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Diabetes Mellitus and Infectious Diseases: Current Evidence and Clinical Implications
Taeeun Kim, Sang-Ho Choi
Diabetes Metab J. 2025;49(5):915-933.   Published online August 27, 2025
DOI: https://doi.org/10.4093/dmj.2025.0508
  • 12,371 View
  • 499 Download
  • 23 Web of Science
  • 26 Crossref
AbstractAbstract PDFPubReader   ePub   
Diabetes mellitus predisposes individuals to a broad spectrum of infections. People with diabetes face a 1.5- to 4-fold increased risk of both common and severe infections, and infections remain the leading cause of morbidity and mortality. Chronic hyperglycemia impairs neutrophil chemotaxis, oxidative burst, and complement activation, while vascular insufficiency and neuropathy compromise tissue perfusion and barrier integrity. These defects, together with altered skin, mucosal, and gut microbiota, influence the marked susceptibility to urinary tract infections (especially renal abscess and emphysematous pyelonephritis), osteomyelitis, diabetic foot infections, pneumonia (including influenza), tuberculosis, skin and soft tissue infections, and lifethreatening syndromes such as emphysematous cholecystitis and rhino-orbital mucormycosis that are almost exclusive to people with diabetes. Outcomes from infections are worse in diabetes. Although the core therapeutic principles align with those for patients without diabetes, management should be individualized. Glycemic control should balance infection risk and hypoglycemia; antimicrobial dosing should account for renal function and drug interactions; and strict antimicrobial stewardship is required. If needed, prompt debridement and multidisciplinary intervention are necessary to mitigate complications and reduce mortality. Preventive care relies on comprehensive vaccination (influenza, pneumococcus, severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2], hepatitis B, herpes zoster, and Tdap/Td) and regular foot surveillance with offloading to avert ulceration.

Citations

Citations to this article as recorded by  
  • Risk of Acute Cholecystitis Based on Combination of Patient Age, Patient Sex, Leukocytosis, and Sonographic Murphy Sign
    Hideaki Ishida, Hiroko Naganuma
    Journal of Ultrasound in Medicine.2026; 45(5): 1117.     CrossRef
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    Yu Li, Guozhong Zhou, Feifei Yang, Rong long, Wei Shi, Yan Dong, Yuanyuan Zhou, Nan Chen, Ying Yang
    BMC Infectious Diseases.2026;[Epub]     CrossRef
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    Qu Liu, Zhenghui Wang, Yujiao Song, Lanlan Liu, Shuang Qiu, Xinxin Niu, Jie Liu, Hailong Jin, Qing Zhang
    Frontiers in Cellular and Infection Microbiology.2026;[Epub]     CrossRef
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    Laura Garriga-Grimau
    The Lancet Respiratory Medicine.2026; 14(7): 573.     CrossRef
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  • Delayed Radiological Resolution: A Comparative Longitudinal Study of Viral Pneumonia Evolution in Diabetic vs. Non-Diabetic Patients
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  • Determinants of COVID-19 and Influenza Vaccination Among People with Diabetes Mellitus in Primary Health Care
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  • Immunometabolic reprogramming in diabetic osteomyelitis: from mechanisms to therapeutics
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    Frontiers in Cellular and Infection Microbiology.2025;[Epub]     CrossRef
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Pathophysiology
Regulation of Systemic Glucose Homeostasis by T Helper Type 2 Cytokines
Yea Eun Kang, Hyun Jin Kim, Minho Shong
Diabetes Metab J. 2019;43(5):549-559.   Published online October 24, 2019
DOI: https://doi.org/10.4093/dmj.2019.0157
  • 13,348 View
  • 130 Download
  • 12 Web of Science
  • 13 Crossref
AbstractAbstract PDFPubReader   ePub   

Obesity results in an inflammatory microenvironment in adipose tissue, leading to the deterioration of tissue protective mechanisms. Although recent studies suggested the importance of type 2 immunity in an anti-inflammatory microenvironment in adipose tissue, the regulatory effects of T helper 2 (Th2) cytokines on systemic metabolic regulation are not fully understood. Recently, we identified the roles of the Th2 cytokine (interleukin 4 [IL-4] and IL-13)-induced adipokine, growth differentiation factor 15 (GDF15), in adipose tissue in regulating systemic glucose metabolism via signal transducer and activator of transcription 6 (STAT6) activation. Moreover, we showed that mitochondrial oxidative phosphorylation is required to maintain these macrophage-regulating autocrine and paracrine signaling pathways via Th2 cytokine-induced secretion of GDF15. In this review, we discuss how the type 2 immune response and Th2 cytokines regulate metabolism in adipose tissue. Specifically, we review the systemic regulatory roles of Th2 cytokines in metabolic disease and the role of mitochondria in maintenance of type 2 responses in adipose tissue homeostasis.

Citations

Citations to this article as recorded by  
  • Role of the Th2-like Immune Response in Obesity: IL-4 as a Metabolic Regulator and IL-13 as an Effector of Muscle Energy Metabolism
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  • Growth and differentiation factor-15: A link between inflammaging and cardiovascular disease
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Double Diabetes.
Sang Youl Rhee, Young Seol Kim
Korean Diabetes J. 2009;33(1):1-8.   Published online February 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.1.1
  • 3,480 View
  • 48 Download
AbstractAbstract PDF
Generally, most cases of diabetes mellitus (DM) are classified as either type 1 DM or type 2 DM based on their pathophysiolgic features. However, it is not always possible to classify this disease clearly according to current diagnostic criteria. Recently, the existence of non-typical diabetes has been found in patients with simultaneous features of both type 1 and type 2 DM. In these patients, obvious evidence of insulin resistance, positivity of islet autoantibody, and progressive beta cell loss are observed concurrently. Moreover, this non-typical diabetes that usually occurs among children and adolescents has been defined as 'double diabetes', and its worldwide incidence has been on the increase as of late. Thus, there has been heightened interest among researchers about this ambiguous condition.
Original Article
Five Year Follow-up of ICA and GADA in Childhood onset Type 1 DM.
Si Hyung Lee, Ji Sung Yoon, Mi Jung Eun, Jin Ho Kim, Yong Ho Park, Kyu Chang Won, Ihn Ho Jo, Hyoung Woo Lee
Korean Diabetes J. 2003;27(5):395-404.   Published online October 1, 2003
  • 2,096 View
  • 27 Download
AbstractAbstract PDF
BACKGROUND
Type 1 diabetes develops due to the destruction of insulin-secreting beta-cells by an autoimmune process, in which both genetic and environmental factors are involved. In children with newly diagnosed type 1 DM, the prevalence of ICA (Islet cell cytoplasmic antibody) is 60~86% and is highest at the time of onset after which it decreases. But, GADA (glutamic acid decarboxylase anti- bodies) are characterized by substantial fluctuations in the humoral immune response over a long period after clinical manifestation. This study was performed to evaluate the persistence of type 1 DM associated autoantibodies, including ICA and GADA, and their relation to clinical characteristics of the disease after clinical manifestation. METHODS: Eighteen childhood onset type 1 diabetes patients (mean age 13.7 years; duration 3.9 years) were included in this study. ICA was measured by indirect immunofluorescence using conventional ICA-IgG and positive samples were titered by serial dilutions. Also the sera were screened for GADA by radioimmuno-assay. RESULTS: The positivities of ICA and GADA at the time of study were 55.6% and 61%, falling to 44.4% and 41.2% 5 years later, respectively. There was no case of an ICA negative patient becoming positive or whose ICA titer was increased later. One case of a GADA negative patient became positive later. Initial c-peptide levels didn't have any correlation with initial ICA titers or ICA prevalence, but did with initial GADA titer. There were significant correlations between initial GADA titer and ICA prevalence (p<0.001), and between initial GADA titer or ICA titer and later ICA persistence (p<0.05). CONCLUSION: ICA and GADA persisted long after the clinical diagnosis of type 1 diabetes. And the persistence of autoantibody positivity showed a weak relation with endogenous insulin secretion and clinical characteristics, both at and after diagnosis of overt type 1 diabetes.

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