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FRI215 Rifampin Induced Adrenal Insufficiency

Disclosure: S.R. Campbell: None. R.M. Tierney: None. J. Lim: None. Introduction: Rifampin is a main component of antimycobacterial therapy in active tuberculosis disease. Although adrenal insufficiency can be caused by infiltration of the pituitary or adrenal glands by Mycobacterium tuberculosis, ri...

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Autores principales: Campbell, Spencer Ramon, Tierney, Ryan M, Lim, Jonea
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554501/
http://dx.doi.org/10.1210/jendso/bvad114.210
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author Campbell, Spencer Ramon
Tierney, Ryan M
Lim, Jonea
author_facet Campbell, Spencer Ramon
Tierney, Ryan M
Lim, Jonea
author_sort Campbell, Spencer Ramon
collection PubMed
description Disclosure: S.R. Campbell: None. R.M. Tierney: None. J. Lim: None. Introduction: Rifampin is a main component of antimycobacterial therapy in active tuberculosis disease. Although adrenal insufficiency can be caused by infiltration of the pituitary or adrenal glands by Mycobacterium tuberculosis, rifampin has also been suggested as a potential causative agent. This case shows a rare example of rifampin-induced adrenal insufficiency in the setting of active tuberculosis disease. Case Presentation: A 42-year-old man with a history of gout and anemia presented with fevers, chills, unintentional weight loss, and productive cough for two weeks. He immigrated from Guatemala 20 years prior and was treated for tuberculosis disease as a child. Upon presentation, he was borderline hypertensive with chest CT showing bilateral nodular opacities in a pattern suggestive of atypical pneumonia. Acid fast bacilli stains were positive and cultures grew Mycobacterium tuberculosis. The patient was started on rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) therapy. Serum cortisol levels on day 4 of RIPE therapy were appropriate in the setting of acute illness (>20 mcg/dl). On day 6 of RIPE therapy, the patient became hypotensive requiring vasopressor support. Labs at that time showed hyponatremia, hypokalemia, and inappropriately low cortisol levels (<20 mcg/dl). ACTH stimulation testing was performed and was blunted with values of 14.50 mcg/dL at 30 minutes and 16.32 mcg/dl at 60 minutes. CT abdomen was also performed and showed no evidence of infiltration. He was started on IV hydrocortisone 50 mg every 6 hours with plans to taper after shock resolved. Following steroid taper, the patient again became hypotensive requiring vasopressors. IV hydrocortisone was resumed, and RIPE therapy was held. He was restarted on PO hydrocortisone 40 mg every 12 hours. Isoniazid, ethambutol, pyrazinamide, and rifampin were sequentially resumed. Pyrazinamide was replaced with moxifloxacin due to recurrent gout flares. The reintroduction of rifampin and rifabutin both resulted in fevers leading to the stoppage of rifamycin therapy. The patient was discharged with stable vital signs on isoniazid 300 mg daily, ethambutol 800 mg daily, moxifloxacin 400 mg daily, and hydrocortisone 30 mg every 12 hours with plans to follow-up with the State Department of Health, internal medicine, and endocrinology. Conclusion: Many drugs are known to cause adrenal insufficiency. There are a few examples in which rifampin has been suggested as a potential cause of adrenal insufficiency. Classically, adrenal insufficiency has been associated with infiltration of the adrenal glands or pituitary gland with Mycobacterium tuberculosis. This case, however, shows further clinical evidence of adrenal insufficiency caused by rifampin therapy and highlights the need for further research to be done to study this adverse effect. Presentation: Friday, June 16, 2023
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spelling pubmed-105545012023-10-06 FRI215 Rifampin Induced Adrenal Insufficiency Campbell, Spencer Ramon Tierney, Ryan M Lim, Jonea J Endocr Soc Adrenal (Excluding Mineralocorticoids) Disclosure: S.R. Campbell: None. R.M. Tierney: None. J. Lim: None. Introduction: Rifampin is a main component of antimycobacterial therapy in active tuberculosis disease. Although adrenal insufficiency can be caused by infiltration of the pituitary or adrenal glands by Mycobacterium tuberculosis, rifampin has also been suggested as a potential causative agent. This case shows a rare example of rifampin-induced adrenal insufficiency in the setting of active tuberculosis disease. Case Presentation: A 42-year-old man with a history of gout and anemia presented with fevers, chills, unintentional weight loss, and productive cough for two weeks. He immigrated from Guatemala 20 years prior and was treated for tuberculosis disease as a child. Upon presentation, he was borderline hypertensive with chest CT showing bilateral nodular opacities in a pattern suggestive of atypical pneumonia. Acid fast bacilli stains were positive and cultures grew Mycobacterium tuberculosis. The patient was started on rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) therapy. Serum cortisol levels on day 4 of RIPE therapy were appropriate in the setting of acute illness (>20 mcg/dl). On day 6 of RIPE therapy, the patient became hypotensive requiring vasopressor support. Labs at that time showed hyponatremia, hypokalemia, and inappropriately low cortisol levels (<20 mcg/dl). ACTH stimulation testing was performed and was blunted with values of 14.50 mcg/dL at 30 minutes and 16.32 mcg/dl at 60 minutes. CT abdomen was also performed and showed no evidence of infiltration. He was started on IV hydrocortisone 50 mg every 6 hours with plans to taper after shock resolved. Following steroid taper, the patient again became hypotensive requiring vasopressors. IV hydrocortisone was resumed, and RIPE therapy was held. He was restarted on PO hydrocortisone 40 mg every 12 hours. Isoniazid, ethambutol, pyrazinamide, and rifampin were sequentially resumed. Pyrazinamide was replaced with moxifloxacin due to recurrent gout flares. The reintroduction of rifampin and rifabutin both resulted in fevers leading to the stoppage of rifamycin therapy. The patient was discharged with stable vital signs on isoniazid 300 mg daily, ethambutol 800 mg daily, moxifloxacin 400 mg daily, and hydrocortisone 30 mg every 12 hours with plans to follow-up with the State Department of Health, internal medicine, and endocrinology. Conclusion: Many drugs are known to cause adrenal insufficiency. There are a few examples in which rifampin has been suggested as a potential cause of adrenal insufficiency. Classically, adrenal insufficiency has been associated with infiltration of the adrenal glands or pituitary gland with Mycobacterium tuberculosis. This case, however, shows further clinical evidence of adrenal insufficiency caused by rifampin therapy and highlights the need for further research to be done to study this adverse effect. Presentation: Friday, June 16, 2023 Oxford University Press 2023-10-05 /pmc/articles/PMC10554501/ http://dx.doi.org/10.1210/jendso/bvad114.210 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Adrenal (Excluding Mineralocorticoids)
Campbell, Spencer Ramon
Tierney, Ryan M
Lim, Jonea
FRI215 Rifampin Induced Adrenal Insufficiency
title FRI215 Rifampin Induced Adrenal Insufficiency
title_full FRI215 Rifampin Induced Adrenal Insufficiency
title_fullStr FRI215 Rifampin Induced Adrenal Insufficiency
title_full_unstemmed FRI215 Rifampin Induced Adrenal Insufficiency
title_short FRI215 Rifampin Induced Adrenal Insufficiency
title_sort fri215 rifampin induced adrenal insufficiency
topic Adrenal (Excluding Mineralocorticoids)
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554501/
http://dx.doi.org/10.1210/jendso/bvad114.210
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