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Year : 2017  |  Volume : 14  |  Issue : 1  |  Page : 8-12

The adrenal gland and the patient with pulmonary tuberculosis infected with human immunodeficiency virus

1 Department of Medicine, Endocrinology, Diabetes and Metabolism Unit, College of Medicine, University of Lagos, Surulere, Lagos, Nigeria
2 Department of Medicine, Endocrinology, Diabetes and Metabolism Unit, Lagos State University College of Medicine, Ikeja, Lagos, Nigeria

Correspondence Address:
Ifedayo Adeola Odeniyi
Department of Medicine, Endocrinology, Diabetes and Metabolism Unit, College of Medicine, University of Lagos, PMB 12003, Surulere, Lagos
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2468-6859.199167

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Background: The adrenal gland is not spared from the involvement by tuberculosis. One of the recognized causes of adrenal insufficiency (AI) is tuberculosis. AI, mostly at the subclinical level, is common in persons with pulmonary tuberculosis (PTB) infection, occurring in about 23% of patients. Coinfection with PTB and human immunodeficiency virus (HIV) may compromise adrenocortical function and produce significant adrenocortical insufficiency. Objective: To determine if coinfection with tuberculosis and HIV have a compound effect on adrenocortical function in persons with HIV and PTB coinfection. Materials and Methods: Persons with sputum-positive PTB, treatment naive, who met our inclusion criteria, were selected. All the recruited patients were screened for HIV and those positive for HIV infection had confirmatory test. A baseline blood samples for cortisol, fasting plasma glucose, full blood count, and electrolytes were collected between 8.00 h and 9.00 h immediately before administration of adrenocorticotropic hormone (ACTH). The persons received an intravenous bolus injection of 1 μg ACTH (Alliance Pharmaceuticals Ltd., Chippenham, Wiltshire SN15 2BB) and blood sample was drawn for cortisol level at 30 min. Results: Forty-four people with PTB infection and forty people with PTB and HIV coinfection met the inclusion criteria of the study. The adrenal response to 1 μg ACTH stimulation in participants with PTB and PTB and HIV coinfection showed that the mean basal cortisol level in the 2 groups was not statistically significant; however, 30-min post-ACTH stimulation cortisol level was 630.84 ± 372.17 and 980.36 ± 344.82 nmol/L (P < 0.001) and increment was 367.79 ± 334.87 and 740.77 ± 317.97 nmol/L (P < 0.001), respectively. Fourteen persons (31.8%) with PTB has subnormal adrenal response to ACTH stimulation while only 2 (5%) persons with PTB and HIV coinfection has subnormal response. Conclusion: AI, at subclinical level, was less frequent in those with PTB and HIV co-infection.

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