Corticotropin-releasing factor (CRF): Stimulation in normal controls and in patients with Cushing's syndrome

Müller, O. A.; Hartwimmer, Johanna; Hauer, A.; Kaliebe, T.; Schopohl, Jochen; Stalla, Günter; Werder, Klaus von

doi:10.1016/0306-4530(86)90031-4

Cited by 27 publications

(17 citation statements)

References 24 publications

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“…Disease states affecting the HPA axis (eg cortisolproducing adrenal tumor, panic disorder, and subtypes of depression) in which ACTH and cortisol response to CRF is lower than in controls show normalization of response to a standard (100 mg or 1.0 mg/kg) dose of CRF following successful surgical and or pharmacological treatment (Muller et al, 1986;Curtis et al, 1997;Zobel et al, 1999). It is not known whether these responses would remain normal following higher doses of CRF.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Schluger

Bart

Green

et al. 2003

Neuropsychopharmacol

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Opiate addiction is associated with abnormal function of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis. In general, addiction and withdrawal are associated with abnormal HPA responsivity as demonstrated by baseline, dexamethasone, and metyrapone testing. Following stabilization in methadone maintenance treatment, normalization of HPA axis responsivity is observed. To further investigate HPA axis function associated with heroin addiction and its treatment, saline placebo and human corticotropin-releasing factor (hCRF) were administered intravenously in two doses, one dose lower (0.5 mg/kg) and one dose higher (2.0 mg/kg) than the dose used in standard clinical diagnostics (100 mg), to 16 normal male volunteer controls (NV) and eight male stable-dose methadone-maintained former heroin addicts without ongoing drug or alcohol abuse or dependence (MM). Plasma adrenocorticotrophic hormone (ACTH) and cortisol levels were determined at serial time points. There was no difference in hormonal measurements between the two groups following placebo. NV as well as MM displayed a dose-response effect in plasma ACTH and cortisol levels. MM displayed a significantly greater increase in plasma ACTH levels than the NV following high-dose but not low-dose hCRF (po0.05). There was no significant difference in plasma cortisol levels between the two groups following high-dose hCRF. Thus, despite earlier documented normalization of behavioral function and of several measures of neuroendocrine function during long-term methadone maintenance, some abnormalities in HPA axis responsivity that may be a consequence of heroin exposure, or that may have existed prior to the addiction, can persist during stable methadone treatment.

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Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Schluger

Bart

Green

et al. 2003

Neuropsychopharmacol

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“…Only six patients who had normal responses to hypoglycaemia had blunted responses to CRH and three patients with blunted responses to hypoglycaemia had no response to CRH. The close correlation between the two tests is surprising, since evaluation criteria based on the ITT were used for both tests and peak plasma ACTH and cortisol responses after maximal CRH stimulation are not as high as those after hypoglycaemia [83,84]. The responses to hypoglycaemia are greater, as this activates not only endogenous CRH but also other stimuli of corticotrophin secretion such as vasopressin [85].…”

Section: Crh Testingmentioning

confidence: 99%

Peri‐operative steroid supplementation

Nicholson¹,

Burrin²,

Hall³

1998

Anaesthesia

141

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“…ACTH release in pituitary Cushing’s disease appears rarely to be CRH dependent; therefore, CRHR1 antagonists would not be expected to have a major therapeutic effect in decreasing ACTH secretion and controlling hypercortisolism in most of these patients. Similarly, ectopic ACTH does not appear either to be CRH dependent, so CRHR1 medications would not be expected to play a primary role in controlling the ectopic ACTH production [18, 19]. In the rare cases of ectopic CRH production driving pituitary ACTH secretion, however, it is possible that CRHR1 antagonists would normalize ACTH and cortisol production.…”

Section: Crh In Pituitary and Adrenal Diseasesmentioning

confidence: 99%

“…These lesions do not respond to normal negative feedback signals of elevated cortisol levels. Exogenous CRH stimulation in pituitary Cushing’s disease is seen in approximately 85% of the patients [14,15,16,17,18], but normal circadian stimulation of the adenoma by CRH from the hypothalamus is lost. ACTH release in pituitary Cushing’s disease appears rarely to be CRH dependent; therefore, CRHR1 antagonists would not be expected to have a major therapeutic effect in decreasing ACTH secretion and controlling hypercortisolism in most of these patients.…”

Section: Crh In Pituitary and Adrenal Diseasesmentioning

confidence: 99%

Nonpeptide Corticotropin-Releasing Hormone Receptor Type 1 Antagonists and Their Applications in Psychosomatic Disorders

Contoreggi¹,

Rice²,

Chrousos³

2004

Neuroendocrinology

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Overproduction of corticotropin-releasing hormone (CRH) and stress system abnormalities are seen in psychiatric diseases such as depression, anxiety, eating disorders, and addiction. Investigations of CRH type 1 receptor (CRHR1) nonpeptide antagonists suggest therapeutic potential for treatment of these and other neuropsychiatric diseases. However, overproduction of CRH in the brain and on its periphery and disruption of the hypothalamic-pituitary-adrenal axis are also found in ‘somatic’ disorders. Some rare forms of Cushing’s disease and related pituitary/adrenal disorders are obvious applications for CRHR1 antagonists. In addition, however, these antagonists may also be effective in treating more common somatic diseases. Patients with obesity and metabolic syndrome who often have subtle, but chronic hypothalamic-pituitary-adrenal hyperactivity, which may reflect central dysregulation of CRH and consequently glucocorticoid hypersecretion, could possibly be treated by administration of CRHR1 antagonists. Hormonal, autonomic, and immune aberrations are also present in chronic inflammatory, autoimmune, and allergic diseases, with considerable evidence linking CRH with the observed abnormalities. Furthermore, autonomic dysregulation is a prominent feature of common gastrointestinal disorders, such as irritable bowel syndrome and peptic ulcer disease. Patients with irritable bowel syndrome and other gastrointestinal disorders frequently develop altered pain perception and affective symptoms. CRH acts peripherally to modulate bowel activity both directly through the autonomic system and centrally by processing viscerosensory and visceromotor neural signals. This review presents clinical and preclinical evidence for the role of CRH in the pathophysiology of these disorders and for potential diagnostic and therapeutic applications of CRHR1 antagonists. Recognition of a dysfunctional stress system in these and other diseases will alter the understanding and treatment of ‘psychosomatic’ disorders.

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Corticotropin-releasing factor (CRF): Stimulation in normal controls and in patients with Cushing's syndrome

Cited by 27 publications

References 24 publications

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Peri‐operative steroid supplementation

Nonpeptide Corticotropin-Releasing Hormone Receptor Type 1 Antagonists and Their Applications in Psychosomatic Disorders

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