In this study 24 hour oesophageal pH and pressure monitoring was used to assess oesophageal motility and acid clearance in 27 patients with reflux oesophagitis (Savary-Miller grades I-IV), before and after healing of oesophagitis. After the first 24 hour study patients were treated with omeprazole 40
Abstract. Class specific anti‐IgA (anti‐α) antibodies were found in seven out of sixteen patients in whom serum IgA was not demonstrable by the Mancini method (sensitivity down to 0.02 mg/ml). Allotype specific anti‐IgA [anti‐A2m(l)] antibodies were found in an eighth patient. The anti‐IgA antibodies proved to be of the IgG class. In the eight patients with anti‐IgA antibodies, the presence of these antibodies could not be ascribed to immunization by administration of blood products. Isoimmunization in pregnancy and absorption of colostral IgA or animal IgA were other possible causes of anti‐IgA antibodies.–Using a combined IgA/anti‐IgA radioimmunoassay very low IgA levels (0.00013‐0.020 mg/ml) were demonstrable in patients without anti‐IgA antibodies whose serum IgA levels could not be determined by the Mancini method.–IgA metabolism was studied in five IgA‐deficient patients. In two patients the rate of degradation of 132I‐IgA almost equalled that in individuals with a normal serum IgA level. In three patients, however, the rate of degradation was greatly increased. In their sera, in contrast to the first two, class specific anti‐a antibodies were demonstrated.–One of these patients showed an anaphylactic reaction immediately after intravenous injection of mI‐IgA. Only this patient showed complement fixation by the IgA/anti‐IgA complex and IgA stimulation of lymphocytes.–The presence of anti‐IgA antibodies has some important practical implications for those patients who need blood products.
Whether the oesophageal motor response to reflux, as recorded over 24 hours, is impaired in patients with reflux oesophagitis was investigated. Twenty three patients with oesophagitis (Savary-Miller grades I-IV) and 23 control subjects matched for age and sex underwent 24 hour ambulatory pH and pressure monitoring. All contractions occurring in the 2 minute period after the onset of each reflux episode were analysed automatically using dedicated computer algorithms. A total of 2085 reflux episodes occurred -1513 in patients and 572 in controls. Oesophageal acid exposure was greater (p<0-01) in patients than in controls (mean (SEM) % time pH<4 13-3 (1-7) and 5 3 (09)%, respectively). The mean duration of the supine reflux episodes was longer (p<0-01) in patients (11.2 (2.8) minutes) than in controls (5.1 (1.8) minutes). In the upright period, no significant differences in the motor response to reflux were found.
Using conventional manometry and 24-hr ambulatory pressure and pH monitoring, we investigated esophageal motility and the esophageal motor response to reflux in 11 patients with reflux esophagitis Savary-Miller grade III and IV, and an age- and sex-matched group of 11 healthy controls. The patients had a significantly increased esophageal acid exposure. Conventional manometry showed a significantly decreased LES pressure and distal peristaltic amplitude in patients. The 24-hr monitoring yielded a significant decrease in peristaltic contraction duration and peristaltic propagation velocity in the patient group. Distal peristaltic amplitude was not decreased. Analysis of the contractions occurring in the 2-min period after each reflux episode showed a reduced number of contractions during the upright period, caused by a significantly decreased number of peristaltic contractions. During the supine period, there was a trend towards an increased number of contractions. It is concluded that esophageal motor activity and the response to reflux are impaired in patients with high-grade reflux esophagitis. However, the abnormalities found are only minor and are unlikely to play an important role in the pathogenesis of reflux esophagitis.
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