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A patient receiving oral contraceptive hormone therapy developed a hepatic adenoma. Widespread haemorrhages, which were apparently unrelated to trauma, developed in the adenoma. Attention is drawn to the increasing incidence of Pill-associated hepatic tumours, and to the possibility of a fatal haemorrhage.
The proliferative rates of terminal duct cells were studied by tritiated thymidine labeling in vitro in 104 specimens of benign breast tissue from 92 women, The tritiated thymidine labeling index showed a cyclic pattern consistent with regulation by female sex hormones. It was low during the segment of the menstrual cycle encompassing days 2 through 15 (early cycle) and often was elevated during the segment encompassing days 16 through 1 (late cycle). The early cycle geometric mean index for morphologically normal terminal ducts was 0.19,and for ducts of fibroadenomas it was 0.77. The geomitric means for latecycle were 1.03 and 1.67 respectively. The difference for normal ducts between early and late cycles was highly significant (p less than 0.001). For both normal ducts and fibroadenomas the tritiated thymidine labeling index correlated negatively with the age of the patient, and the higher index value of fibroadenoma ducts relative to normal ducts was entirely accounted for by the younger mean age of the fibroadenoma patients. Oral use of contraceptive hormones could not be shown to change the index in either normal ducts or fibroadenoma ducts. Based on a postulated duration of DNA synthesis of 12 hours, the mean turnover time of the cells of normal terminal ducts would be approximately 22 days for 20 year old women with regular menstrual cycles, and would increase to 147 day at age 40. The mean potential doubling times of fibroadenomas would be approximately 33 days. The index values of other benign ductal proliferative lesions of the breast were similar to those of fibroadenomas and normal terminal ducts.
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An exudative retinal process was noticed in a 38-year-old woman who had taken oral hormonal contraceptives for about 8 years. An incidental finding was a fundus albipunctatus in combination with an euryblepharon. There was further a strange shading in the colour of fundus, perhaps identical with the well known Mizuophenomenon. It seems that the macula is starting point of this phenomenon (Fig. 3). Possibly exudative processes in the plexus chorioidei of brain, also are due to complications in the ZNS from contraceptives.
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We have effectuated a chromogenic and immunologic determination of alpha 2-At III and antiplasmin in plasma into three groups of patients. The 1st group is constituted of 93 subjects which never take oral hormone contraceptives. The 2nd group is constituted of 56 subjects who are taking oral hormone contraceptives. The 3rd group is constituted of 55 subjects in pregnancy (VI-VIII months). The results show a light difference, in the immunologic assay, between I in equilibrium or formed of II and I in equilibrium or formed of III, but there is not a significant difference in the chromogenic determination. Data have not evidenced significant variations in the antiplasmin too, except for the group of subjects in pregnancy.
A 38 year old previously well woman had sudden onset of upper abdominal pain and fever. Ultrasound examination revealed a necrotizing lesion in the liver. Arteriography revealed findings consistent with an adenoma or focal nodular hyperplasia. A right lobectomy and wedge resection of a similar lesion in the left lobe were done. Microscopy of both lesions indicated focal nodular hyperplasia. Adenoma is said to be related to the contraceptive oral hormone; focal nodular hyperplasia not. But it is possible that both may have an increased incidence of bleeding in the users of the oral contraceptive hormones.
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Estrogens are known to change the level of specific circulating proteinthyroid binding globulin (TBG). In view of this, a study was conducted of the effect of some hormonal oral contraceptives on the thyroid function by using routine procedures: thyroid scintigraphy, protein bound iodine (PBI), determination of thyroid hormones thyroxine and triiodothyronine. No statistically significant difference was found between the experimental (N = 84) and the control (N = 34) group.
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In man both basal gonadotrophin levels and the pituitary responses to LHRH remained relatively constant throughout life. In women the pituitary sensitivity varied in the menstrual cycle due to the typical cyclic variation of oestradiol and progesterone. The max delta LH increase to 100 mug LHRH was observed in the periovulatory period (183 +/- 41 mU/ml); it was also significantly higher in the luteal (49 +/- 7 mu/ml) than in the early follicular phase (18 +/- 3 mU/ml). The effect of exogenous sex steroid hormones taken as contraceptive drugs was then studied in 15 women. Significantly lower LH and FSH basal values as well as responses to LHRH were observed in 8 normal women under oral combined contraceptives. Conversely, in 7 women under oral sequential contraceptives, basal LH and FSH remained in the normal range. The LH-FSH responses were increased and delayed when these tests were performed during the period of estrogen treatment. Thus, with combined oral contraceptives, constant and high levels of estrogens and progesterone not only inhibit the LH peak, but also decrease the basal LH-FSH levels and responses to releasing hormone. Conversely, with sequential oral contraceptives, the low level of estradiol does not inhibit these responses and even enhances them. In menopausal women both basal and gonadotrophin responses to LHRH were increased indicating an important pituitary reserve. In menstruating women a significant estradiol increase is observed 2 and 4 hours after a 100 mug LHRH injection, both during the follicular and the luteal phases whereas progesterone increases only in the luteal phase. In men, testosterone was found to increase 4 hours after a 100 mug LHRH injection. These studies show that in normal subjects, sex steroid hormones are important regulators of the sensitivity of the pituitary responsiveness to releasing hormone.
75 women received different preparates of contraceptives (Non-Ovlon, Ovosiston, Gravistat, Deposistion--VEB Jenapharm Jena, GDR) for two years. In the last month of the application of the sexual steroids and one month later the lysozyme titer in the sera was tested to determine a reverse or stop-effect. An elevation of the muramidase could be shown in all cases. This findings are interpreted in relation to a non manifest influence of sexualsteroids on the lysozyme.
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Three sources of information are available pertaining to the effect of oral contraceptive hormones on the breast: 1) toxicity experiments in animals; 2) histologic examinations of breast tissue from women taking hormones; and 3) epidemiologic studies of women using hormones. Animals treated with hormones at doses equivalent to the human contraceptive level have not developed cancer of the breast at a greater than expected frequency. Monkeys, the one experimental animal with a reproductive cycle similar to humans, have not developed cancer during long-term hormone administration except for a single animal which likely represents a chance occurrence. In humans, histologic studies of breast tissue have failed to identify abnormalities which could be attributed to hormones with rare exceptions of secretory change indistinguishable from normal lactating breast. Epidemiologic studies have usually shown a decreased frequency of benign breast disease and neither an increase nor a decrease in carcinoma of the breast. The one exception to the latter statement is a possible increased risk of cancer in long-term users who have had previous surgery for benign breast disease.
The increased incidence of liver tumors in women of childbearing age who have been using oral contraceptives for many years suggests an environmental causation. The causative agent may be the steroidal oral contraceptives. Two lesions are recognized: focal nodular hyperplasia and hepatic adenoma. This paper concentrates on focal nodular hyperplasia, with two cases added to the four previously described cases. It is postulated that the estrogen component causes vascular lesions characterized by myointimal hyperplasia and thrombosis, leading to infarct, necrosis, and subsequent nodular hepatic regeneration. The clinical feature highlighted is the long history of gastrointestinal disturbance associated with negative gastrointestinal investigation with the possible exception of cholelithiasis. It is suggested that gray-scale ultrasonography is an effective screening method that also aids in a definitive diagnosis. As these tumors are often incidental findings it is emphasized that the liver should always be inspected at laparoscopy. Ultimately, diagnosis by biopsy or excision is essential as it may well be possible to treat cases of focal nodular hyperplasia of the liver conservatively, once oral contraceptives have been discontinued.