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.
恶性和炎性胸腔积液中胸膜纤维化的机制仍不清楚。我们检测了胸腔积液合并肺癌患者以及其他患有炎性疾病(肺炎旁胸腔积液和结核性胸膜炎)患者的III型前胶原N端氨基肽(PIIIP)和IV型胶原7S水平。恶性胸腔积液患者的PIIIP水平和PIIIP/IV型胶原7S比值显著低于炎性胸腔积液患者(p < 0.01),但IV型胶原7S水平无差异。结核性胸膜炎患者的PIIIP与IV型胶原7S的比值高于肺炎旁胸腔积液患者(p < 0.05)。这些数据表明,由于III型胶原产生增加,炎性胸腔积液中胸膜纤维化粘连可能加速;恶性和炎性胸腔积液中的基底膜损伤可能由类似损害所致。我们得出结论,高水平的PIIIP和高PIIIP/IV型胶原7S比值可能提示炎性胸膜炎的存在,而后者可能提示结核性胸膜炎的存在。