[Hypothalamo-hypophyseal amenorrhea. I. The clinical and laboratory manifestations]. / Amenorrea hipotálamo-hipofisaria. I. Manifestaciones clínicas y de laboratorio.

This study included 15 women 18-36 years old with primary or secondary amenorrhea, low FSH and LH, a negative response to clormadinone and serum prolactin (Prl) levels less than 20.0 ng/ml. The following tests were performed on alternate days: LH and FSH determinations every 20 minutes (pulses) during 2-4 hours (n = 15); LH and FSH response to a single dose of GnRH 100 micrograms IV (n = 15) and after administration of 100 micrograms IM of GnRH daily during four consecutive days (n = 7); TRH test 200 micrograms IV (n = 9); oral metoclopramide-Prl induced response (10 mg) (n = 2); one to three basal determinations of cortisol, estradiol (E2), T3, T4, and TSH (n = 15). All patients had serum E2 levels less than 10.0 pg/ml and none showed a regular LH or FSH pulsatility. In seven patients (group A) serum LH had a 10-30 fold increase above basal levels in response to GnRH, while the other eight patients (group B) showed no response at all; serum FSH changes were most irregular in both group. In group A no other hormonal deficiencies were detected, while in group B only three patients had an isolated LH-FSH deficiency, and in the other five this deficiency was accompanied by Prl, TSH, and/or ACTH lack. The present results suggest that: 1) group A represents isolated GnRH deficiency and the amenorrhea has hypothalamic etiology; 2) group B had LH-FSH deficiency of pituitary origin, in most cases associated to other pituitary hormone deficiencies; 3) the lack of LH response to an initial single dose of GnRH is not an absolute indicator of hypophyseal amenorrhea.

[Endocrine behavior of battered children in the acute stage of the aggression]. / Comportamiento endocrino del niño maltratado en la fase aguda de la agresión.

To date the cause of growth retardation of children who have suffered physical abuse and emotional deprivation is unknown. Hypophyseal disturbances in these patients have been proposed of the cause but there are still several concerns on the dynamics of growth hormone secretion in these children. In this study, eleven out of sixteen patients had a low height without important diminution of corporal weight. Growth hormone under basal conditions was found to be elevated in battered children compared with a control group (15.2 +/- 4.7 ng/mL vs 9.6 +/- 1.9 ng/mL, p = 0.025). Two weeks after hospitalization a tendency towards normalization was apparent (13.8 +/- 3.0, NS vs controls). Cortisol, thyroid hormones T3 and T4 as well as thyrotrophin did not show significant changes under basal conditions with respect to control patients although there were some isolated cases with abnormal values. While chronic stress could adversely affect hypophyseal trophic hormone secretion, our study did not show either this were effect nor a clear association between growth retardation and a characteristic abnormal endocrine pattern. It seems that the cause growth and developmental retardation in battered children is of a multifactorial.