No abstract

Meperidine is a potent narcotic related chemically and pharmacologically to morphine and atropine. To examine its gastric antisecretory activity a study designed to test the effect of meperidine on basal acid secretion was carried out: 100 mg of meperidine given intramuscularly reduced basal acid output (BAO) by 66.3% at 1 hr (P less than 0.001), 64.9% at 2 hr (P less than 0.001), and 44.9% at 3 hr (P = 0.005). This degree of reduction of BAO by this dose of meperidine did not differ from that produced by 30 mg of propantheline intramuscularly. These results demonstrate that meperidine in standard classical doses is a potent inhibitor of BAO in man.

We report on five patients with Aarskog syndrome who show previously undescribed umbilical features. Two of the five patients had protruding umbilicus, while the other three had a characteristic umbilicus consisting of a smooth depression with radiating branches of the cicatrix, and a flat cushion. These umbilical configurations have not previously been described in association with Aarskog syndrome. The flat configuration of the umbilicus could be a characteristic umbilical finding associated with Aarskog syndrome as well as the protruding umbilicus.

Introduction: Polycystic ovary syndrome (PCOS) is the most frequent cause of hyperandrogenism in women of reproductive age. Among its metabolic complications, vitamin D deficiency has been described in relation with insulin resistance’s pathophysiology and other metabolic risk factors. However, it is not clear if this deficiency is inherent to PCOS or it depends on adiposity degree. As well, it is also suggested that vitamin D could regulate leptin levels and high leptin levels should be associated with vitamin D defiency in obesity. Our aim was to evaluate the relationship between vitamin D, leptin and obesity degree in PCOS patients. Subjects and methods: In 84 PCOS women (19 -37 years) and 49 controls (22-45 years), 25 hidroxi-vitamin D (25 OH-D) was measured by direct chemoluminiscence. Body mass index (BMI) was calculated; 20% of PCOS women were overweight and 46% were obese. Waist circumference (WC) was measured as an indicator of abdominal obesity. The lipid accumulation product (LAP) index, a secondary marker of insulin resistance, was calculated (LAP: [waist (cm) - 58] x triglycerides (mmol/l)). In a subgroup of 26 patients, leptin levels were determined by ELISA method. Statistical analysis was performed through SPSS 22. Results: Variables are expressed as mean ± SD or median (range) according to distribution. The following parameters were higher in PCOS women than in controls, BMI: 29.3 (18.6-48.2) vs 22.4 (18.1-37.4) kg/m2; WC 95 ± 16 vs 82 ± 11 cm and LAP: 47.9 (1.1-198.2) vs 17.5 (6.8-93.4) cm.mmol/L, p<0.0001 in all cases. 25 OH-D was lower in PCOS: 14.5 (10.0-39.0) vs 17.0 (10.0-38.8) ng/ml, p=0.024. Leptin levels in PCOS women were 10.1 ± 5.4, 26.4 ± 7.0 and 33.8 ± 16.9 ng/ml in normal weight, overweight and obese patients, respectively. After a logistic binary regression analysis, differences in 25 OH-D between groups were lost when BMI and WC were considered (p=0.556; RR=0.978; IC95% [0.909-1.063]). 25 OH-D levels were negatively associated with WC (r=-0.286, p=0.006), LAP (r=-0.333, p=0.002) and leptin (r=-0.462, p=0.017). Conclusions: although 25 OH-D levels were lower in PCOS women than in controls and negatively associated with LAP, an insulin resistant marker, the fact than differences between groups was lost after correction by BMI and WC, in addition to the correlation found between 25 OH-D and leptin levels, indicates that obesity degree and abdominal fat distribution should be responsible of decreased vitamin D levels in PCOS.