acid-phosphatase and Pulmonary-Disease--Chronic-Obstructive

The activity of α1-antitrypsin (AAT) and the lysosomal enzymes, cathepsin D (CTS D), arylsulfatase (ASA), and acid phosphatase, (AcP) was determined in patients with COPD (GOLD category A). Moreover, the diagnostic usefulness of these parameters in blood serum was assessed along with establishing whether smoking cessation affects these parameters. The study included 70 patients with COPD who ceased smoking (study group) and two control groups of 33 subjects each: nonsmokers without COPD (control I) and patients with COPD who continued smoking (control II). In control I, blood was taken once and in control II, at the start of the experiment and after the 1st, 2nd, and 3rd months. AAT in the patients exhibited higher activity than in the healthy subjects at all time points. AAT activity in the patients before the start of the experiment was ~80% higher (P < 0.001) than in control I. No statistically significant differences in CTS D, ASA, and AcP activity were found. COPD involves increased AAT activity and unchanged activities of the assessed lysosomal enzymes. Three-month tobacco abstinence does not affect these parameters in peripheral blood. Determining the AAT levels in blood serum can be used in the diagnostics of COPD.

Topics: Acid Phosphatase; Adult; alpha 1-Antitrypsin; Arylsulfatases; Cathepsin D; Female; Humans; Lysosomes; Male; Middle Aged; Pulmonary Disease, Chronic Obstructive; Serum; Smoking Cessation

To evaluate bone and calcium-phosphorus metabolism, bone tissue density (BTD) in smokers and non-smokers with chronic obstructive pulmonary disease (COPD).. The study included 120 patients with COPD; smokers (n=68), smokers in the past (n=8) and non-smokers (n=44). Control 80 healthy subjects were matched by age and sex. Bone metabolism was estimated by concentration of osteocalcin (OC), markers of bone resorption (TRAP, betaCrossLaps-betaCL).. Smoking aggravates disturbance of calcium metabolism in COPD leading to hypocalcaemia and hypercalciuria. In smokers with COPD bone remodeling dysfunction is caused by suppression of osteogenesis and enhancement of resorption, in non-smokers--intensification of both resorption and osteogenesis. The analysis of correlations has shown that there is a close correlation between the level of TRAP, bone mineral density scores and indices of pack-years (r = -075, p < 0.01; r = -0.6, p < 0.01, respectively). Anamnesis of smoking has a positive correlation with TRAP (r = 0.85, p < 0.001) and a negative correlation with bone density (r = -0.8, p < 0.01) and OC (r = -0.55, p < 0.01).. Duration of smoking (total pack-years) is an additional marker of osteopenic syndrome in COPD. This is confirmed by close correlation of this parameter with bone density and markers of bone resorption.

Topics: Acid Phosphatase; Aged; Biomarkers; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Bone Resorption; Calcium; Female; Humans; Hypercalcemia; Male; Osteocalcin; Phosphorus; Pulmonary Disease, Chronic Obstructive; Smoking