Effect of exocrine pancreatic function on resting energy expenditure in cystic fibrosis.

AIM: To prove the hypothesis that exocrine pancreatic function determines resting energy expenditure (REE) in cystic fibrosis (CF). METHOD: Thirty-eight CF individuals, 9-34 (19.98 +/- 1.0) years, were divided into three groups: Six pancreatic sufficient patients (PS; group A), 21 pancreatic insufficient patients (PI), whose pulmonary function was comparable to that of group A (group B1) and 11 PI patients, whose pulmonary function was significantly worse than that of group A (group B2). REE was estimated by indirect calorimetry. Predicted REE was based on Schofield equations. Measured REE was expressed as % of the predicted. BMI, BMI z-scores, serum albumin, cholesterol and triglycerides levels were related to REE. Results were expressed as mean +/- standard error. RESULTS: Groups B1 and B2 had significantly higher REE% (111.7 +/- 2.75% and 119.94 +/- 3.8, respectively) as opposed to group A (98.9 +/- 3.81%; p = 0.022 and 0.035, respectively) whose REE% was similar to that predicted. REE% between group B1 and B2 was not statistically significant. In groups A, B1 and B, mean FEV1% was 86.33 +/- 10.1%, 90.24 +/- 4.39%, 44.54 +/- 3.47%, respectively, mean BMI was 25.6 +/- 2.06, 19.48 +/- 0.64 and 20.09 +/- 8.8, respectively, BMI z-scores were 0.75 +/- 0.51, -0.52 +/- 0.24 and -1.07 +/- 0.37, respectively. Significant correlation was demonstrated between REE%, BMI z-scores and cholesterol levels in group A. CONCLUSION: Clinically stable CF patients, who had comparable pulmonary function, exhibited increased REE% only in the presence of exocrine pancreatic insufficiency. REE% strongly correlated with BMI z-scores in pancreatic sufficiency. These findings support the hypothesis that pancreatic rather than pulmonary function may determine nutritional status as well as REE in CF.

Growth of asthmatic children before long-term treatment with inhaled corticosteroids.

The aim of this study was to examine the growth of asthmatic children before any long-term inhaled corticosteroid treatment. We studied 436 asthmatic children (254 boys and 182 girls), age range 3.9-15.4 years, that had not been treated with long-term inhaled corticosteroids. In each child height and weight were measured, and the height standard deviation score (HSDS) and the weight for height ratio (%WFH) were calculated. We also estimated asthma severity and tested atopic status by skin testing. Children were grouped into three age groups: prepuberty (3.9-7.9 years), peripuberty (8-11.9 years), and puberty (12-15.5 years). HSDS was correlated to asthma severity and duration, atopic status, and other coexisting allergic diseases. Seven hundred ten healthy children (345 boys, 365 girls) ages 4.1-15.5 years were used as controls for height and weight. There was no statistically significant difference in HSDS and %WFH between patients and controls, except for HSDS of pubertal female patients that was significantly less than that of controls, x: 0.06 (0.80) vs. x: 0.40 (0.90), respectively, p < 0.02. There was also no significant correlation between HSDS or %WFH and severity or duration of the disease, allergy status and other coexisting allergic diseases. However, there was significant difference in menarcheal age between asthmatic girls x: 12.49 (0.12) and controls x: 12.00 (0.10), p < 0.001. In conclusion, our data show that the growth of asthmatic children before any long-term treatment with inhaled corticosteroids is not different from the control population, except for the asthmatic girls of pubertal age who are shorter than control girls probably because of delay in pubertal maturation.