PubMed HealthSearch

Biomedical subjects

G Zanconato

Publications and source records attributed to G Zanconato.

2 recordsLinked to original sources

[Obstetric-gynecologic problems in the developing countries].

The integrated health programmes in the developing countries give priority to the improvement of women's living conditions and of maternal and child health medical attention. The Authors, as specialists in Obstetrics and Gynecology active in an African country, present the most frequent pathological situations which, in their experience, can lead to the death of the pregnant woman. The social reality of the underdeveloped world and the high Total Fertility rates, due partly to the absence of a contraceptive culture, too often see the woman of reproductive age threatened by the complication deriving from abortion, ectopic pregnancy and labour. The obstetrician needs to know how to solve these emergencies and how to train the local personnel in order to guarantee as much as he can the essential obstetrical functions.

Child Health Services

A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol.

A syndrome is described whose features, suggestive of primary mineralcorticoid excess, included hypertension, hypokalemia, low PRA, and responsiveness to spironolactone. Aldosterone levels were subnormal but as yet there has been no evidence of overproduction of other mineralocorticoids by chemical analysis or by bioassay of plasma and urinary extracts. The steroidal abnormalities that were observed involved peripheral matabolism rather than secretion. One patient exhibited a transient delay in reduction of the 3-keto group in the A ring, and both patients exhibited a decrease in the metabolism of cortisol to biologically inactive cortisone. This was shown by the marked decrease in the excretion of urinary metabolites bearing an 11-keto group and a decrease in the oxidation of 11 alpha-[3H]cortisol to tritiated water. The defect appeared not to be a deficiency of the 11 beta-oxidoreductase system itself, since the reverse reaction of conversion of cortisone to cortisol proceeded normally, but, rater, an alteration in the equilibrium position of 11 beta-oxidoreduction in favor of the reduced form. This was also expressed by a prolongation of the half-time of disappearance of cortisol. The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion. The decreased rate of conversion of cortisol to cortisone serves as a biochemical marker of this hypertensive syndrome.

17-Hydroxycorticosteroids