Skin collagen synthesis is depressed in patients with severe sepsis.

Abstract

Skin is an essential barrier in maintaining a stable internal environment. Adequate regenerative capacity is crucial to overcome the homeostatic challenges caused by a septic insult. In sepsis, coagulation and inflammation are activated to restore homeostasis, but it is not known whether sepsis also alters tissue regeneration processes such as skin collagen synthesis. In this prospective observational study, we measured aminoterminal propeptides of collagens I and III (PINP, PIIINP) from blister fluid of sepsis patients. Blister fluid was obtained from experimental blisters induced on intact abdominal skin 4 times: within the first 48 hours from the first organ failure, on the fifth day, and at 3 and 6 months thereafter. Forty-four patients with severe sepsis were enrolled. The median age was 63 years (25th-75th percentile, 53-71 years). The median Acute Physiology and Chronic Health Evaluation II score on admission was 26 (22-30). Thirty-day mortality was 25%. Fifteen healthy adults were used as controls. Median PIIINP and PINP levels in septic patients were lower in comparison with controls in the first blister (40.8 microg/L [25th-75th percentile, 22.2-77.1 microg/L], P = 0.028 and 69.9 microg/L [32.4-112.7 microg/L], P < 0.001, respectively) and in the blister induced on day 5 (38.8 microg/L [19.9-68.5 microg/L], P < 0.001 and 90.0 [35.1-138.8 microg/L], P < 0.001, respectively). The survivors revealed an overexpression at 3 months, whereas normal values of PIIINP and PINP were reestablished at 6 months. Skin collagen synthesis is depressed during severe sepsis and is followed by a compensatory response 3 and 6 months after the onset of sepsis.