Sex hormone alterations and systemic inflammation in chronic obstructive pulmonary disease.

OBJECTIVE: Decreased anabolic hormone levels are described in chronic obstructive pulmonary disease (COPD), leading to important clinical consequences. The aim of this study was to evaluate the alterations in sex hormone levels in men with COPD to compare with age-matched control subjects, the determinants of these alterations, the relationship between hypogonadism and markers of systemic inflammation [interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha)] and the androgen status during an acute exacerbation of COPD. METHODS: A total of 103 COPD patients and 30 control subjects were admitted to the study. 83 stable COPD patients and 30 control subjects were evaluated as outpatients. 20 patients with COPD exacerbation were hospitalised and evaluated before discharge and after 1 month. RESULTS: Testosterone and dehydroepiandrosteronesulphate (DHEAS) levels of both COPD groups were lower than that of the control group. Luteinizing hormone (LH), follicle stimulating hormone (FSH) levels were increased during exacerbation. Testosterone and DHEAS levels increased and LH decreased in follow-up measurements of COPD exacerbation group. Testosterone and DHEAS levels were lower in severe COPD [forced expiratory volume in 1 s (FEV(1)) < 50%], in patients with severe hypoxaemia (PaO(2) < 60 mmHg) and in hypercapnic patients. Circulating IL-6 and TNF-alpha concentrations were higher in both stable and exacerbation phase COPD groups than controls. There was no correlation between sex hormones and TNF-alpha or IL-6. CONCLUSION: The alterations in sex hormone levels in COPD are particularly related to FEV(1), hypoxaemia and hypercapnia. There are significant differences in hormone levels during stable and exacerbation phases of COPD; the hormonal changes are marked during exacerbation and partially regress after 1 month when the disease is stabilised.

Circulating leptin and body composition in chronic obstructive pulmonary disease.

Nutritional depletion and weight loss are two features of chronic obstructive pulmonary disease (COPD), and the association between low body mass index (BMI) and poor prognosis in patients with COPD is a common clinical observation. Mechanisms of weight loss are still unclear in COPD. Excessive energy expenditure partly due to increased work of breathing was shown, but other mechanisms have been searched for. Leptin is a hormone secreted by adipocytes that plays an important role in energy homeostasis and regulates body weight through control of appetite and energy expenditure. The aim of this study was to evaluate the association of circulating leptin levels and measures of body composition in COPD patients. Thirty male COPD outpatients (mean age 66.3 +/- 8.4) and 20 controls (mean age 65.9 +/- 10.8) were included in the study. After standard spirometry and body composition measurements, serum leptin concentration was measured by ELISA assay. COPD patients were grouped according to BMI. Mean BMI was 19.01 +/- 2.26 kg/m2 in group 1 (COPD patients with low BMI), 26.85 +/- 4.51 in group 2 COPD (COPD patients with normal/high BMI) and 27.64 +/- 2.75 kg/m2 in healthy controls (group 3). Mean serum leptin concentration was 1.41 +/- 1.86 ng/ml in group 1, 2.60 +/- 1.38 ng/ml in group 2 and 2.82 +/- 1.46 ng/ml in group 3 (p = 0.002). Leptin correlated to not only BMI but also body weight, waist circumference, triceps and biceps skinfold thickness and body fat percent (p < 0.05 for all). Results of this study suggest that the cause of weight loss is not increased circulating leptin in COPD. Instead, leptin remains regulated in COPD and further decreased in patients with low BMI, probably as a compensatory mechanism to preserve body fat content, which should be evaluated in further studies.

Pulmonary function tests in Parkinson's disease.

Morbidity and mortality are usually caused by respiratory disorders in Parkinson's disease (PD) because of pulmonary functional impairments. The purpose of this study was to determine the effects of PD on ventilatory function and that the use of pulmonary function tests (PFT) may serve as an indicator of PD severity. PFT have been performed in 21 patients with PD (15 non-smoker and six exsmoker with 36.17 +/- 26.54 pack-years of smoking history; mean age 64.67 +/- 10.76 years) and 16 normal age-matched control subjects who never smoked. The clinical disability was indicated by a Hoehn-Yahr (H-Y) scale. MEF25% [maximal flow rate at 25% of remaining forced vital capacity (FVC)] and FEV1 (the volume of air expired during the first second of the FVC) in exsmoker PD group was lower than non-smoker PD group (P < 0.05). The two effort dependent variables' peak expiratory flow (PEF) and the maximal flow rate at 75% of the remaining FVC (MEF75%) percent predicted values were 70.66 +/- 24.15 and 69.05 +/- 24.39 in non-smoker PD group whereas 90.18 +/- 17.24 and 90.00 +/- 18.97% predicted were in control group, respectively (P < 0.05). The maximal voluntary ventilation (MVV) was found to be 52.83 +/- 15.52 and 91.52 +/- 13.80% in PD and control group, respectively (P < 0.0001). MVV was the most effected parameter that was inversely correlated with the PD severity (r=-0.87, P < 0.0001). We concluded that less coordinated and less explosive muscle force has contributed to decrease in PEF and MEF75% values, and MVV decreases in PD as a result of the impaired performance and reduced efficiency during repetitive motor tasks which in part reflects abnormal agonist-antagonist muscle activity. So, spirometric studies may serve as a useful indicator of patients' neurophysiological conditions for the purpose of anticipating and preventing complications because of pulmonary impairment.