Hydrolysis of peripheral leucine enkephalin in allergic asthma.

Plasma hydrolysis of leucine enkephalin was studied in a group of patients affected by seasonal allergic asthma in acute and quiescent stage; data were compared with those obtained from a control group of healthy volunteers. Results obtained indicate a statistically significant reduction of leu-enkephalin hydrolysis in allergic subjects. In the quiescent stage, substrate degradation is reduced, and the pattern of the hydrolysis by-products is modified with respect to normal controls. In the acute stage, hydrolysis is further reduced, and the pattern of the hydrolysis by-products is further modified with respect to the quiescent stage. The variations of leu-enkephalin hydrolysis appear to be controlled by decreased activity of proteolytic enzymes and by increased activity of the low-molecular-weight plasma inhibitors active on these enzymes. The sum of these processes is conducive to a distribution of enkephalin-hydrolyzing enzymes, as well as a hydrolysis pattern, that appears to be specific for the allergic subjects and distinct from that seen in the controls.

Leucine enkephalin degradation in allergopathic versus normal human plasma.

The enzyme hydrolysis of labelled leu-enkephalin in the presence of plasma enzymes was studied by kinetic and chromatographic techniques in a group of allergopathic patients in the acute and quiescent stage; data obtained have been compared with those obtained with normal controls. Results shown indicate that in the quiescent stage substrate degradation is reduced, and that the pattern of the hydrolysis by-products is modified with respect to the controls. In the acute as compared to the quiescent stage, enkephalin hydrolysis is further reduced, and the pattern of hydrolysis by-products is further modified. ANOVA analysis of these data indicates that the dependency of hydrolysis reduction upon the grouping of subjects (i.e., controls, quiescent and acute stage) is statistically very significant. Reduced substrate hydrolysis, and modified hydrolysis pattern, appears to be associated with decreased activity of the enzymes involved and more significantly with increased activity of the low molecular weight plasma inhibitors. The combination of these two factors appears to define a hydrolysis pattern characteristic of the allergopathic subjects, similar in the quiescent and acute phase, and different from that observed in the controls.

Co-morbidity contributes to predict mortality of patients with chronic obstructive pulmonary disease.

The aim of this study was to assess the prognostic role of co-morbidity in severe chronic obstructive pulmonary disease (COPD). A cohort of 270 COPD patients, mean (+/-SD) age 67+/-9 yrs, consecutively discharged from a University Hospital after an acute exacerbation was studied. Mean (+/-SD) forced expiratory volume in one second (FEV1) was 34+/-16% of predicted and FEV1/forced vital capacity (FVC) was 40.5+/-13.8%. The most common co-morbid diseases were: hypertension (28%), diabetes mellitus (14%), and ischaemic heart disease (10%). Clinical, electrocardiogram (ECG), and respiratory function data taken at the time of discharge were collected from the clinical records. The Charlson's index was used to quantify co-morbidity. Follow-up was conducted by means of telephone calls. Multivariate survival analysis was used to identify the independent predictors of death. The median survival of the cohort was 3.1 yrs. Death was predicted by the following variables: age (hazard rate (HR) 1.04; 95% confidence intervals (95% CI) 1.02-1.05), ECG signs of right ventricular hypertrophy (HR 1.76; 95% CI 1.30-2.38), chronic renal failure (HR 1.79; 95% CI 1.05-3.02), ECG signs of myocardial infarction or ischaemia (HR 1.42; 95% CI 1.02-1.96), FEV1 < 590 mL (HR 1.49; 95% CI 0.97-2.27). A score based upon these variables predicted mortality at 5 yrs with a sensitivity of 63% and a specificity of 77%. Selected co-morbid diseases and electrocardiogram signs of right ventricular hypertrophy play a major prognostic role in advanced chronic obstructive pulmonary disease. The clinical assessment of patients with chronic obstructive pulmonary disease should include these important and easily measurable variables.

Maximal inspiratory pressure in elite soccer players.

The respiratory muscle strength of elite athletes has been assessed only for some competitive sports and different conclusions have been reported. The aim of this study was to evaluate the inspiratory muscle strength in a group of professional soccer players in comparison with a group of sedentary subjects. Maximal Inspiratory Pressure (PImax) was measured both at Functional Residual Capacity (FRC) and at Residual Volume (RV) in 130 subjects: 27 of these were elite soccer players (all males, aged 22 +/- 3 years) and 103 were normal sedentary subjects (77 males and 26 females, aged 44 +/- 19 years). Predictive linear models were produced by a stepwise regression analysis in the whole sample of subjects. Both PImaxFRC and PImaxRV models included female gender and ageing as negative predictors, and Body Mass Index (BMI) as positive predictor of the inspiratory pressures. The model predicting PImaxFRC was slightly more accurate than the model predicting PImaxRV (r-squared: 0.38 vs 0.36, respectively). After adjustment for the variables entered in these models, PImaxFRC and PImaxRV were respectively 1.54 KPa and 1.08 KPa higher in soccer players than in sedentary subjects but this result was statistically significant (p < 0.02) only for PImaxFRC. We conclude that the inspiratory muscle strength is increased in soccer players and PImax measured at FRC seems more sensitive in order to discriminate between subjects with different level of physical activity.