Purpose: The cause of choledochal (cystic or fusiform) malformation is not known.A favoured hypothesis suggests that abnormal reflux of activated pancreatic secretions via a common pancreatobiliary channelmay initiate...Purpose: The cause of choledochal (cystic or fusiform) malformation is not known.A favoured hypothesis suggests that abnormal reflux of activated pancreatic secretions via a common pancreatobiliary channelmay initiate mucosal injury and mural weakness leading to bile duct dilatation, at normal intraduct pressures.However, bile duct pressures in both normal or disease states are not known in such children.Methods: Intraoperative choledochal pressure (CP) measurements were made before any other manipulation.Bile was cultured and its amylase content measured.Biochemical liver function (bilirubin, aspartate aminotransferase, γ-glutamyl transpeptidase, and alkaline phosphatase)was measured.Datawere quoted as median (interquartile range).Statistical tests were parametric, where appropriate, and P =.05 was regarded as significant.Results: Twenty-five children (age 2.5 [1.25-5.91] years) with choledochal (cystic [n = 13] and fusiform [n = 12]) malformation coming to surgery were studied.Median CP was 13 (8.5-17)-mm Hg.Median bile amylase was 6722 (241-18,000) IU/L.Choledochal pressure inversely correlated with bile amylase (r = -0.60, P =.001), serum aspartate aminotransferase (r = 0.46, P =.01), and log γ-glutamyl transpeptidase (r = 0.4, P =.04) but not with bilirubin (P =.11), alkaline phosphatase (P =.20), or age (P =.11).No difference in CP, bile amylase, or liver biochemistry could be identified between the 2 biliary phenotypes.All bile cultures were sterile.Conclusions: Increased CP is inversely related to the level of bile amylase (and hence degree of the functional common channel).This suggests that obstructive stenosis at the level of the pancreato-biliary junction (but not the ampulla) may be a causal factor in a proportion of choledochal malformations.展开更多
Objective: To determine whether obese, nonhirsute adolescents with oligomenorrhea exhibit similar increased LH pulse secretion patterns compared with obese girls with polycystic ovary syndrome (PCOS). Design: Prospect...Objective: To determine whether obese, nonhirsute adolescents with oligomenorrhea exhibit similar increased LH pulse secretion patterns compared with obese girls with polycystic ovary syndrome (PCOS). Design: Prospective, observational study. Setting: Tertiary university hospital. Patient(s): Nine obese girls with oligomenorrhea, 15 with PCOS, and 10 controls. Intervention(s): Twenty-four-hour IV blood sampling for LH (every 10 minutes); measurement of steroid hormones (every 12 hours); and injection of leuprolide acetate (10 μ gm/kg SC). Main Outcome Measure(s): Twenty-four-hour,wake, and sleep LH mean serum concentration, pulse frequency, amplitude; steroid hormones, including free androgen index (FAI); and pre-and post-leuprolide acetate 17-hydroxyprog-esterone measurements. Result(s): Twenty-four-hour LH pulse frequency in oligomenorrheic girls (18.6 ± 1.2) (mean ± SE) was comparable to that in girls with PCOS (20.9 ± 0.7) and greater than in normal girls (13.4 ± 0.8). The pulse number during both sleep and wake was identical in oligomenorrheic and PCOS girls and significantly greater than that of normal girls. Mean 24- hourLH level, serum androgen levels, and FAI in oligomenorrheic girls were equivalent to those of normal controls and lower than those of PCOS girls. Conclusion(s): These preliminary results indicate that obese girls with oligomenorrhea exhibit increased LH pulse frequency in the absence of clinical and/or biochemical evidence of hyperandrogenism.展开更多
文摘Purpose: The cause of choledochal (cystic or fusiform) malformation is not known.A favoured hypothesis suggests that abnormal reflux of activated pancreatic secretions via a common pancreatobiliary channelmay initiate mucosal injury and mural weakness leading to bile duct dilatation, at normal intraduct pressures.However, bile duct pressures in both normal or disease states are not known in such children.Methods: Intraoperative choledochal pressure (CP) measurements were made before any other manipulation.Bile was cultured and its amylase content measured.Biochemical liver function (bilirubin, aspartate aminotransferase, γ-glutamyl transpeptidase, and alkaline phosphatase)was measured.Datawere quoted as median (interquartile range).Statistical tests were parametric, where appropriate, and P =.05 was regarded as significant.Results: Twenty-five children (age 2.5 [1.25-5.91] years) with choledochal (cystic [n = 13] and fusiform [n = 12]) malformation coming to surgery were studied.Median CP was 13 (8.5-17)-mm Hg.Median bile amylase was 6722 (241-18,000) IU/L.Choledochal pressure inversely correlated with bile amylase (r = -0.60, P =.001), serum aspartate aminotransferase (r = 0.46, P =.01), and log γ-glutamyl transpeptidase (r = 0.4, P =.04) but not with bilirubin (P =.11), alkaline phosphatase (P =.20), or age (P =.11).No difference in CP, bile amylase, or liver biochemistry could be identified between the 2 biliary phenotypes.All bile cultures were sterile.Conclusions: Increased CP is inversely related to the level of bile amylase (and hence degree of the functional common channel).This suggests that obstructive stenosis at the level of the pancreato-biliary junction (but not the ampulla) may be a causal factor in a proportion of choledochal malformations.
文摘Objective: To determine whether obese, nonhirsute adolescents with oligomenorrhea exhibit similar increased LH pulse secretion patterns compared with obese girls with polycystic ovary syndrome (PCOS). Design: Prospective, observational study. Setting: Tertiary university hospital. Patient(s): Nine obese girls with oligomenorrhea, 15 with PCOS, and 10 controls. Intervention(s): Twenty-four-hour IV blood sampling for LH (every 10 minutes); measurement of steroid hormones (every 12 hours); and injection of leuprolide acetate (10 μ gm/kg SC). Main Outcome Measure(s): Twenty-four-hour,wake, and sleep LH mean serum concentration, pulse frequency, amplitude; steroid hormones, including free androgen index (FAI); and pre-and post-leuprolide acetate 17-hydroxyprog-esterone measurements. Result(s): Twenty-four-hour LH pulse frequency in oligomenorrheic girls (18.6 ± 1.2) (mean ± SE) was comparable to that in girls with PCOS (20.9 ± 0.7) and greater than in normal girls (13.4 ± 0.8). The pulse number during both sleep and wake was identical in oligomenorrheic and PCOS girls and significantly greater than that of normal girls. Mean 24- hourLH level, serum androgen levels, and FAI in oligomenorrheic girls were equivalent to those of normal controls and lower than those of PCOS girls. Conclusion(s): These preliminary results indicate that obese girls with oligomenorrhea exhibit increased LH pulse frequency in the absence of clinical and/or biochemical evidence of hyperandrogenism.
