CONCURRENT 3β-Hydroxysteroid DEHYDROGENASE DEFICIENCY IN ADRENAL AND SCLEROCYSTIC OVARY

Axelrod, Leonard R.; Goldzieher, Joseph W.; Ross, Steven

doi:10.1530/acta.0.0480392

Cited by 46 publications

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“…Prevention of cyst formation in rabbits of the present study by AGP therefore, may have resulted from the inhibi¬ tion of oestrogen synthesis by this compound. Cystic ovaries in rabbits possessed subnormal 3ß-HSD concentration and specific activity, which agrees with similar observations in humans (Axelrod & Goldzieher 1962;Axelrod et al 1965) and rats (Shapiro & Leathern 1971) with this condition. However, ovarian weight was elevated 3-and 7-fold in rabbits bearing cystic ovaries produced by hCG and PMS, respectively, thus total capacity for ovarian A4-3-ketosteroid production was en¬ hanced.…”

Section: Resultssupporting

confidence: 87%

Prevention of cystic ovary induction in rabbits by aminoglutethimide

Albrecht

1980

Acta Endocrinologica

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Polycystic ovaries were induced in thyroidectomized rabbits by the administration of either 25 IU human chorionic gonadotrophin or 10 IU pregnant mare serum daily for a period of 20 days. Cystic ovaries in rabbits exhibited subnormal (P < 0.01) ovarian \ g=D\ 5-3\ g=b\ \ x=r eq-\ hydroxysteroid dehydrogenase (3\g=b\-HSD)concentration and specific activity. Since weight of cystic ovaries was markedly elevated, however, total capacity for \g=D\4-3-ketosteroid production was enhanced. Concomitant administration of chorionic gonadotrophin and aminoglutethimide phosphate to thyroidectomized rabbits prevented the formation of cystic ovaries indicating that a steroid, or steroids formed beyond cholesterol in the biosynthesic pathway is necessary for the experimental induction of cystic ovaries in this laboratory animal.Cystic ovaries induced in hypothyroid rats by the administration of human chorionic gonadotrophin (hCG) exhibit subnormal ovarian A5-3ß-hydroxysteroid dehydrogenase (3ß-HSD) concentration (Shapiro & Leathern 1971) and aromatization of androstenedione to oestradiol (Callard 8c Leathern 1965; Adams & Senseman 1976) indicating modifi¬ cations in ovarian steroidogenesis. Cystic ovaries are also formed in hypothyroid rabbits by either hCG or pregnant mare serum (PMS) administra¬ tion (Laird 1967), but their capacity for steroid synthesis has not been described.In the present study, ovarian 3ß-HSD activity was determined in rabbits following follicular cyst induction by thyroidectomy and either hCG, or PMS treatment to determine the potential for A4-3-ketosteroid production. As ovarian cyst formation is prevented in rats by the antioestrogen, ethamoxytriphetol (Leathern & Adams 1963), the current study also determined if inhibition of ste¬ roid formation by aminoglutethimide phosphate (AGP) administration would prevent cystic ovary formation in rabbits. Materials and MethodsImmature New Zealand white rabbits weighing 1 -1.2 kg were purchased from a local breeder. The animals were housed singly in air-conditioned quarters (22°C) with a controlled lighting schedule (lights on 6 a.m.; off 6 p.m.) and fed rabbit chow (Ralston Purina Co.) and water ad libitum, supplemented twice weekly with lettuce and carrots. The animals were permitted a 5-6 day adapta¬ tion period, then either surgically thyroidectomized un¬ der iv injected sodium pentobarbital anaesthesia (Nembutal, 50 mg/kg b.w., Abbott Laboratories) or left un¬ treated (euthyroid). Thirty days after surgery euthyroid and thyroidectomized rabbits received for 20 days one of the following regimens: (1) no treatment; (2) 25 IU hCG (chorionic gonadotrophin, Sigma) in 0.1 ml saline in¬ jected sc daily; (3) 10 IU PMS (Equinex, Ayerst) in 0.1 ml saline injected sc daily; (4) 100 mg AGP (Elipten, CIBA) in 0.2 ml olive oil injected sc twice daily, or (5) 25 IU hCG daily plus 100 mg AGP injected sc twice daily. The rabbits were killed by cervical dislocation between 9 and 11 a.m. on the day following the last injection; ovaries were immediately removed, dissected free o...

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Section: Resultssupporting

confidence: 87%

Prevention of cystic ovary induction in rabbits by aminoglutethimide

Albrecht

1980

Acta Endocrinologica

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“…Continued anovulation was also observed in CLAH patients and may involve the formation of ovarian cysts. Androgen is involved in polycystic ovary syndrome in patients with congenital adrenal hyperplasia (17,18). However, in our cases, androgen was not a likely factor, because serum levels of androgen were undetectable.…”

Section: Discussionmentioning

confidence: 52%

Mechanism for the development of ovarian cysts in patients with congenital lipoid adrenal hyperplasia

Shima

Tanae

Miki

et al. 2000

European Journal of Endocrinology

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Objective: Although ovarian cysts commonly occur in patients with congenital lipoid adrenal hyperplasia (CLAH), the mechanism of development remains to be determined. To clarify the pathogenesis of the ovarian cysts, endocrinological examinations were performed in patients with CLAH. Methods: The subjects were three Japanese CLAH patients. Basal body temperature, serum and urinary gonadotropin levels, serum and/or urinary ovarian hormones and mutations of the steroidogenic acute regulatory protein (StAR) gene were examined. Results: The basal body temperature was not biphasic in any patient. Basal LH levels were high in all CLAH patients and markedly responded to LH-releasing hormone in two patients. Urinary gonadotropin analysis revealed repetitive LH surges in the menstrual cycles of the CLAH patients. No increase in the urinary pregnanediol suggested anovulation in all patients, and bilateral ovarian cysts were found in two of the subjects. Examination of the StAR gene revealed a frameshift mutation 840delA at codon 238, a nonsense mutation Q258X at codon 258, a homozygotic mutation at Q258X, and a compound heterozygotic mutation with 251insG and Q258X. Conclusions: We concluded that the development of ovarian cysts may be derived from continued anovulation in CLAH patients. Elevated LH levels may be explained by increased sensitivity of the anterior pituitary to circulating estrogen.

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“…Females with 3f)-HSD deficiency experience menstrual disturbances and hirsutism (Axelrod et al 1965;. Menstruation normalizes once cyclic estrogen-progesterone therapy is begun.…”

Section: P-hydroxysteroid Dehydrogenase Deficiencymentioning

confidence: 99%

“…Menstrual disturbances, hirsutism, polycystic ovaries, acne, and clitoromegaly have been shown to be caused by a mild 3f)-HSD deficiency in some pubertal and postpubertal women (Axelrod et al 1965;Rosenfield et al 1980a;Lobo and Goebelsmann 1980a. These symptoms respond to treatment with steroid replacement therapy.…”

Section: P-hydroxysteroid Dehydrogenase Deficiencymentioning

confidence: 99%

Congenital Adrenal Hyperplasia

New

Levine

1984

Monographs on Endocrinology

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This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically those of translation, reprinting, fe-use of illustrations, broadcasting, reproduction by photocopying machine or similar means, and storage in data banks. Under §54 of the German Copyright Law where copies are made for other than private use. a fee is payable to 'Verwertungsgesellschaft Wort'. Munich. 1[. Springer-Verlag Berlin. Heidelberg 1984 Softcover reprint of the hardcover 1 st edition 1984The use of registered names, trademarks, etc. in this publication does not imply. even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.Product Liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature.

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CONCURRENT 3β-Hydroxysteroid DEHYDROGENASE DEFICIENCY IN ADRENAL AND SCLEROCYSTIC OVARY

Cited by 46 publications

References 0 publications

Prevention of cystic ovary induction in rabbits by aminoglutethimide

Prevention of cystic ovary induction in rabbits by aminoglutethimide

Mechanism for the development of ovarian cysts in patients with congenital lipoid adrenal hyperplasia

Congenital Adrenal Hyperplasia

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