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At least 127 records · Page 7Linked to original sources
PubMed2002

Risk factors for ulcer development in patients with non-ulcer dyspepsia: a prospective two year follow up study of 209 patients.

BACKGROUND AND AIMS: A subset of non-ulcer dyspepsia (NUD) disorders can evolve into peptic ulcer disease. This prospective study attempted to determine the independent risk factors for ulcer formation in NUD patients, and compared the natural history of Helicobacter pylori positive and negative NUD subjects. METHODS: From May 1997 to April 1999, consecutive NUD patients were enrolled into the study. Endoscopy was performed routinely on enrolment, at the end of the second and 12th months, and whenever there was a dyspepsia attack. Patients were prospectively followed up for two years. RESULTS: Peptic ulcers occurred in 16 of 209 NUD patients during the two year follow up period. Multivariate analysis of 13 host and bacterial factors demonstrated that advanced age (odds ratio 2.90), H pylori infection (odds ratio 3.59), and use of non-steroidal anti-inflammatory drugs (NSAID; odds ratio 4.46) were independently significant in predicting subsequent peptic ulcer development. NUD patients with all three risk factors had a 75% (3/4) risk of developing peptic ulcer but the ulcer incidence in patients without any of the risk parameters was only 1.2% (1/84). The resolution rate of symptoms in the H pylori positive NUD patients was similar to the H pylori negative patients (57.9% v 49.1%; 95% confidence interval (CI) -5 to 22). However, rates for subsequent peptic ulcer and erosion development were significantly higher in H pylori positive patients than in H pylori negative patients (ulcer 12.6% v 3.5%, 95% CI 1-16; erosion 23.2% v 12.3%, 95% CI 1-21). CONCLUSION: A small but significant proportion of NUD patients develop peptic ulcer after long term follow up. H pylori infection, NSAID use, and advanced age are independent risk factors for subsequent ulcer formation. Follow up endoscopy is strongly indicated for an NUD patient with multiple risk factors for ulcer formation when symptoms recur.

Age Factors↗
PubMed2000

Pentoxifylline accelerates gastric ulcer healing in rats: roles of tumor necrosis factor alpha and neutrophils during the early phase of ulcer healing.

BACKGROUND/AIMS: Pentoxifylline has many anti-inflammatory properties including inhibition of production of tumor necrosis factor alpha (TNF-alpha). Although pentoxifylline prevents several types of gastric mucosal injury, the effect of this drug on ulcer healing is unknown. In this study, we examined the effect of pentoxifylline on healing of acetic acid induced gastric ulcers in rats. METHODS: Rats with gastric ulcer received an intraperitoneal injection of 10 mg/kg pentoxifylline once daily for 14 days or for only the first 7 days or the last 7 days of the 14-day treatment period. Some rats were given antirat neutrophil antiserum intraperitoneally every other day. Ulcer size, myeloperoxidase activity, and concentration and location of TNF-alpha in ulcer tissue were assessed. RESULTS: Administration of pentoxifylline for 14 days or for the first 7 days, but not for the last 7 days, of the 14-day treatment period accelerated ulcer healing. TNF-alpha was detected mainly in monocytes/macrophages and in some neutrophils at ulcer bases and margins. Pentoxifylline markedly decreased the concentration of TNF-alpha as well as the myeloperoxidase activity in ulcer tissue on days 2 and 4. Antirat neutrophil antiserum inhibited neutrophil infiltration into ulcer tissue and accelerated ulcer healing. CONCLUSION: Pentoxifylline accelerates healing of acetic acid induced gastric ulcer in rats. This effect may be due in part to reduction of neutrophil infiltration and inhibition of production of TNF-alpha by inflammatory cells. Early-phase inhibition of inflammatory response may accelerate ulcer healing.

Acetic Acid↗
PubMedDate not supplied

Evaluation of pressure ulcer prevalence rates for hospice patients post-implementation of pressure ulcer protocols.

Hospice patients may be particularly at risk for pressure ulcer development due to several factors. Identifying populations at risk for pressure ulcer development, such as hospice patients, and providing prevention and risk protocols for these populations can substantially reduce the prevalence and incidence of pressure ulcers. However, are hospice patients prone for skin breakdown despite prevention and treatment efforts? This study examines the prevalence of pressure ulcers in hospice patients following the implementation of pressure ulcer prevention and treatment protocols. Levine's theory of conservation of structural integrity formed the theoretical framework for this descriptive study. A midwestern hospital-based hospice agency was the site for this study. All patients 18 years of age and older were included in the study. Pressure ulcer prevalence audits were done at four, eight, 12, and 18 months after protocols were outlined by the hospice staff. Results of the audits revealed prevalence rates of 14.8 percent, 8.5 percent, 13.6 percent, and 23.8 percent, at each of the aforementioned audits. 10 of 15 patients who were pressure ulcer positive were males; the sacral location was most common (seven of 19 ulcers occurred sacrally) with the ischial location being the next common (six of 19 ulcers were ischially located). No ulcers occurred above the waist or in patients below 51 years of age. Recommendations from this study urge that particular prevention attention be given to protocols which address "sitting," due to the predominance of ulcers located in the sacral and ischial regions. In addition, the author concludes that perhaps, pressure ulcers may occur in this population despite the best of efforts to prevent them.

Aged↗
PubMed1991

Young onset peptic ulcer disease and non-ulcer dyspepsia are separate entities.

The characteristics of peptic ulcer and non-ulcer dyspepsia in young men were studied in 202 consecutive conscripts who attended Central Military Hospital in Helsinki because of long-standing upper abdominal complaints. Active peptic ulceration (APU) was found in 48 patients, inactive peptic ulcer disease (IPU) was diagnosed in 77 patients, non-ulcer dyspepsia (NUD) was diagnosed in 52 patients. In 25 cases the reason for symptoms was another disease, and these patients were excluded from the study. A control series (CON) consisted of 30 symptomless healthy young male volunteers. The likelihood of discriminating between peptic ulcer disease and non-ulcer dyspepsia in a young male patient with dyspepsia are indicated by odds ratios (OR) and its 95% confidence limits (CL 95). Active peptic ulcer disease differs from NUD, e.g., by 1) presence of antrum gastritis, OR 41.5 (CL 95: 10.1-171), 2) Helicobacter pylori in the gastric mucosa, OR 31.0 (7.4-130), 3) Lewisa+ phenotype, OR 8.9 (1.7-45.4), 4) serum pepsinogen I (S-PGI) greater than 100 micrograms/l, OR 4.6 (1.7-12.4), 5) non-secretor status, OR 4.3 (1.6-11.6), and 6) O-blood group, OR 3.0 (1.2-7.7). In conclusion, the status of gastroduodenal mucosa, gastric secretion pattern and distribution of some genetic markers in patient series indicate that young onset peptic ulcer and non-ulcer dyspepsia are two separate entities. Helicobacter-positive antrum gastritis is the best determinant of ulcer risk, but also high S-PGI, Lewisa+ phenotype, non-secretor status and O-blood group are signs of increased risk of peptic ulcer.

Adolescent↗
PubMed1996

The prevalence of esophagitis in patients with duodenal ulcer or ulcer-like dyspepsia.

OBJECTIVE: It has been reported that 30-72% of patients with duodenal ulcer disease also have esophagitis. However, many of these reports included patients who had severe or complicated ulcer disease, so that the high prevalence may reflect pyloric stenosis or gastric hyper-secretion. The objective of this study was to determine the prevalence of esophagitis in unselected patients with duodenal ulcer disease or ulcer-like dyspepsia. METHOD: A prospective study of endoscopic and histological esophagitis in consecutive patients with either duodenal ulcer disease or with ulcer-like dyspepsia. RESULTS: Of 27 patients with duodenal ulcer disease, 33% had endoscopic esophagitis, 26% had histological esophagitis, and 48% had esophagitis by either criterion. Of 66 patients with ulcer-like dyspepsia, 35% had endoscopic esophagitis, 47% had histological esophagitis, and 62% had esophagitis by either criterion. Esophagitis was independent of patients' Helicobacter pylori status. CONCLUSIONS: Esophagitis is common in patients with duodenal ulcer disease, and the prevalence is similar in patients with ulcer-like dyspepsia. In addition to causing heartburn, esophagitis may also be cause ulcer-like epigastric pain. Concomitant esophagitis may account for the persisting or recurring dyspepsia that has been reported in up to one-third of duodenal ulcer patients after successful eradication of H. pylori.

Adult↗
PubMed2001

Effect of Helicobacter pylori eradication on the ulcer recurrence rate after simple closure of perforated duodenal ulcer: retrospective and prospective randomized controlled studies.

BACKGROUND: The possible advantage of eradication of Helicobacter pylori in patients with perforated duodenal ulcer is unknown. This study was planned to assess the prevalence of H. pylori after simple closure of a perforated duodenal ulcer and to study the effect of H. pylori eradication on ulcer persistence and recurrence. METHODS: Some 202 patients were followed prospectively for 2 years after simple closure of a perforated duodenal ulcer (prospective group). A second group of 60 patients was reviewed 5 years or more after perforation closure (retrospective group). The prevalence of H. pylori in patients with perforated duodenal ulcer was compared with that in controls. Patients in the prospective group were randomized to receive either ranitidine alone or quadruple therapy (ranitidine, colloidal bismuth subcitrate, metronidazole and tetracycline) after operation. The incidence of H. pylori infection after the two treatments and the association with residual or recurrent ulcer were studied. In the retrospective group long-term ulcer recurrence was correlated with H. pylori status. RESULTS: The prevalence of H. pylori in patients with perforated duodenal ulcer was not significantly different from that in controls. At every interval of follow-up in the prospective group and in the retrospective group the H. pylori infection rate was significantly higher in patients who had recurrent or residual ulcers. CONCLUSION: Eradication of H. pylori after simple closure of a perforated duodenal ulcer should reduce the incidence of residual and recurrent ulcers.

Adolescent↗
PubMed1996

Simultaneous evaluation of gastric and duodenal ulcers-healing activities of anti-ulcer agents in rats.

We investigated the effects of cimetidine, omeprazole and atropine, antisecretory anti-ulcer agents, on the healing of gastric and duodenal ulcers simultaneously induced in the same rats. Furthermore, we examined the effect of histamine, an acid secretory agent, on the healing of both ulcers. When the effects of test drugs were assessed on the 15th day after local application of acetic acid, repeated oral administration of cimetidine (50 and 100 mg/kg twice daily) or omeprazole (25 and 50 mg/kg once daily) markedly accelerated the healing of both gastric and duodenal ulcers. Atropine (10 mg/kg twice daily, p.o.) showed a healing effect on duodenal ulcers only. The repeated subcutaneous administration of histamine (30 mg/kg 3 times daily) apparently delayed the healing of duodenal ulcers but not gastric ulcers. In conclusion, this experimental chronic ulcer model in rats is useful for directly comparing the effects of anti-ulcer drugs on the healing of gastric and duodenal ulcers. In addition, the increase in acid secretion appears to have a greater influence on the delay of ulcer healing in the duodenum than in the stomach.

Acetic Acid↗
PubMed1999

Relapse of duodenal ulcers after successful eradication of Helicobacter pylori in gastric ulcer patients.

Relapse of duodenal ulcers was observed endoscopically after Helicobacter pylori eradication therapy for gastric ulcer patients in 2 of 32 successful cases. One patient, a 40-year-old woman, received dual therapy with lansoprazole 60mg and amoxicillin 1000mg for 2 weeks because of an intractable, easily-relapsing gastric ulcer accompanied by duodenal ulcer scars that had not relapsed for 5 years. The H. pylori status was assessed by a rapid urease test, light microscopy, culture, and anti-H. pylori antibody. At 24 months after the cure of H. pylori she had upper abdominal pain and showed relapse not of the gastric ulcer but of the duodenal ulcer. The H. pylori status remained negative. The other patient, a 44-year-old man, showed an active gastric ulcer and duodenal ulcer scars at the first endoscopy. He received the same regimen as described above. Ten weeks after completion of the eradication therapy, endoscopy showed healing of the gastric ulcer and relapse of the duodenal ulcer despite successful eradication. These two cases suggest that H. pylori eradication modifies the pathophysiological condition of gastric acid secretion and facilitates relapse of duodenal ulcers.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1964

STASIS GASTRIC ULCER: A COMPLICATION OF DUODENAL ULCER.

A causal relation between gastric stasis and gastric ulceration is suggested by the literature reviewed. In obstructive duodenal ulcer disease it is important to know that a concomitant gastric ulcer may be present and causing the symptoms. In combined ulcers, symptoms are more severe and treatment is more difficult.A clinical study of 60 cases of stasis gastric ulcer associated with chronic duodenal ulcer disease is presented. Twenty-six of these patients with gastric ulcers were bleeding at the time of their admission. The mortality rate was at least twice that for solitary ulcer. Early warning symptoms of stasis were fatigue, anorexia, fullness and weight loss; vomiting was a late manifestation. X-ray findings were often inaccurate; evidence of retention was reported in only 21. Gastric residue measurements were particularly useful in showing gastric retention.Since the basic disease in combined ulcers is the duodenal lesion, surgical treatment is primarily that for duodenal ulcer.

Duodenal Ulcer↗
PubMedDate not supplied

Is neuropathic ulceration the key to understanding increased mortality due to ischaemic heart disease in diabetic foot ulcer patients? A population approach using a proportionate model.

Ischaemic heart disease (IHD) is the commonest cause of death in diabetic foot ulcer patients and non-ulcerated diabetic patients, yet the mortality rate of diabetic foot ulcer patients is over twice that of non-ulcerated patients. As the cause of this increased mortality is not understood, we plotted the ratio of deaths due to ischaemic heart disease (IHDn) to other causes of death (i.e. IHDn:OCDn) against age for 242 diabetic foot ulcer patients and 121 controls (non-ulcerated diabetic patients). The IHDn:OCDn ratio rose above 1.0 from age 40 years onwards for diabetic foot ulcer patients, but from age 70 years onwards for controls, demonstrating differentially increased mortalities due to IHD. A population model involving summation of IHDn:OCDn ratios for neuropathic and neuroischaemic diabetic foot ulcer patients calculated an overall increased mortality rate of 1.8 compared with that of non-ulcerated diabetics. The model predicted that a 25% reduction in neuropathic diabetic foot ulcer patients dying from IHD would eliminate the increased mortality, demonstrating that neuropathic rather than ischaemic ulceration defines the cause of increased mortality among diabetic foot ulcer patients.

Adult↗
PubMed1986

Ventilatory function in chronic peptic ulcer. A controlled study of ventilatory function in patients with gastric and duodenal ulcer.

The aim of this study was to determine if a defect in ventilatory function is present in patients with chronic peptic ulcer and if so, is it present in both gastric and duodenal ulcer and is it related to smoking. Fifty-six patients with peptic ulceration (27 gastric ulcer, 29 duodenal ulcer), together with 56 healthy controls matched for age, sex, and smoking status, were studied. Ventilatory function was measured and the ABH blood group antigen secretor status was determined. Vital capacity and forced expiratory volume in 1 s were significantly reduced in both smokers and nonsmokers with gastric ulcer when compared with controls; total lung capacity was lower than controls only in smokers with gastric ulcer. In duodenal ulcer patients, a trend similar to that observed in gastric ulcer patients was present. It is concluded that a defect in ventilatory function is present in patients with chronic gastric ulcer; a lesser defect is present in patients with duodenal ulcer.

ABO Blood-Group System↗
PubMed1997

Preliminary clinical study on gastric ulcer scars and ulcer relapses after Helicobacter pylori eradication therapy.

To determine the effect of Helicobacter pylori eradication on the healing of gastric ulcers, endoscopic examinations of gastric ulcer scars and ulcer relapse after eradication therapies or antisecretory therapy were carried out in 24 H. pylori-positive patients with recurrent gastric ulcers located in the gastric angle. Sixteen patients were initially treated with 2-week triple eradication therapy. Subsequently, seven of eight noneradicated cases were retreated with triple therapy, which included metronidazole. Eight patients received antisecretory monotherapy. Endoscopic examinations were performed at 4 weeks and 6 months after the treatments. Gastric ulcer scars were classified endoscopically into three types: Sa, a central depression surrounded by a coarse pattern: Sb, a coarse regenerated pattern; and Sc, a fine pattern indicating matured scar of high quality. Transformations of the scar patterns and ulcer relapse were assessed in 19 patients who showed an ulcer scar at 4 weeks after initial therapy. Thirteen cases in which H. pylori was successfully eradicated, either after initial or re-eradication therapies, mainly showed Sc scars and had no ulcer relapse. Sa scar was mainly observed during H. pylori-positive conditions. Transformation from the Sa to the Sc was observed after successful re-eradication. Ulcer relapses occurred in three patients who showed Sa scar after antisecretory therapy. Although a random study would be needed to obtain a definite conclusion, we suspect that the H. pylori-negative condition after eradication therapies may result in good ulcer healing and may subsequently reduce ulcer relapse.

Anti-Bacterial Agents↗
PubMed1996

Ranitidine bismuth citrate plus clarithromycin is effective for healing duodenal ulcers, eradicating H. pylori and reducing ulcer recurrence. RBC H. pylori Study Group.

AIM: To compare the efficacy of the coadministration of ranitidine bismuth citrate plus the antibiotic clarithromycin, with ranitidine bismuth citrate alone or clarithromycin alone for the healing of duodenal ulcers, eradication of H. pylori and the reduction of ulcer recurrence. METHODS: This two-phase, randomized, double-blind, placebo-controlled, multicentre study consisted of a 4-week treatment phase followed by a 24-week post-treatment observation phase. Patients with an active duodenal ulcer were treated with either ranitidine bismuth citrate 400 mg b.d. for 4 weeks plus clarithromycin 500 mg t.d.s. for the first 2 weeks; ranitidine bismuth citrate 400 mg b.d. for 4 weeks plus placebo t.d.s. for first 2 weeks; placebo b.d. for 4 weeks plus clarithromycin 500 mg t.d.s. for the first 2 weeks; or placebo b.d. for 4 weeks plus placebo t.d.s. for the first 2 weeks. RESULTS: Ulcer healing rates after 4 weeks of treatment were highest with ranitidine bismuth citrate plus clarithromycin (82%) followed by ranitidine bismuth citrate alone (74%; P = 0.373), clarithromycin alone (73%; P = 0.33) and placebo (52%; P = 0.007). Ranitidine bismuth citrate plus clarithromycin provided significantly better ulcer symptom relief compared with clarithromycin alone or placebo (P < 0.05). The coadministration of ranitidine bismuth citrate plus clarithromycin resulted in significantly higher H. pylori eradication rates 4 weeks post-treatment (82%) than did treatment with either ranitidine bismuth citrate alone (0%; P < 0.001), clarithromycin alone (36%; P = 0.008) or placebo (0%; P < 0.001). Ulcer recurrence rates 24 weeks post-treatment were lower following treatment with ranitidine bismuth citrate plus clarithromycin (21%) compared with ranitidine bismuth citrate alone (86%; P < 0.001), clarithromycin alone (40%; P = 0.062) or placebo (88%; P = 0.006). All treatments were well tolerated. CONCLUSIONS: The coadministration of ranitidine bismuth citrate plus clarithromycin is a simple, well-tolerated and effective treatment for active H. pylori-associated duodenal ulcer disease. This treatment regimen effectively heals duodenal ulcers, provides effective symptom relief, eradicates H. pylori infection and reduces the rate of ulcer recurrence. The eradication of H. pylori infection in patients with recently healed duodenal ulcers is associated with a significant reduction in the rate of ulcer recurrence.

Adolescent↗
PubMed2005

Standard treatment for Helicobacter pylori infection is suboptimal in non-ulcer dyspepsia compared with duodenal ulcer in Chinese.

BACKGROUND: Recent studies suggest that the Helicobacter pylori eradication rate in patients with non-ulcer dyspepsia is lower when compared to patients with peptic ulcer diseases. AIM: The aim of this study was to study the efficacy of triple therapy for H. pylori infection in patients with duodenal ulcer vs. patients with non-ulcer dyspepsia. METHODS: A total of 582 Chinese patients with proven H. pylori infection were recruited to receive: omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg all given twice daily for 7 days (OCA regime). Endoscopy with rapid urease test, histology and culture were performed before treatment. Post-treatment H. pylori status was determined by (13)C-urea breath test. Metronidazole, clarithromycin and amoxicillin resistance was defined as minimum inhibitory concentration (MIC) of >8 microg/mL, >1 microg/mL and >1 microg/mL, respectively. RESULTS: A significantly higher (intention-to-treat/per-protocol) eradication rate was found in patients with duodenal ulcer than those with non-ulcer dyspepsia (91/94% vs. 84/88% respectively, P = 0.011 and P = 0.016). Clarithromycin resistance rate was higher in patients with non-ulcer dyspepsia than those with duodenal ulcer (14% vs. 6%, P = 0.015). Clarithromycin resistance (40% vs. 5%, P < 0.001, OR 12, 95% CI: 5.7-24.3) and the diagnosis of non-ulcer dyspepsia (91% vs. 84%, P = 0.011, OR 2.0, 95% CI: 1.2-3.3) significantly affected the success of H. pylori eradication. CONCLUSION: Clarithromycin resistance accounts for the significantly lower and suboptimal H. pylori eradication rate of OCA regimen in Chinese patients with non-ulcer dyspepsia compared to those with duodenal ulcer.

Adolescent↗
PubMed1997

Anti-ulcer activity of cromakalim (BRL 34915), a potassium-channel opener, against experimentally induced gastric and duodenal ulcers in rats and guinea-pigs.

The effect of cromakalim, a potassium-channel opener, was studied on pylorus ligation-induced, aspirin-induced and water-immersion plus restraint stress-induced gastric ulcers in rats and on histamine-induced duodenal ulcer in guinea-pigs. Pretreatment with cromakalim (50-500 micrograms kg-1, p.o.) resulted in a significant reduction in the incidence of gastric and duodenal ulceration in each model. The anti-ulcer activity of cromakalim was comparable with that of cimetidine. Cromakalim at 100, 250 and 500 micrograms kg-1 caused a reduction in the volume of the gastric content in pylorus-ligated rats, and a dose of 250 micrograms kg-1 resulted in a significant reduction in total acidity (28.81 +/- 11.73 mEq L-1, P < 0.02) in the pylorus ligation model. A significant reduction in total acid output was observed at doses of 250 micrograms kg-1 (84.27 +/- 22.33 mEqH+, P < 0.02) and 500 micrograms kg-1 (120.17 +/- 24.49 mEqH+, P < 0.01) in pylorus-ligated rats. A significant reduction in the ulcer index in pylorus-ligated rats was observed at all cromakalim doses: 50 micrograms kg-1 (0.23 +/- 0.09, P < 0.05), 100 micrograms kg-1 (0.15 +/- 0.09, P < 0.02), 250 micrograms kg-1 (0.12 +/- 0.05, P < 0.01) and 500 micrograms kg-1 (0.14 +/- 0.03, P < 0.02). A significant reduction in the ulcer index of aspirin-treated rats was also observed at all cromakalim dose levels: 50 micrograms kg-1 (0.39 +/- 0.03, P < 0.01), 100 micrograms kg-1 (0.28 +/- 0.06, P < 0.01), 250 micrograms kg-1 (0.22 +/- 0.04, P < 0.001) and 500 micrograms kg-1 (0.28 +/- 0.03, P < 0.01). In the water-immersion plus restraint stress-induced gastric ulcer model, cromakalim significantly reduced gastric ulceration at all the dose levels: 50 micrograms kg-1 (28.2 +/- 2.12, P < 0.001), 100 micrograms kg-1 (20.24 +/- 1.71, P < 0.01), 250 micrograms kg-1 (19.95 +/- 1.46, P < 0.001) and 500 micrograms kg-1 (21.61 +/- 3.00, P < 0.001) but there was no consistent reduction of gastric bleeding. In addition to gastric ulcers, duodenal lesions were also reduced by pretreatment with cromakalim at all dose levels: 50 micrograms kg-1 (97.87 +/- 20.03 mm2, P < 0.02), 100 micrograms kg-1 (70.72 +/- 12.82 mm2, P < 0.02), 250 micrograms kg-1 (48.32 +/- 8.42 mm2, P < 0.01) and 500 micrograms kg-1 (55.50 +/- 12.50 mm2, P < 0.01). Cromakalim at a dose of 100 micrograms kg-1 also reduced total acidity (99.36 +/- 9.12 mEqL-1, P < 0.02) and total acid output (172.22 +/- 45.33 mEq of H+, P < 0.05) in this model. These findings demonstrate the anti-ulcer activity of cromakalim in different experimental models and suggest its potential use in ulcer therapy.

Animals↗
PubMed2000

Does the depth of gastric ulceration influence a modified dual therapy with amoxicillin and lansoprazole for Helicobacter pylori-associated gastric ulcer?

PURPOSE: To clarify whether the depth of ulceration evaluated by endoscopic ultrasonography (EUS) influences a modified dual therapy with amoxicillin and lansoprazole for the treatment of Helicobacter pylori-positive patients with gastric ulcer. PATIENTS AND METHODS: Twenty-two consecutive cases of gastric ulcer (nine superficial ulcers and 13 deep ulcers) in H pylori-positive patients were studied. Ten of 22 patients received a two-week eradication therapy with amoxicillin 1500 mg/day, lansoprazole 30 mg/day and a new antiulcer agent with features in common with sucralfate, ecabet sodium, 2.0 g/day. They continued to receive the same doses of lansoprazole and ecabet sodium for the next six weeks. The other 12 patients received the same therapy except for those who underwent the four-week amoxicillin treatment. All patients underwent EUS both at the start of the study and eight weeks later. They then received ecabet sodium alone for the next six months as a maintenance therapy, followed by a six-month interval with no treatment. The final endoscopy was done one year after H pylori eradication therapy was completed to evaluate H pylori status and ulcer recurrence. RESULTS: The rates of endoscopic healing and H pylori eradication in the nine patients with superficial ulcer were 100%, irrespective of the period of amoxicillin treatment. In contrast, the rates of endoscopic evidence of healing and H pylori eradication in the 13 patients with deep ulcer were different for each period of amoxicillin treatment; that is, the rates of reduction in ulcer determined by echo and H pylori eradication in the four patients treated with the two-week amoxicillin course were significantly lower (P=0.03) than those in the nine patients treated with the four-week course. CONCLUSION: Ulcer depth is likely to influence the success of amoxicillin treatment for H pylori-positive patients with gastric ulcer.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2002

Cost-effectiveness of wound management in France: pressure ulcers and venous leg ulcers.

OBJECTIVES: This study set out to define realistic protocols of care for the treatment of chronic venous leg ulcers and pressure ulcers in France and, by developing cost-effectiveness models, to compare the different protocols of care for the two ulcer groups, enabling a calculation of direct medical costs per ulcer healed in a typical French health insurance plan. METHOD: Clinical outcomes and some treatment patterns were obtained from published literature. Validations of different treatment patterns were developed using an expert consensus panel similar to the Delphi approach. Costs were calculated based on national averages and estimates from the UK and Germany. The models were used to measure costs per healed ulcer over a 12-week period. RESULTS: For both the pressure ulcer and venous leg ulcer models, three protocols of care were identified. For pressure ulcers and venous leg ulcers, the hydrocolloid DuoDERM (ConvaTec, also known as Granuflex in the UK and Varihesive in Germany) was most cost-effective in France. CONCLUSION: The combination of published data and expert consensus opinion is a valid technique, and in this case suggests that treating pressure ulcers and venous leg ulcers with hydrocolloid dressings is more cost-effective than treating them with saline gauze, in spite of the lower unit cost of the latter.

Biological Dressings↗
PubMed1984

Serum group I pepsinogen (PG I) levels and their changes in the healing process of the ulcer in patients with and without unoperated recurrent ulcer.

We measured serum group I pepsinogen (PG I) levels in subjects with endoscopically normal gastric and duodenal mucosa and patients with peptic ulcer. The release mechanism of PG I into blood stream was also investigated. The mean (+/- S.E.) serum PG I level in 136 subjects with endoscopically normal mucosa was 61 +/- 2 ng/ml and the normal range was calculated to be 30-109 ng/ml from the frequency distribution. In the patients with unoperated recurrent duodenal ulcer, the serum PG I levels remained high with the healing process of the ulcer. On the other hand, in the patients with non-recurrent duodenal ulcer and those with recurrent or non-recurrent gastric ulcer, the serum PG I levels decreased with the healing process of the ulcer gradually and significantly from the value in the active stage. These findings suggest that duodenal ulcer patients with high levels of serum PG I throughout the healing process of the ulcer tend to have the recurrence. Therefore, the serial measurements of serum PG I with the healing process will be helpful for the prediction of ulcer recurrence. Administration of atropine caused a significant decrease in serum PG I in the patients with duodenal ulcer, which suggests the vagal control of PG I release in duodenal ulcer patients.

Adolescent↗