Delayed restoration of epidermal barrier function after suction blister injury in patients with diabetes mellitus

Summary Aims Diabetes mellitus is a risk factor for compromised wound healing. The present study examines the restoration of the epidermal barrier function using the suction blister wound model. Methods The healing process was evaluated over time by measuring water evaporation (WE) and blood flow (B...

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Published inDiabetic medicine Vol. 16; no. 7; pp. 563 - 567
Main Authors Koivukangas, V., Annala, A. -P., Salmela, P. I., Oikarinen, A.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.07.1999
Blackwell
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Summary:Summary Aims Diabetes mellitus is a risk factor for compromised wound healing. The present study examines the restoration of the epidermal barrier function using the suction blister wound model. Methods The healing process was evaluated over time by measuring water evaporation (WE) and blood flow (BF) in the wound area. Seventeen Type 1 diabetic males and 11 non‐diabetic control males were studied. Results At the onset, the WE of diabetic patients was 116 ± 11 g.m–2.h–1 and that of controls 95 ± 13 g.m–2.h–1 (P < 0.001). On the second day, the WE of diabetic patients was 90 ± 21 g.m–2.h–1 and that of controls 60 ± 24 g.m–2.h–1 (P < 0.02). The most profound difference was encountered during the fourth day, when the WE of diabetic patients was 40 ± 17 g.m–2.h–1 and that of controls 14 ± 8 g.m–2.h–1 (P < 0.001). The value recorded on the fourth day was 37% of the onset value in diabetic patients and 16% in controls (P < 0.001). Eight days after wounding the values were close to that of normal skin in both diabetic and control subjects. At the onset, the BF was 93 ± 20 (arbitrary units) in diabetic men and 112 ± 18 in controls (P = 0.02). On the second, fourth and eighth day there was no significant differences. Conclusions The results suggest that restoration of the epidermal barrier function is delayed in the patients with diabetes. There were also a trend toward an initially weaker inflammatory response.
Bibliography:istex:6D2AD3C468377D9FAE199EDF4F825684EEAAA089
ArticleID:DME117
ark:/67375/WNG-GLV65Z16-2
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ISSN:0742-3071
1464-5491
DOI:10.1046/j.1464-5491.1999.00117.x