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Cited by 257

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Infections and Diabetes: Mechanisms and Prospects for Prevention

Pozzilli, P., Leslie, R.D.G.·1994·Diabetic Medicine

Abstract

Infections remain a serious hazard for the diabetic patient. Good metabolic control is a major factor in limiting the development and spread of infections and, most importantly, the development of diabetic complications which predispose to infections. In some patients recurrent infections can pose a problem, particularly if there is evidence of secondary immunodeficiency. In these patients adjuvant therapies, including Biological Response Modifiers (BRMS) should be considered. Several factors could predispose diabetic patients to infections. These factors include: genetic susceptibility to infection; altered cellular and humoral immune defence mechanisms; local factors including poor blood supply and nerve damage, and alterations in metabolism associated with diabetes. In the context of a diabetic patient all or some of these factors may operate. The purpose of this review is to assess the relative contribution of these potential mechanisms in leading to infection in patients with diabetes.

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Metadata

Authors
Pozzilli, P., & Leslie, R. D. G.
Venue
Diabetic Medicine
Publisher
Wiley
Published
1994-12
Volume
11
Issue
10
Pages
935-941
ISSN
  • 0742-3071 (ISSN-L)
  • 1464-5491
OpenAlex
W2168727631
Cited by
257
References
0
FWCI
1.12
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Infections and Diabetes: Mechanisms and Prospects for Prevention. https://app.cochat.ai/papers/10.1111/j.1464-5491.1994.tb00250.x
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Pozzilli, P., & Leslie, R. D. G. (1994). Infections and Diabetes: Mechanisms and Prospects for Prevention. Diabetic Medicine. https://doi.org/10.1111/j.1464-5491.1994.tb00250.x

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.