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1 nical trials for the treatment of congenital adrenal hyperplasia.
2 st tumors (TART) in patients with congenital adrenal hyperplasia.
3 ermed corticotropin-independent macronodular adrenal hyperplasia.
4 rm of early severe hypertension with massive adrenal hyperplasia.
5 by enhancing our understanding of congenital adrenal hyperplasia.
6 is of primary aldosteronism with and without adrenal hyperplasia.
7 f severe aldosteronism and massive bilateral adrenal hyperplasia.
8 d primarily in male patients with congenital adrenal hyperplasia.
9 and with bilateral nonpigmented multinodular adrenal hyperplasia.
10 5 patients with cortisol-secreting bilateral adrenal hyperplasias.
11 with corticotropin-independent macronodular adrenal hyperplasia (12 men and 21 women who were 30 to
12 acranial pressure, a diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) with tes
13 oximately 95% of individuals with congenital adrenal hyperplasia, a common autosomal recessive metabo
14 proximately 95% of cases of human congenital adrenal hyperplasia, a disorder of adrenal steroidogenes
15 orticotropin (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a heterogeneous condition
16 e, cause the majority of cases in congenital adrenal hyperplasia, an autosomal recessive disorder.
17 (21 percent) of the patients with congenital adrenal hyperplasia and in 19 (95 percent) of the patien
20 deficiency, salt-wasting forms of congenital adrenal hyperplasia, and adrenal hypoplasia congenita al
21 l lipodystrophy and non classical congenital adrenal hyperplasia, and an essential splice site mutati
22 en shown in patients with classic congenital adrenal hyperplasia, and the degree of adrenomedullary i
23 une maladies such as preeclampsia, bilateral adrenal hyperplasia, and the rejection of organ transpla
24 es of corticotropin-independent macronodular adrenal hyperplasia appear to be genetic, most often wit
25 olism associated with bilateral macronodular adrenal hyperplasia appears to be corticotropin-dependen
27 terone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), remains a matter of debate.
29 h dysregulation of one pathway may result in adrenal hyperplasia, but accumulation of a second or mul
30 wo inherited endocrine disorders, congenital adrenal hyperplasia (CAH) and apparent mineralocorticoid
31 is the mainstay of treatment for congenital adrenal hyperplasia (CAH) but has a narrow therapeutic i
35 classic 21-hydroxylase deficiency congenital adrenal hyperplasia (CAH) is treated with glucocorticoid
36 ionale for neonatal screening for congenital adrenal hyperplasia (CAH) owing to low sensitivity in sa
39 of female genital virilization is congenital adrenal hyperplasia (CAH), in which excess androgen prod
44 tensively studied the genetics of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency
45 n found in the testes of men with congenital adrenal hyperplasia; characteristic clinical and radiolo
46 concerns; for males with classic congenital adrenal hyperplasia, common issues include testicular ad
49 metanephrines in 38 children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25
50 levels of androgens, as occurs in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
52 virilization of girls affected by congenital adrenal hyperplasia due to P450 oxidoreductase deficienc
55 Although results for surgery for congenital adrenal hyperplasia have been less than satisfactory whe
57 ared various regimens for classic congenital adrenal hyperplasia in adults, thus therapy is individua
60 The reduced ACTH response together with the adrenal hyperplasia in the IL-6 transgenic mice suggests
61 gene result in the disease congenital lipoid adrenal hyperplasia, in which steroid hormone biosynthes
62 Challenges in the treatment of congenital adrenal hyperplasia include avoidance of glucocorticoid
63 on of corticotropin-independent macronodular adrenal hyperplasia indicated that ARMC5 mutations influ
68 ular pathogenesis of this form of congenital adrenal hyperplasia is caused by mutations in the gene e
69 Management of adolescents with congenital adrenal hyperplasia is especially challenging because ch
71 ficiency, the most common type of congenital adrenal hyperplasia, is in place in many countries, howe
72 d to be elevated in patients with congenital adrenal hyperplasia; it is unknown whether patients with
73 del for the human disorder lipoid congenital adrenal hyperplasia (lipoid CAH), we used targeted gene
78 CCX structures in 22 salt-losing, congenital adrenal hyperplasia patients revealed a significant incr
79 caused by autoimmune destruction, congenital adrenal hyperplasia, pharmacological inhibition (eg, hig
81 In the group of patients with congenital adrenal hyperplasia, plasma epinephrine and metanephrine
82 ntly been discovered in primary macronodular adrenal hyperplasia (PMAH), a cause of Cushing syndrome.
83 rders of androgen excess, such as congenital adrenal hyperplasia, premature adrenarche and polycystic
84 education of females with classic congenital adrenal hyperplasia regarding their genital anatomy and
87 ercent lower in the patients with congenital adrenal hyperplasia than in the normal subjects (P<0.05)
88 fic loss of ZNRF3, but not RNF43, results in adrenal hyperplasia that depends on Porcupine-mediated W
89 erone, with increased activity in congenital adrenal hyperplasia variants associated with 17alpha-hyd
90 f StAR (A218V) that causes lipoid congenital adrenal hyperplasia was incorporated into the His-tag pr
92 21A2, the disease-causing gene in congenital adrenal hyperplasia, we now provide a full structural ex
93 Material/Forty-one patients with congenital adrenal hyperplasia were evaluated by gray-scale and col
94 lications of this gene resulted in bilateral adrenal hyperplasias, whereas somatic PRKACA mutations r
96 the underlying molecular basis of congenital adrenal hyperplasia with apparent combined P450C17 and P