[Association of oncological markers in colon cancer].
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Biomedical subjects
Publications and source records attributed to G Latella.
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The aim of the present investigation was to study systemic metabolic consequences following rectosigmoid bladder (RSB) operation. RSB after cystectomy has recently been employed with increasing frequency in the Urologic Clinic of the University of Rome inasmuch as, compared with ureterosigmoidostomy (USS), it shows a lower incidence of complications. Acid base balance, serum electrolytes and renal function were studied in 22 patients submitted to RSB and in 25 submitted to USS. Urine from patients with RSB and urine-feces mixture from patients with USS was also analyzed. Metabolic acidosis occurred in 86 per cent of patients with RSB and in 80 per cent of patients with USS but was significantly less severe (p less than 0.01) in patients with RSB (pH 7.34 +/- SD 0.04) than in those with USS (pH 7.29 +/- 0.07). This finding corresponded to a significantly lower intestinal loss of HCO3- in the RSB than in the USS group. The frequency of hyperchloremia was very low in both groups of patients whereas the incidence of an increased anion gap was surprisingly high. Data obtained demonstrate that metabolic acidosis develops even after RSB surgery thus indicating that the reduction in the area of the colonic mucosa in contact with the urine is not in itself sufficient to prevent the metabolic changes. Nevertheless patients with RSB were usually asymptomatic, insofar as metabolic alterations were not severe in any of the cases. In conclusion, RSB ensures good functional results and may be considered a satisfactory solution in those patients in whom radical cystectomy is mandatory. Nonetheless, even in these patients, constant clinical surveillance and monitoring of the metabolic situation is necessary.
The normal colon absorbs water, sodium and chloride and secretes potassium and bicarbonate. In ulcerative colitis (UC), modifications occur in the absorption of water, sodium and chloride, whereas the secretion of potassium remains unchanged. There appear to be no data in the literature on bicarbonate secretion. Since some 25% of chloride absorption is coupled with bicarbonate secretion by an anion exchange mechanism, the impairment in chloride absorption should be accompanied by modifications in bicarbonate secretion. Faecal bicarbonate was therefore measured in 20 patients with active UC and 15 normal control subjects. Faecal pH, pCO2 and electrolytes (Na+, K+, Cl-, HCO3-), blood acid-base balance, urinary pH and bicarbonate were determined on the same day in all patients. Faecal pH and bicarbonate were significantly reduced in UC versus controls: pH 6.06 +/- 0.39 versus 6.52 +/- 0.43; HCO3- 8.4 +/- 5.2 versus 34.6 +/- 12.3 mEq/l (mean +/- SD), whereas sodium and chloride were increased. Faecal potassium concentration was normal, but potassium output was increased. Metabolic alkalosis was observed in 8 patients and a normal acid-base balance in the remaining 12. Urinary pH was acid and urinary bicarbonate negligible in all patients. No correlation was observed between plasma, faecal and urinary bicarbonate. Data emerging from this study show that the faecal excretion of bicarbonate is reduced in patients with active UC. A possible explanation for this finding may be impairment of the colonic anion exchange mechanism induced by inflammation of the mucosa. The role of organic anions is also hypothesized. The acid-base balance does not seem to be directly affected by the decrease in faecal bicarbonate loss.
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We evaluated the relationship existing between the site of intestinal lesions and systemic acid-base balance in 78 patients with active Crohn's disease. Patients with enteritis had a normal acid-base balance, while mild and moderate metabolic alkalosis were present in enterocolitis and colitis. These findings appeared to be related to the electrolyte fecal losses. In enteritis fecal sodium and chloride concentrations were within the normal range (Na 29.2 +/- 18.5; Cl 16.6 +/- 11.2 mEq/l) while in colitis they were significantly higher (Na 52.8 +/- 20.8; Cl 29.6 +/- 12.7 mEq/l). Intermediate values were observed in enterocolitis. The fecal potassium concentrations were similar in the three groups of patients, with a slightly lower concentration in enterocolitis and colitis. The fecal K/Na ratio was normal in enteritis and reversed in enterocolitis and colitis. This study suggests that a relationship exists between the site of lesions, fecal electrolyte losses, and systemic acid-base balance in Crohn's disease. Systemic metabolic alkalosis and an abnormal fecal K/Na ratio occurred in patients with colonic involvement, indicating the important role played by the colon in acid-base and electrolyte homeostasis.
We describe a simple method for the collection of stool water using dialysis membrane tubing placed directly into the feces. When the membrane was placed in pure aqueous solutions or in homogenized feces stored at 4 degrees C, equilibration for solutes was complete in 24 h. Exchangeable ions, short chain fatty acids, osmolality, and pH were measured in the fecal water of 8 normal subjects and 36 patients affected by different diarrheal diseases. The composition of fecal water collected by this method was almost identical to that obtained by ultrafiltration of feces immediately after collection. Differences, when present, were minimal (about 4%) and practically irrelevant. This in vitro dialysis method is simple, inexpensive, and seems particularly suitable for the measurement of osmolality, electrolytes, and short chain fatty acid concentrations in large numbers of fecal samples.
BACKGROUND: Whilst upper gastrointestinal disturbances are frequently observed in patients with diabetes mellitus, little is known about the prevalence of Helicobacter pylori infection and peptic disease in these patients. AIM: To evaluate prevalence of Helicobacter pylori infection and peptic disease lesions in diabetics with dyspeptic symptoms. PATIENTS AND METHODS: Study population comprises 74 consecutive diabetes mellitus patients with dyspepsia and 117 consecutive non diabetic dyspeptic patients. Upon enrolment, each patient completed an interview screening questionnaire to obtain information concerning presence and severity of dyspepsia. All patients underwent upper gastrointestinal endoscopy with biopsy specimens being collected from gastric antrum and body Helicobacter pylori was evaluated in each patient by rapid urease test and histology (Giemsa). Gastritis was classified according to the Sydney System. Statistical analysis was performed by chi-square, Fisher exact or t test and logistic regression analysis. A p value <0.05 was considered significant. RESULTS: Prevalence of Helicobacter pylori infection was found to be significantly higher in diabetics than in controls. The prevalence rate of endoscopic lesions was comparable in the two groups, but the association between endoscopic lesions and Helicobacter pylori infection was significantly higher in diabetics. Overall, the presence of chronic gastritis, both non atrophic and atrophic, as well as intestinal metaplasia were comparable in the two groups of patients, whilst the association between chronic gastritis and Helicobacter pylori infection or gastritis activity were significantly higher in diabetics. In neither group, was any correlation found between severity of dyspepsia and presence of endoscopic lesions, chronic gastritis or Helicobacter pylori infection. CONCLUSIONS: These data show a higher prevalence of Helicobacter pylori infection in diabetes mellitus patients with dyspepsia. Helicobacter pylori infection was significantly associated both with the presence of endoscopic lesions and chronic gastritis in diabetic patients, but not in the controls.
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