. Twenty‐six patients with premature ovarian failure (last menstrual period before the age of 30 years) were evaluated clinically and endocrinologically and, in addition, ovarian biopsies were obtained in 15 out of the 26 patients. Only 1 of the patients revealed a family history of early menopause. The typical menstrual pattern indicated a normal age at menarche with regular periods for various length of time followed either by amenorrhoea abruptly or by a period of oligomenorrhoea before the onset of amenorrhoea. All patients showed normal or slightly underdeveloped secondary sexual characteristics, and it should be noted that 2 patients had been pregnant previously. It was characteristic of all patients that the excretion of total gonadotropins was constantly increased and that the excretion of total oestrogens was low, whereas both the adrenal and thyroid function were normal. All patients were X‐chromatin positive. In 13 out of the 15 patients, in whom ovarian biopsies were obtained, the histological examination revealed a normal stroma without or with very few primordial and atretic follicles, a picture very similar to that characteristic of the postmenopausal ovary. In the last 2 patients, however, the histological examination showed a quite different picture, viz. a normal stroma with numerous primordial and primary follicles and even a few growing follicles. In spite of these morphologically normal follicles, it was not possible to stimulate the follicular development and to induce ovulation even with very high doses of human gonadotrophins. It is, therefore, concluded that the presence of a few growing follicles in the ovaries does not seem to exclude the diagnosis of premature ovarian failure. Only 14 out of the 26 patients had the typical symptoms of the climacteric, and even in these cases the nuisance was only of a mild to moderate degree. It is generally agreed that all patients with symptoms should receive substitution therapy, but the essential risk of ischaemic heart disease and osteoporosis, together with the unquestionable psychological effect of having regular menstrual bleeding, have led us to the conclusion that this therapy is indicated in all cases of premature ovarian failure. Cyclical treatment either with a sequential preparation or with oestrogens alone is the treatment of choice.

A case of Turner's syndrome (45,XO) with two pregnancies is reported. There was no evidence of mosaicism after chromosomal investigation of 5 different tissues (2 ovaries, blood, skin, uterus). Pregnancy occurred in both cases after withdrawal of substitutional hormone therapy. The first pregnancy ended with abortion of a macerated hydrocephalic female fetus. Chromosome studies could not be carried out. The second pregnancy ended with delivery by caesarian section of a normal boy (46,XY). Prenatal chromosome analysis was not carried out for ethical reasons.

A case history of monozygotic twins is presented. Twin A showed gonadal dysgenesis and chromosomal mosaicism (45,X0/46,XX). Twin B was a phenotypical normal female with the karyotype 46,XX. Fifteen previous reports of monozygotic twins with gonadal dysgenesis are reviewed. Dissimilar phenotypes seem to be the rule rather than the exception, and mosaicism is found in the majority of cases with dissimilar phenotype. The assumption is made that the chromosome disorder leading to gonadal dysgenesis arises postzygotically, eigher before or after the process leading to twinning.

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