Thyroid Hormone Profile in HIV, Hepatitis B Virus, and Hepatitis C Virus Mono- and Co-Infected Patients in Edo State, Nigeria
Iweka FK, Omolumen LE, Okogun GRA, Iyevhobu KO*, Dada FL, Esan EO and Obohwemu OK
Abstract
Background: Thyroid dysfunction is increasingly recognized as a complication of chronic viral infections, particularly HIV, hepatitis B virus (HBV), and hepatitis C virus (HCV). The interaction between viral infections and the hypothalamic-pituitary-thyroid axis remains incompletely understood, especially in sub-Saharan African populations. This study evaluated thyroid hormone profiles in mono- and coinfected patients compared with healthy controls in Edo State, Nigeria.
Methods: A cross-sectional study involving 660 subjects was conducted across four hospitals in Edo State. Study groups comprised 100 HIV-positive subjects on HAART, 50 HIV HAART-naïve subjects, 100 HBV-positive subjects, 100 HCV-positive subjects, 50 HBV/HCV co-infected subjects, 50 HIV/HBV co-infected subjects, 50 HIV/HCV co-infected subjects, and 100 apparently healthy controls. Plasma thyroid stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were determined by enzyme immunoassay (EIA). Data were analyzed using one-way ANOVA and Duncan's Multiple Range post-hoc test at p≤0.05.
Results: TSH levels were significantly elevated in HIV subjects on HAART (4.16±0.7 mIU/L) and HBV (5.23±0.7 mIU/L) and HCV (4.08±0.8 mIU/L) subjects compared with controls (3.10±0.7mIU/L; p<0.05), but significantly decreased in HIV HAART-naïve (2.47±1.0), HBV/HCV co-infected (2.98±0.8), HIV/HBV co-infected (2.09±0.7), and HIV/HCV co-infected (2.12±1.1) subjects. T3 levels were significantly decreased in HIV on HAART (0.56±0.2 ng/dl), HBV (0.54±0.1 ng/dl), and HCV (0.43±0.1 ng/dl) subjects compared with controls (1.53±0.3 ng/dl), but significantly elevated in all co-infected groups. T4 levels were significantly decreased in HIV and HBV mono-infected subjects but markedly elevated in all co-infected groups (HBV/HCV: 12.93±2.2; HIV/HBV: 12.46±3.2; HIV/HCV: 12.88±2.0 μg/dl) compared with controls (6.81±1.9 μg/dl;p<0.05).
Conclusion: Viral infections significantly alter thyroid hormone profiles, with distinct patterns observed between mono-infected and coinfected subjects. HAART-treated HIV subjects show elevated TSH suggesting subclinical hypothyroidism, while co-infected subjects demonstrate a paradoxical hyperthyroid-like pattern with elevated T3 and T4. These findings highlight the need for routine thyroid function monitoring in viral infection patients, particularly those with co-infections.
