Serum concentration of 7S collagen and prognosis in patients with the adult respiratory distress syndrome.

Abstract

Background -7S collagen, an N-terminal peptide of type IV collagen, is a primary constituent of the basement membrane. To evaluate whether the serum concentration of 7S collagen reflects the severity of inflammatory lung disease, the serum concentration of 7S collagen was measured in patients with adult respiratory distress syndrome (ARDS) and idiopathic pulmonary fibrosis (IPF). Methods -A radioimmunoassay was used for the measurement of 7S collagen. Gas exchange abnormality was expressed as the arterial oxygen tension (PaO2) divided by the fractional concentration of inspired oxygen (FiO2). Results -The mean (SD) concentration of 7S collagen was 2-7 (0 9) ng/ml in 10 healthy subjects, 5 0 (1P5) ng/ml in 11 patients with IPF, and 14-8 (9 7) ng/ml in 13 patients with ARDS. Significant differences were observed between the patients with ARDS and both healthy subjects and the patients with IPF. In the patients with ARDS serum concentrations of 7S collagen were strongly related to PaO2/FiO2 (r= -0-61). Moreover, the mean (SD) serum concentration of 7S collagen in the eight patients with ARDS who died (19-5 (10-2) ng/ml) was considerably higher than that of the five who survived (7-1 (2'1) ng/ml).Conclusion -These results suggest that serum levels of the 7S fragment of type IV collagen may have some prognostic value in ARDS. (Thorax 1994;49:144-146) Type IV collagen is a major constituent of all basement membranes where it forms a network structure, partly because of interactions between the N-terminal domains of adjacent molecules. These domains, known as 7S collagen,' are known to be comparatively resistant to proteases. It has therefore been proposed that serum concentrations of 7S collagen reflect degradation or synthesis of the basement membrane, or both.2'As type IV collagen exists in the basement membrane of pulmonary capillaries and alveoli, we hypothesised that serum concentrations of 7S collagen in patients with inflammatory lung disease may reflect the extent of damage to the pulmonary basement membrane. In this study serum concentrations of 7S collagen were measured in patients with adult respiratory distress syndrome (ARDS) and those with idiopathic pulmonary fibrosis (IPF), and the use of 7S collagen in assessing the severity of these diseases was evaluated.

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

“…1) and bronchoalveolar lavage (BAL) TNF-α, IL-1β, IL-2, IL-4, IL-6 and IL-8 levels than survivors [49,50]. Although cytokine levels may not reflect activity, these findings are similar to those reported by others (table 4) and agree with studies indicating that the evolution of ARDS is determined by the extent of initial pulmonary HDR in the form of alveolar denudation, basement membrane destruction, vascular permeability and quantity of intra-alveolar exudate [74][75][76][77].…”

Expression of matrix metalloproteinases in pigs with hyperoxia-induced acute lung injury

“…Among these, type IV collagen is the major component of the basement membrane. Both epithelial and endothelial basement membrane destruction are important in the pathogenesis of idiopathic pulmonary fibrosis (IPF) [24] or ARDS [25]. Thus, the present study focused on the type IV collagenolytic MMPs such as MMP-2 and MMP-9.…”

Matrix Metalloproteinase Inhibitor Prevents Acute Lung Injury After Cardiopulmonary Bypass

“…19,20 Although the progression of neutrophil-mediated lung injury is very complex, it is evident that the destruction of the endothelial basement membrane has a central role. 13,14 The basement membrane of the capillary endothelium and the alveolar epithelium is a complex of type IV collagen. MMPs and serine proteases are the primary neutrophil products that can target the basement membrane.…”

“…12 MMPs released from activated neutrophils degrade type IV collagen, which provides the framework for the basement membrane of pulmonary capillaries, and interstitial collagen and proteoglycan. 13,14 Aside from direct collagenolysis, MMPs inactivate endogenous antiproteases, allowing unrestricted protease activity. 15 Studies by Golub et al have confirmed that, by nonantimicrobial mechanisms, chemically modified tetracyclines (CMTs) can directly inhibit MMPs and prevent activation of pro-MMPs to MMPs by scavenging reactive oxygen species.…”