PubMed · 16149493
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Yuzuru Kato. 2005. [Beta-endorphin (beta-end)].. https://pubmed.ncbi.nlm.nih.gov/16149493/
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AIMS: Metyrapone causes a decrease in the serum cortisol level without affecting ACTH production in ectopic tumors. We report a case who presented with Cushing's syndrome due to an ectopic ACTH-producing thymic carcinoid. In the present case, it was demonstrated that metyrapone administration resulted in a significant decrease in the plasma ACTH and serum cortisol levels. We hypothesized that the steroid hormone may promote proopiomelanocortin (POMC) gene expression in the carcinoid cells. METHODS: An 11-year-old boy presented with Cushing's syndrome. Prior to the detection of a thymic tumor, metyrapone was administered to ameliorate the symptoms of Cushing's syndrome. Interestingly, plasma ACTH as well as serum cortisol levels immediately decreased after metyrapone administration. The levels of cortisol and ACTH were observed to be normal after complete surgical resection of the tumor. Biological characterization of the tumor cells was by in vitro analysis. RESULTS: Thein vitro culture of the tumor cells showed an increased expression of POMC in the presence of cortisol. A CpG methylation assay showed that the demethylation of the POMC promoter was induced by a steroid hormone. CONCLUSION: These findings suggest that the ectopic ACTH-producing tumor may partly be regulated by the elevated levels of cortisol.
OBJECTIVE: To report the preparation and use of etomidate in a patient with Cushing's syndrome caused by an ectopic adrenocorticotropic hormone (ACTH)-producing tumor. CASE SUMMARY: A 73-year-old man with a 5 year history of prostate cancer was admitted for symptoms consistent with Cushing's syndrome. He was started on oral metyrapone for elevated serum cortisol, ACTH, and 24 hour urinary unbound cortisol levels. Shortly after starting metyrapone, he was transferred to the medical intensive care unit for new-onset atrial fibrillation, neutropenic fever, and respiratory failure. A nasogastric tube could not be inserted to administer metyrapone. Intravenous etomidate 4 mg/h (0.06 mg/kg/h) was initiated to decrease cortisol production and provide sedation for mechanical ventilation. Despite supportive treatment, the patient died from multiple organ dysfunction. DISCUSSION: For patients exhibiting signs and symptoms of Cushing's syndrome who have no enteral access, administering etomidate intravenously may be a viable alternative treatment route. Although several articles report the use of etomidate to control cortisol overproduction, the intravenous preparation and stability are discussed only vaguely. In our patient, etomidate was infused via a 30 mL syringe, 2 mg/mL undiluted through a central venous catheter; syringe use was limited to 24 hours. Etomidate should be infused only with continuous monitoring of hemodynamics and periodic assessment of adrenal function. CONCLUSIONS: When oral or enteral medications cannot be administered and sedation is required in critically ill patients, etomidate is an appropriate intravenous agent for hypercortisolemia. There were no obvious problems with stability when undiluted etomidate 2 mg/mL was infused through a dedicated central venous catheter lumen.
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