Objective assessment of gastroesophageal reflux after extended Heller myotomy and total fundoplication for achalasia with the use of 24-hour combined multichannel intraluminal impedance and pH monitoring (MII-pH).

This study aims to evaluate by the use of 24-hour combined multichannel intraluminal impedance and pH monitoring (MII-pH) the efficacy of the Nissen fundoplication in controlling both acid and nonacid gastroesophageal reflux (GER) in patients that underwent Heller myotomy for achalasia. It has been demonstrated that fundoplication prevents the pathologic acid GER after Heller myotomy, but no objective data exists on the efficacy of this antireflux surgery in controlling all types of reflux events. The study population consisted of 20 patients that underwent laparoscopic Heller myotomy and Nissen fundoplication for achalasia. All patients were investigated with manometry and MII-pH. MII-pH showed no evidence of postoperative pathologic GER. The overall number of GER episodes was normal in both the upright and recumbent position. This reduction was obtained because of the postoperative control of both the acid and nonacid reflux episodes. The Nissen fundoplication adequately controls both acid and nonacid GER after extended Heller myotomy. Further controls with MII-pH are warranted to check at a longer follow-up for the efficacy of this antireflux procedure in achalasic patients.

Total fundoplication does not obstruct the esophageal secondary peristalsis: investigation with pre- and postoperative 24-hour pH-multichannel intraluminal impedance.

AIM: To determine the impact of total fundoplication on the spontaneous esophageal clearance, known as secondary peristalsis. BACKGROUND: Although there is general agreement that total fundoplication is not an obstacle to bolus swallowing (primary peristalsis), whether it is an obstacle to spontaneous esophageal clearance (secondary peristalsis) is still not clear. Based on 24-hour monitoring, multichannel intraluminal impedance was used to calculate the time of spontaneous bolus clearance (BCT). METHODS: Mean BCT was prospectively calculated in 15 consecutive patients before and after total fundoplication. BCT was calculated in seconds including all the gastroesophageal reflux episodes, whereas bolus swallows (solid meals and liquid swallows) were excluded from the analysis. RESULTS: BCT was extrapolated from 1,057 episodes in the 623 h of study. Overall, BCT did not change after surgery (13.6 +/- 4 vs. 15.2 +/- 10 s; p = nonsignificant) and in the upright (12.2 +/- 3 vs. 16.5 +/- 7 s; p = nonsignificant) and recumbent position (22.9 +/- 9 vs. 23.0 +/- 9 s; p = nonsignificant). CONCLUSIONS: In this study total fundoplication did not affect the BCT by combined 24-hour ph monitoring and multichannel intraluminal impedance.

Non-alcoholic fatty liver disease in young adult severely obese non-diabetic patients in South Italy.

BACKGROUND/AIMS: In the absence of other causes, obesity increases the risk of liver disease. We evaluated the prevalence and degree of metabolic and hepatic abnormalities associated with non-alcoholic fatty liver disease (NAFLD) in type II-III obesity in a metropolitan area of South Italy. METHODS: 187 (81 M, 106 F) young adult non-diabetic obese patients, age range 18-50 years (mean 31.9 +/- 8.8), body mass index (BMI) > or =30 (mean 47.5 +/- 9.6), consecutively admitted from January 2000 to April 2003 to the Obesity Outpatients Clinic entered into the study. Patients were divided into two groups: (1) BMI 30.0-39.9, and (2) BMI> or =40. Ultrasound detected liver steatosis was classified as: (I) mild; (II) moderate, and (III) severe. RESULTS: All patients, except 4, showed a variable degree of steatosis: mild was more frequent among females, severe steatosis present only in grade III obesity, with higher prevalence in males than in females (p < 0.001). Mean serum transaminases, in particular alanine aminotransferase (ALT), increased according to BMI and degree of steatosis. Homeostasis Model Assessment (HOMA) index, ferritin and fibrinogen levels increased with BMI, particularly in severe steatosis. In group 2, patients with BMI> or =40 showed a positive correlation between ferritin, aspartate aminotransferase (AST) (r = 0.46, p < 0.018), ALT (r = 0.41, p < 0.036) and gamma-glutamyltransferase (gammaGT) (r = 0.51, p < 0.007), between serum triglycerides (TG) and AST (r = 0.28, p < 0.036), ALT (r = 0.30, p < 0.02) and between HOMA and ALT (r = 0.30, p < 0.03) and gammaGT (r = 0.35, p < 0.012). In group 2 patients with severe steatosis the prevalence of metabolic syndrome according to Adult Treatment Panel III (ATP III) was 40%. CONCLUSION: These data suggest that, in young adult non-diabetic grade III obese patients, fatty liver is always present and strictly related to insulin resistance which, in the presence of severe liver steatosis, is also related to serum ferritin.

Calcification processes in the chick otoconia and calcium binding proteins: patterns of tetracycline incorporation and calbindin-D28K distribution.

In order to clarify the otoconia formation and turnover, tetracycline, an antibiotic that precipitates at calcifying fronts and serves as a fluorescent marker, was injected into eggs at different stages of chick embryonic development, as well as into postnatal chicken and into adult animals. The changes in the intensity, location patterns and time course of fluorescent labelling in each examined stage in the otolithic organs was studied. The presence and distribution of calbindin (CB)-D28K, one of the calcium-binding proteins constantly found in the mammalian and chicken cochlea and also in otolithic membrane of some adult mammals, was studied. Results in embryonal stages, postnatal and adult animals allow us to postulate that otoliths are mainly produced during the embryonal phase, but they may also be produced throughout the whole life span. Results also indicate that otoconia are dynamic structures which undergo turnover. The correspondence between the patterns of CB-D28K immunoreactivity and tetracycline fluorescence may indicate that CB-D28K participates in the formation of otoconia.