The PPAR‐gamma activator rosiglitazone fails to lower plasma ACTH levels in patients with Nelson's syndrome

Mullan, Karen; Leslie, Hilary; McCance, David R.; Sheridan, B.; Atkinson, A. B.

doi:10.1111/j.1365-2265.2006.02501.x

Cited by 41 publications

(26 citation statements)

References 8 publications

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“…Mullan et al presented a series of 7 patients with Nelson's syndrome for whom 8 mg of rosiglitazone orally, once daily for 12 weeks, led to no statistically significant decrease in plasma ACTH levels. 57 Of note, the US Food and Drug Administration limits the maximal dose of rosiglitazone in humans …”

Section: Medical Therapymentioning

confidence: 99%

Nelson's syndrome: a review of the clinical manifestations, pathophysiology, and treatment strategies

Patel¹,

Eloy

Liu

2015

FOC

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Nelson's syndrome is a rare clinical manifestation that occurs in 8%–47% of patients as a complication of bilateral adrenalectomy, a procedure that is used to control hypercortisolism in patients with Cushing's disease. First described in 1958 by Dr. Don Nelson, the disease has since become associated with a clinical triad of hyperpigmentation, excessive adrenocorticotropin secretion, and a corticotroph adenoma. Even so, for the past several years the diagnostic criteria and management of Nelson's syndrome have been inadequately studied. The primary treatment for Nelson's syndrome is transsphenoidal surgery. Other stand-alone therapies, which in many cases have been used as adjuvant treatments with surgery, include radiotherapy, radiosurgery, and pharmacotherapy. Prophylactic radiotherapy at the time of bilateral adrenalectomy can prevent Nelson's syndrome (protective effect). The most promising pharmacological agents are temozolomide, octreotide, and pasireotide, but these agents are often administered after transsphenoidal surgery. In murine models, rosiglitazone has shown some efficacy, but these results have not yet been found in human studies. In this article, the authors review the clinical manifestations, pathophysiology, diagnostic criteria, and efficacy of multimodal treatment strategies for Nelson's syndrome.

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Section: Medical Therapymentioning

confidence: 99%

Nelson's syndrome: a review of the clinical manifestations, pathophysiology, and treatment strategies

Patel¹,

Eloy

Liu

2015

FOC

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“…However, treatment of Cushing's disease patients with pioglitazone for one month has recently been demonstrated to be ineffective both at serum ACTH/cortisol levels and urinary free cortisol levels [31]. Moreover, rosiglitazone treatment failed to lower plasma ACTH levels in patients with Nelson's syndrome [32], indicating the limitation of PPAR-γ ligands as the therapeutics for Cushing's disease. Although ATRA has been shown to be effective on patients with Cushing's disease [16], our observation indicates that Am80 cannot be used as a therapeutic for the Cushing's disease.…”

Section: Roles Of Transcription Factors Tpit and Neurod1 On The Am80-mentioning

confidence: 99%

Retinoic acid receptor-α up-regulates proopiomelanocortin gene expression in AtT20 corticotroph cells

et al. 2014

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“…One report showed that two out of three patients responded to rosiglitazone with lowering of plasma ACTH levels, but one of these subsequently escaped (43). Rosiglitazone at maximum licensed doses has not been found to be effective (44). We have shown recently that even higher than licensed doses of rosiglitazone (12 mg/day) are not effective in reducing plasma ACTH levels, and by inference tumour growth (45) (figure 1).…”

Section: Medicalmentioning

confidence: 99%

Nelson's Syndrome

Munir

Newell‐Price

2007

Arq Bras Endocrinol Metab

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Nelson's syndrome is a potentially severe complication of bilateral adrenalectomy performed in the treatment of Cushing's disease, and its management remains difficult. Of all of the features of Nelson's syndrome, the one that causes most concern is the development of a locally aggressive pituitary tumour, which, unusually for pituitary disease, may occasionally cause death from the tumour itself. This feature is especially pertinent given the increasing use in Cushing's disease of laparoscopic bilateral adrenal surgery as a highly effective treatment modality to control cortisol-excess. Despite numerous studies and reports, there is no formal consensus of what defines Nelson's syndrome. Thus, some will define Nelson's syndrome according to the classical description with an evolving pituitary mass after bilateral adrenalectomy, whereas others will rely on increasing plasma ACTH levels, even in the absence of a clear pituitary mass lesion on MRI. These factors need to be borne in mind when considering the reports of Nelson's syndrome, as there is great heterogeneity, and it is likely that overall the modern 'Nelson's syndrome' represents a different disease entity from that of the last century. In the present paper, clinical and epidemiological features of Nelson's syndrome, as well as its treatment modalities, are reviewed.

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The PPAR‐gamma activator rosiglitazone fails to lower plasma ACTH levels in patients with Nelson's syndrome

Abstract: This study showed no effect of rosiglitazone treatment at maximum approved doses in lowering plasma ACTH levels in patients post bilateral adrenalectomy for Cushing's disease.

Cited by 41 publications

References 8 publications

Nelson's syndrome: a review of the clinical manifestations, pathophysiology, and treatment strategies

Nelson's syndrome: a review of the clinical manifestations, pathophysiology, and treatment strategies

Retinoic acid receptor-α up-regulates proopiomelanocortin gene expression in AtT20 corticotroph cells

Nelson's Syndrome

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