BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Skin collagen synthesis is depressed during severe sepsis and is followed by a compensatory response 3 and 6 months after the onset of sepsis.
BACKGROUND: 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. METHODS: In this prospective observational study, we measured aminoterminal propeptides of collagens I and III (PINP, PIIINP) from blister fluid of sepsispatients. 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. RESULTS: 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. CONCLUSIONS: Skin collagen synthesis is depressed during severe sepsis and is followed by a compensatory response 3 and 6 months after the onset of sepsis.