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189. Adrenal function in hirsute women treated with a combination of cyproterone acetate and ethinylestradiol
852
Abstracts
184. Pituifary fuoction in !%eehaak syndrome SHAHMANESH.M.. POURMAND.M. and ALI. Z.. Department of Medicine. Pahlavi University. Shiraz. Iran Pituitary function in post partum pituitary necrosis IS not well described. Ten patients. aged 35-50 years (mean 39) with the typical clinical picture of Sheehan% syndrome and a mean duration of amenorrhoea. loss of secondary sexual hair and absence of lactation of 1.5-18 years (mean 11.2) were tested. All presented with clinical and biochemical evidence of hypothyroidism. Through an indwelling venous catheter, 2001cg of thyrotrophin releasing hormone (Roche. 7 patients). 100~8 of Luteinizing hormone releaseing hormone (Ayerst. IO patients) and 0.0.5-0.1 units soluble insulin per kg body weight (8 patients) were injected simultaneously. Blood. withdrawn at 3Omin intervals for 2 h. was assayed for LH. FSH. TSH and prolactin by radioimmunoassays. cortisol by competitive binding assay and glucose. All subjects had a hypoglycaemic response below 32 mg per 100 ml. There was a significant rise in the maximal secretion from basal levels (paired t test) in blood cortisol. LH. FSH and TSH in the subjects. A greater than 100”,, rise tn basal hormone levels was seen in 8 out of IO subjects for LH. 4 out of 10 subjects for FSH. 4 out of 7 subjects for TSH and 3 out of 8 for cortisol. The prolactin response did not exceed 130’,, in any of the subjects. II is concluded that the functional capacity of pituttary cells is partially present after post partum necrosis. Absence of a rise in prolactin levels. may however, be useful in the diagnosis bf Sheehan‘s syndrome. (We wish to thank the NIAMDD. D. W. Butt and Dr Stockeli Hartree for supply of radioimmunoassay materials.) 187. Ultrastructure of prostatic carcinoma during hormonnl treatment VIHKO. P.. KONTTURI. M. and KORHONEN. L. K.. Departments of Anatomy and Surgery. University of Oulu. SF-90220 Oulu 22. Finland We have reported previously the effects of castration and oestrogen on the ultrastructural cytology of carcinoma of the prostate. The follow up period was from I to I2 months. The success of treatment was not determined by the histological type or degree of differentiation of the carcinoma. The aim of the hormonal therapy is to destroy the malignant cells. Electron microscopy (EM) reveals the signs of cell injury more clearly than light microscopy (LM). In the present study 30 patients were followed from I to 36 months. The LM and EM morphology as well as histochemical reactions for acid phosphatase were studied from needle biopsies. The object was to observe the effect of treatment. If the effect of treatment was positive. autophagocytosis, residual bodies and decrease in secretion were observed in the cancer cells within two months. The first signs of injury were observed in the endoplasmic reticulum. i.e. in the apparatus for protein synthesis. The nuclear changes being the main criteria at the LM level. were not constant and were more delayed in comparison with the changes in cellular orpanelles at the EM level.
188. Effect of cyproheptrdk aad clemastioe on plasma cortisol in normal pemom and in patieots with Cusbing’s synlroy WINKELMANN. W.. ALLOLIO. B.. HACKENBERG. K.. HEESEN. D.. KAULEN. D. and MIES. R.. Department
Internal Med. II. University of K(ifn and Medical Clinic. Department Endocrinology. University of Essen. Federal Republic of Germany An inhibitory effect of the serotonin antagomst cyproheptadine on the hypoglycemia-induced increase of plasma cortisol (F) and ACTH could be demonstrated in humans.
But cyproheptadine has not only a serotonin-antagonistic but also a histamine-antagonistic effect. We examined the influence of cyproheptadine and the antihistamine clemastine on basal F plasma levels as well as on the vasopressininduced F increase. in normal persons and in patients with Gushing’s syndrome. F was measured by radioimmunoassay. Followinp a cyproheptadine infusion (5Smg within 9Omini 15 normals showed a significant F decrease from 14.1 + 4.9 to 8.6 rt 2.9pgdl. Clemastine (4 mg by infusion) led to a comparable F decrease (9.5 + 3.8 vs 5.4 + 3.gpgidl). The vasopressin-induced F increase in normals was completely abolished by cyproheptadine and only partially by clemastine. In 6 patients with Cushinp’s syndrome cyproheptadine had no effect on the increased plasma F levels. In addition. the vasopressin-induced F increase from 25.3 + 7.7 to maximally 49.0 + 16.3 ,ug:dl in IO patients with Gushing’s syndrome was not influenced by cyproheptadine and clemastine. respectively. The inhibttory efTect of cyprohcptadme on vasopresssin-induced F Increase in normal persons indicates that this substance can influence ACTH secretion by direct action on the adenohypophysis. The effect of the histamine antagonist clemastine in comparable dosape on the vasopressinInduced F increase is less pronounced. The cyproheptadine etTect. thus. appears to be related mainly to the serotonm antagonistic capacity of this substance. The abolished effect of cyproheptadine in Cushin8.s syndrome could be explained by an exaggerated ACTH response in these cases. (Supported by Landesamt ftir Forschunp NRW.I 189. Adrenal function in hirsute women treated with a combination of cyproterone acetate and etbinylestradiol HANSSON. U.. ENEROTH. P. and HAGENFELDI, K.. Department of Obstetrics and Gynecology and Hormonlaboratoriet. Karolinska sjukhuset. 10401 Stockholm. Sweden Treatment with cyproterone acetate (CPA) in large doses in children with precocious puberty has resulted in depression of adrenal function. impairment of cortisol response to exogenous ACTH and inhibition of ACTH secretion. Therefore the adrenal function has been studied in a 8roup of hirsute women treated with a combination of 5Omg CPA and 5Opg of ethinyl~tradiol in a reversed sequential therapy. Basal levels of tort isol. tort icosterone. It desoxs cortisol. tesrosterone. dihydrotestosterone. androstendione. dihydroepiandrostendione and l7-OH-progesterone were determined before treatment and during therapy. Dexamethazone suppression tests and ACTH stimulation tests were also performed. After 3 months of treatment no changes were found in basal levels of I Idesoxycortisol. testosterone. dihydrot~tosterone. dihydroepiandrostendione and I ‘J-OH-progesterone. The androstendione levels were markedly decreased (P e 0.01) and cortisol and corticosterone levels were markedly increased (P c 0.01) during treatment. The ratio between cortisol and corticosterone was unchanged which could indicate a cross reaction as the reason for the corticosterone increase. Although the basal levels were increased. all subjects showed a normal suppression on dexamethazont and a normal response to ACTH injection after 3 months of treatment. These alterations in the cortisol levels indicate an increased stimulation of the adrenal cortex and/or a declining turnover of the adrenal cortical steroids. The presented data are in contrast to the findings in children and may indicate a different hormonal homeostatic adrenocortical regulation in women. tw.ovuiatt stcmidogcacshin patients with byperprolactiaaemia before ad rfter brotnoergocrypti~ thPy VAIDYA. R. A., ALOORKAR. S. D.. MEWERJI. p. K.. RAIKAR. R. S.. SHETH. A. R.. SHAH. H. P. and JOSHI.
Abstracts
184. Pituifary fuoction in !%eehaak syndrome SHAHMANESH.M.. POURMAND.M. and ALI. Z.. Department of Medicine. Pahlavi University. Shiraz. Iran Pituitary function in post partum pituitary necrosis IS not well described. Ten patients. aged 35-50 years (mean 39) with the typical clinical picture of Sheehan% syndrome and a mean duration of amenorrhoea. loss of secondary sexual hair and absence of lactation of 1.5-18 years (mean 11.2) were tested. All presented with clinical and biochemical evidence of hypothyroidism. Through an indwelling venous catheter, 2001cg of thyrotrophin releasing hormone (Roche. 7 patients). 100~8 of Luteinizing hormone releaseing hormone (Ayerst. IO patients) and 0.0.5-0.1 units soluble insulin per kg body weight (8 patients) were injected simultaneously. Blood. withdrawn at 3Omin intervals for 2 h. was assayed for LH. FSH. TSH and prolactin by radioimmunoassays. cortisol by competitive binding assay and glucose. All subjects had a hypoglycaemic response below 32 mg per 100 ml. There was a significant rise in the maximal secretion from basal levels (paired t test) in blood cortisol. LH. FSH and TSH in the subjects. A greater than 100”,, rise tn basal hormone levels was seen in 8 out of IO subjects for LH. 4 out of 10 subjects for FSH. 4 out of 7 subjects for TSH and 3 out of 8 for cortisol. The prolactin response did not exceed 130’,, in any of the subjects. II is concluded that the functional capacity of pituttary cells is partially present after post partum necrosis. Absence of a rise in prolactin levels. may however, be useful in the diagnosis bf Sheehan‘s syndrome. (We wish to thank the NIAMDD. D. W. Butt and Dr Stockeli Hartree for supply of radioimmunoassay materials.) 187. Ultrastructure of prostatic carcinoma during hormonnl treatment VIHKO. P.. KONTTURI. M. and KORHONEN. L. K.. Departments of Anatomy and Surgery. University of Oulu. SF-90220 Oulu 22. Finland We have reported previously the effects of castration and oestrogen on the ultrastructural cytology of carcinoma of the prostate. The follow up period was from I to I2 months. The success of treatment was not determined by the histological type or degree of differentiation of the carcinoma. The aim of the hormonal therapy is to destroy the malignant cells. Electron microscopy (EM) reveals the signs of cell injury more clearly than light microscopy (LM). In the present study 30 patients were followed from I to 36 months. The LM and EM morphology as well as histochemical reactions for acid phosphatase were studied from needle biopsies. The object was to observe the effect of treatment. If the effect of treatment was positive. autophagocytosis, residual bodies and decrease in secretion were observed in the cancer cells within two months. The first signs of injury were observed in the endoplasmic reticulum. i.e. in the apparatus for protein synthesis. The nuclear changes being the main criteria at the LM level. were not constant and were more delayed in comparison with the changes in cellular orpanelles at the EM level.
188. Effect of cyproheptrdk aad clemastioe on plasma cortisol in normal pemom and in patieots with Cusbing’s synlroy WINKELMANN. W.. ALLOLIO. B.. HACKENBERG. K.. HEESEN. D.. KAULEN. D. and MIES. R.. Department
Internal Med. II. University of K(ifn and Medical Clinic. Department Endocrinology. University of Essen. Federal Republic of Germany An inhibitory effect of the serotonin antagomst cyproheptadine on the hypoglycemia-induced increase of plasma cortisol (F) and ACTH could be demonstrated in humans.
But cyproheptadine has not only a serotonin-antagonistic but also a histamine-antagonistic effect. We examined the influence of cyproheptadine and the antihistamine clemastine on basal F plasma levels as well as on the vasopressininduced F increase. in normal persons and in patients with Gushing’s syndrome. F was measured by radioimmunoassay. Followinp a cyproheptadine infusion (5Smg within 9Omini 15 normals showed a significant F decrease from 14.1 + 4.9 to 8.6 rt 2.9pgdl. Clemastine (4 mg by infusion) led to a comparable F decrease (9.5 + 3.8 vs 5.4 + 3.gpgidl). The vasopressin-induced F increase in normals was completely abolished by cyproheptadine and only partially by clemastine. In 6 patients with Cushinp’s syndrome cyproheptadine had no effect on the increased plasma F levels. In addition. the vasopressin-induced F increase from 25.3 + 7.7 to maximally 49.0 + 16.3 ,ug:dl in IO patients with Gushing’s syndrome was not influenced by cyproheptadine and clemastine. respectively. The inhibttory efTect of cyprohcptadme on vasopresssin-induced F Increase in normal persons indicates that this substance can influence ACTH secretion by direct action on the adenohypophysis. The effect of the histamine antagonist clemastine in comparable dosape on the vasopressinInduced F increase is less pronounced. The cyproheptadine etTect. thus. appears to be related mainly to the serotonm antagonistic capacity of this substance. The abolished effect of cyproheptadine in Cushin8.s syndrome could be explained by an exaggerated ACTH response in these cases. (Supported by Landesamt ftir Forschunp NRW.I 189. Adrenal function in hirsute women treated with a combination of cyproterone acetate and etbinylestradiol HANSSON. U.. ENEROTH. P. and HAGENFELDI, K.. Department of Obstetrics and Gynecology and Hormonlaboratoriet. Karolinska sjukhuset. 10401 Stockholm. Sweden Treatment with cyproterone acetate (CPA) in large doses in children with precocious puberty has resulted in depression of adrenal function. impairment of cortisol response to exogenous ACTH and inhibition of ACTH secretion. Therefore the adrenal function has been studied in a 8roup of hirsute women treated with a combination of 5Omg CPA and 5Opg of ethinyl~tradiol in a reversed sequential therapy. Basal levels of tort isol. tort icosterone. It desoxs cortisol. tesrosterone. dihydrotestosterone. androstendione. dihydroepiandrostendione and l7-OH-progesterone were determined before treatment and during therapy. Dexamethazone suppression tests and ACTH stimulation tests were also performed. After 3 months of treatment no changes were found in basal levels of I Idesoxycortisol. testosterone. dihydrot~tosterone. dihydroepiandrostendione and I ‘J-OH-progesterone. The androstendione levels were markedly decreased (P e 0.01) and cortisol and corticosterone levels were markedly increased (P c 0.01) during treatment. The ratio between cortisol and corticosterone was unchanged which could indicate a cross reaction as the reason for the corticosterone increase. Although the basal levels were increased. all subjects showed a normal suppression on dexamethazont and a normal response to ACTH injection after 3 months of treatment. These alterations in the cortisol levels indicate an increased stimulation of the adrenal cortex and/or a declining turnover of the adrenal cortical steroids. The presented data are in contrast to the findings in children and may indicate a different hormonal homeostatic adrenocortical regulation in women. tw.ovuiatt stcmidogcacshin patients with byperprolactiaaemia before ad rfter brotnoergocrypti~ thPy VAIDYA. R. A., ALOORKAR. S. D.. MEWERJI. p. K.. RAIKAR. R. S.. SHETH. A. R.. SHAH. H. P. and JOSHI.