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Presents abstracts of articles adapted from the April 1998 edition of the periodical `European Journal of Clinical Nutrition,' which focused on clinical nutrition.

External hemorrhoids thrombosis affects 8% of women during last trimester pregnancy and 20% of women immediately after delivery. Their treatment is medical with local treatment (with corticoid and anesthetic), defecation regulation and paracetamol. NSAID can be used after delivery in absence of breath-feeding. Local excision is not possible in most of the cases because of inflammation. Surgery has to be an exception because medical treatment is sufficient in almost all cases. Anal fissure is the most frequent differential diagnosis, encountered in 15% after all deliveries. Symptoms associate anal pain during and after defecation with blood on toilet paper. The only identified risk factor for hemorrhoids thrombosis (and anal fissure) is dyschesia. We have to think about it., (Copyright © 2011. Published by Elsevier Masson SAS.)

Dysphagia can be caused by a number of disorders, benign or malignant, that involve either the oropharynx or the esophagus. The cause of dysphagia can be determinated with an accuracy on the basis of a careful history alone in most cases. In patients without endoscopic abnormality, eosinophilic esophagitis must be suspected. Esophageal manometry is especially useful for the diagnosis of achalasia. There are no specific treatment for motility disorders other than achalasia and its variants.

Background: Obesity is a predisposing factor to gastro-esophageal reflux disease (GERD), but esophageal function remains poorly studied in morbidly obese patients and could be modified by bariatric surgery., Methods: Every morbidly obese patient (BMI > or =40 kg/m2 or > or =35 in association with co-morbidity) was prospectively included with an evaluation of GERD symptoms, endoscopy, 24-hour pH monitoring and esophageal manometry before and after adjustable gastric banding (AGB) or Roux-en-Y gastric bypass (RYGBP)., Results: Before surgery, 100 patients were included (84 F, age 38.4 +/- 10.9 years, BMI 45.1 +/- 6.02 kg/m2), of whom 73% reported GERD symptoms. Endoscopy evidenced hiatus hernia in 39.4% and esophagitis in 6.4%. The DeMeester score was pathological in 53.3%; 69% of patients had lower esophageal sphincter (LES) pressure <15 mmHg and 7 had esophageal dyskinesia. BMI was significantly related to the DeMeester score (P = 0.018) but not to LES tone or esophageal dyskinesia. Postoperative data were available in 27 patients (AGB n = 12/60, RYGBP n = 15/36). The DeMeester score (normal < 14.72) was significantly decreased after RYGBP (24.8 +/- 13.7 before vs. 5.8 +/- 4.9 after; P < 0.001) but tended to increase after AGB (11.5 +/- 5.1 before vs. 51.7 +/- 70.7 after; P = 0.09), with severe dyskinesia in 2 cases., Conclusion: GERD and LES incompetence are highly prevalent in morbidly obese patients. Preliminary postoperative data show different effects of RYGBP and AGB on esophageal function, with worsening of pH-metric data with occasional severe dyskinesia after AGB.

Laparoscopic adjustable gastric banding (LAGB) has become an increasingly popular option to treat morbid obesity. Esophageal dysmotility secondary to LAGB has been described, but is usually reversible after removal of the band. Long-term esophageal dysmotility persisting after removal of the band is an unusual and not yet described complication. We report the case of a 58-year-old obese patient who developed severe dysphagia and vomiting associated with atypical esophageal dysmotility 22 months after gastric band placement. Radiological exploration revealed no acute band slippage but only a pseudoachalasia. Device deflation and then band removal were required in an attempt to treat her symptoms. Esophageal dysmotility persisted for several months after band removal and was still present after a Roux-en-Y gastric bypass performed as revisional operation. Possible mechanisms generating this complication and clinical implications are discussed.

Objective: To study in morbid obesity the relationship between the degree of gastro-oesophageal reflux (GER) and the excess of body weight, or the related factors such as the energy intake or the fat distribution (waist-hip ratio)., Methods: In 20 morbid obese subjects (body weight: 125 +/- 32 kg) consulting in a weight-loss programme, anthropometric measurements, 3-hr oesophageal pHmetry, double isotope labelled meal for studying gastric emptying, study of gastric acid and pepsin secretions using PEG 4,000 as marker, and upper endoscopy were performed., Results: Nine out of the 20 patients had more than 10 GER per 3-hr period. Seven patients had at least one GER symptom per day. In 6 patients, pH was under 4 for more than 10% of the time. The total number of GER and the number of GER of more than 5 min duration were correlated to the body mass index (P = 0.016 and P < 0.05 respectively). The number of GER was also correlated to the android type of overweight (P < 0.03). These relationships persisted when sex, age, smoking, and obesity complications (such as diabetes) were taken into account. There was a positive correlation between the number of GER and energy and lipid intake (energy intake: 3,119 +/- 1,082 kcal/day; P < 0.003 for both). The degree of GER was positively related to basal acid output (P = 0.049), and to sham feeding-stimulated acid output (P = 0.05); it was negatively related to gastric emptying half time, but was not correlated with basal or stimulated pepsin output. A relationship was found between body mass index (BMI) and gastric emptying half time for solid (P = 0.002) and liquid phases (P = 0.001)., Conclusion: GER seems to be common in long lasting morbid obesity. The number of refluxes increased with waist/hip ratio, BMI and energy or fat intake. GER was also increased by decreased gastric emptying rate, which was in part determined by BMI. The real prevalence of GER in morbid obeses must be determined by a large prospective study.

The term inflammatory bowel diseases applies to two intestinal diseases (ulcerative colitis and Crohn's disease) localized to the colon. Clinical, morphological and histological data often point to one or the other of these diseases, but they are not always distinguishable, and intermediate forms classified under one name or the other are numerous. Lower digestive tract endoscopy and biopsies are determinant (1) for the diagnosis, as they provide a precise description of the lesions for each segment and evaluate their severity; (2) to monitor the course of the disease under treatment and detect precancerous lesions.

The present study intended to investigate the effect of antroduodenal acidification on gastric acid secretion and emptying, gastrin and somatostatin release in response to food in healthy subjects as well as in duodenal ulcer patients. Ten duodenal ulcer patients and 9 normal controls were studied twice: the same 400 ml liquid protein meal (proteins: 10 g) was introduced into the stomach; then intragastric pH was either maintained at pH 4.5 or allowed to decrease in response to the meal. Acid secretion was calculated using the intragastric titration method (for which the intragastric pH is fixed at pH 4.5) and using the serial dilution indicator method (which allows antral acidification) respectively. Gastric emptying was estimated according to: a) iterative measurements of intragastric meal residual volume; b) volume passing through the pylorus. These two tests were performed in a random order and during each, plasma gastrin and somatostatin responses to the meal were determined. In healthy subjects, antral acidification following the meal was associated with a significantly lower acid secretion (17.3 +/- 0.9 mmol/h; m +/- SEM) than when the pH was maintained at pH 4.5 (20.2 +/- 1.3; p less than 0.05). Moreover, gastric emptying was slower when the pH was allowed to decrease (t 1/2: 26.2 +/- 1.4 min) than when the pH was constant (t 1/2: 20.5 +/- 2.2 min; p less than 0.05). By contrast, in the duodenal ulcer group, neither acid output nor gastric emptying were significantly different in the two situations.(ABSTRACT TRUNCATED AT 250 WORDS)

The high basal and meal-induced acid secretions in duodenal ulcer patients has led to the concept that vagal hyperactivity is a common factor in the pathogenesis of peptic ulcer. For these reasons, since pancreatic polypeptide secretion is known to be under vagal control, we studied the pancreatic polypeptide release after intragastric administration of two protein meals (10 and 20 g protein in 400 ml) in 18 duodenal ulcer patients and in 17 normal subjects. After a 10 g protein meal was administered, gastric pH was either maintained at pH 4.5 or allowed to decrease. The 20 g protein meal induced a higher pancreatic polypeptide release than did the 10 g protein meal (p less than 0.05): the integrated pancreatic polypeptide responses were 1.07 +/- 0.5 and 3.21 +/- 0.58 nmol/l/60 min respectively in the duodenal ulcer group and 0.46 +/- 0.21 and 2.67 +/- 0.69 nmol/l/60 min respectively in the control group. On the other hand, the responses to the two protein meals in duodenal ulcer patients were not different from those obtained in normal subjects, despite the higher meal-induced acid secretions in the duodenal ulcer group. pancreatic polypeptide increase was not larger when gastric pH was fixed than when it was allowed to decrease, 0.56 +/- 0.21 and 1.7 +/- 0.63 nmol/l/60 min respectively in normal subjects and 1.07 +/- 0.5 and 1.07 +/- 0.49 nmol/l/60 min respectively in duodenal ulcer patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenal ulcer is a recurrent disease with seasonal periodicity for pain and complications such as hemorrhage and perforation. Ulcer craters or symptoms seem to occur preferentially in early spring and autumn. Since acid secretion is one of the pathogenetic factors of the disease, we analyzed retrospectively basal and maximal (pentagastrin) acid secretion data obtained in 341 consecutive patients according to the month in which they were obtained. The patients were classified according to the activity of their ulcer (active, non active) and to the level of the peak acid secretion (hypersecretors, normosecretors). Basal acid concentration and output, and peak acid output were, both overall and month by month, higher in patients with active duodenal ulcer disease than in those who were non active, and in hypersecretors than in normosecretors. For all 341 patients as well as for normosecretors and non active ulcer patients, a triannual rhythm was detected for stimulated acid concentration and peak acid output. The highest values were noted in February, June, and October (period: 4 months). The amplitude of these rhythms was 3 to 4 percent, with differences between highest and lowest values of 30.4 mmol/l for concentration and 17.1 mmol/h for peak acid output. These rhythms for acid secretion during the year may contribute to the periodicity of duodenal ulcer events and should be analyzed in association with other factors which could be implied in ulcerogenesis. Moreover, this seasonal periodicity of acid secretion in duodenal ulcer should be taken into account in all therapeutic trials in which acid secretion is analyzed.