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Review
. 2024 Jul;67(7):1168-1180.
doi: 10.1007/s00125-024-06102-x. Epub 2024 Feb 20.

Diabetes and infection: review of the epidemiology, mechanisms and principles of treatment

Affiliations
Review

Diabetes and infection: review of the epidemiology, mechanisms and principles of treatment

Richard I G Holt et al. Diabetologia. 2024 Jul.

Abstract

An association between diabetes and infection has been recognised for many years, with infection being an important cause of death and morbidity in people with diabetes. The COVID-19 pandemic has re-kindled an interest in the complex relationship between diabetes and infection. Some infections occur almost exclusively in people with diabetes, often with high mortality rates without early diagnosis and treatment. However, more commonly, diabetes is a complicating factor in many infections. A reciprocal relationship occurs whereby certain infections and their treatments may also increase the risk of diabetes. People with diabetes have a 1.5- to 4-fold increased risk of infection. The risks are the most pronounced for kidney infection, osteomyelitis and foot infection, but are also increased for pneumonia, influenza, tuberculosis, skin infection and general sepsis. Outcomes from infection are worse in people with diabetes, with the most notable example being a twofold higher rate of death from COVID-19. Hyperglycaemia has deleterious effects on the immune response. Vascular insufficiency and neuropathy, together with altered skin, mucosal and gut microbial colonisation, contribute to the increased risk of infection. Vaccination is important in people with diabetes although the efficacy of certain immunisations may be compromised, particularly in the presence of hyperglycaemia. The principles of treatment largely follow those of the general population with certain notable exceptions.

Keywords: Antimicrobials; Bacteria; Diabetes; Epidemiology; Infection; Pathogenesis; Review; Virus.

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Figures

Fig. 1
Fig. 1
Mechanisms by which infection may worsen glycaemia. Stress hormones include glucagon, growth hormone, catecholamines and glucocorticoid. Cytokines include tumour necrosis factor-α and interleukin-1. This figure is available as part of a downloadable slideset
Fig. 2
Fig. 2
Age-standardised rates of hospitalisation (per 10,000 people) for influenza (a) and community-acquired pneumonia (b) in men (blue) and women (red) with diabetes in Hong Kong between 2001 and 2016 [4]. Similar trends have also been observed in the USA [7]. Data for average annual percentage change (AAPC) with 95% CI are also shown. This figure has been reproduced from [4] with permission from Springer Nature. This figure is available as part of a downloadable slideset
Fig. 3
Fig. 3
Mechanisms that increase the risk of infection in people with diabetes. Diabetes and its complications impair both innate and adaptive immune systems. The green boxes illustrate how host factors associated with diabetes can affect aspects of the immune system (shown in blue boxes). Some of these host factors affect the likelihood of infection (see processes shown above the skin and epithelial lining) and some affect the response to an infection (see processes shown below the skin and epithelial lining). APC, antigen-presenting cells; NK, natural killer. This figure is available as part of a downloadable slideset

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