Abnormal degrees of gastro-oesophageal reflux (GOR) were detected by 24 hour intraoesophageal pH measurement in 12 of 14 children (mean age 7-9 years; range 5 months-16 years) affected by cystic fibrosis and complaining of symptoms suggesting GOR. These patients underwent combined recording of distal oesophageal motility and intraluminal pH in order to investigate mechanisms of GOR. Inappropriate lower oesophageal sphincter relaxation was the most common mechanism of reflux in all patients. Other mechanisms (appropriate relaxation or lowered pressure of the lower oesophageal sphincter, increased intragastric pressure) were detected less frequently. Frequency of inappropriate lower oesophageal sphincter relaxations was significantly higher in patients with cystic fibrosis than in other study groups (symptomatic GOR, GOR disease complicated by respiratory complaints). Inappropriate lower oesophageal sphincter relaxations occurred with the same frequency in patients with cystic fibrosis and in a group of children with GOR disease complicated by oesophagitis. Abnormalities of distal oesophageal contractions such as decreased amplitude or uncoordinated waves were also recorded in cystic fibrosis patients. Seven patients with cystic fibrosis completed a therapeutic trial for eight weeks consisting of postural treatment and oral cisapride, a new prokinetic drug. The oesophageal acid exposure improved in only three patients. We conclude that pathologic GOR is commonly asssociated with cystic fibrosis. The predominant reflux mechanism in these patients is a transient inappropriate lower oesophageal sphincter relaxation rather than a low steady state basal lower oesophageal sphincter pressure.
Summary: Serum and plasma myoglobin and creatine kinase-MB catalytic activity were analysed in 157 patients admitted within 2 hours of the onset of ehest pain (58 were retrospectively recognized s acute myocardial infarction).Serum and plasma values were highly correlated for both myoglobin and creatine kinase-MB.Plasma myoglobin appared to be more sensitive than creatine kinase-MB for the early diagnosis of acute myocardial infarction; using a cut-off value of 100 μ §/1, 90% of acute myocardial infarction cases were correctly recognized by plasma myoglobin 6 hours after the onset of ehest pain, with a diagnostic specificity of 100% for non-acute myocardial infarction ehest pain subjects. Plasma creatine kinase-MB showed a diagnostic sensitivity of 62% and a diagnostic specificity of 95% in the same group of patients.We suggest the inclusion of the plasma myoglobin immunonephelometric assay together with plasma creatine kinase-MB activity analysis in protocols for the early diagnosis of acute myocardial infarction.
In 10 children with cystic fibrosis and persisting steatorrhoea, supplementation with taurine (30-40 mg/kg/day) was given for two months as an adjunct to the usual pancreatic enzyme treatment. A three day fat and energy balance was performed in patients with cystic fibrosis, before and after the supplementation, and in seven healthy controls who did not receive taurine. Faecal fat was measured by a gravimetric method and stool energy was determined using a bomb calorimeter. Patients with cystic fibrosis, before and after taurine, and healthy controls received the same fat and energy intake (calculated by a dietitian). In patients with cystic fibrosis taurine did not produce any improvement of steatorrhoea (mean (SD) faecal fat 8.7 (3.3) v 11.2 (7.0) g/day, respectively before and after the supplementation), of faecal energy loss (0.978 (0.468) v 1.133 (0.539) MJ/day), of faecal fat expressed as percent of fat intake (13.4 (5.6) v 15.1 (9.8)%), and of faecal energy expressed as percent of energy intake (9.9 (3.6) v 11.2 (5.7)%). Healthy controls had significant lower fat (3.5 (2.3) g/day) and energy 0.576 (0.355) MJ/day faecal losses. In conclusion, taurine failed to decrease significantly fat and energy losses. Our study does not support the use of taurine supplementation in the nutritional management of cystic fibrosis.
The aim of the study was the evaluation of the relationship between chemical fat analysis and some more rapid tests proposed to estimate steatorrhoea. Stool collections (72 h) were obtained on 32 occasions in 22 patients with cystic fibrosis and in seven healthy children. A very close relationship was found between faecal fat, as measured by standard chemical methods, and faecal energy (r = 0.95, P < 0.001). We conclude that the determination of faecal energy, easier to measure than faecal fat, can provide reliable information about the extent of steatorrhoea in cystic fibrosis.
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