Prevalencia familiar de patologías metabólicas en paciente con síndrome de ovario poliquístico / Prevalence of metabolic disorders among family members of patients with polycystic ovary syndrome

Background: About 60 percent of patients with polycystic ovary syndrome (PCOS) have insulin resistance, predisposing them to the premature coronary disease and type 2 -diabetes mellitus. However, the history of metabolic disorders in family members of patients with PCOS has been seldom documented in the literature. Aim: To evaluate the family profile of metabolic disorders of PCOS patients and to determine their relative risk of developing one of them in comparison to a control group. Patients and Methods: Sixty PCOS patients were evaluated. The control group were 60 normal women. The data were obtained from the clinical history and personal interview with the patients, the controls and their relatives (brothers, parents and grandparents). The metabolic disorders considered were: dyslipidemia, obesity, hypertension and diabetes. Results: The ages were similar between groups (PCOS: 24.0 ñ 6.3; control group: 24.8 ñ 6.2 years). The prevalence of metabolic disorders was 62 percent in the relatives of the PCOS patients and 27.8 percent in the relatives of the control group (p <0.005). The probability to develop a metabolic disorder within the family was 2.7 (2.2-3.3) fold higher in the PCOS group compared to the control group. The risk of developing hypertension, dyslipidemia, obesity and diabetes was 2.1 (1.5-2.9); 1.8 (1.5-2.7); 3.6 (2.6-4.9) and 2.7 (1.8-3.9), respectively, in the PCOS group compared to the control group. Conclusions: The probability of finding a metabolic disorder in the families of PCOS patients, is 2.7 fold higher than in the control group families. The metabolic disorders are more frequent in parents and grandparents of the PCOS patients than in those of normal women

Síndrome de ovario poliquístico: la importancia de establecer su diagnóstico / Polycystic ovary syndrome: the importance of establishing diagnosis

Polycystic ovary syndrome (PCOS) is a very common disorder that occurs up to 10 percent of premenopausal women. Although PCOS is known to be associated with a higher reproductive morbility and increased risk of hormone dependent-cancer, its diagnosis is particularly important because PCOS is strongly linked to insulin resistance. This involves a major risk of early metabolic and cardiovascular complications. On the other hand, the prevalence of metabolic disorders associated with insulin resistance is higher in family members of patients with PCOS than in those of normal women, which suggests that the treatment of this syndrome should be preventive rather than symptomatic. For that reason, PCOS might be considered a signal of a family disorder, a route to diabetes and a public health problem

Evaluación del efecto agudo de la administración de GnRH sobre la secreción de leptina en mujeres sanas e hiperandrogénicas / Assessment of acute effect of GnRH administration on leptin secretion in normal and hyperandrogenic women

Background: Several studies suggest that leptin modulates the reproductive axis function. Leptin may stimulate release of GnRH from hypothalamus and of gonadotrophins from the pituitary. A synchronicity of LH and leptin pulses has been described in healthy women and in patients with polycystic ovarian syndrome (PCOS), suggesting a relationship between the episodic secretion of LH and leptin. In vitro experimental studies have demonstrated that leptin administration promotes GnRH-LH release. However it is not established whether GnRH promotes the episodic secretion of leptin. Aim: To assess the response of LH and leptin to the administration of a GnRH bolus in hyperandrogenic and healthy women. Patients and methods: Eleven hyperandrogenic and eleven healthy women of similar age and body mass index (BMI) were studied. Under basal conditions three blood samples were collected every 30 min before and after the administration of a GnRH bolus (100 µg). LH and leptin concentrations were measured in all samples. Testosterone, SHBG and estradiol were determined in the first sample. For data analysis, the increment of LH and leptin between 0-30 and 0-60 min. was calculated. The LH and leptin areas under the curve (AUC) before and after GnRH administration were also calculated in both groups. Results: After GnRH administration. an increment in LH concentrations was observed in both groups; however, leptin concentrations were not modified. In both groups LH area under the curve increased after GnRH administration; however, the leptin area was not modified. Conclusions: These results suggest that circulating leptin concentration is not modulated by GnRH-LH