Separation of Antibody-Bound and Free Human Follicle-Stimulating and Luteinizing Hormones by Ethanol-Ammonium Acetate

Römmler, A.; Saxena, Brij B.

doi:10.1530/acta.0.0720643

Cited by 20 publications

(5 citation statements)

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“…Urinary aldosterone was measured according to previously described methods (5), as were plasma FSH and LH (6). Urinary excretion of 17-hydroxycorticosteroids and 17-ketosteroids was measured by established methods (7,8).…”

Section: Methodsmentioning

confidence: 99%

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Prepubertal Diagnosis of Steroid 5α-Reductase Deficiency*

Saenger

Goldman

Levine

et al. 1978

The Journal of Clinical Endocrinology & Metabolism

101

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The diagnosis of 5 alpha-reductase deficiency was proven in two prepubertal patients with male pseudohermaphroditism (MPH). Both had a 46-XY karyotype and were reared as females; one child had been castrated in infancy. Clitoromegaly, urogenital sinus, and short vaginal pouch were present in both; inguinal gonads were palpable in one. The diagnosis was made biochemically by observing characteristic changes in five parameters: 1) abnormally high testosterone to dihydrotestosterone (T:DHT) ratio after hCG stimulation (35 and 53 vs. normal, 11 +/- 3), 2) abnormally high 5 beta-T metabolites in urine (8.1 and 6.0 vs. normal, less than 1),3) deficient conversion of T to DHT during [3H] T infusion (0.3 and 0.4% vs. normal, 5.3 +/- 3), 4) deficient conversion of [14 C] T to 5 alpha-reduced metabolites by nongenital skin fibroblasts (2.2 and 1.9 pmol/microgram DNA/nmol substrate vs. 68.4+/- 7.8 Pmol/microgram DNA/nmol substrate in normal controls), and 5) deficient conversion of [14C]T to DHT in genital skin slices. The fact that this syndrome represents a defect in T metabolism rather in in T binding is demonstrated by the observation that binding of [3H]DHT to cytosol of skin fibroblasts was normal (4.2 dpm/micrograms DNA vs. normal male values of 3.7 +/- 0.64). Thus, the present report suggests that 5 alpha-reductase deficiency can be diagnosed during childhood and even after castration by metabolic studies of nongenital skin fibroblasts and determination of the conversion ratio of [3H]T to [3H]DHT in plasma.

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Section: Methodsmentioning

confidence: 99%

“…Infusion of [1,2,6, H]T (specific activity, 85 Ci/mmol) by the constant infusion technique as described by Tait and Horton (9, 10) was utilized to measure the plasma conversion of T to DHT.…”

Section: Measurement Of the Conversion Of Testosterone (T) To Dhtmentioning

confidence: 99%

Prepubertal Diagnosis of Steroid 5α-Reductase Deficiency*

Saenger

Goldman

Levine

et al. 1978

The Journal of Clinical Endocrinology & Metabolism

101

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“…The concentrations of LH in samples of effluent were estimated by a modification of the radioimmunoassay described by Rommler & Saxena (1973). In this method 'ethanolammonium acetate' is used to precipitate antibody-bound, but not free, labelled LH.…”

Section: Methodsmentioning

confidence: 99%

Steroid Priming of the Luteinizing Hormone Response to Luteinizing Hormone Releasing Hormone

Beck¹,

Bay²,

Smith³

et al. 1978

Journal of Endocrinology

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Perifusion experiments were performed to study the stimulatory effects of luteinizing hormone releasing hormone (LH-RH) on the release of LH from anterior pituitary tissue. Exposure of pituitary tissue from normal male rats to LH-RH (5 ng/ml for 5 min) induced a small release of LH; in tissue from ovariectomized rats receiving no pretreatment, the release was more than three times greater and in tissue from gonadectomized male or female rats pretreated with oestradiol benzoate and progesterone, the release was six times greater than that observed in normal rats. Further exposure of pituitary tissue from gonadectomized steroid-pretreated male and female rats to LH-RH (5 ng/ml) induced an increase in the level of LH even greater than that seen after the initial exposure (priming action of LH-RH); in tissue from ovariectomized rats receiving no pretreatment, less LH was released than after the first exposure to LH-RH and in tissue from normal male rats the response was unchanged.

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“…All determinations were performed in duplicate, and serial samples from the same subject were determined in the same batch of assays. Precision, accuracy and sensitivity of the radioimmunoassays for each hormone were as described before (5,12,17,19).…”

Section: Materials a N D M E T H O D Smentioning

confidence: 99%

TRH‐Induced Hyperprolactinemia and Pituitary‐Ovarian Function

Ylikorkala

Dawood

Kivinen

1980

Intl J Gynecology & Obste

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To elucidate the role of prolactin in the control of pituitary-ovarian function, eight healthy women were given 80 mg of synthetic thyrotropin-releasing hormone (TRH) orally on two consecutive days during the luteal phase of their menstrual cycle. TRH elevated serum prolactin to a mean concentration of 43.8 ng/ml on the first day and to 15.5 ng/ml on the second day. The reduced response to the second TRH dose was statistically significant (p < 0.05). Accompanying changes in concentrations of gonadotropins or ovarian steroids were not consistent. Short-term oral administration of TRH and/or the temporary hyperprolactinemia induced by its use do not modify the pituitary-ovarian function during the luteal phase of the menstrual cycle.

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Separation of Antibody-Bound and Free Human Follicle-Stimulating and Luteinizing Hormones by Ethanol-Ammonium Acetate

Cited by 20 publications

References 0 publications

Prepubertal Diagnosis of Steroid 5α-Reductase Deficiency*

Prepubertal Diagnosis of Steroid 5α-Reductase Deficiency*

Steroid Priming of the Luteinizing Hormone Response to Luteinizing Hormone Releasing Hormone

TRH‐Induced Hyperprolactinemia and Pituitary‐Ovarian Function

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