Eradication of Helicobacter pylori in peptic ulcer patients

The aim of this study was to compare in an open trial the efficacy of 2 x 500 mg clarithromycin + 2 x 1000 mg amoxicillin + 40 mg pantoprazole/day given for 7 days (I. group, 48 cases), with that of 2 x 500 mg clarithromycin + 2 x 400 mg ranitidine bismuth citrate/day given for 14 days (II. group, 51 cases). The diagnosis of peptic ulcer was established endoscopically. HP infection was confirmed the modified Giemsa stain and rapid urease test. After eradication all patients were given 2 x 150 mg ranitidine for one month. Controls were performed 4-6 weeks after eradication. Peptic ulcer healing was proven in the group I in 93.0% and in the group II in 91.6% (p > 0.05). On intention-to-treat basis, HP was eradicated in 80.3% (confidence interval, CI: 73-92.7%) in the I. and 80.3% (confidence interval: 76-95%) in the II. group (p > 0.05). Per protocol analysis revealed eradication rates of 88.3% (CI: 81-97.6%) and 85.4% (CI: 80-97%) (p > 0.05). Side effects were recorded in 9.5% and 14.5% of the cases. Both regimens were equally effective in the eradication of HP and healing of peptic ulcers.     

Survey on Helicobacter pylori and peptic ulcer in Spain

OBJECTIVE: The goal of this study is to determine, through a national survey, the degree of acceptance among gastroenterologists of the relationship between Helicobacter pylori and peptic ulcer, and how they manage their patients according to this association. STUDY DESIGN: An observational study through a self-administered questionnaire. PARTICIPANTS: The questionnaire was distributed to 690 gastroenterologists from all over Spain. The questionnaire was answered by 687 specialists. RESULTS: Most (98.1%) Spanish specialists accept the relationship, 1.5% are reluctant, and 0.3% are irresolute. Eradication treatments are prescribed by 96.4% of the gastroenterologists, mainly omeprazole+amoxicillin, in 1994, though only 40.8% of gastroenterologists always prescribe it for H. pylori positive peptic ulcer. A control of the effectiveness of the treatment is undertaken by 84.3% of gastroenterologists. CONCLUSIONS: The relationship between H. pylori and ulcer is accepted by Spanish gastroenterologists, as well as eradication therapy.     

Helicobacter pylori infection and peptic ulcer disease in cirrhosis

An increased frequency of peptic ulcer disease is noted in patients with cirrhosis, but the role of H. pylori in this disorder remains to be determined. The diagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, and histological methods. The severity of cirrhosis was assessed by Pugh's modification of Child's criteria. Upper gastrointestinal endoscopy was performed consecutively to evaluate the presence of varices and gastroduodenal mucosa. H. pylori status was assessed by histology, urease test, and serology. In all, 130 patients with cirrhosis were recruited into the study; there were 86 males and 44 females with a mean (SD) age of 54.4 (12.7) years. The H. pylori prevalence was 76.2%. There was no difference in age between the H. pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no difference among cirrhotics with Child A (77.8%), Child B (72.9%), and Child C (78.6%) (P = 0.8), and neither was there a difference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs 73.7%, P = 0.84). The prevalence of H. pylori in cirrhotics with and without varices did not show a statistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pylori prevalence between cirrhotic patients with and without peptic ulcers (84.4% vs 69.7%, P = 0.09). In conclusion, the prevalence of H. pylori or peptic ulcer is independent of the severity of cirrhotic liver disease. The association between H. pylori infection and peptic ulcer disease is weak in cirrhosis.     

The impact of Helicobacter pylori eradication on peptic ulcer healing

OBJECTIVE: Current literature was reviewed analyzing the outcome of peptic ulcer healing in relation to the results of the posttherapeutic Helicobacter pylori (HP) status. METHODS: Literature was reviewed along with an analysis of 60 studies, comprising a total of 4329 patients. RESULTS: Successful Helicobacter pylori eradication was found to induce a better response in peptic ulcer healing, regardless of diagnosis: gastric ulcer 88% vs 73% (odds ratio [OR] 2.7, p < 0.01), duodenal ulcer 95% vs 76% (OR 5.6, p < 0.0001), and peptic ulcer 95% vs 76% (OR 6.6, p < 0.0001), for patients having their HP infection successfully cured versus those remaining HP-positive, respectively (Fisher's exact test). For all evaluated time points (< or = 6, 7-8, and 10-12 wk after beginning treatment), HP-negative patients had higher healing rates than HP-positive patients (95% vs 82%, 94% vs 69%, and 96% vs 78% with corresponding OR of 4.2, 6.5, and 7.4, all p < 0.0001, Fisher's exact test). The use of concomitant acid suppression therapy during initial HP eradication provided a benefit on peptic ulcer healing only for patients with persistent HP infection (improved healing rates of 78% vs 67%; otherwise rates were 94-96%). Likewise, prolonged acid inhibition in HP treatment failures after the initial HP treatment phase resulted in 7-20% improved healing rates, whereas patients becoming HP-negative did not profit. CONCLUSION: Successful HP eradication therapy accelerates peptic ulcer healing even without concomitant acid suppression.     

Effect of genetic differences in omeprazole metabolism on cure rates for Helicobacter pylori infection and peptic ulcer

We report a 65-year-old woman with thyrotropin (TSH) secreting pituitary adenoma, who was diagnosed based on the lack of inhibition of serum TSH despite an increased serum free thyroxine (T4), a low response of serum TSH to thyrotropin releasing hormone, and a pituitary tumor as revealed by magnetic resonance imaging. The pituitary adenoma was, however, inoperable due to chronic respiratory failure. The treatment with octreotide in a dose of 100 microg b.i.d. resulted in inhibition of serum TSH and free T4 to euthyroid levels and considerable shrinkage of the pituitary tumor. These effects were continued over 8 months after the start of octreotide therapy without any adverse effects. These findings add further evidence that octreotide is useful for treating inoperable TSH secreting pituitary adenoma.     

Helicobacter pylori in peptic ulcer disease: report of an NIH consensus conference

Preoperative electromyographic examinations of superior levator muscle were done in 36 ptotic patients using the Neurematic 2000 electromyograph. Shortening of the levator palpebrae superior was done through a combined internal and external route. In 12 patients of mild ptosis the spike voltage was all above 30 mv during contraction. When the spike voltage was above 100 mv, better operative results were obtained. In 24 patients whose ptosis was moderate or severe, the graphs of contraction generally showed simple phases with low amplitude. In 9 patients whose spike voltage was below 30 mv, their palpebral fissure did not reach the anticipated width after the operation. On the contrary, in 15 patients whose spike voltage was above 30 mv the operative results were satisfactory. It is concluded that in patients whose ptosis is moderate or severe, the operative procedure should be based on electromyographic examinations. If the spike voltage of the superior levator muscls is higher than 30 mv on contraction, simple shortening of the levator will be successful. If the spike voltage is lower than 30 mv and the graph presents simple phase or electro-tranquilization, then suspension of the frontalis muscle is preferable.     

Epidemiology of peptic ulcer disease in cirrhotic patients: role of Helicobacter pylori infection

OBJECTIVE: The aim of this study was to investigate the clinical and epidemiological factors associated with the appearance of peptic ulcer in patients with cirrhosis and, in particular, the role of Helicobacter pylori infection. METHODS: A total of 201 of 220 consecutive patients included in a prospective study that aimed to evaluate the effect of dietary intervention on cirrhotic complications and survival underwent upper gastrointestinal endoscopy. At entry, an epidemiological and clinical questionnaire was completed and the presence of peptic ulcer disease or esophageal varices at endoscopy was prospectively collected. Sera were obtained and stored at -70 degrees C until analyzed, being tested afterward for Helicobacter pylori antibodies using a commercial ELISA kit. RESULTS: Eleven of 201 patients had borderline anti-Helicobacter pylori IgG titers and were excluded from further analysis. In the remaining 190 patients, point prevalence of peptic ulcer was 10.5% and lifetime prevalence 24.7%. Multivariate analysis selected male sex (OR 2.3; 95%CI 1.09-4.89) and Helicobacter pylori seropositivity (OR: 1.7, 95%CI 1.02-2.81) as the variables independently related to peptic ulcer disease. CONCLUSIONS: Male sex and seropositivity for Helicobacter pylori are the major risk factors for peptic ulcer in cirrhosis.     

The impact of peptic ulcer disease and infection with Helicobacter pylori on life expectancy

OBJECTIVE: Knowledge about the influence of H. pylori-related disease on life expectancy might affect physician behavior in dealing with such disease. The aim of this study was to assess how life expectancy is influenced by H. pylori infection and peptic ulcer disease. METHODS: The declining exponential approximation of life expectancy was used to model the effects of H. pylori and various peptic ulcer disease conditions on life expectancy. Deaths from peptic ulcer and gastric cancer were determined from the Vital Statistics of the United States. H. pylori prevalence rates were derived from the existing literature. RESULTS: Cure of active peptic ulcer increases life expectancy by 2.3 yr in persons aged 40-44 yr and 121 days in persons aged 70-74 yr. More substantial impact occurs in complicated ulcer, with increases in life expectancy ranging between 26.1 and 6.3 yr. Primary prevention of H. pylori could increase life expectancy by 190 days in those aged 40-44 yr and 26 days in 70-74-yr-old subjects. CONCLUSION: The benefit of ulcer cure or H. pylori prevention diminishes as age advances. Cure of ulcers in young patients or in those who have sustained complications results in an appreciable increase in life expectancy. Successful primary prevention of H. pylori in selected populations could substantially increase life expectancy.     

Treatment of Helicobacter pylori reduces the rate of rebleeding in peptic ulcer disease

BACKGROUND: We evaluated whether therapy designed to eradicate Helicobacter pylori infection resulted in a reduction in rebleeding in patients with peptic ulcer disease. Patients presenting because of major upper gastrointestinal hemorrhage from peptic ulcer and whose ulcers healed in a study in which they were randomized to receive ranitidine alone or triple therapy plus ranitidine were followed up regularly with endoscopy. No maintenance anti-ulcer therapy was given after ulcer healing. METHODS: Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet), and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given. Development of ulcer recurrence with or without recurrent upper gastrointestinal bleeding was evaluated. RESULTS: Thirty-one patients with major upper gastrointestinal bleeding from peptic ulcer were studied; 17 received triple therapy and 14 ranitidine alone. Major rebleeding occurred significantly (p = 0.031) more often in those in the ranitidine group (28.6%), compared with none (0%) in the triple therapy group. CONCLUSION: Eradication of H. pylori infection reduces the rate of ulcer recurrence and rebleeding in complicated ulcer disease.     

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.     

High seroprevalence of Helicobacter pylori in active bronchiectasis

Helicobacter pylori causes chronic inflammation of the gastric mucosa and has been identified in tracheobronchial secretions. Serum IgG against H. pylori was therefore measured prospectively in consecutive subjects with bronchiectasis (n = 100; mean age +/- SD 55.1 +/- 16.7 yr), active pulmonary tuberculosis (n = 87; age, 57.3 +/- 19.1 yr), and healthy volunteers (n = 94; age, 54.6 +/- 7.6 yr). Seropositivity was found in 76.0% of bronchiectatic subjects, which was significantly higher than that of the control (54.3%, p = 0.001) and tuberculous (52.9%, p = 0.0001) groups. Multiple logistic regression, adjusted for age, sex, occupational social class, and number of persons living in the household, showed that H. pylori IgG levels of the bronchiectatic group were still significantly higher than that of the control (p = 0.0014) and tuberculous (p = 0.0154) groups. Multiple regression analysis revealed associations between H. pylori serology and sputum volume (p = 0.03) and age (p = 0.001) in the bronchiectatic patients, but not lung function indices or causes of bronchiectasis. The H. pylori seroprevalence in bronchiectasis was significantly (p = 0.0002) higher in patients who produced more (83.1%) than those who produced less than 5 ml sputum/24 h (58.6%). This is the first report of a high H. pylori seroprevalence in bronchiectasis which appears to be specific. Further studies are indicated to evaluate the possible pathogenic role of H. pylori in bronchiectasis.     

Lack of correlation between vacuolating cytotoxin activity, cagA gene in Helicobacter pylori, and peptic ulcer disease in children

To determine the prevalence of the cagA gene and vacuolating cytotoxin in Helicobacter pylori isolates obtained from children and to characterize the relationship between cagA, cytotoxin production, and ulcerogenesis, pediatric Helicobacter pylori isolates were tested for cagA by the polymerase chain reaction and for vacuolating cytotoxin by a cell culture assay. Helicobacter pylori isolates were obtained from 33 children referred for upper gastrointestinal endoscopy. Twenty-six of these isolates were tested for cagA by the polymerase chain reaction; all 26 (100%) were positive. Of the 26 children from whom these isolates were obtained, 26 (100%) had chronic gastritis and 12 (46%) had duodenal ulcers. Nine (30%) of 30 isolates tested showed expression of vacuolating cytotoxin, only three of which came from patients with duodenal ulceration (odds ratio 0.81, 95% confidence interval 0.1-5.3). Of the 23 cagA-positive isolates tested for cytotoxin, only nine (39%) were positive. There was no association between vacuolating cytotoxin and clinical symptoms, nor was cytotoxicity associated with ulcerogenesis. In summary, the findings suggest that cagA is not a marker of duodenal ulceration or of vacuolating cytotoxin production in children referred for endoscopy.     

Racial differences in fetal morphometry in Singapore

A systematic collection of fetal morphometric measurements was started seven years ago in 1987 with the prospective entry of data into personal computer-based stations in the Department of Obstetrics and Gynaecology, Singapore General Hospital. A cross-sectional study was done, comparing 2392 Chinese fetuses with 2117 Malay fetuses and 459 Indian fetuses from 18 to 40 weeks. The mean values of the head circumference (HC), abdominal circumference (AC) and femur length (FL) of the 3 ethnic groups were analysed. There were no statistical significant differences in the head circumference and abdominal circumference of Chinese, Malay and Indian fetuses in Singapore. The Chinese and Malay fetal femur length appeared similar but were apparently shorter than the Indian femur length. Nomograms of head circumference, abdominal circumference and femur length were constructed for application to fetuses of all 3 ethnic groups.     

Immediate eradication of Helicobacter pylori in patients with previously documented peptic ulcer disease: clinical and economic effects

The introduction of adenovirus 5 E1A into the SKOV3ip1 ovarian cancer cell line was shown previously to suppress HER2/neu expression and reduce the malignant potential of these cells (Yu et al., Cancer Res., 53: 891-898, 1993). In this report, we show that reduction of p185 in cells stably expressing E1A protein was coincident with increased sensitivity to cytotoxic agents. The LD50 of cisplatin was reduced 6-fold, and the LD50 of paclitaxel and doxorubicin was reduced 10-fold in E1A-expressing cells compared with control cells. The growth of SKOV3ip1 and control cells was unchanged in the presence of 150 ng/ml of tumor necrosis factor-alpha, whereas the growth of E1A-expressing cells was reduced by 30 to 40%. When we used a physiologically obtainable concentration of paclitaxel (0.5 microM), DNA laddering consistent with apoptotic cell death was seen after a 24-h exposure in the E1A-expressing cells, whereas laddering and DNA fragmentation were only detected in DNA from control cells after longer exposure (48 h) at a 20-fold higher concentration of paclitaxel. The SKOV3ip1 cells do not express p53 protein; hence, the induction of apoptosis by paclitaxel is through a p53-independent pathway. Despite their diverse mechanisms of action, the cytotoxic effects of cisplatin, doxorubicin, paclitaxel, and tumor necrosis factor-alpha were enhanced by the expression of E1A proteins in the SKOV3ip1 ovarian cancer cells. This suggests that these agents share a common final pathway of cell killing, which may represent a potential therapeutic target in resistant ovarian cancers.