https://orcid.org/0000-0002-3183-1259
Figures & data
Table 1. Incidence, YLD, death and YLL in patients with NCDs in 2017.Citation4-7,Citation10,Citation11
Citation13,Citation16,Citation17,Citation19-22,Citation31,Citation32
Figure 1. Immunologic differences in (a) older individuals and (b) those with chronic diseases.
a) The effect of aging on the immune response.Citation33 The immune system becomes compromised and dysfunctional with increasing age (immunosenescence), due to a decline in key immune cells that regulate innate and adaptive immune responses.Citation33 In the older population, the efficiency of APC migration is reduced along with the ability of APCs to form stable contacts with T cells. This results in poor activation and differentiation of T cells. The thymic output is reduced in older patients due to thymic involution that occurs with age, and bone marrow output is also adversely affected with age, leading to a decrease in T-cell and B-cell populations and reduced downstream effects.Citation33 All these factors have a significant negative impact on the immunity of aged individuals.
b) Potential mechanisms for immune impairment in patients with diabetes and CKD.Citation16,Citation23,Citation24,Citation34,Citation35 Similarly, the immune system can also become comprised in patients with chronic diseases.Citation16,Citation23,Citation24,Citation34,Citation35 Hyperglycemia in diabetes affects the innate immune system by reducing the production of type I interferon and interleukin-22, which are involved in antiviral activity, chronic inflammation and insulin sensitivity.Citation16,Citation24 Altered immune responses in patients with CKD, such as a reduction in T and B cells and increased pro-inflammatory cytokines, leave patients more susceptible to infection.Citation23,Citation35 Infections, such as influenza, increase the risk of adverse coronary and cardiovascular events via direct and indirect mechanisms on the vasculature.Citation34 Together, this increases the risk of worse outcomes for patients with diabetes and CKD.
APC, antigen-presenting cell; BCR, B-cell receptor; CKD, chronic kidney disease; MHC, major histocompatibility complex; TCR, T-cell receptor.
Figure 2. The effect of VPDs.
VPDs and infections can ultimately result in cardiovascular events.Citation34,Citation42-46 Infection with pathogens associated with influenza-like illness leads to an increased pro-inflammatory response that exacerbates plaque formation in the blood vessels and procoagulant effects, which then contributes to accelerated atherosclerosis.Citation34 Influenza has also been shown to lower the anti-inflammatory properties of HDL cholesterol particles, which further drives the infiltration of macrophages through the arterial wall.Citation43 In addition, there is some evidence that influenza may increase the risk of tachycardia, which is associated with major adverse cardiovascular events in hypertensive patients.Citation43,Citation45 Other viral infections may have similar outcomes: for example, the varicella zoster virus has been shown to directly cause pathologic vascular remodeling, resulting in a thickened intima and vascular occlusion, leading to subsequent thrombosis and rupture.Citation44,Citation46 Varicella zoster virus also induces systemic inflammatory responses, which cause disruption to pre-existing atherosclerotic plaques and stimulate mediators of the coagulation system.Citation42,Citation46 Altogether, these events increase the risk of stroke.Citation42,Citation44,Citation46
HDL, high-density lipoprotein; MI, myocardial infarction; VPD, vaccine-preventable disease.
Table 2. Recommendations for vaccinations in adults with key chronic diseases provided by various guidelines across the world.Citation66-88