Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The differential regulation of immunoactive FSH and LH secretion by endogenous GnRH was studied using a GnRH antagonist, [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]GnRH (the NAL-ARG antagonist), in normal women in the early follicular phase of the menstrual cycle, and their responses were compared to those in two groups of control women. Pulsatile LH secretion was examined as an index of the completeness of blockade of endogenous GnRH secretion. There was a dose-dependent decrease in both the frequency and amplitude of LH pulses. At the highest dose, LH pulses were completely abolished within 20 min after sc administration of the GnRH antagonist and for a minimum of 8 h in all women. The mean plasma LH levels were reduced within the first 4 h after antagonist administration at all doses (P less than 0.001). The duration of LH suppression was influenced by antagonist dose, with a continued effect 24 h after administration of the 500 micrograms/kg dose only. The maximum degree of LH suppression was 40% after 50 micrograms/kg (n = 6), 60% after 150 micrograms/kg (n = 6), and 59% after 500 micrograms/kg (n = 5). In contrast, plasma immunoreactive FSH levels did not change after these doses of the NAL-ARG GnRH antagonist. The maximum degree of FSH suppression was 16%, and the changes in plasma FSH concentrations were not dose dependent. Serum antagonist concentrations rose within 30 min after its administration to mean peak levels of 7.5 +/- 2.1 (+/- SE), 20.4 +/- 6.1, and 151 +/- 21 ng/mL after the 50, 150, and 500 micrograms/kg doses, respectively. The half-time of the disappearance of the NAL-ARG GnRH antagonist from plasma was 8.8 +/- 1.5 h. While there were no effects of antagonist administration on hematological, hepatic, or renal function, three women developed urticaria distant from the site of injection when administered the highest dose. We conclude that blockade of GnRH receptors by a GnRH antagonist 1) effectively antagonizes the action of GnRH, as assessed by its ability to block pulsatile LH secretion and reduce mean plasma LH levels; and 2) inhibits LH release to a considerably greater degree than FSH release, providing further evidence of possible GnRH-independent FSH secretion.
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PMID:Evidence of differential control of FSH and LH secretion by gonadotropin-releasing hormone (GnRH) from the use of a GnRH antagonist. 313 43

The aim of the present study was to evaluate the estrogen dermatitis of women who have chronic skin disorders with exacerbations or premenstrual dermatitis in a cyclic pattern. Twenty-three women exhibiting skin disorders of pruritus, urticaria, eczema, papulovesicular eruption, hirsutism-acne with hyperpigmentation (hirsutism and/or its related disorders such as acne) and 18 healthy control subjects were included in the study. Sensitivity to estrogen was described in 14 of 23 women. Of the 14 estrogen sensitive women, nine had a premenstrual flare of their skin lesions and five had a chronic dermatitis with exacerbations. In the evaluation of endocrine profile, mean serum testosterone and LH levels of the patient group were significantly higher than controls (2.814 +/- 0.839 vs. 1.561 +/- 0.645 nm/l, P < 0.001; 10.843 +/- 2.538 vs. 4.539 +/- 1.215 IU/l, P < 0.0001). The LH/FSH ratio of the patient group was also significantly higher than controls (1.765 +/- 0.329 vs. 0.810 +/- 0.0116, P < 0.0001). Mean serum progesterone level of the patient group was significantly lower than the control group (0.499 +/- 0.201 vs. 0.977 +/- 0.396 ng/ml, P < 0.001). Hyperandrogenism and anovulation were the two more common outcomes in the patient group. Skin lesions of estrogen sensitive women were all cured with the administration of tamoxifen 20 mg daily for 7 days premenstrually.
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PMID:Estrogen dermatitis. 907 30