Adjunctive Therapeutic Effects of Zinc Supplementation in Tuberculosis Treatment among Adults in Calabar, Nigeria

Tuberculosis (TB) is a contagious bacterial disease caused by Mycobacterium tuberculosis, which most commonly affects the lungs. It is the leading killer from a single infectious agent worldwide, especially in Asia and Africa. Each year globally, about 1.3 million people die of TB. Majority of the cases are pulmonary TB (PTB) with approximately 15% being extra pulmonary (ETB). The infection is an insidious; chronic process which may take several weeks or months to become clinically patent. The symptoms of PTB include cough, chest pain and hemoptysis.  Systemic symptoms of TB include fevers, chills, night sweats, easy fatigability, loss of appetite and weight loss. Tuberculosis has long been associated with malnutrition. Micronutrients including Zinc; deficiency is considered to be the most frequent cause of secondary immunodeficiency and infection related to morbidity such as tuberculosis. Zinc deficiency affects the host defences in a variety of ways. It results in decreased phagocytosis and leads to a reduced number of circulating T-cells and reduced tuberculin reactivity, at least in animals. In vitro cellular killing by macrophages was found to be reduced during zinc deficiency and rapidly restored after zinc supplementation. This article aimed to describe the convalescence of patients with tuberculosis who received Zinc supplementation in comparison to those that did not during the course of tuberculosis treatment in Calabar, Cross River State, Nigeria.

Eligible patients (81) out of the 182 assessed were randomized to receive anti-TB drug regimen plus oral administration of individual zinc, 25 mg daily for 60 days (intervention group), while the control group received anti-tuberculosis drug regimen only for 60 days. Both qualitative and quantitative data were collected. Clinical examination, Karnofsky performance scale index, direct sputum examination, anthropometric measurements and blood collection for haematological and zinc assessment were carried out before and 2 months after anti-TB treatment began. The mean serum zinc levels at 2 months of TB treatment were significantly higher in the intervention group (14.4 ± 0.37 µmol/L) in comparison with the control (12.9 ± 0.37 µmol/L); (p = 0.004). A significant difference (p = 0.010) in the serum concentrations of zinc was observed between the two groups when adjustments were made for TB-HIV co-infection. Risk reduction of about 41% for acid fast bacilli (AFB) positivity (RR: 0.59; 95% CI 0.23 to 1.46) was observed after 2 months of anti-TB treatment in favour of the intervention group. There was a significant improvement in the haematological parameters as evidenced by significant higher proportion of patients in the intervention group than the control group with values above the lower ranges for these parameters. Therefore, irrespective of HIV status in individuals with TB, zinc supplementation significantly increases clinical outcomes, haematological parameters, improves nutritional status as proxied by anthropometric indices and leads to faster sputum smear conversion. The article adds to the growing body of evidence in support of the beneficial role of zinc in TB control.

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