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Sildenafil shows an intense and prolonged inhibitory effect on the smooth muscle cells of corpus cavernosum arterioles by blocking phosphodiesterase type 5 that inactivates the nitric oxide-stimulated cyclic guanosine monophosphate. We investigated if this inhibitory effect is also displayed on smooth muscle cells of the esophagus. In 16 normal subjects (9 men and 7 women, mean age 34 years, range 22-56) esophageal motility was recorded by means of a low-compliance manometric system with side holes for the esophageal body and a sleeve for the lower esophageal sphincter (LES). After a basal period of 60 min, a tablet of sildenafil 50-mg ground and dissolved in water was infused in the stomach in eight subjects (group A) and a placebo tablet in the other eight subjects (group B), randomly and in a double-blind manner; the recording continued for another 60 min. LES tone and postdeglutitive residual pressure, as well as amplitude, propagation velocity, and onset latency of contractions were measured each minute, the values averaged every 5 min, and the mean of the entire basal and postinfusion periods was calculated. The postinfusion values were compared with the basal values in each group and with the corresponding values of the other groups. The percent variations of postinfusion values with respect to basal values were also compared. Sildenafil induced a statistically significant decrease of LES tone, residual pressure, wave amplitude, and propagation velocity and a significant increase of onset latency of pressure waves in comparison with the values of the basal period and placebo. The inhibitory effect reached its maximum 10-15 min after the infusion and lasted about 1 hr. In conclusion, sildenafil markedly inhibits the motor activity of the esophageal musculature by decreasing LES pressure, wave amplitude, and propagation velocity and increasing the onset latency of pressure waves.

This study was carried out to compare the measurements and the diagnostic accuracy of the traditional expensive IRMS and the new economical LARA system using two doses of [13C]urea + two different test meals in patients undergoing upper gastrointestinal endoscopy, both before and after anti-Helicobacter treatment. A total of 354 dyspeptic patients underwent endoscopy with gastric biopsies to diagnose H. pylori infection by CLO-test and histology. No patients had taken antibiotics, bismuth, or antisecretory drugs in the 4 weeks before testing. After overnight fasting, breath samples were collected simultaneously in both plastic and glass tubes at baseline and at 30 and 60 min after urea ingestion. In 237 patients 100 mg [13C]urea + Ensure and in 117 patients 75 mg [13C]urea + citric acid were given. The test was also performed with the two urea dosages and meals in 67 and 64 infected patients, respectively, four weeks after anti-Helicobacter therapy. H. pylori was considered eradicated when both biopsy-based tests were negative. A delta value >5 per thousand was considered positive. Breath samples with insufficient CO2 levels at both 30 and 60 min were excluded from final analysis (N = 37 in pre- and N = 8 in posttreatment). There was excellent agreement between overall delta values of the two machines with both [13C]urea 100 mg + Ensure and [13C]urea 75 mg + citric acid. The 95% CI of the difference against the mean was wider with the former (mean -1.3, +6.3, and -9.4) than with the latter urea dosage and test meal (mean -1.2, +5.2 and -8.1). LARA and IRMS were equally effective (P = NS) in distinguishing infected from uninfected patients before therapy using both doses of [13C]urea and test meals (sensitivity ranged from 95% to 99% and specificity from 95% to 97%). This good performance was maintained in the posttreatment phase (sensitivity ranged from 90% to 100% and specificity from 90% to 97%), without any statistical difference among the various combinations (P = NS). The LARA system is a valid alternative to IRMS in the diagnosis of H. pylori infection. Both machines provide highly reliable results after 30 min, so that the 60 min sample can be avoided. The dose of 75 mg + citric acid suffices to ensure an accurate UBT. The test performed with both devices and [13C]urea dosages is very effective also for posttherapy evaluation of H. pylori status.

Several techniques have been developed to diagnose Helicobacter pylori infection and two noninvasive methods are available: carbon 13-urea breath test (UBT) and serology. Measurement of IgG serum antibodies by enzyme-linked immunosorbent assay (ELISA) is a reliable and inexpensive method for detection of infection. The aim of this study was to assess the seroconversion by different techniques after five to eight years. In 1990, 588 of 1,010 asymptomatic donors were found to be seronegative by ELISA, based on an H. pylori whole-cell suspension lysate (sensitivity and specificity: 92% and 97%). In 1995 serum samples from 418 of 588 seronegative donors were collected and retested using the same antigen. 411 of 418 samples were frankly negative, and 7 donors were found to be seroconverted. This group of seven sera represents the object of the study. They were retested by ELISA and western blotting using a different antigen (NCTC). To standardize our techniques, sera from 43 H. pylori positive and 47 H. pylori negative patients according to culture, histology, urease test, and UBT were used. The cutoff for ELISA-NCTC was 0.53 AI (absorbance index) (mean value + 2 SD), and for western blotting was negativity for CagA or <10 bands (sensitivity and specificity: 95% and 96%; 98% and 81% for ELISA and western blotting respectively). According to the results obtained in 1990 and 1995, seven donors were found to be seroconverted by ELISA using sonicated antigen; in five the seroconversion was confirmed by ELISA using NCTC antigen and in two there was concordance with WB. Four of the seven donors were contacted and asked to undergo UBT and a further serum sample was drawn to be reassessed in 1998. A seroconversion was found in all four donors by ELISA, while WB and UBT confirmed the seroconversion in only three of four donors. In conclusion the in-house ELISA used performed well compared to other theoretically better serologic assays and confirmed the low seroconversion rate for H. pylori infection in adult populations living in developed countries.

Glanzmann's thrombasthenia (GT) is a rare familial thrombocytic disease inherited as an autosomal recessive disorder that can induce hemorrhages due to a defect of platelet aggregation, resulting from the absence or reduced concentration of the membrane glycoproteic receptor binding the fibrinogen (integrin alpha(IIb)beta3). The gastrointestinal tract is the site of bleeding in only about 10% of cases but the related mortality is high (12.8%). Among the deaths due to hemorrhage, digestive bleeding causes 57.1%. According to reported data, the source of bleeding may be from preexisting gastroduodenal chronic and acute lesions. We report a case of severe and relapsing upper digestive bleeding in a woman with GT and coexisting thrombocytopenia (from HCV-related liver cirrhosis) and H. pylori-positive duodenal ulcer.

Gastroduodenal motility of 16 patients complaining of functional dyspepsia and Helicobacter pylori gastritis was recorded by means of a low-compliance manometric system with four recording ports in the stomach and four in the duodenum. Clarithromycin (CLA) 250 mg (group A: 8 patients) or normal saline solution (group B: 8 patients) was infused intravenously randomly and in double-blind manner 30 min after the end of the first recorded activity front (AF) of the migrating motor complex or, in the absence of AFs, after 200 min of recording, continuing the recording until an AF was observed during the subsequent 200 min. CLA administration was followed by a typical gastroduodenal AF in a significantly higher number of patients than saline administration. In addition, the time-lag between the drug administration and the appearance of AFs was 22 min +/-7.4 (mean +/- SD), significantly shorter than after saline (109+/-56 min) and the CLA-related duodenal AFs showed a duration of 7.4 min +/-1.6 in group A, significantly longer than that of the spontaneous AFs (3.5 min +/-1), while in group B AF duration after saline was not significantly different from that of the spontaneous ones. In conclusion, clarithromycin is able to stimulate cyclic interdigestive gastroduodenal motility. This prokinetic property of clarithromycin is not unexpected because it is a macrolide like erythromycin, the prokinetic activity of which is well known, and could be utilized for therapeutic uses.

Emerging evidence suggests that infection by CagA-positive Helicobacter pylori strains is related to the development of more serious gastroduodenal diseases, thus conferring to the determination of anti-CagA antibodies a relevant clinical significance in serological screenings. The detection of anti-CagA positivity in sera negative for anti-H. pylori antibodies raises the question of whether this apparently nonsense result is merely due to a false positive reaction. To address this issue, we compared three different methods for the detection of anti-CagA antibodies. In all, 272 selected sera from patients with precisely defined H. pylori status (positive or negative concordance of five tests, ie, histology by Giemsa in both antrum and corpus, rapid urease test, culture, [13C]urea breath test, IgG ELISA) were tested for anti-CagA reactivity by three different techniques (western immunoblotting, ELISA, and recombinant immunoblotting assay). In order to assess the sensibility and specificity of each tests, we considered as "true" anti-CagA positive sera those with two out of three positive results. Sera from 70% of H. pylori-positive patients and 10% from H. pylori-negative patients turned out to be "true" positives for anti-CagA antibodies. The three methods showed similar excellent results, in terms of both sensitivity and specificity, always over 93%. It is confirmed that a proportion of patients with a negative conventional serology against H. pylori possess anti-CagA antibodies in their sera. In this paper we demonstrate that it can happen even in patients without any biological signs of actual H. pylori infection. The possibility that this can be due to a false positive laboratory result is very likely ruled out by the accuracy of the three methods used. The clinical management of these patients needs further study on larger series.

To determine the clinical significance of Helicobacter pylori seropositivity and seronegativity in healthy blood donors, we carried out a serological evaluation of Helicobacter pylori status and endoscopy in a healthy blood donors population. In all, 1010 donors were screened for Helicobacter pylori by IgG ELISA and assessed for pepsinogen I and gastrin levels by RIA; 298 IgG seropositive and 61 seronegative subjects underwent endoscopy with biopsies. Of 359, 165 were also tested for CagA by western blotting. Of the 298 IgG seropositives, 274 were shown to be infected on biopsy testing. Endoscopy revealed 70 peptic ulcers, 41 cases of erosive duodenitis, and two gastric cancers. In all 105 seropositive donors were tested for CagA and 69 were CagA positive [34/58 gastritis (58.6%), 24/35 duodenal ulcer (68.6%) and 11/12 gastric ulcer (91.6%)]. Histologically active/chronic gastritis was associated with CagA: 88.4% vs 50% (CagA seropositive vs seronegative). Of the 61 IgG seronegatives, 59 were negative on biopsy testing. At endoscopy three had duodenitis. Of the 60/61 IgG seronegatives tested for CagA, one had a moderate reaction. Duodenal ulcer donors showed higher pepsinogen I levels than donors without duodenal ulcers (97.7 microg/ml vs 80.9 microg/ml respectively). Screening for Helicobacter pylori and anti-CagA seropositivity and pepsinogen I can identify individuals likely to have gastroduodenal pathology even in the absence of symptoms.

Nitric oxide is thought to play an important role in modulating the inflammatory process. Recently an increase in the inducible form of nitric oxide synthase (iNOS) has been found in the rat trinitrobenzene sulfonic acid model of experimental colitis, and inhibition of nitric oxide synthase activity resulted in an amelioration of tissue injury. The aim of our study was to evaluate in vivo intracolonic release of nitric oxide in this model of colitis. Experimental colitis was induced in male Sprague-Dawley rats by a single intracolonic administration of trinitrobenzene sulfonic acid. Nitrite levels were determined in rectal dialysates by HPLC. The tissue myeloperoxidase and iNOS and the luminal leukotriene B4 were also measured. Nitrite levels were significantly increased in rectal dialysates during colitis and correlated significantly with tissue myeloperoxidase and iNOS activity. The correlation between nitrite dialysate levels and wall iNOS activity confirms that nitrite in dialysates is produced by inflammatory cells and not by colonic bacterial flora. Determination of nitrite levels in rectal dialysates seems a valuable method to monitor colonic inflammation in rat trinitrobenzene sulfonic acid colitis.

In 153 consecutive patients with cirrhosis we assessed: (1) the prevalence of IgG to Helicobacter pylori and compared it with that found in 1010 blood donors resident in the same area; and (2) the relationships of IgG to Helicobacter pylori with clinical and endoscopic features and with the risk of peptic ulcer. The IgG to Helicobacter pylori prevalence of cirrhotics was significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was not associated with sex, cirrhosis etiology, Child class, gammaglobulins and hypertensive gastropathy. In both groups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Among patients with cirrhosis a significantly higher prevalence of Helicobacter pylori was found in patients with previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) and patients with peptic ulcer (P = 0.0004). Multivariate analysis identified increasing age and male sex as risk factors for a positive Helicobacter pylori serology and no independent risk factors for peptic ulcer. The high prevalence of Helicobacter pylori-positive serology found in the present series is related to age and sex and might also be explained by previous hospital admissions and/or upper gastrointestinal endoscopy. Our results do not confirm the role of Helicobacter pylori as risk factor for peptic ulcer in patients with liver cirrhosis.

The aim of this study was to compare the sensitivity, specificity, and diagnostic accuracy of serum interleukin-6, interleukin-8, beta 2-microglobulin, and C-reactive protein in the assessment of the severity of acute pancreatitis using commercial kits for their respective assays. Thirty-eight patients with acute pancreatitis (25 men, 13 women, mean age 59 years, range 16-97) were studied; the diagnosis was based on prolonged upper abdominal pain associated with a twofold increase of serum lipase, and it was confirmed by imaging techniques. According to the Atlanta criteria, 15 patients had severe illness and 23 had mild disease. The four serum markers were determined in all patients on admission, as well as daily for the following five days. On the first day of the disease, the sensitivity (calculated on patients with severe pancreatitis), specificity (calculated on patients with mild pancreatitis), and the diagnostic accuracy of these serum markers for establishing the severity of acute pancreatitis were 100%, 86%, and 91% for interleukin-6 (cutoff level 2.7 pg/ml); 100%, 81% and 88% for interleukin-8 (cutoff level 30 pg/ml); 58%, 81%, and 73% for beta 2-microglobulin (cutoff level 2.1 mg/liter); and 8%, 95%, and 64% for C-reactive protein (cutoff level 11 mg/dl). The results of our study indicate that, when assayed during the first 24 hr of disease onset, interleukin-6 and interleukin-8 are better markers than beta 2-microglobulin or C-reactive protein for evaluating the severity of acute pancreatitis.

We have carried out a large prospective study of the frequency of H. pylori infection and HIV-1 status in a community of ex-drug abusers including subjects with (N = 210) and without (N = 259) upper gastrointestinal symptoms, endoscopy and serology. Control groups were patients with upper gastrointestinal symptoms not at high risk of HIV-1 infection (N = 219) and asymptomatic blood donors (n = 322). H. pylori was present in 52% of symptomatic community residents having endoscopy and 55% of the control patients with symptoms but not at high risk of HIV-1 infection. H. pylori was less common in HIV-1-positive patients (40%) than those who were negative (66%; P < 0.001). In patients with AIDS (33%), the frequency of H. pylori infection was reduced compared to HIV-1-positive patients without AIDS (53%; P = 0.05). All the residents with AIDS had upper gastrointestinal symptoms. In community residents, peptic ulcer was always associated with H. pylori infection. By H. pylori serology, there was no difference in the frequency of infection in asymptomatic residents (56%) whether HIV-1 positive (55%) or HIV-1 negative (58%) compared with those residents with symptoms. Overall, H. pylori was less common in HIV-1-positive residents (49%) than those who were HIV-1 negative (61%; p < 0.05). This difference was due mainly to the low frequency of infection in residents with AIDS (33%). H. pylori infection is common in HIV-1 positive patients, and only slightly reduced when compared with at-risk HIV-1-negative subjects. Peptic ulcer is associated with H. pylori in HIV-1 infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Fish oil has been recently proposed as a possible effective treatment in inflammatory bowel disease (IBD); however, a lot of annoying side effects (ie, belching, halitosis, diarrhea, etc) affect patient compliance. We carried out a study of patient tolerance in a group of Crohn's disease (CD) patients with a new fish oil derivative consisting of 500-mg capsules of eicosapentaenoic-docosahexaenoic (EPA 40%-DHA 20%), a free fatty acid mixture (Purepa), and we also evaluated its incorporation into phospholipids, both in plasma and in red cell membranes. Five groups of 10 CD patients in remission received nine Purepa capsules daily in four different preparations (A: uncoated, B: coated, pH 5.5; C: coated, pH 5.5, 60 min time release; D: coated, pH 6.9) and 12 x 1-g capsules daily of a triglyceride preparation (Max-EPA, EPA 18%-DHA 10%), respectively. We coated three of the four Purepa preparations in order to delay the release of contents in an attempt to minimize the side effects. After six weeks of treatment, the group taking Purepa capsules, coated, pH 5.5, 60 min time release (group C) showed the best incorporation of EPA and DHA in red blood cell phospholipid membranes (EPA from 0.2 to 4.4%, DHA from 3.7 to 6.3%), and no side effects were registered, whereas in all other groups side effects were experienced in 50% or more of subjects. This new preparation will make it possible to treat patients for long periods.

Concentrations of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha) were determined by solid-phase ELISA in tissue homogenates of mucosal biopsy specimens obtained from pelvic ileal pouches in 13 patients with pouchitis (reservoir ileitis) and 17 with pouches without pouchitis. Normal ileal mucosa was used as a control. IL-1 beta was detected in all tissue homogenates from patients with pouchitis compared with only 29% from pouches without pouchitis and none from controls. IL-6 and IL-8 were present in all pouchitis specimens, in 70% of the specimens from nonpouchitis and only 30% of specimens from controls. TNF-alpha was undetectable in all specimens examined. The concentrations of IL-1 beta, IL-6, and IL-8 were significantly greater (P < 0.001) in biopsy specimens from pouchitis compared to those from pouches without pouchitis or normal ileal mucosa and in patients with pouchitis tissue levels of IL-1 beta significantly correlated with IL-6 (P < 0.05) and IL-8 (P < 0.01). Furthermore IL-1 and IL-8 levels were significantly higher in tissue specimens from nonpouchitis pouches than in those from normal ileal mucosa (P < 0.02). These results suggest that an enhanced cellular immunity operates in vivo at the mucosal level in pouchitis as in the case of ulcerative colitis.

The activation of circulating polymorphonuclear leukocytes was determined in terms of superoxide radical generation and granulocyte elastase release in untreated patients with ulcerative colitis (N = 10) and Crohn's disease (N = 9) in remission and in control subjects (N = 10). Superoxide radical generation was determined by monitoring spectrophotometrically the reduction of ferricytochrome, after stimulation of cells with phorbol myristate acetate. Plasma elastase concentration was measured by a solid-phase enzyme immunoassay technique as the complex with alpha-1-proteinase inhibitor. Superoxide formation by polymorphonuclear leukocytes from patients with ulcerative colitis and Crohn's disease was significantly lower compared with controls [median (range) nmol/min/mg protein: Crohn's disease 7.8 (7.1-9.6); ulcerative colitis 8.25 (7.4-10.3); controls 14.7 (13.6-15.8)] (P < 0.001), while no difference was found between the two groups of patients. In contrast plasma elastase levels in patients with ulcerative colitis and Crohn's disease were similar to that of controls. This defective respiratory burst of polymorphonuclear leukocytes in patients with inflammatory bowel disease in remission, in absence of an altered degranulation, could represent an important factor for the pathogenesis of these diseases.

We studied the behavior of serum amylase and lipase in 66 consecutive patients with acute pancreatitis in order to assess the ability of these tests and of the serum lipase-amylase ratio to establish the etiology and predict the severity of acute pancreatitis. Forty-two patients had biliary acute pancreatitis, 14 had alcoholic acute pancreatitis, and the remaining 10 nonbiliary, nonalcoholic (NBNA) acute pancreatitis. Serum amylase and lipase were abnormally high in all patients. The elevations of both serum amylase and lipase were significantly lower in patients with alcoholic pancreatitis than in those with biliary pancreatitis, although a considerable overlap was observed between the two groups. No statistically significant differences were found between NBNA patients and those with either biliary or alcoholic forms of the disease. The serum lipase-amylase ratios in patients with alcoholic pancreatitis ranged from 0.2 to 5.6, in those with biliary pancreatitis from 0.1 to 7.9, and in those with NBNA pancreatitis from 0.1 to 4.4. These differences were not statistically significant. No differences in serum enzyme levels were observed among patients without apparent imaging signs of acute pancreatitis (N = 20), those with signs of pancreatic edema (N = 36), and those with necrotizing pancreatitis (N = 10). The results indicate that serum amylase and lipase concentrations are not able to establish either the etiology or to predict the severity of acute pancreatitis as assessed by imaging techniques. Furthermore, the serum lipase-amylase ratio is not useful in distinguishing acute episodes of alcoholic from nonalcoholic acute pancreatitis.

Rectal treatment with enemas, foams, and suppositories is the most efficient method of delivering an adequate quantity of locally active drugs to the distal colon. In a pilot study carried out by colonoscopy in four patients, it was observed that 4 g 5-ASA in 20 ml foam spread up or beyond the splenic flexure and more extensively than 2 g 5-ASA in 10 ml foam. Therefore we have undertaken a study in order to compare by scintigraphy the colonic distribution of 4 g 5-ASA foam versus 4 g 5-ASA in 100 ml liquid enemas in 10 patients with ulcerative colitis using a crossover randomized design. Both preparations were labeled with 100 MBq [99mTc]sulfur colloid before administration. Anterior scans were taken at intervals for 4 hr. Activity, expressed as a percentage of total radioactivity, was measured in the rectum, sigmoid, descending, transverse, and ascending colon. Six patients had the same extent of spread with the two formulations; in three patients with foam and in one patient with enema a greater spread was observed. The foam reached the upper limit of disease in all cases, while enema failed in two cases. The maximum spread with foam was observed within 30 min in nine of 10 patients compared with seven of 10 after enema. Compared to enema, foam distributes more uniformly and seems to persist longer in the descending and sigmoid colon. The 5-ASA colonic foam shows some more favorable characteristics than enema for the local treatment of left-sided ulcerative colitis.

Treatment of Crohn's disease (CD) in clinical remission is still a debated issue. Previous studies have shown a high risk of relapse for patients with CD in clinical remission (CDAI less than 150) but with some abnormally high laboratory parameters as well as a possible beneficial role of low-dosage steroid treatment in this group of patients. Furthermore, good results have been reported on the efficacy of 5-aminosalicylic acid (5-ASA) in moderately active CD. In our study we verified the efficacy of a slow-release oral 5-ASA preparation in preventing relapses in a group of patients in clinical remission but with raised laboratory parameters. Forty-four patients were randomized in a double-blind manner to receive either 5-ASA (2 g/day) or placebo for four months. Location of disease and previous steroid treatment were similar in both groups. One patient in the 5-ASA group discontinued the drug because of uterine bleeding. During the study period, 13 of 22 placebo-treated patients and 11 of 21 5-ASA-treated patients relapsed (corrected chi square = NS). Considering the location of disease, three of 10 patients in the 5-ASA group and six of nine patients in the placebo group with ileal CD relapsed (therapeutic gain with 5-ASA: 36.6%; 95% allowance for error from -6% to 79.2%). Moreover, in seven patients with ileal CD who remained in remission, we found a statistically significant decrease in alpha 1 acid glycoprotein and C-reactive protein from the second month of the study.(ABSTRACT TRUNCATED AT 250 WORDS)

The in vitro antioxidant capacity of sulfasalazine (SASP), its metabolites (SP, 5-ASA), and olsalazine (OAZ), was studied by evaluating their effects on superoxide (O2-.) production. Assay systems were the xanthine-xanthine oxidase (X/XOD) reaction and phorbol myristate acetate (PMA)-activated polymorphonuclear leukocytes (PMNs), using the cytochrome c (cyt-c) reduction assay and a luminol-dependent chemiluminescence method. 5-ASA, SASP, and OAZ showed a dose-dependent scavenger effect in both O2-. generating systems, 5-ASA being the most powerful (greater than 50% of inhibition in the PMNs system and greater than 70% in the X/XOD system at 10 microM concentration). SP had an inhibitory effect only in the PMNs system but did not modify the activity of xanthine oxidase, thus excluding a scavenger action. These data suggest that the scavenger effect of 5-ASA, SASP, and OAZ may be an important mechanism of action.

The relationship between intestinal permeability to an oral dose (100 mu Ci) of [51CR]EDTA and the inflammatory activity of Crohn's disease was studied in 63 adult patients (32 unresected and 31 resected) who underwent 162 evaluations. The results of the [51CR]EDTA test were compared with the serum levels of the acute-phase reactant proteins (APRP) and with the result of the [111In]leukocyte scanning, respectively, as an indirect and direct method to assess intestinal inflammation. In a group of healthy adult controls, the upper normal value for the 24-hr urinary [51CR]EDTA excretion was 3.61 (97.5% percentile) and the mean coefficient of variation was 21%. Sensitivity and specificity of the [51CR]EDTA test in identifying active inflammation expressed by increased serum levels of APRP were, respectively, 97% and 54% in the unresected group and 68% and 52% in the resected group of patients. The low specificity of the test was due to the presence of increased [51CR]EDTA urinary excretion in about half the cases with normal serum levels of APRP. The [111In]leukocyte scanning was performed in a subgroup of 11 patients (three unresected and eight resected) with normal serum levels of APRP, six with increased and five with normal [51CR]EDTA urinary excretion. All six patients with increased intestinal permeability had a positive 111In image of mild to moderate degree of activity. A positive 111In scan was present in two of the five patients with normal permeability; these were two resected patients.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to examine the effect of adrenergic influences on gastric inhibitory polypeptide (GIP) secretion, a series of glucose tolerance tests was carried out in seven healthy volunteers during intravenous infusion of epinephrine (6 microgram/min), epinephrine plus phentolamine (5 mg stat + 0.5 mg/min), epinephrine plus propranolol (5 mg stat + 0.08 mg/min), and saline. No drug infusion modified fasting GIP levels. Alpha-adrenergic stimulation (epinephrine + propranolol) significantly reduced the GIP response (P less than 0.02) and completely inhibited the insulin response (P less than 0.005) to oral glucose, compared with control experiments. Epinephrine alone and epinephrine + phentolamine did not influence glucose-stimulated GIP. These results suggest the possibility that the adrenergic nervous system may have a role in the regulation of GIP secretion in man.

A controlled trial has been carried out in order to compare the efficacy of enemas containing a high dosage of 5-ASA (4 g) versus enemas containing hydrocortisone 100 mg. The trial was conducted on 86 patients, 44 of whom received 5-ASA and 42 received hydrocortisone. The results were favorable in terms of clinical, sigmoidoscopic, and histologic criteria for 5-ASA treatment. Other aspects have been investigated, such as retrograde spread of enemas which have been shown to reach the left colon. No nephrotoxicity was detected. The long term experience confirmed the preliminary positive results.

We have investigated the gastric secretory activity and the emptying half-time of a liquid meal in 17 selected patients with reflex esophagitis compared to 10 controls. The basal acid output and the basal and maximal secretory volume were higher in the patient group (P less than 0.05, P = 0.05, and P less than 0.01, respectively), while the maximal acid output and the basal and maximal acid concentration were not different in the two groups. The gastric emptying half-time of a liquid meal was higher in the patient group (P less than 0.001). Our results show that gastric function may be altered in reflux esophagitis patients and suggest particularly that a delayed emptying of liquids may play a role in the pathogenesis of the disease in some patients.

In order to study the reliability of urinary zinc levels as an index of zinc metabolism and status in Crohn's disease, we evaluated plasma and urinary zinc concentrations, urinary 3-methylhistidine excretion, and Crohn's disease activity index (CDAI) in 42 patients affected by Crohn's disease. Plasma zinc correlated directly with albuminemia (P = 0.01) and inversely with CDAI (P = 0.001). Urinary zinc excretion correlated with urinary 3-methylhistidine (P = 0.001) and plasma zinc levels (P = 0.01), and inversely with CDAI (P = 0.05). However, from multiple regression analysis, it was found that zincemia is influenced by CDAI and not by albumin, whereas zincuria is related to urinary 3-methylhistidine and plasma zinc, and not to CDAI. Our conclusion is that, in Crohn's disease, zincuria can be an index of zinc status when used together with measurements of lean body mass and turnover and factors influencing plasma ultrafiltrable zinc fraction.

This paper reports the results of a multicenter prospective study of 188 consecutive patients affected by gastric ulcer, verified by endoscopy, in whom the frequency of a mycotic infection of the lesion was evaluated as well as the eventual influence of such pathology on the efficiency of medical treatment, the healing rate, and the healing time. A mycotic infection, defined as penetration of the periulcerous mucosa by the fungi, was found in only 13 patients (6.9%). No significant differences were found in the healing rate and healing time among these patients treated with H2-receptor antagonists and a control group of 43 matched gastric ulcer patients treated in the same period with the same therapy. It would appear from the data that mycotic infections of the gastric ulcer do not modify the efficiency of medical treatment.