Burki N K, Diamond L
Am Rev Respir Dis. 1977 Aug;116(2):327-31. doi: 10.1164/arrd.1977.116.2.327.
Serum creatine phosphokinase activity was measured in 2 groups of asthmatics. The first group consisted of 12 asthmatics followed as outpatients for periods of up to 16 months. Serum creatine phosphokinase activity increased in 8 patients and correlated with the severity of subjective symptoms and objective measurement of airway obstruction, as represented by the forced expiratory volume in 1 second. In the second group, consisting of 5 asthmatic patients studied during hospitalization for acute exacerbations of asthma, serum creatine phosphokinase activity was increased on admission in all the patients and decreased as symptoms and airway obstruction improved and alveolar ventilation decreased. Analysis of creatine phosphokinase isoenzymes showed the increase in every instance to be due entirely to skeletal muscle isoenzyme. The results of additional laboratory tests and further evaluation suggested that the increased serum creatine phosphokinase activity was not derived from the myocardium and was not related to parenteral therapy, specific drugs, hyperthermia, or hyperkalemia. The increase in serum creatine phosphokinase during exacerbations of asthma is probably derived from respiratory muscles, owing to the increased work of breathing.
对两组哮喘患者的血清肌酸磷酸激酶活性进行了测定。第一组由12名哮喘患者组成,作为门诊患者随访长达16个月。8名患者的血清肌酸磷酸激酶活性升高,且与主观症状的严重程度以及气道阻塞的客观测量结果相关,后者以一秒用力呼气量表示。第二组由5名因哮喘急性加重住院治疗的哮喘患者组成,所有患者入院时血清肌酸磷酸激酶活性均升高,随着症状和气道阻塞改善以及肺泡通气量下降而降低。肌酸磷酸激酶同工酶分析表明,每次升高完全是由于骨骼肌同工酶所致。其他实验室检查和进一步评估结果提示,血清肌酸磷酸激酶活性升高并非源自心肌,且与肠外治疗、特定药物、体温过高或高钾血症无关。哮喘发作期间血清肌酸磷酸激酶升高可能源于呼吸肌,这是由于呼吸功增加所致。