Abstract
Tuberculosis-diabetes co-morbidity (TB-DM) has been a hurdle in the elimination of tuberculosis worldwide. Individuals with Type 2 diabetes mellitus (T2DM) can become vulnerable to bacterial infections, due to compromised cell mediated immunity [1, 2]. Therefore, individuals with diabetes are at an increased risk for developing an active tuberculosis (TB) disease when infected with Mycobacterium tuberculosis (Mtb). It is estimated that these individuals with T2DM are about three times more likely to develop the active TB compared to individuals without diabetes. Approximately 10% of all TB cases are linked to diabetes and the risk of death from TB is roughly double for those with diabetes, especially in middle to low-income areas [3, 4]. Patients with both T2DM and TB have worse outcomes, including slower bacteria conversion, lower rate of cure, higher chances to relapse, increased risk of mortality, and even escalated drug resistance. While it is known that diabetes causes immune dysfunction, there are still many questions as to how diabetes worsens TB outcomes. It is reported that diabetes might change the appropriate mechanisms of immunological factors that maintain host immune defenses towards infectious agents, the production of specific cytokines, increased formation of reactive oxygen species, as well as reduced levels of the antioxidant glutathione (GSH). In this review, we explore recent research that helps explain the reasons for tuberculosis-diabetes (TB-DM) comorbidity as well as the possible causes for the increased risk of mortality and finally possible prophylactic treatments.