ライフサイエンスコーパス: adrenal hyperplasia

1 st tumors (TART) in patients with congenital adrenal hyperplasia.

2 ermed corticotropin-independent macronodular adrenal hyperplasia.

3 rm of early severe hypertension with massive adrenal hyperplasia.

4 by enhancing our understanding of congenital adrenal hyperplasia.

5 is of primary aldosteronism with and without adrenal hyperplasia.

6 f severe aldosteronism and massive bilateral adrenal hyperplasia.

7 d primarily in male patients with congenital adrenal hyperplasia.

8 and with bilateral nonpigmented multinodular adrenal hyperplasia.

9 5 patients with cortisol-secreting bilateral adrenal hyperplasias.

10 with corticotropin-independent macronodular adrenal hyperplasia (12 men and 21 women who were 30 to

11 acranial pressure, a diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) with tes

12 oximately 95% of individuals with congenital adrenal hyperplasia, a common autosomal recessive metabo

13 proximately 95% of cases of human congenital adrenal hyperplasia, a disorder of adrenal steroidogenes

14 orticotropin (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a heterogeneous condition

15 e, cause the majority of cases in congenital adrenal hyperplasia, an autosomal recessive disorder.

16 (21 percent) of the patients with congenital adrenal hyperplasia and in 19 (95 percent) of the patien

17 Despite compensatory adrenal hyperplasia and increased adrenal secretion of c

18 deficiency, salt-wasting forms of congenital adrenal hyperplasia, and adrenal hypoplasia congenita al

19 l lipodystrophy and non classical congenital adrenal hyperplasia, and an essential splice site mutati

20 en shown in patients with classic congenital adrenal hyperplasia, and the degree of adrenomedullary i

21 es of corticotropin-independent macronodular adrenal hyperplasia appear to be genetic, most often wit

22 olism associated with bilateral macronodular adrenal hyperplasia appears to be corticotropin-dependen

23 ly accepted medical management of congenital adrenal hyperplasia are described.

24 terone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), remains a matter of debate.

25 nts, 10 (50%) had APA and 10 (50%) bilateral adrenal hyperplasia (BAH).

26 h dysregulation of one pathway may result in adrenal hyperplasia, but accumulation of a second or mul

27 wo inherited endocrine disorders, congenital adrenal hyperplasia (CAH) and apparent mineralocorticoid

28 is the mainstay of treatment for congenital adrenal hyperplasia (CAH) but has a narrow therapeutic i

29 Congenital adrenal hyperplasia (CAH) due to deficiency of 21-hydrox

30 ionale for neonatal screening for congenital adrenal hyperplasia (CAH) owing to low sensitivity in sa

31 ned for 21-hydroxylase deficiency congenital adrenal hyperplasia (CAH) worldwide.

32 of female genital virilization is congenital adrenal hyperplasia (CAH), in which excess androgen prod

33 Congenital adrenal hyperplasia (CAH), resulting from mutations in C

34 100 CYP21A2 variants give rise to congenital adrenal hyperplasia (CAH).

35 nadequately treated patients with congenital adrenal hyperplasia (CAH).

36 adolescents and young adults with congenital adrenal hyperplasia (CAH).

37 tensively studied the genetics of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency

38 n found in the testes of men with congenital adrenal hyperplasia; characteristic clinical and radiolo

39 concerns; for males with classic congenital adrenal hyperplasia, common issues include testicular ad

40 Congenital adrenal hyperplasia compromises both the development and

41 Congenital adrenal hyperplasia describes a group of inherited autos

42 metanephrines in 38 children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25

43 levels of androgens, as occurs in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

44 rotein in 15 patients with congenital lipoid adrenal hyperplasia from 10 countries.

45 c mutations causing many cases of congenital adrenal hyperplasia have been identified.

46 Although results for surgery for congenital adrenal hyperplasia have been less than satisfactory whe

47 ttenuated, late-onset, acquired, and cryptic adrenal hyperplasia, have been published thus far.

48 ared various regimens for classic congenital adrenal hyperplasia in adults, thus therapy is individua

49 aldosterone-producing adenoma and idiopathic adrenal hyperplasia in most cases.

50 The reduced ACTH response together with the adrenal hyperplasia in the IL-6 transgenic mice suggests

51 gene result in the disease congenital lipoid adrenal hyperplasia, in which steroid hormone biosynthes

52 Challenges in the treatment of congenital adrenal hyperplasia include avoidance of glucocorticoid

53 on of corticotropin-independent macronodular adrenal hyperplasia indicated that ARMC5 mutations influ

54 The management of congenital adrenal hyperplasia involves suppression of adrenal andr

55 Congenital adrenal hyperplasia is a family of inborn errors of ster

56 Congenital adrenal hyperplasia is a group of autosomal recessive di

57 Bilateral macronodular adrenal hyperplasia is a rare cause of primary adrenal C

58 ular pathogenesis of this form of congenital adrenal hyperplasia is caused by mutations in the gene e

59 Management of adolescents with congenital adrenal hyperplasia is especially challenging because ch

60 ction are normal in patients with congenital adrenal hyperplasia is not known.

61 ficiency, the most common type of congenital adrenal hyperplasia, is in place in many countries, howe

62 d to be elevated in patients with congenital adrenal hyperplasia; it is unknown whether patients with

63 del for the human disorder lipoid congenital adrenal hyperplasia (lipoid CAH), we used targeted gene

64 s cause potentially lethal congenital lipoid adrenal hyperplasia (lipoid CAH).

65 Corticotropin-independent macronodular adrenal hyperplasia may be an incidental finding or it m

66 PPNAD is a bilateral adrenal hyperplasia often associated with Carney complex

67 Women with congenital adrenal hyperplasia often develop the polycystic ovary s

68 CCX structures in 22 salt-losing, congenital adrenal hyperplasia patients revealed a significant incr

69 The congenital lipoid adrenal hyperplasia phenotype is the result of two separ

70 In the group of patients with congenital adrenal hyperplasia, plasma epinephrine and metanephrine

71 ntly been discovered in primary macronodular adrenal hyperplasia (PMAH), a cause of Cushing syndrome.

72 education of females with classic congenital adrenal hyperplasia regarding their genital anatomy and

73 Patients with non-classic congenital adrenal hyperplasia require reassessment regarding the n

74 Congenital lipoid adrenal hyperplasia results in severe impairment of ster

75 ercent lower in the patients with congenital adrenal hyperplasia than in the normal subjects (P<0.05)

76 f StAR (A218V) that causes lipoid congenital adrenal hyperplasia was incorporated into the His-tag pr

77 In a patient with congenital adrenal hyperplasia, we discovered a TNXB-TNXA recombina

78 21A2, the disease-causing gene in congenital adrenal hyperplasia, we now provide a full structural ex

79 Material/Forty-one patients with congenital adrenal hyperplasia were evaluated by gray-scale and col

80 lications of this gene resulted in bilateral adrenal hyperplasias, whereas somatic PRKACA mutations r

81 In three patients with congenital adrenal hyperplasia who had undergone bilateral adrenale

82 the underlying molecular basis of congenital adrenal hyperplasia with apparent combined P450C17 and P

83 Congenital adrenal hyperplasia with apparent combined P450C17 and P