Titlebook: Congenital Adrenal Hyperplasia; Maria I. New,Lenore S. Levine Book 1984 Springer-Verlag Berlin, Heidelberg 1984 Adrenogenitales Syndrom.gl

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書目名稱Congenital Adrenal Hyperplasia影響因子(影響力)




書目名稱Congenital Adrenal Hyperplasia影響因子(影響力)學科排名




書目名稱Congenital Adrenal Hyperplasia網(wǎng)絡公開度




書目名稱Congenital Adrenal Hyperplasia網(wǎng)絡公開度學科排名




書目名稱Congenital Adrenal Hyperplasia被引頻次




書目名稱Congenital Adrenal Hyperplasia被引頻次學科排名




書目名稱Congenital Adrenal Hyperplasia年度引用




書目名稱Congenital Adrenal Hyperplasia年度引用學科排名




書目名稱Congenital Adrenal Hyperplasia讀者反饋




書目名稱Congenital Adrenal Hyperplasia讀者反饋學科排名

輕彈

Recent Advances: The Fasciculata and Glomerulosa as Two Distinct Glands, (1970) suggested that an 11 .-hydroxylase defect might occur only in the fasciculata, sparing the glomerulosa from an 11 .-hydroxylase deficiency. The hypothesis accounts for the rise in aldosterone secretion observed in a patient with 11 .-hydroxylase deficiency after excessive DOC levels were sup

Carcinogen

Treatment,he efficacy of cortisone therapy for CAH due to 21-hydroxylase deficiency (Wilkins et al. 1950; Bartter et al. 1951; Bartter 1977), glucocorticoid therapy has been the keystone of treatment for this disorder. Glucocorticoid administration both replaces the deficient Cortisol and suppresses ACTH over

具體

Pubertal Development,nological age (John and Verkauf 1971; Ghali et al. 1977; Klingensmith et al. 1977; Pang et al. 1977 a). The pattern of gonadotropin response to LH-RH is appropriate for age in well-controlled prepubertal and pubertal female patients (Kirkland et al. 1974; Reiter et al. 1975). These normal findings s

Cubicle

Genetics,traits (Childs et al. 1956; Prader 1958; Wilkins 1962). Males and females are equally at risk (Baulieu et al. 1967). Although there are exceptions (Rosen- bloom and Smith 1966), the clinical presentation—simple virilizing or salt-wasting—is usually consistent within one family. In Europe and the USA

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Prenatal Diagnosis,niotic fluid of the affected fetus, several investigators have attempted the prenatal diagnosis by measurement of various hormones (New and Levine 1973). Most recently, elevated levels of 17-OHP (Frasier et al. 1975; Nagamani et al. 1978; Hughes and Laurence 1979; Pang et al. 1980b) and Δ. (Pang et

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莎草

,Electron–Specimen Interactions., suppressed by treatment, natriuresis occurs and renin-angiotensin levels consequently rise, stimulating the glomerulosa to synthesize aldosterone (Fig. 9). Because the glomerulosa, unlike the fasciculata, is spared the 11 .-hydroxylase defect, it can respond to this stimulation with an appropriate

febrile

條街道往前推

,Electron–Specimen Interactions.,t 50—80% of patients with 21-hydroxylase deficiency (Cohen 1969; Rimoin and Schimke 1971; Fife and Rappaport 1983). A very high incidence of salt-wasting CAH has been found among the Yupiks (Hirschfeld and Fleshman 1969).