Subject(s)
Fatty Liver/genetics , Histocompatibility Antigens Class I/genetics , Iron Overload/genetics , Membrane Proteins/genetics , Amino Acid Substitution , Fatty Liver/complications , Hemochromatosis/complications , Hemochromatosis/genetics , Hemochromatosis/metabolism , Hemochromatosis Protein , Homozygote , Humans , Iron/metabolism , Iron Overload/complications , Iron Overload/metabolism , Male , Metabolic Syndrome/complications , Metabolic Syndrome/genetics , Middle Aged , Point MutationABSTRACT
OBJECTIVE: The secretin-cholecystokinin test is the "gold standard" to evaluate exocrine pancreatic function. But this direct duodenal intubation test is invasive, particularly in children, time-consuming, and expensive. For several years, indirect noninvasive tests of pancreatic insufficiency have been developed, such as fecal chymotrypsin (FChT) and fecal elastase-1 (FEL-1) measurements. Generally, elastase-1 is truly admitted to be the most relevant test of exocrine pancreatic status. However, so far, no consensus for stool collection protocol exists. The aim of our study was to investigate the diagnostic advantage from measuring fecal proteases in stool samples collected for two or three consecutive days in comparison to one single stool sample collected at random. DESIGN: A total of 69 children were divided into group A (stool samples collected for three consecutive days) and group B (stool samples collected for two consecutive days). These two groups included pancreatic-sufficient patients (PS) and severe pancreatic-insufficient patients (PI). One single determination of fecal chymotrypsin activity and of fecal elastase-1 concentration was realized on each stool. RESULTS: The same relatively important intraindividual variability of fecal proteases was observed in group A and B (mean coefficients of variation (CVs) 36% vs. 40.2% for chymotrypsin, 22.2% vs. 26.8% for elastase-1). No significant PS or severe PI diagnostic discordance was observed between 1, 2, or 3 days of stool collections. CONCLUSION: Our study clearly shows that the determination of fecal proteases on one single stool collected at random is sufficient to evaluate pancreatic exocrine status for PS and severe PI.
Subject(s)
Chymotrypsin/analysis , Exocrine Pancreatic Insufficiency/diagnosis , Feces/enzymology , Pancreas, Exocrine/enzymology , Pancreatic Elastase/analysis , Adolescent , Child , Child, Preschool , Exocrine Pancreatic Insufficiency/enzymology , Female , Humans , Infant , Infant, Newborn , Male , Random Allocation , Reproducibility of ResultsABSTRACT
The objective of this study was to describe long-term detraining effects on lipid profile in previously highly endurance-trained athletes. The study design was longitudinal, with a 2-yr follow-up study of changes in lipid profile during hard training and detraining. Ten subjects trained for 2 yr (22 h/wk; two 47-wk training periods with a 5-wk recovery period), and the 10 others stopped training after wk 47. Main blood lipid profile parameters, energy intake, and body composition were measured at baseline (wk 1) and at wk 24, 47, 52, 76, and 99. Although food caloric intake was reduced (2411 +/- 256 vs. 5697 +/- 455 kcal/d, detraining vs. training), detraining induced a decrease in high density lipoprotein cholesterol and increases in fat mass (by 6.5 +/- 1.1 kg), body mass index, leptin, low density lipoprotein cholesterol, low density lipoprotein/high density lipoprotein ratio, and apolipoprotein B, although insulin resistance (determined by homeostasis model assessment) stabilization had previously occurred. Further disorders appeared in triglycerides (TG) metabolism during detraining, with a persistent increase in TG (from 1.0 +/- 0.3 to 1.4 +/- 0.3 mmol/liter), whereas glycerol decreased (from 88 +/- 9 to 73 +/- 8 micromol/liter), and very low density lipoprotein-TG, chylomicrons, and apolipoprotein C(3) remained stable. Plasma lipoprotein lipase activity decreased whereas hepatic lipase activity remained stable. As well as a rapid loss of endurance-training benefits for the cholesterolemic profile, detraining also induced disorders in TG metabolism, possibly as a result of the elevated TG turnover acquired with long-term hard training.
