Abstract

A bidirectional communication between the immune and endocrine systems exists and facilitates optimum responses in the host during infections. This is in part achieved through changes in secretion patterns of hypothalamic hormones induced by inflammatory cytokines. The aim of this study was to elucidate the immune–endocrine alterations during tuberculosis (TB) treatment in patients with cured and failed TB treatment outcomes. Blood samples were collected from 27 cured and 10 failed patients and hormone as well as cytokine concentrations quantified at baseline, week 4, and month 6 of TB treatment. Hormone profiles of the two treatment outcome groups were different from each other prior to as well as during TB treatment. Treatment response effects were observed for cortisol, estradiol, T3, T4 ghrelin, leptin, amylin, adiponectin, and dehydroepiandrosterone (DHEA). Trends suggest that T4, amylin, and DHEA concentrations were different between treatment outcomes, although these did not reach statistical significance. Relationships between endocrine and inflammatory markers and the biological pathways involved differed between cured and failed treatment patients. These results highlight the complex interaction between the endocrine and immune system during active TB disease and throughout treatment and suggest that endocrine markers in conjunction with inflammatory markers may be useful in predicting unfavorable treatment outcomes.

Highlights

  • Tuberculosis (TB), caused by Mycobacterium tuberculosis (M.tb), is a major global health threat, in developing countries and continues to claim approximately two million lives every year [1]

  • We found that the body mass index (BMI) increased, in both groups, during TB treatment, and were not different between the two groups at any of the three time points (Table 1)

  • In an attempt to understand these interactions during M.tb infection, Santucci et al investigated the multifaceted immune– endocrine–metabolic alterations in patients with different sever­ities of pulmonary TB [11]

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Summary

Introduction

Tuberculosis (TB), caused by Mycobacterium tuberculosis (M.tb), is a major global health threat, in developing countries and continues to claim approximately two million lives every year [1]. Rapidly increasing rates of recurrent TB episodes and increasing rates of multi-drug resistant (MDR) TB present a startling public health emergency [2]

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