Tsuchiya Y, Nishikawa M, Iwamoto K, Kirioka T, Noguchi M, Watanabe A, Nishiwaki K, Nozaki Y, Nakane Y
Department of Respiratory Medicine, Nishio Municipal Hospital, Aichi, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1997 Jun;35(6):622-6.
The mechanism of pleural fibrosis in malignant and inflammatory pleural effusion remains unclear. We measured the levels of type III procollagen N-terminal amino peptide (PIIIP) and type IV collagen 7S in patients who had pleural effusion and lung carcinoma, and in others who had inflammatory diseases (parapneumonic and tuberculous pleuritis). The PIIIP level and the PIIIP/type IV collagen 7S ratio in patients with malignant pleural effusion were significantly lower than those in patients with inflammatory pleural effusion (p < 0.01), but the levels of type IV collagen 7S did not differ. The ratio of PIIIP to type IV collagen 7S was higher in patients with tuberculous pleuritis than in those with parapneumonic pleuritis (p < 0.05). These data indicate that pleural fibrotic adhesion may be accelerated in inflammatory pleural effusion because of elevated production of type III collagen; basement membrane injury in malignant and inflammatory pleural effusion may be caused by similar damage. We conclude that a high level of PIIIP and a high PIIIP/type IV collagen 7S ratio may indicate the presence of inflammatory pleuritis, and that the latter may indicate the presence of tuberculous pleuritis.