Symptoms and pathophysiological correlations in patients with constipation and functional dyspepsia.

INTRODUCTION: Patients with constipation often report dyspeptic symptoms, but whether constipation is associated with specific dyspeptic symptoms and altered gastrointestinal (GI) motility, remains to be established. Our aim was to study symptoms association and GI motility parameters in patients with constipation and functional dyspepsia. PATIENTS AND METHOD: 42 patients with different symptoms and severity of constipation and dyspepsia were enrolled. Scintigraphic gastric emptying, colonic transit time and gallbladder contraction were studied in all subjects. RESULTS: No significant association was observed between individual symptoms of constipation and dyspepsia. Patients with more severe constipation did not have higher dyspepsia severity scores. Colonic transit time, gastric half emptying and gallbladder contraction were not significantly correlated. Although patients with severe nausea had faster colonic transit than those with absent/mild symptom (19 +/- 2 vs. 48 +/- 7 h; p < 0.05), the multivariate analysis only revealed a significant association between severe postprandial fullness, delayed t1/2 (OR 1.05, CI 1-1.1) and impaired gallbladder contraction (OR 0.94, CI 0.89-0.99). CONCLUSIONS: Constipation was not associated with severity, or any particular dyspeptic symptom. Although motor abnormalities of both colon and proximal GI tract regions existed in the subset of constipated dyspeptic patients, they did not seem associated with the genesis of different dyspeptic symptoms.

Gastroduodenal lesions and Helicobacter pylori infection in dyspeptic patients with and without chronic renal failure.

BACKGROUND: Patients with chronic renal failure (CRF) often have dyspeptic symptoms and may develop peptic disease or digestive disorders leading to severe gastrointestinal complications. The primary aim of this study was to evaluate the prevalence of peptic lesions and Helicobacter pylori infection, and the severity of dyspeptic symptoms, in dyspeptic patients with and without CRF. Our secondary aim was to investigate whether uremic status may affect the diagnostic efficiency of the [13]C-urea breath test ([13]C-UBT). PATIENTS AND METHODS: We consecutively enrolled in the study 50 dyspeptic patients with chronic kidney failure (mean age 52 +/- 5 years), of whom 11 were on hemodialysis treatment (HD), and 93 subjects (mean age 54 +/- 7 years) with chronic dyspepsia and normal renal function (NRF). All patients completed an oriented and validated questionnaire scoring the severity of nine dyspeptic symptoms (i.e. epigastric pain, epigastric burning, postprandial fullness, early satiety, bloating, belching, nausea and vomiting) and underwent upper endoscopy with multiple bioptic sampling for rapid urease test and histological examination, [13]C-UBT and HpSA test. RESULTS: The prevalences of peptic lesions and H. pylori infection and mean symptom score were 74%, 52% and 3.5 +/- 3, respectively, in dyspeptic patients with CRF and 18%, 36% and 8 +/- 5, respectively, in dyspeptic patients with NRF. The diagnostic accuracy of [13]C-UBT with respect to histological diagnosis was 94% and 97% for dyspeptic patients with and without renal failure, respectively. CONCLUSIONS: 1, A high frequency of peptic lesions and low symptom scores were observed in uremic patients in spite of H. pylori infection; 2, uremic status did not affect the diagnostic accuracy of [13]C-UBT.

High prevalence of non-HFE gene-associated haemochromatosis in patients from southern Italy.

Hereditary haemochromatosis is an autosomal recessive disorder of iron regulation that results in abnormal intestinal iron absorption with progressive iron overloading of parenchymal cells. Two specific, single point mutations of the HFE gene (C282Y and H63D) have been described in haemochromatosis patients. Epidemiological studies have revealed a strict association between hereditary haemochromatosis and C282Y homozygosis or C282Y/H63D compound heterozygosis, suggesting that these mutations may provide a useful tool for diagnosis. However, recent investigations from southern Europe have reported lower allelic frequencies of the C282Y mutation among haemochromatosis patients, apparently depending on the geographical area of the population analysed. To assess the predictive value of the detection of the C282Y and H63D HFE mutations in our geographical area, we have evaluated their occurrence in 46 haemochromatosis patients from southern Italy. We found that only 19.6% of our patients were homozygous for the C282Y mutation and 21.7% were compound C282Y/H63D heterozygotes. Among the remaining 59%, approximately 40% did not display any of the known HFE mutations. We conclude that, in southern Italy, another genetic determinant/s must be responsible for many haemochromatosis cases and that a genetic screening for the C282Y and H63D HFE mutations is not sufficient for hereditary haemochromatosis diagnosis.

Effect of chronic administration of tacrolimus and cyclosporine on human gastrointestinal permeability.

The antirejection drug tacrolimus (FK506) has been reported to impair intestinal permeability in an early stage after orthotopic liver transplantation (OLT), and cyclosporine (CsA) has shown a similar effect in animals. We studied the chronic effect of FK506 and CsA on gastroduodenal and intestinal permeability and on blood endotoxin levels in patients 2 to 3 years after OLT. Thirty-two OLT patients (22 men and 10 women; mean age, 44.8 +/- 7.1) who had received CsA (n = 19) or FK506 (n = 13) and 10 healthy volunteers (6 male and 4 female, mean age 41.7 +/- 5.4) were assessed for gastroduodenal permeability by recovery in urine of sucrose after oral administration and for intestinal permeability by recovery in urine after oral loads of rhamnose and lactulose, which evaluate the intracellular and paracellular routes, respectively. In all subjects, plasma levels of endotoxins also were assessed. Gastroduodenal permeability was similar in patients and controls (0.03 +/- 0.003 versus 0.04 +/- 0.01%, P = NS). In regard to intestinal permeability, passage through the intracellular route was significantly reduced in OLT patients compared with controls (1.13 +/- 0.06 versus 2.74 +/- 0.17%, P <.01), but paracellular permeability was unchanged (0.14 +/- 0.007 versus 0.13 +/- 0.01%, P = NS). Serum endotoxin levels were similar in all subjects. We conclude that chronic administration of FK506 or CsA induces a clinically irrelevant, selective dysfunction of monosaccharide absorption, but does not affect gastroduodenal or intestinal permeability.

Effects of carbonated water on functional dyspepsia and constipation.

OBJECTIVE: The effects of carbonated beverages on the gastrointestinal tract have been poorly investigated. Therefore, this study aims to assess the effect of carbonated water intake in patients with functional dyspepsia and constipation. METHODS: Twenty-one patients with dyspepsia and secondary constipation were randomized into two groups in a double-blind fashion. One group (10 subjects) drank carbonated water and the other (11 subjects) tap water for almost 15 days. Patients were evaluated for dyspepsia and constipation scores, and underwent a satiety test by a liquid meal, radionuclide gastric emptying, sonographic gallbladder emptying and colonic transit time, using radio-opaque markers. RESULTS: The dyspepsia score was significantly reduced with carbonated water (before = 7.9 +/- 2.8 after = 5.4 +/- 1.7; 0.05) and remained unmodified after tap water (9.7 +/- 5.3 9.9 +/- 4.0). The constipation score also decreased significantly ( 0.05) after carbonated water (16.0 +/- 3.9 12.1 +/- 4.4; 0.05) and was not significantly different with tap water (14.7 +/- 5.1 13.7 +/- 4.7). Satiety was significantly reduced with carbonated water (before = 447 +/- 146 kcal after = 590 +/- 245; 0.01). Gallbladder emptying (delta percent contraction) was significantly improved only with carbonated water (39.9 +/- 16.1% 53.6 +/- 16.7%; 0.01). CONCLUSION: In patients complaining of functional dyspepsia and constipation, carbonated water decreases satiety and improves dyspepsia, constipation and gallbladder emptying.

Diagnosis of chronic atrophic gastritis by morphometric image analysis. A new method to overcome the confounding effect of the inflammatory infiltrate.

The risk of gastric cancer increases with the severity of gastric mucosal atrophy. Atrophy is a 'loss of properly specialized glands'. These glands may be substituted by metaplastic cells and by interstitial fibrosis, or displaced by an inflammatory infiltrate. Agreement among pathologists for the diagnosis of atrophy is poor (kappacoefficient < 0.4), probably because inflammatory infiltrate can confound the identification of gland loss. The aim of this study was to evaluate interstitial fibrosis by image analysis, and thereby overcoming the confounding effect of the inflammatory infiltrate. Gastric biopsies of 40 controls (20 children and 20 adults) and 111 patients with chronic atrophic gastritis were examined. Patients underwent another biopsy a year later. Gastric sections were examined by conventional histology (updated Sydney system) and image analysis to detect collagen and non-collagen fibres. There were no significant intra- or inter-operator differences in the evaluation by image analysis of fibre content in either controls or patients. In both controls and patients, the mean percentage of collagen fibres was lower in the gastric body (9%) than in the antrum (10%). In the antrum it was 14%, 17% and 20% in patients with mild, moderate and severe atrophy, respectively. A year later, histology showed that the grade of atrophy had decreased in 42%, probably due to the regression of inflammation, and increased in 10% of cases, but interstitial fibrosis (expressed as collagen fibre content) was practically unchanged. The use of image analysis of gastric biopsies appears to be a reliable method with which to measure interstitial fibrosis, even in the presence of an inflammatory infiltrate. This study highlights the difference between 'real gastric atrophy', where glands are replaced by collagen fibres, and 'apparent gastric atrophy', where glands are displaced by an inflammatory infiltrate.