ライフサイエンスコーパス: hypercortisolism

1 tropic hormone, indicating primary (adrenal) hypercortisolism.

2 mpact of clinical conditions associated with hypercortisolism.

3 ipates in PRKAR1A-mediated tumorigenesis and hypercortisolism.

4 g to high bone mass despite hypogonadism and hypercortisolism.

5 thways that each are driven and sustained by hypercortisolism.

6 iately high, considering the degree of their hypercortisolism.

7 y imaging can help identify tumor sources of hypercortisolism.

8 rophin-releasing hormone expression, chronic hypercortisolism, adrenocortical hyperplasia, glucose in

9 wareness have broadened our understanding of hypercortisolism and its role in the pathophysiology of

10 The phenomena of basal hypercortisolism and of dexamethasone resistance have lo

11 glucocorticoid sensitivity in the absence of hypercortisolism and to the pathogenesis of AIDS.

12 e development of adrenal cortex hyperplasia, hypercortisolism, and spleen atrophy, which was attenuat

13 ngal infections that arise in the setting of hypercortisolism, and the ways in which glucocorticoids

14 lectomy for symptomatic relief of persistent hypercortisolism appears to be an effective treatment op

15 Hypercortisolism as a causative factor in the developmen

16 with multiple glucose-lowering agents, have hypercortisolism as a causative factor in their poorly m

17 Thus, the hypercortisolism associated with bilateral macronodular

18 In contrast, patients with cholestasis show hypercortisolism associated with disease severity as mir

19 nt in glucose homeostasis and recommend that hypercortisolism be added to the Ominous Octet to form t

20 as well as metabolic disturbances mimicking hypercortisolism caused by Cushing disease.

21 These results suggest that neurogenic hypercortisolism contributes to a rapid systemic and fun

22 evelopment of primary aldosteronism (PA) and hypercortisolism [Cushing's syndrome (CS)] in humans, we

23 ential diagnosis and treatment of endogenous hypercortisolism--Cushing's syndrome.

24 Despite their hypercortisolism, depressed patients had normal levels o

25 We propose a reverberating cycle in which hypercortisolism disrupts the normal circadian rhythm ca

26 The primary treatment of Cushing disease (hypercortisolism due to ACTH-producing adenomas, which i

27 eatment of Cushing's disease, being cured of hypercortisolism for a minimum of 10 years at study entr

28 Psychologic stress and clinical hypercortisolism have been related to direct effects on

29 iseases (such as primary hyperaldosteronism, hypercortisolism, hyperandrogenism, or hyperestrogenism)

30 itive impairments associated with endogenous hypercortisolism in humans.

31 l implication of expanding the definition of hypercortisolism in patient populations with compromised

32 roxylase (11betaHSD) inhibitor used to treat hypercortisolism in pregnant, lactating, and neonatal po

33 nt of a buffalo hump cannot be attributed to hypercortisolism in these eight men.

34 e cause in approximately 65% of the cases of hypercortisolism) is adenoma resection and medical thera

35 tropin) and corticotropin-dependent forms of hypercortisolism (midnormal to elevated corticotropin le

36 rm effects and comorbidities associated with hypercortisolism need ongoing care.

37 unction, hyperparathyroidism, acromegaly and hypercortisolism on bone.

38 It is proposed that the negative impact of hypercortisolism on neurocognitive function mediates thi

39 isolation were associated in our study with hypercortisolism or feedback resistance.

40 t detectable in 40 patients with subclinical hypercortisolism or in 82 patients with other adrenal tu

41 quately treated hyperandrogenism, iatrogenic hypercortisolism, or both.

42 ho had received curative treatment and whose hypercortisolism remained in remission for more than 10

43 cians who treat patients with ACC and severe hypercortisolism should recognize that uncontrolled horm

44 n help distinguish between adrenal causes of hypercortisolism (suppressed corticotropin) and corticot