Minimally invasive direct coronary bypass surgery via distal mini-sternotomy : Promising clinical results with anaortic, multivessel, all-arterial technique.

BACKGROUND: Minimally invasive direct coronary artery bypass grafting (MIDCAB) was developed to decrease perioperative morbidity, some of which may be related to the use of cardiopulmonary bypass and to cross-clamping of the aorta. We report our initial experience with multivessel MIDCAB via distal mini-sternotomy (DIMS). DIMS is performed to gain access to the left and right internal thoracic arteries and to reach the left anterior descending coronary artery (LAD), diagonal branches, and right coronary artery (RCA). METHODS: Between January 2016 and January 2017, 12 patients with significant coronary artery disease of the LAD and the RCA underwent multivessel, all-arterial MIDCAB through a distal midline skin incision from the fourth intercostal space to the xyphoid process, with L­ or T­shaped division of the sternum. The mean age of the patients was 61.5 ± 5.2 years (range: 52-71 years). RESULTS: We performed all-arterial revascularization using the left internal mammary artery in 12 patients, the radial artery in ten, and the right internal mammary artery in two patients. The mean number of grafts per patient was 2.08 ± 0.4 (range: 2-3). The mean length of the skin incision was 8.5 ± 1.3 cm (range: 7-11 cm). There was no perioperative ischemia, postoperative bleeding, or arrhythmia events. No postoperative cognitive dysfunction occurred. The mean hospital stay was 5.6 days. No major adverse cardiac events (MACE) occurred at the 12-month follow-up. At follow-up, all patients were in New York Heart Association class I and there were no wound complications. CONCLUSION: Although MIDCAB-DIMS is technically more demanding than conventional procedures and our experience is limited, we conclude that this technique can be used safely in selected patients, with promising 12-month follow-up results.

Nonsteroidal anti-inflammatory drugs-induced failure of lower esophageal and pyloric sphincter and counteraction of sphincters failure with stable gatric pentadecapeptide BPC 157 in rats.

The sphincters failure is a part of NSAIDs-toxicity that can be accordingly counteracted. We used a safe stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419), LD1 not achieved, since successful in inflammatory bowel disease trials, and counteracts esophagitis, sphincters failure, gastrointestinal ulcer and skin ulcer, external and internal fistulas in rats, and particularly counteracts all NSAIDs-lesions. We assessed lower esophageal sphincter and pyloric sphincter pressure (cmH2O) in rats treated with various NSAIDs regimens, at corresponding time points, known to produce stomach, small intestine lesions, hepatotoxicity and encephalopathy. Assessment was after diclofenac (12.5 mg/kg, 40 mg/kg intraperitoneal challenge), ibuprofen (400 mg/day/kg intraperitoneally for 4 weeks), paracetamol (5.0 g/kg intraperitoneal challenge), aspirin (400 mg/kg intraperitoneally or intragastrically), celecoxib (0.5 mg/kg, 1.0 mg/kg intraperitoneally). BPC 157 (10 µg/kg, 10 ng/kg) was given immediately after NSAIDs (intraperitoneally or intragastrically) or given in drinking water. Regularly, in all control NSAIDs fall of pressure occurred in both sphincters rapidly and then persisted. By contrast, in all NSAIDs-rats that received BPC 157, initial fall of pressure was minimized and pressure values restored to normal values. All tested NSAIDs decrease pressure in both sphincters, whilst BPC 157 counteracts their effects and restored both sphincters function.

Randomised clinical trial: a comparative dose-finding study of three arms of dual release mesalazine for maintaining remission in ulcerative colitis.

BACKGROUND: Comparative data regarding different regimens of oral mesalazine (mesalamine) for maintaining remission in ulcerative colitis are limited. AIM: To evaluate whether 3.0 g mesalazine once-daily (OD) is superior to the standard treatment of 0.5 g mesalazine three times daily (t.d.s.) and to prove the therapeutic equivalence of OD vs. t.d.s. dosing of total 1.5 g mesalazine for remission maintenance in patients with ulcerative colitis. METHODS: A 1-year, multicentre, double-blind, double-dummy study was undertaken in patients with endoscopically and histologically confirmed ulcerative colitis in remission. Patients were randomised to oral mesalazine 3.0 g OD, 1.5 g OD or 0.5 g t.d.s. The primary efficacy endpoint was the proportion of patients still in clinical remission at the final visit, with clinical relapse being defined as CAI score >4 and an increase of ≥3 from baseline. RESULTS: The primary efficacy endpoint occurred in 162/217 3.0 g OD patients (75%), 129/212 1.5 g OD patients (61%) and 150/218 0.5 g t.d.s. patients (69%) in the intention-to-treat population, and in 152/177 (86%), 121/182 (67%) and 144/185 (78%) in the per protocol population respectively; 3.0 g OD was superior to both low-dose regimens for the primary endpoint (i.e. P < 0.001, 3.0 g OD vs. 1.5 g OD; P = 0.024, 3.0 g OD vs. 0.5 g t.d.s.; superiority test, per protocol population). Safety analysis, including comprehensive renal monitoring, revealed no concern in any treatment group. CONCLUSION: Mesalazine 3.0 g once daily was the most effective dose for maintenance of remission in ulcerative colitis of the three regimens assessed, with no penalty in terms of safety.

The status of antimicrobial resistance of Helicobacter pylori in eastern Europe.

OBJECTIVE: To evaluate the primary, secondary and combined resistance to five antimicrobial agents of 2340 Helicobacter pylori isolates from 19 centers in 10 countries in eastern Europe. METHODS: Data were available for centers in Bulgaria, Croatia, the Czech Republic, Estonia, Greece, Lithuania, Poland, Russia, Slovenia and Turkey. Susceptibility was tested by agar dilution (seven countries), E test (five countries) and disk diffusion (three countries) methods. Resistance breakpoints (mg/L) were: metronidazole 8, clarithromycin 1, amoxicillin 0.5, tetracycline 4, and ciprofloxacin 1 or 4 in most centers. Primary and post-treatment resistance was assessed in 2003 and 337 isolates respectively. Results for 282 children and 201 adults were compared. RESULTS: Primary resistance rates since 1998 were: metronidazole 37.9%, clarithromycin 9.5%, amoxicillin 0.9%, tetracycline 1.9%, ciprofloxacin 3.9%, and both metronidazole and clarithromycin 6.1%. Isolates from centers in Slovenia and Lithuania exhibited low resistance rates. Since 1998, amoxicillin resistance has been detected in the southeastern region. From 1996, metronidazole resistance increased significantly from 30.5% to 36.4%, while clarithromycin resistance increased slightly from 8.9% to 10.6%. In centers in Greece, Poland, and Bulgaria, the mean metronidazole resistance was slightly higher in adults than in children (39% versus 31.2%, P > 0.05); this trend was not found for clarithromycin or amoxicillin (P > 0.20). Post-treatment resistance rates exhibited wide variations. CONCLUSIONS: In eastern Europe, primary H. pylori resistance to metronidazole is considerable, and that to clarithromycin is similar to or slightly higher than that in western Europe. Resistance to amoxicillin, ciprofloxacin and tetracycline was detected in several centers. Primary and post-treatment resistance rates vary greatly between centers.

A model of the gastric gland ejection cycle: low ejection fractions require reduction of the glandular dead space.

This paper was inspired by the reported results of authors from Uppsala and Lund that gastric glands in rats rhythmically contract 3-7 cycles per minute and develop luminal pressures more than 10 mmHg. To ensure that pepsinogen is not retained in the acid-rich section of the gland, ejection fractions would need to be more than 50% of the gland volume. We have tried to calculate the ejection fraction of such contractions. Dimensions of human gastric glands were measured on the fresh frozen samples of macroscopically and histologically normal gastric mucosa. In total, 18 specimens (from nine persons) were measured under the microscope. The density of glands was 135 +/- 11 (mean +/- S.D.) glands per mm( 2) of gastric mucosa. A typical gastric gland is a tubular structure 1.2 +/- 0.22 mm long and 0.03-0.05 mm wide. We have used 1 mm for length and 0.03 mm for the gland diameter to calculate that each gland approximates a volume of 707 pl, suggesting that the total glandular volume for 15 million glands reaches 10.6 ml. Further calculations based on one to five contractions per minute on an average and on the total volume of gastric glands of 10 ml showed that only ejection fractions less than 10% deliver daily volumes less than 3 l. The presented model of the gastric gland activity is based on the idea that the low ejection fractions require a reduction of the glandular dead space. The reduced luminal pressure during the gland relaxation might cause backflux of hydrophobic viscoelastic mucus through the gland aperture. Repeated glandular contractions and relaxations would move the mucus all the way to the gland bottom, filling the gland cavity below the neck with an axial semisolid mucous cylinder. This filling would reduce the gland dead space. During contractions, the gland would eject mainly the peripheral, the more liquid part of its content. The decreasing luminal pressure in the relaxing gland would pull the outlet mucus inside, protecting gland apertures from the gastric juice.

Gastropathy and diarrhea in diabetic patients: the presence of helicobacteriosis and PAS-positive vascular deposits in gastric and duodenal mucosa.

AIM: To determine the presence of vascular periodic acid-Schiff's reagent (PAS) positive deposits in the gastric and duodenal mucosa of diabetic patients and controls. METHODS: Forty-six poorly controlled diabetic patients with digestive symptoms, aged 23 to 63 years (32 type I patients on insulin therapy with a mean diabetes duration of 14.2 +/- 3.1 years (mean +/- SE) and 13 type II patients with a mean diabetes duration of 7.2 +/- 2.3 years) were included. Of these, 17 had mainly gastropathic symptoms while 13 had diarrhea, and the remaining 16 patients had nonspecific symptoms. Forty control individuals of similar age and gender were included. Biopsy specimens were taken from areas of grossly normal gastric and duodenal mucosa. RESULTS: Gastric mucosa samples were pathological in 38 of 46 diabetic patients (18 cases of chronic active H. pylori antral gastritis, 13 cases of chronic active H. pylori pangastritis and 7 cases of nonspecific chronic gastritis). Duodenal mucosa samples were pathological in 32/46 diabetic patients. In the control group, 21 of 40 gastric samples (5 cases of chronic active H. pylori antral gastritis, 3 cases of chronic active H. pylori pangastritis and 13 cases of H. pylori-negative chronic gastritis) and 12/40 duodenal samples were pathological. Both helicobacteriosis and gastric and duodenal mucosa pathologies were significantly (p < 0.01) more common in diabetic patients than in controls. No significant associations were found between histological findings of gastric mucosa and of duodenal mucosa in diabetics and the control group. PAS-positive material in the vascular wall of gastric (16/46 vs. 2/40 in controls) and duodenal mucosa specimens (25/46 vs. 5/40 in controls) was significantly more common among diabetics (p = 0.001 for gastric and p < 0.001 for duodenal mucosa). No significant association was found between the presence of gastropathy or diarrhea compared to the presence of neuropathy, retinopathy, nephropathy or the type of diabetes. CONCLUSION: Endoscopic specimens from the gastroduodenum of diabetic patients revealed a large quantity of PAS positive vascular deposits, probably reflecting the condition of the mucosal vessels in our patients.

Amoxycillin, clarithromycin and either sucralfate or pantoprazole for eradication of Helicobacter pylori in duodenal ulcer (a randomized controlled trial).

BACKGROUND: Sucralfate enhances the anti-Helicobacter pylori activity of antimicrobials and has an inhibitory effect on H. pylori. AIM: To evaluate the efficacy and safety of one-week sucralfate-based eradication therapy for H. pylori infection in patients with duodenal ulcers, compared with treatment based on pantoprazole, in a randomized controlled multicenter study. METHODS: One hundred and twenty patients with active duodenal ulcers and H. pylori infection were treated with amoxycillin 1 g b.d. plus clarithromycin 500 mg b.d. for the first 7 days. Patients were randomly assigned to receive either sucralfate 1 g t.d.s. for 4 weeks (SAC group; n = 60) or pantoprazole (PAC group; n = 60) 40 mg b.d. for the first 7 days and 40 mg o.d. for the next 3 weeks. The patient's H. pylori status was determined by a urease test and histological investigation before the treatment, and again 4 weeks after cessation of all medication. RESULTS: One hundred and eleven patients completed the study. H. pylori infection was eradicated in 76.4% (42/55) of patients in the SAC group (ITT analysis: 70%, 95% CI: 58-80%) vs. 85.7% (48/56) of patients in the PAC group (ITT analysis: 80%, 95% CI: 70-89) (N.S.). All ulcers had healed. There were no significant differences between the two regimens regarding the occurrence of adverse effects. CONCLUSION: Our study shows that one-week triple therapy with amoxycillin, clarithromycin and either pantoprazole or sucralfate are effective regimens to cure H. pylori infection in patients with duodenal ulcer.

Histochemical changes in the rectal mucosa of diabetic patients with and without diarrhea or constipation.

Sixty-four diabetic patients, 35 with diarrhea, 15 with constipation and 14 without stool problems, and forty healthy subjects, were subjected to rectosigmoidoscopy. During rectosigmoidoscopy, rectal biopsy specimens for histological and histochemical analysis were obtained. Histological findings of nonspecific colitis in 25 out of 64 diabetic patients were uniformly distributed among the three groups (p = 0.959). However, the finding was slightly more common in diabetic patients than in controls (eight out of 40 control subjects, p = 0.043). A positive PAS reaction was observed in 30 out of 64 diabetic patients and was also uniformly distributed among the three groups (p = 0.508), but was significantly more common among diabetic patients than controls (three out of 40, p < 0.001). A positive reaction to cholesterol was found in 46 out of 64 diabetic patients, also uniformly distributed among the three groups (p = 0.773). It was significantly more common in diabetic patients than in controls (nine out of 40, p < 0.001). Reactions of the rectal mucosa histological specimens to glycogen and triglycerides were negative, both in diabetic patients and in controls. In conclusion, it appears that stool problems among our diabetic patients were not related to the positivity of PAS or to the positive cholesterol reaction in the rectal mucosa histological specimens. Since positive findings of both reactions were more common in specimens taken from diabetic patients than in controls, positive reactions might be related to metabolic disturbances in diabetic patients.

Pantoprazole, amoxycillin and either azithromycin or clarithromycin for eradication of Helicobacter pylori in duodenal ulcer.

BACKGROUND: Studies have shown that 1-week triple therapy consisting of a proton pump inhibitor, amoxycillin and clarithromycin may cure Helicobacter pylori infection in the majority of patients. AIM: To establish whether pantoprazole plus amoxycillin in association with either azithromycin or clarithromycin is useful in curing H. pylori infection in patients with a duodenal ulcer. METHODS: One hundred and ten patients with active duodenal ulcers and H. pylori infection were treated with pantoprazole (days 1-7, 40 mg b.d.; days 8-28 40 mg o.d.) plus amoxycillin 1 g b.d. for the first 7 days. Patients were randomly assigned to receive either azithromycin 500 mg o.d. for the first 6 days (PAAz group; n=55) or clarithromycin 500 mg b.d. for the first 7 days of treatment (PAC group; n=55). H. pylori status was determined by urease test and histology before the treatment, and again 4 weeks after cessation of any medication. RESULTS: One hundred and three patients completed the study. H. pylori infection was eradicated in 78% (39/50) of patients in the PAAz group (ITT analysis: 71%, 95% CI: 61-83%) vs. 81% (43/53) of patients in the PAC group (ITT analysis: 78%, 95% CI: 69-90%) (N.S.). All ulcers had healed. CONCLUSION: Our study shows that 1-week triple therapy with pantoprazole, amoxycillin and either azithromycin or clarithromycin is not satisfactory (<80% ITT H. pylori eradication rate).

High dose omeprazole plus amoxicillin and azithromycin in eradication of Helicobacter pylori in duodenal ulcers.

BACKGROUND: The aim of our study was to establish whether one-week triple therapy regimen (omeprazole, amoxicillin, azithromycin) with low dose (2 x 20 mg/day) or high dose omeprazole (2 x 40 mg/day) is more effective in curing H. pylori infection in patients with active duodenal ulcer disease. METHODS: One hundred and twenty patients with duodenal ulcer and H. pylori infection were treated with amoxicillin 2 x 1000 mg/day for the first 7 days plus azithromycin 500 mg/day for the first 6 days. Patients were randomly assigned to receive either omeprazole 2 x 20 mg/day for the first 7 days (group A; n = 60) or omeprazole 2 x 40 mg/day for the first 7 days (group B; n = 60). After 7 days all patients in both groups continued treatment with omeprazole (40 mg/day (days 8-14) and 20 mg/day (days 15-28)). H. pylori status was determined by urease test and histology before the treatment and 4 weeks after cessation of any medication. RESULTS: One hundred and thirteen patients completed the study. H. pylori infection was eradicated in 73.2% [41/56] of patients in group A (intention-to-treat [ITT] analysis: 68.3%; 95% CI: 58.6-80.4%) vs. 82.5% [47/57] of patients in group B (ITT analysis: 78.3%; 95% CI: 67.8-87.9%; NS). All ulcers had healed after 4 weeks of omeprazole treatment. Side effects, usually minor, were recorded in 12.5% (group A) and in 14% (group B) of patients (NS), but therapy was discontinued for only one patient in group B (NS). CONCLUSION: There was no statistically significant difference between one-week triple therapy regimen (omeprazole, amoxicillin, azithromycin) with high dose omeprazole (2 x 40 mg/day) and regimen with low dose omeprazole (2 x 20 mg/day) in curing H. pylori infection in patients with active duodenal ulcer disease.

Pantoprazole versus omeprazole in the treatment of reflux esophagitis.

Pantoprazole is a new proton pump inhibitor with a potent antisecretory activity, well defined pharmacokinetics and safety profile. The aim of this single blind, randomized clinical trial was to compare the efficacy of pantoprazole (PAN) 40 mg/day and omeprazole (OME) 20 mg/day in patients with grade I and II GERD (Savary-Miller classification). A total of 120 patients were included (PAN = 60 and OME = 60). In the per protocol/analysis, healing rates at 4 weeks were 76.3% PAN and 71.2% OME (ns), and at 8 weeks 94.7% PAN and 92.9% OME (ns). In the intention to treat analysis, healing rates at 4 weeks were 75% PAN and 70% OME (ns), and at 8 weeks 90% PAN and 86.6% OME (ns). Both pantoprazole and omeprazole were well tolerated with no serious drug related adverse events. Pantoprazole 40 mg/day was found to be safe and effective therapy comparable to omeprazole 20 mg/day in the short-term treatment for reflux esophagitis (grade I and II).

Omeprazole, azithromycin and either amoxycillin or metronidazole in eradication of Helicobacter pylori in duodenal ulcer patients.

BACKGROUND: Azithromycin is a new generation, acid stable, macrolide antibiotic that achieves remarkably high concentrations in gastric tissue (above the minimal inhibitory concentration for Helicobacter pylori) after oral administration. AIM: To establish whether azithromycin plus omeprazole in association with either amoxycillin or metronidazole are useful in curing H. pylori infection in patients with a duodenal ulcer. METHODS: One hundred patients with active duodenal ulcers and H. pylori infection were treated with omeprazole (days 1-10, 40 mg b.d.; days 11-24, 40 mg o.m.; days 25-42, 20 mg o.m.) plus azithromycin 500 mg o.m. for the first 6 days. Patients were randomly assigned to receive either amoxycillin 1 g b.d. (OAzA group: n = 50) or metronidazole 400 mg t.d.s. (OAzM group: n = 50) during the first 10 days of treatment. H. pylori status was determined by urease test and histology before the treatment and 6 weeks after completion of therapy. RESULTS: Ninety-seven patients completed the study. H. pylori infection was eradicated in 85% (41/48) of patients in the OAzA group (intention-to-treat analysis 82%) vs. 74% (36/49) of patients in the OAzM group (intention-to-treat analysis: 72%) (N.S.). All ulcers had healed after 6 weeks of omeprazole treatment. Side-effects, usually minor, were recorded in 13% (OAzA group) and 47% (OAzM group) of patients (P < 0.001), but therapy was discontinued for only one patient in the OAzA group (N.S.). CONCLUSION: Ten days of treatment with omeprazole plus (for the first 6 days) azithromycin and either amoxycillin or metronidazole provides effective regimens to cure H. pylori infection in patients with duodenal ulcer disease.

Infection with Helicobacter pylori and long-term use of non-steroidal antiinflammatory drugs.

The use of nonsteroidal anti inflammatory drugs (NSAID) is associated with an increased risk of peptic ulcer and of ulcer complications. However, the relation between Helicobacter pylori infection and gastroduodenal damage associated with NSAID use is unclear. This study investigated the prevalence of Helicobacter pylori infection in patients with arthritis (n = 85) taking NSAID, trying to find out whether the patients taking NSAID and infected with H. pylori were more likely to have dyspepsia, mucosal damage or chronic active gastritis than those without H. pylori infection. H. pylori was identified by biopsy, rapid urease test and histologic test. Dispeptic symptoms were assessed according to a standardized questionnaire. Gastroduodenal mucosal damage was graded endoscopically (using a modified Lanza scale) and the diagnosis of chronic gastritis was based on the histologic criteria of the Sydney system. The frequency of H. pylori infection was found to increase with age. No statistically significant difference was observed in the presence of damage to gastroduodenal mucosa between the patients with and without H. pylori infection. H. pylori infection was found to be associated with an increased frequency and severity of dyspeptic symptoms in patients with arthritis taking long-term NSAID. Chronic active gastritis was only present in patients with H. pylori infection. H. pylori infection was shown to be associated with an increased frequency and severity of dyspeptic symptoms in patients with arthritis on long-term NSAID therapy, without causing an increased damage to gastroduodenal mucosa.

Omeprazole, azithromycin and amoxicillin or amoxicillin plus clavulanic acid in eradication of Helicobacter pylori in duodenal ulcer disease.

Treatment with omeprazole (OME), azithromycin (AZI) and amoxicillin (AMO) resulted in encouraging Helicobacter pylori cure rates in pilot and control studies. The aim of this study was to establish whether OME + AZI in combination with either AMO or ACA (amoxicillin plus clavulanic acid) are effective in curing H. pylori infection. A hundred patients with active duodenal ulcer and H. pylori infection were treated with OME (day 1-10: 2 x 40 mg/day, day 11-24: 40 mg/day, day 25-42: 20 mg/day) plus AZI 500 mg/day for the first 6 days. Patients were randomly assigned to either AMO 2 x 1000 mg/day (group A, n = 50) or ACA 2 x 1250 mg/day (group B, n = 50) during the first 10 days of treatment. H. pylori status was determined by urease test and histology before and 6 weeks after completion of therapy. Ninety-five patients completed the study. H. pylori infection was eradicated in 85.4% (41/48) patients from group A (intention-to-treat (ITT) analysis: 82%) versus 91.5% (43/47) patients from group B (ITT) analysis: 86%) (NS). All ulcer had healed after 42 days of omeprazole treatment. Side effects, usually minor, were recorded in 12.5% (group A) and 14.9% (group B) of patients (NS). Therapy had to be discontinued in two patients (one in group A and one group B) only. Ten-days treatment with OME and AZI (for the first 6 days) with AMO or ACA are simple and highly effective regimens to cure H. pylori infection in patients with duodenal ulcer disease.

[Omeprazole and azithromycin with and without metronidazole in the eradication of Helicobacter pylori in duodenal ulcer disease]. / Omeprazol i azitromicin s metronidazolom ili bez njega za eradikaciju Helicobactera pylori u duodenalnoj ulkusnoj bolesti.

This prospective, single blind, randomized study was designed to compare the efficacy and tolerance of two therapeutic schedules for eradication of H. pylori in patients with duodenal ulcer. Patients were randomized into two groups. Group 1 (n = 25) was treated with omeprazole 20 mg each morning for 28 days, azithromycin 500 mg/day for 5 days and metronidazole 3 x 500 mg/day for 5 days. Group 2 (n = 25) was treated with omeprazole 20 mg/day for 28 days and azithromycin 500 mg/day for 5 days. H. pylori status was determined by rapid urease test and histology before and 1, 6 and 12 months after the therapy. After 4 weeks of treatment ulcers healed in 96% (24/25) of patients in the first group and in 92% (23/25) of patients in the second group. One and 12 months after the treatment, eradication of Helicobacter pylori was achieved in 72% (18/25) of patients in the first group and in 64% (16/25) of patients in the second group. In 12 months after the treatment ulcer recurred in 43.7% (7/16) of patients in whom H. pylori was not eradicated and in 2.9% (1/34) of patients with eradicated H. pylori. The side effects were minor and/or transitory and did not require discontinuation of the treatment.

Another therapeutic schedule in eradication of Helicobacter pylori.

In this study, the efficacy and tolerability of two different therapeutic schedules in eradicating Helicobacter pylori and healing duodenal ulcer were evaluated. The study included 60 patients with duodenal ulcer and Helicobacter pylori infection. They were randomly allocated to either of two groups: group 1 (N = 30) received omeprazole 20 mg for 28 days, amoxicillin 3 x 500 mg for 7 days and metronidazole 3 x 500 mg for 5 days, and group 2 (N = 30) received omeprazole 20 mg for 28 days, ACA (amoxicillin 500 mg plus clavulanic acid 125 mg) 3 x 625 mg for 7 days and metronidazole 3 x 500 mg for 5 days. Endoscopic examination, bioptic urease test and histologic examination were performed before, and 30 and 90 days after the treatment. Endoscopic examination was also performed one month after the beginning of the treatment, when healing of duodenal ulcer was observed in 90% (27/30) of the group 1 patients and in 93.3% (28/30) of the group 2 patients. The Helicobacter pylori eradication achieved in group 1 and 2 was 76.7% (23/30) and 83.3% (25/30), respectively. Side effects were present in 20% (6/30) of the group 1 patients and in 23.3% (7/30) of the group 2 patients. Side effects were mild and did not require interruption of the treatment. A higher rate of eradication was achieved in group 2 than in group 1, but the difference was not statistically significant.

Lansoprazole versus omeprazole in the treatment of reflux esophagitis.

To evaluate the therapeutic potential of the newly developed proton pump inhibitor lansoprazole in patients with reflux esophagitis (grade I and II according to Savary Müller criteria), the authors performed a single blind, randomized clinical trial comparing 20 mg omeprazole and 30 mg lansoprazole, involving 60 patients at two clinical hospitals. The treatment period was or 8 weeks, and main efficacy variables were healing of endoscopic changes and relief of reflux symptoms. No significant difference in terms of healing and relief of reflux symptoms was found either after 4 or after 8 weeks of treatment. In conclusion, 30 mg lansoprazole daily was found to be safe and effective therapy comparable to omeprazole in the short-term treatment for reflux esophagitis (grade I and II).

Biochemical parameters in the early differentiation of the etiology of acute pancreatitis.

OBJECTIVES: We undertook a retrospective study to define the usefulness of various biochemical parameters in differentiation between alcoholic and nonalcoholic acute pancreatitis. METHODS: One hundred sixty-seven patients were divided into groups A (alcoholic pancreatitis) and NA (nonalcoholic pancreatitis). Group NA was further subdivided into groups B (biliary pancreatitis) and NANB (nonalcoholic, nonbiliary pancreatitis). The values of serum and urine amylase, serum lipase, AST, ALT, alkaline phosphatase, gamma glutamyl transferase, bilirubin, lipase/amylase ratio, and erythrocyte mean corpuscular volume were investigated. RESULTS: Serum amylase, ALT, AST, alkaline phosphatase (p < 0.001), and urine amylase (p < 0.01) were significantly lower in patients with alcoholic pancreatitis. Erythrocyte mean corpuscular volume and lipase/amylase ratio were significantly higher in patients with alcoholic pancreatitis (p < 0.001). There were no differences in lipase, bilirubin, and gamma glutamyl transferase between patients with alcoholic pancreatitis and those with nonalcoholic pancreatitis. Multivariate analysis showed that a combination of three variables (lipase/amylase ratio, erythrocyte mean corpuscular volume, and alkaline phosphatase) differentiated between alcoholic and nonalcoholic pancreatitis. CONCLUSIONS: Various biochemical parameters used together and with other clinical features can help in the early differentiation between alcoholic and nonalcoholic acute pancreatitis.