Abstract

Mycobacterium tuberculosis and human immunodeficiency virus (HIV) are known to cause abnormal thyroid function. There is little information on whether HIV infection aggravates alteration of thyroid function in patients with MDR-TB. This study was carried out to determine if HIV co-infection alters serum levels of thyroid hormones (T3, T4) and thyroid stimulating hormone (TSH) in patients with MDR-TB patients and to find out the frequency of subclinical thyroid dysfunction before the commencement of MDR-TB therapy. This observational and cross-sectional study involved all the newly admitted patients in MDR-TB Referral Centre, University College Hospital, Ibadan, Nigeria between July 2010 and December 2014. Serum levels of thyroid stimulating hormone (TSH), free thyroxine (fT4) and free triiodothyronine (fT3) were determined using ELISA. Enrolled were 115 patients with MDR-TB, out of which 22 (19.13%) had MDR-TB/HIV co-infection. Sick euthyroid syndrome (SES), subclinical hypothyroidism and subclinical hyperthyroidism were observed in 5 (4.35%), 9 (7.83%) and 2 (1.74%) patients respectively. The median level of TSH was insignificantly higher while the median levels of T3 and T4 were insignificantly lower in patients with MDR-TB/HIV co-infection compared with patients with MDRT-TB only. It could be concluded from this study that patients with MDR-TB/HIV co-infection have a similar thyroid function as patients having MDR-TB without HIV infection before commencement of MDR-TB drug regimen. Also, there is a possibility of subclinical thyroid dysfunction in patients with MDR-TB/HIV co-infection even, before the commencement of MDR-TB therapy.

Highlights

  • Multidrug-resistant tuberculosis (MDR-TB) continues to be a public health problem because of its increasing trend[1,2]

  • The median level of thyroid stimulating hormone (TSH) was insignificantly higher while the median levels of T3 and T4 were insignificantly lower in patients with MDR-TB/human immunodeficiency virus (HIV) co-infection compared with patients with MDRT-TB only

  • Our observation shows that the effect of

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Summary

Introduction

Multidrug-resistant tuberculosis (MDR-TB) continues to be a public health problem because of its increasing trend[1,2]. African Health Sciences Vol 16 Issue 2, June 2016 for the alteration is still unknown[8,10], though the following mechanisms were suggested; viz: decreased T4 to T3 conversion, decreased TSH production and action of drugs such as ethionamide and prothionamide used for the treatment of MDR-TB on the thyroid causing hypothyroidism by inhibiting thyroid hormone synthesis through inhibition of iodine organification[11,12,13]. Thyroid function in multidrug-resistant tuberculosis patients with or without human immunodeficiency virus (HIV) infection before commencement of MDR-TB drug regimen.

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