60 min after initiating eating increased postprandial symptom scores measured 30 min after the completion of food consumption (P=0.01). Postprandial increase in CCK (P=0.002) and PP (P=0.02) was associated with postprandial symptoms.Conclusion:Meal size can be reduced in overweight/obese subjects by pharmacologically accelerating GE. This may be a reasonable target in obesity management. [ABSTRACT FROM AUTHOR]

Background: Left ventricular hypertrophy (LVH) is a well known cardiac risk factor. There are no data available as to the epidemiology of this disease in the general hypertensive population in Spain., Methods: A randomized sample (n = 267) of a general hypertensive population under the age of 80 years was followed in a Basic Health Care Area located in the center of Barcelona, Spain. A Doppler-echocardiographic study of the patients was carried out. The patients were considered to have LVH when they demonstrated an index > 134 g/m2 of left ventricular mass in males and > 110 g/m2 in females. The odds ratio (OR) was estimated on presentation of LVH associated with exposure to different factors., Results: A prevalence of LVH diagnosed by echocardiogram was observed in 64% (confidence interval 95% from 58.3 to 69.8%). The independent risk factors associated with the presence of LVH were female sex, age and systolic blood pressure., Conclusions: Left ventricular hypertrophy is a frequent cardiovascular risk factor in the general hypertensive population in Spain. A systematic search by echocardiography cannot be recommended in primary health care until cost-effectiveness studies have been performed.

The peripheral plasma levels of 20alpha-dihydroprogesterone (20alpha-DHP), progesterone (P) and 17-hydroxyprogesterone (17-OHP) were measured by radioimmunoassay techniques in 440 samples during normal human pregnancy between weeks 4 and 41. The levels of 20alpha--DHP in plasma from the 4th to the 6th week were between 6.0 and 6.6 ng/ml. From then until the 21st week the average plasma 20alpha-DHP concentrations remained at the same level between 4.0 and 6.3 ng/ml; they then rose significantly to and beyond term, levels reaching over 40 ng/ml. The range of mean plasma concentration of P during the first trimester of pregnancy fell to a nadir in the 9th week (170 ng/ml) then rose with increased gestation until the 39th week (190.4 ng/ml) followed by a slight and not significant drop. Single measurements of plasma 17--OHP from the 4th to the 6th week of pregnancy gave value between 2.8 and 3.6 ng/ml, but from the 7th week the mean plasma 17--OHP levels gradually declined, then from week 30 the 17-OHP concentration increased to reach a mean level of 7.63 ng/ml in the 41st week. The ratio P/20alpha--DHP increased from the 4th (3.5:1) to the 24th week (15.6:1) and then decreased from 25th week (7.9:1) towards term (3.2:1).