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  • Title: Secondary amenorrhoea and oral contraceptives.
    Author: Ingerslev M, Jeppesen T, Ramsing EM.
    Journal: Acta Obstet Gynecol Scand; 1976; 55(3):233-8. PubMed ID: 945653.
    Abstract:
    Eight-seven cases of secondary amenorrhoea of more than 6 months' duration developing after treatment with oral contraceptives (group I) were compared with 227 cases of secondary amenorrhoea not preceded by treatment with combined tablets (group II). The two groups were collected during the same period. The average age of the patients was 4 years higher in group I than in group II. Oligomenorrhoea and previously occurred in 30% of group I and in 46% of group II. Pronounced predisposing factors., such as psychogenic trauma and stress with or without considerable change in body weight, were encountered in 26% in group I and 56% in group II. The incidence of increased urinary output of 17-keto steroids, 17-ketogenic steroids and of hirsutism was slightly higher in group II. The percentage of eosinophilic cells in vaginal scrapings was low in 20% in group I as compared with 46% in group II. Spontaneous return of pituitary-ovarian function occurred in 40% in both groups. Patients recovering spontaneously in group I presented a maximum during the first few months, followed by a steady and fairly uniform decline. Spontaneous recovery in group II was more or less independent of time. It seems reasonable to believe that oral contraceptives did promote or contribute to the development of secondary amenorrhoea in about 50%, representing cases with various predisposing factors. A causal relation between oral contraceptives and secondary amenorrhoea was indicated in the remaining 50% because of perfectly normal ovarian function before treatment and absence of predisposing factors. 87 cases (Group 1) of secondary amenorrhea starting immediately after treatment with estrogen-gestagen tablets and 227 cases (Group 2) with secondary amenorrhea not preceded by hormonal therapy were studied. In all cases the amenorrhea had been of more than 6 months' duration. Endocrine studies included urinary output of 17-keto steroids, 17-ketogenic steroids, and total gonadotropins. Basal metabolic rate, protein bound iodine (PBI), and triiodothyronine were measured and the percentage of eosinophilic cells in vaginal scrapings was assessed. Radiological examination of the sella turcica and visual field testing were carried out. Group 1 patients averaged 4 years older than those in Group 2. In 28% of cases, treatment with oral contraceptives had been given for menstrual irregularities only. Oligomenorrhea had been present previously in 30% of Group 1 and in 46% of Group 2 patients (p equals .05). Increased urinary output of 17-keto steroids and 17-ketogenic steroids, and of hirsutism were slightly higher in Group 2. Eosinophilic cells in vaginal scrapings were low in 20% of Group 1 patients and in 46% of Group 2 patients. Psychogenic factors or severe stress had been noted in 26% of Group 1 and in 56% of Group 2 patients (p equals .0125). Galctorrhea had occurred in 1 patient in Group 1 and in 4 in Group 2. Spontaneous recovery of pituitary-ovarian function occurred in 40% of both groups. Type of menstrual pattern before therapy in Group 1 did not alter spontaneous re covery rates. But when the interval between menarche and start of hormonal therapy had been shorter than 5 years the spontaneous recovery was greater, 32 vs. 42%, when it had been longer than 5 years. Other predisposing factors may explain the development of secondary amenorrhea in about 50% of cases occurring after treatment with oral contraceptives . In the other 50%, a causal relationship of the therapy is suggested.
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