American Diabetes Association
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Temporal Trends in Incident Hospitalization for Diabetes-Related Foot Ulcer in Type 2 Diabetes: The Fremantle Diabetes Study

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posted on 2021-01-13, 18:47 authored by Emma J Hamilton, Wendy A Davis, Ranita Siru, Mendel Baba, Paul E Norman, Timothy ME Davis
Objective: To determine whether, reflecting trends in other chronic complications, incident hospitalization for diabetes-related foot ulcer (DFU) has declined over recent decades in type 2 diabetes.

Research design and methods: Participants with type 2 diabetes from the community-based Fremantle Diabetes Study Phases I (FDS1; 1,296 participants, mean age 64.0 years, 48.6% males, recruited 1993-1996) and II (FDS2; 1,509 participants, mean age 65.4 years, 51.8% males, recruited 2008-2011) were followed from entry to first hospitalization for/with DFU, death or 5 years (whichever came first). Incident rate ratios (IRRs) and incident rate differences (IRDs) were calculated for FDS2 versus FDS1 overall and in 10-year age-groups. Cox proportional hazards modelling determined independent predictors of first DFU hospitalization in the combined cohort.

Results: Incident DFU hospitalization (95% CI) was 1.9 (0.9-3.3) /1,000 person-years in FDS1 during 5,879 person-years of follow-up, and 4.5 (3.0-6.4) /1,000 person-years in FDS2 during 6,915 person-years of follow-up. The crude IRR (95% CI) was 2.40 (1.17-5.28), P=0.013) and IRD 2.6 (0.7-4.5) /1,000 person-years (P=0.010). The highest incidence rate (IR) for any age-group was 23.6/1,000 person-years in FDS2 participants aged 31-40 years. Age at diabetes diagnosis (inverse), HbA1c, insulin use, height, ln(urinary albumin:creatinine), absence of any foot pulse, previous peripheral revascularization and peripheral sensory neuropathy (PSN) were independent predictors of incident hospitalization for/with DFU.

Conclusions: Incident DFU hospitalizations complicating type 2 diabetes increased between FDS Phases, especially in younger participants, and were more likely in those with PSN, peripheral arterial disease and suboptimal glycemic control at baseline.


Seeding funding for FDS1 was provided by the Raine Foundation University of Western Australia and FDS2 was funded by the National Health and Medical Research Council of Australia (project grants 513781 and 1042231). TMED is supported by a Medical Research Future Fund Practitioner Fellowship. EJH is supported by a Raine Clinician Research Fellowship. The funding bodies had no involvement in the study design, data collection, analysis and interpretation of results or writing this manuscript.


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