Decrease of collagen deposition in wound repair in type 1 diabetes independent of glycemic control.
OBJECTIVE
Type 1 and type 2 diabetes mellitus and glycemic control influence wound healing in humans.


METHODS
Experimental study using a human wound-healing model.


METHODS
Collaboration among a multidisciplinary wound-healing department, department of medicine, and research laboratories. PATIENTS, CONTROL SUBJECTS, AND METHODS: In 34 patients with type 1 (insulin-dependent) and 25 with type 2 (non-insulin-dependent) diabetes and 5 nondiabetic control subjects matched with the type 2 diabetic patients, wound-healing capacity was determined as subcutaneous accumulation of collagen measured as hydroxyproline. Two expanded polytetrafluoroethylene tubes were implanted and removed 10 days later. The hydroxyproline level was determined by means of high-performance liquid chromatography; the collagenase activity, by using a radiolabeled collagen substrate. Proliferation of fibroblasts cultured from the wounds was studied in patient groups.


RESULTS
The deposition of hydroxyproline decreased by 40% (P =.03) in type 1 compared with type 2 diabetes (median, 0.70 vs 1.16 nmol/mg; interquartile range, 0.48-1.04 vs 0.56-1.63 nmol/mg), which in turn did not differ significantly from that of controls (median, 1.35 nmol/mg; interquartile range, 0.72-1.88 nmol/mg). The decreased collagen deposition in type 1 diabetes was not caused by increased collagenase activity. The deposition of hydroxyproline did not correlate significantly (r(s) = 0.07; P =.63) with glycosylated hemoglobin levels in either diabetic group. Fibroblast growth was also decreased in type 1 compared with type 2 diabetic patients and controls.


CONCLUSIONS
Collagen deposition in acute wounds is impaired in type 1 diabetes, possibly due to a decreased fibroblast proliferation. In type 2 diabetes, collagen deposition is normal. Glycemic control does not influence collagen deposition in acute wound repair in type 1 or in type 2 diabetes mellitus.
Black
Eva
E
Copenhagen Wound Healing Center, Bispebjerg Hospital, University of Copenhagen, DK 2400 Copenhagen NV, Denmark.
Vibe-Petersen
Jette
J
Jorgensen
Lars N
LN
Madsen
Søren M
SM
Agren
Magnūs S
MS
Holstein
Per E
PE
Perrild
Hans
H
Gottrup
Finn
F
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000502:physiology*; D016022:Case-Control Studies; D003094:Collagen / Q000378:metabolism*; D017364:Collagenases / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D005347:Fibroblasts / Q000502:physiology; D006801:Humans; D006909:Hydroxyproline / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D011138:Polytetrafluoroethylene; D019736:Prostheses and Implants; D014945:Wound Healing / Q000502:physiology*
D001786:Blood Glucose; D011138:Polytetrafluoroethylene; D003094:Collagen; D017364:Collagenases; D006909:Hydroxyproline