Convergence of non-communicable diseases and tuberculosis

Magee, M.J., Salindri, A.D., Gujral, U.P., Auld, S.C., Bao, J., Haw, J.S., Lin, H.H. and Kornfeld, H., 2018. Convergence of non-communicable diseases and tuberculosis: a two-way street?. The International Journal of Tuberculosis and Lung Disease, 22(11), pp.1258-1268.
https://doi.org/10.5588/ijtld.18.0045
  • In 2016, there were 10.4 million global TB cases and 1.7 million TB deaths; over 85% occurred in LMICs.
  • None of the LMICs are projected to meet the 2030 TB-related Sustainable Development Goals.
  • Chronic illness from TB is recognized as a risk factor for NCDs, but empirical evidence on post-TB NCD risk is limited.
  • TB disease can temporarily increase blood glucose levels, potentially leading to hyperglycemia.
  • Antituberculosis treatment may lower blood glucose levels.
  • Active TB may induce hyperglycemia or DM via acute stress response, involving pro-inflammatory cytokines and regulatory hormones.
  • Reactive oxidative species and pro-inflammatory cytokines from TB may increase liver glucose production, resulting in stress hyperglycemia.
  • Pre-existing hyperglycemia in TB patients can lead to exacerbated hyperglycemia or DM.
  • M. tuberculosis may persist in adipose tissue, promoting pro-inflammatory responses and impacting insulin sensitivity.
  • Elevated heme oxygenase-1, associated with TB, is linked to inflammation and increased DM risk.
  • Epigenetic reprogramming is a potential mechanism by which TB increases hyperglycemia or DM risk.
  • The bidirectional association between TB and DM is complex, and understanding is limited.
  • Prospective cohorts are needed to measure metabolic parameters post-TB treatment to determine the incidence of DM and other metabolic disorders.
  • Incident TB might reveal pre-existing predispositions to DM, complicating post-TB DM incidence studies.
  • Proper control groups and ruling out reverse causality are critical for future research.
  • By 2030, COPD-related deaths are projected to surpass lower respiratory tract infections, becoming the third leading cause of death worldwide.
  • The increase in COPD deaths is partly due to rising air pollution and tobacco use, with TB also recognized as a significant contributor to the global burden of chronic lung disease (CLD).
  • In South Africa, a history of pulmonary TB (PTB) was associated with a five-fold increase in chronic bronchitis risk, nearly three times higher than the risk from smoking.
  • Post-TB lung damage can include residual cavitation, bronchiectasis, fibrosis, or scarring, resulting in volume loss.
  • Cigarette smokers have a higher likelihood of TB infection, progression to active disease, and TB-related mortality compared to non-smokers.
  • Fibrotic resolution of PTB, once a protective response, may now be maladaptive with effective anti-tuberculosis treatment.
  • Patients with PTB receiving medical care for TB at least three times had a 1.4-fold increased risk of acute coronary syndrome (ACS) compared to non-infected controls.
  • After adjusting for covariates, TB patients had a 50% greater risk of ischemic stroke and a two-fold increased risk of acute myocardial infarction.
  • Infections may lead to cardiovascular disease (CVD) through systemic inflammation, which can cause atherosclerotic plaque formation or rupture.
  • Inflammatory processes increase the secretion of leukocyte-soluble adhesion molecules, aiding monocyte attachment to endothelial cells.
  • Interleukin (IL) 6, associated with insulin resistance, dyslipidemia, and endothelial dysfunction, inhibits lipoprotein lipase and stimulates lipolysis.
  • Active TB may directly or indirectly affect lipid levels, with TB patients generally having lower serum total cholesterol, HDL cholesterol, and LDL cholesterol levels than healthy controls.
  • TB-related inflammation might trigger LDL oxidation, leading to lower serum LDL levels, or individuals with low cholesterol might be more susceptible to TB due to cholesterol's role in cellular immunity.
  • Reduced HDL levels may negatively impact the immune response, but anti-tuberculosis treatment can normalize lipid parameters in individuals with low lipid levels before treatment.
  • Distinguishing the direct effects of TB from the indirect effects of pre-existing cardiovascular risk factors remains a major research design challenge.

 

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