ライフサイエンスコーパス: hyperaldosteronism

1 -producing adenomas of patients with primary hyperaldosteronism.

2 herapeutic value for curbing HF-exacerbating hyperaldosteronism.

3 l conditions characterized and aggravated by hyperaldosteronism.

4 as a possible therapeutic target for primary hyperaldosteronism.

5 ockout mice exhibit the hallmarks of primary hyperaldosteronism.

6 cluding a large, undiagnosed pool of primary hyperaldosteronism.

7 iagnosis and estimated prevalence of primary hyperaldosteronism.

8 .0001) compared with the 44 subjects without hyperaldosteronism.

9 n promoting hypertension in conjunction with hyperaldosteronism.

10 d gene that causes glucocorticoid-remediable hyperaldosteronism.

11 c alkalosis with normotensive hyperreninemic hyperaldosteronism.

12 related to deteriorating liver function and hyperaldosteronism.

13 was significantly lower in 36 subjects with hyperaldosteronism (1.8+/-1.3% versus 3.9+/-1.9% from ba

14 ma who only presented with clinical signs of hyperaldosteronism after renal transplantation.

15 sh an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as a possi

16 An association between chronic hyperaldosteronism and medullary nephrocalcinosis has ra

17 hat support our proposed association between hyperaldosteronism and nephrocalcinosis.

18 of, and differentiation of causes of primary hyperaldosteronism and the Cushing syndrome.

19 tissue calcification, volume depletion with hyperaldosteronism, and early death.

20 s included hyperphosphatemia, hypercalcemia, hyperaldosteronism, and elevated levels of 1,25-dihydrox

21 th deficits, rapid aging, hyperphosphatemia, hyperaldosteronism, and extensive vascular and soft tiss

22 dohypoaldosteronism, including hyperkalemia, hyperaldosteronism, and metabolic acidosis.

23 demonstrated significant suppression of the hyperaldosteronism as well as marked attenuation of prot

24 enic by a novel mechanism in which secondary hyperaldosteronism, associated with an adrenal-specific

25 It is hypothesized that the hyperaldosteronism attending this model stems from the c

26 is not limited to patients with demonstrable hyperaldosteronism but instead can be effective in resis

27 Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathic hypera

28 Hyperaldosteronism causes endothelial dysfunction indepe

29 Primary and secondary hyperaldosteronism correlate with LV enlargement and hig

30 Hyperaldosteronism correlates positively with vascular r

31 The importance of K for the hyperaldosteronism during dietary Na restriction was ver

32 angiotensin, led to a marked attenuation of hyperaldosteronism during dietary Na restriction.

33 otensin-independent mechanism exists for the hyperaldosteronism during LS; (b) high K is a central co

34 xia-PAH rats and monocrotaline-PAH rats with hyperaldosteronism expressed increased levels of the Rap

35 rs cause endocrine diseases (such as primary hyperaldosteronism, hypercortisolism, hyperandrogenism,

36 normally, intermediary feedback signals for hyperaldosteronism, i.e., both hypotension and high K, a

37 terone synthesis; in systemic blood vessels, hyperaldosteronism induces vascular dysfunction by incre

38 Primary hyperaldosteronism is a well-recognized cause of seconda

39 Primary hyperaldosteronism is an uncommon cause of hypertension

40 Hyperaldosteronism is associated with impaired endotheli

41 Indeed, hyperaldosteronism is associated with impaired pancreati

42 Hyperaldosteronism is associated with impaired vascular

43 Obesity-induced hyperaldosteronism is independent of the known regulator

44 Hyperaldosteronism leads todeleterious effects on the ki

45 been described: glucocorticoid-suppressible hyperaldosteronism, Liddle's syndrome, and apparent mine

46 Previously silent hyperaldosteronism may be unmasked by a successful renal

47 ynthesis seen in glucocorticoid-suppressible hyperaldosteronism may cause hypokalemia, suppressed pla

48 inflammasome, suggesting that the effect of hyperaldosteronism on the inflammasome may be mediated t

49 Hypertensive patients with hyperaldosteronism or normal levels of aldosterone exhib

50 result differs from that expected in primary hyperaldosteronism, our finding argues against low-renin

51 aldosteronism caused by bilateral idiopathic hyperaldosteronism remains unknown.

52 We conclude that chronic hyperaldosteronism should be included as one of the caus

53 Hyperaldosteronism sustains much of the hypertension, bu

54 ednisone to reduce the symptoms of secondary hyperaldosteronism that can occur with AA monotherapy.

55 Here we describe three women with hyperaldosteronism, two who presented in pregnancy and o

56 Hyperaldosteronism was diagnosed on the basis of a renin

57 ng diagnostic evaluation of 26 patients with hyperaldosteronism, we administered adrenocorticotrophic

58 ared with unilateral lesions, while rates of hyperaldosteronism were similar in both groups (4.3% [1

59 de may offer a novel way of treating primary hyperaldosteronism, which avoids the vascular side effec

60 67 years; median age, 46 years) with primary hyperaldosteronism who underwent 1.5-T MR imaging betwee

61 We describe five cases of hyperaldosteronism with a long- standing history in whom