Type 3 Procollagen Peptide in Bronchoalveolar Lavage Fluid: Conclusion

24 Nov
2014

In addition, very high lavage type 3 procollagen peptide levels were observed in several sarvoid patients with erythema nodosum or uveitis—clinical combinations which are infrequently associated with the subsequent development of chronic disease and fibrosis. Thus, we found no evidence to suggest that elevated lavage procollagen peptide levels are of prognostic significance in sarcoidosis patients. In this study, the association between lavage type 3 procollagen peptide and ACE, fibronectin and T-lymphocytes; the presence of very high levels of type 3 procollagen peptide in lavage fluid from some patients presenting with acute symptoms of disease; and finally, the lack of association between lavage type 3 procollagen peptide levels and subsequent functional deterioration suggest that alterations in lavage type 3 procollagen peptide levels may reflect changes in collagen production during the alveolitis phase of disease. storehealthmall.eu

In the majority of sarcoid patients, the alveolitis resolves over time leaving no permanent lung injury. Thus, this inflammatory response, when properly regulated, can be seen to be part of the normal healing process following lung injury. Several studies indicate that there is an increase in the production of type 3 relative to type 1 collagen during the early stages of wound healing. In addition, prostaglandin E2, which may play 4 rple in down-regulating the fibrotic response following ipflammation, enhances the production of type 3 relative to type 1 collagen by fibroblasts. In a study on the collagen composition of lung tissue from patients with adult respiratory distress syndrome, Nerlich et al also noted similarities between alterations in collagen metabolism in acute posttraumatic pulmonary fibrosis and the wound healing process. Thus, it may be that increased type 3 collagen production, as reflected by elevated lavage type 3 procollagen peptide levels, is a normal response during lung inflammation and that chronic disease and fibrosis ensues only when regulation of this response fails.

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