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IN 1935 Stein and Leventhal1 reported 7 cases of amenorrhea associated with polycystic ovaries. In addition 4 of their patients complained of hirsutism, and 3 were obese. After wedge resection of the ovaries, normal menses reappeared in all 7 patients, 5 of whom eventually conceived. The amenorrhea and the polycystic ovaries were thought to be due to an imbalance of the pituitary-ovarian axis. The combination has become known as the Stein–Leventhal syndrome. Secondary amenorrhea as the main clinical symptom of this syndrome was emphasized by Leventhal and Cohen2 in 1951, when they stated that wedge resection was not indicated unless . . .

A 46,X,t(X;X) (qter-->p22;;p22-->qter) karyotype was found in the chromosome analysis of a 22 years old female patient with secondary amenorrhea. Further analysis with fluorescence in situ hybridization indicated that the marker chromosome had one active and one inactive centromere originating from the X chromosome. RBG-banding showed that the derivative X chromosome was preferentially inactivated in cultured lymphocytes.

Eight thalassemic patients, aged 24-35 years, who developed amenorrhea 2-15 years after menarche, were studied. Mean basal serum LH and FSH levels and the peak levels after gonadotropin-releasing hormone were significantly less than corresponding values in normal controls. All patients showed low basal serum levels of estradiol and six had a poor or absent response to human menopausal gonadotropin. One subject had intact pituitary-gonadal function and one patient had an impaired LH and FSH response to gonadotropin-releasing hormone in the presence of a significant increase of estradiol after human menopausal gonadotropin stimulation. The findings regarding pituitary hormones other than gonadotropins suggest that iron overload damages tropic cells unequally and inconsistently. We conclude that both pituitary and gonadal damage may be responsible for the secondary amenorrhea in thalassemic patients.

Cytogenetic investigations were carried out on 103 women presenting with either primary (n = 88) or secondary (n = 15) amenorrhea. A sex chromosome anomaly was found in 26% and 33% of these patients, respectively. Other studies on women with primary amenorrhea have found a similar or even higher percentage of patients with an abnormal karyotype. It is therefore suggested that all women with absence of menstruation after the age of 16 years should be investigated cytogenetically. The surprisingly high percentage of pathological karyotypes among the secondary amenorrhea group does indicate that sex chromosome anomalies cannot be ruled out in women who have had apparently normal ovarian function for at least some time, and therefore more patients from this group should be selected for chromosome analysis.

Amenorrhea, whether primary or secondary, is still a major therapeutic problem. With rare exceptions organotherapy has failed to elicit permanently good results. At best, bleeding is induced upon withdrawal of the experimentally administered hormone without, however, sustained cyclic menstruation thereafter. The ideal treatment has not been attained, because the etiology of amenorrhea remains unknown. Recently Pencharz1 reported maximum stimulation of the immature rat ovary with chorionic gonadotropin combined with diethylstilbestrol. The stimulation exceeded that of any other experimental hormonal stimulus. This combination of hormones was, therefore, given to 12 amenorrheic women in the hope that such therapy might effect more permanent results than were attained with cyclically administered sterols or with equine gonadotropins. The latter hormones had previously yielded very indifferent results in this clinic. Of the 12 patients, 4 complained of primary and 8 of secondary amenorrhea; only 8 were treate...

THE RESULTS of treatment of secondary amenorrhea are often a source of dissatisfaction both to the patient and her physician. We are reporting a case of secondary amenorrhea in which a careful diagnostic survey was completed and an unusually long and tedious course of therapy was given before a completely successful result was achieved. CASE REPORT The patient was first seen in March, 1941, at the age of 17. She was a thin, pale, white schoolgirl who had not had a menstrual period since June, 1940. Menarche occurred at 13 years of age. She had her first 3 periods at 6-month intervals and then had regular 6-week menstrual cycles which terminated abruptly in June, 1940. Her periods had been normal in duration and were never painful. She had never been operated upon and had had only the usual childhood diseases. Physical examination. Physical examination revealed a thin, white girl with no endocrine stigmata.

Ethinyl estradiol was prepared by Inhoffen and Hohlweg1 by the replacement of the 17th carbon atom in estradiol by an ethinyl group. When given subcutaneously in oil, ethinyl estradiol and estradiol are equal in potency, but when given orally, ethinyl estradiol is 15 to 20 times as active as estradiol. Clauberg and Ustun2 reported the use of ethinyl estradiol in secondary amenorrhea and oligomenorrhea and demonstrated proliferative changes in the uterine mucosa following doses of 56 mg. of ethinyl estradiol, given over a period of 20 days. No symptoms of toxicity were reported in their series. Salmon et al.3 administered ethinyl estradiol in the form of enteric-coated tablets and in alcoholic solution to 27 patients with menopausal symptoms and morphologic evidence of estrogen deficiency (tablets, 22 patients; alcoholic solution, 5 patients). Ethinyl estradiol in the form of entericcoated tablets was found to possess high estrogenic potency when administered orally, as demonstrated by the relief of menopa...

In adolescent girls, secondary amenorrhea can result from a variety of physiologic and psychologic disturbances. Previous reports associating amenorrhea and primary hypothyroidism have not distinguished between the alternative etiologic roles of thyroxine deficiency and hyperprolactinemia. We have evaluated two girls with secondary amenorrhea who had clinical and chemical evidence of hypothyroidism. Both had low basal T4's (0.8 and 3.8 μg%), calculated free T4's (0.1 and 0.7 μg%), and T3's (51 and 81 ng%). Both had undetectable basal TSH with normal TSH response to TRH. Basal FSH and LH were normal, as was the response to LHRH. Basal prolactins were 6 and 14 ng/ml, and both girls had growth hormone responses of ≥15 ng/ml in response to insulin-induced hypoglycemia. Pituitary-adrenal function and reserve were also normal. In neither case were there any historical, physical, or laboratory features compatible with anorexia nervosa. After treatment with 1-thyroxine, both girls had a resumption in menses. These two adolescent girls thus appear to have isolated hypothalamic hypothyroidism. The associated secondary amenorrhea demonstrates that thyroid deficiency alone, without hyperprolactinemia, can interfere with normal hypothalamic-pituitary-ovarian function. (Supported by grant RR-125)

A significant correlation between simultaneously determined SP and PP was found in 69 healthy adolescent girls (r=0.562, p < 0.001). 29 were still premenarchal (chronologic age -CA- 10.5-15, bone age -BA- 10-13.5 years -yrs-). 8 had anovulatory cycles (CA 12.8-21, BA 13-18, gynecologic age -GA- 0.1-6.7 yrs) and 4 presented primary and secondary amenorrhea (CA 12-18.8, BA 10-18 yrs). 17 with ovulatory cycles (CA 13-21.4, BA 13-18, GA 0.3-7 yrs) provided progesterone values during the follicular phase (FP) and 11 during the luteal phase (LP). SP and PP concentrations during FP did not differ from premenarchal girls or those with cyclic abnormalities. With respect to FP the coefficient of correlation between SP and PP was r=0.432 (n=58, p < 0.001). The correlation between SP and PP during LP was r=0.783 (n=11, p < 0.01). The regression equation of the log normally distributed values was y=3.49863+1.14611× (y=PP,x=SP). Provisional normal ranges for SP and PP during ovulatory cycles were established. During FP SP and PP ranged from 70-280 and 500-2400 pM/L, while the highest SP and PP levels during LP were 800 and 39000 pM/L. The Wilcoxon test was significant between progesterone during FP and LP both for SP (p < 0.05) and PP (p < 0.001). Conclusion: Serial analyses of SP are suited to characterize phase and type of a cycle. Because of the high correlation it is possible to calculate PP during LP based on SP.

In the past ten years, hyperprolactinemia has been implicated as a possible cause of several common medical problems. One of the first recognized was the so-called amenorrhea-galactorrhea syndrome. Subsequently it was learned that not all patients with elevated prolactin levels have galactorrhea 1 (only about 20% of hyperprolactinemic women and even fewer men lactate), so that the absence of galactorrhea does not rule out an elevated prolactin level. Several studies have now shown that 15% to 30% of women with secondary amenorrhea (without galactorrhea) also have hyperprolactinemia. 2,3 Most recently, prolactin has been implicated as a cause of impotence and/or oligospermia in men. 4 It also seems likely that many pituitary tumors that in the past were thought to be nonfunctioning chromophobe adenomas were actually prolactin-producing. Thus, the number of clinical presentations associated with hyperprolactinemia and the number of patients affected are much greater than were originally estimated. What is

This little book is essentially a research monograph. It is solid yet at the same time baffling and elusive. Conceptually worthwhile, it reports the ketosteroid and hydroxycorticosteroid changes over a considerable period of time in seven women undergoing psychoanalysis, attempting to correlate these changes with phases in the analyses. The researchers have a clear and valid methodological approach, and, unaware of the pitfalls and complexities, recognize that their research falls short of yielding the correlates they seek. Yet the title is misleading, for this work does not fulfill its promise of enlarging the reader's understanding of psychosomatic gynecological disorders, but focuses on seven case histories in which secondary amenorrhea, premenstrual tension, and frigidity were presenting symptoms of serious personality disorders. The rather general and incomplete case reports (in contrast to the excellent and detailed steroid studies) are presented strictly in the opaque language of classical psychoanalysis, often expressing only the

A study of 9 patients with secondary amenorrhea which began after stopping oral contraceptives is presented. None of the women had evidence of organic disease. Urinary 17-oxosteroids and 17-hydroxysteroids were normal. Withdrawal bleeding could be induced by the administration of exogenous gonadal steroids. 7 of the 9 patients underwent diagnostic gonadotrophin stimulation. The response to exogenous gonadotrophins indicated that the women had potentially responsive ovaries and that the cause of the amenorrhea lay in the hypothalamus or pituitary. 2 of the patients were treated with clomiphene and they readily ovulated and conceived. It is postulated that the prolonged inhibition of FSH and LH release that is associated with the use of oral contraceptives may very occasionally cause long-term disruption of hypothalamic cycling just as very rarely may normal pregnancy. In most cases the condition is resolved spontaeously.