Prevalence of Peptic Ulcer in Dyspeptic Patients and the Influence of Age,Sex, and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

We investigated the prevalence of peptic ulcer in dyspeptic patients in China to analyze the influence of age, sex, and Helicobacter pylori (H. pylori) infection. The results showed that the prevalence of gastric and duodenal ulcer increased with age. In patients under 60 years old, the prevalence of duodenal and gastric ulcers in females was markedly lower than that in males, especially the prevalence of duodenal ulcer. The prevalence of duodenal ulcer and gastric ulcer in H. pylori-infected patients was markedly higher than in patients without H. pylori infection. In the patients under 60 years old, sex differences were still seen in both H. pylori-positive and H. pylori-negative patients. The prevalence of gastric and duodenal ulcers was markedly increased with age in both H. pylori-positive and H. pylori-negative patients. Multivariate logistic regression analysis showed that age, male sex, and H. pylori infection were three independent risk factors for gastric and duodenal ulcers.     

Acid peptic disease in the elderly.

Research in epidemiology and related fields highlights three factors contributing to a high prevalence of complications of ulcer disease in the elderly, namely anti-inflammatory drugs (aspirin and NSAIDs), type B gastritis due to H. pylori infection, and smoking; these factors also increase the prevalence of both GU and DU. The major dangers with ulcer disease arise from continued exposure to the causative risk factors, absent or insidious symptoms, difficulties in diagnosis, late presentations, high rates of complications (often the presenting features), high preoperative and perioperative mortality, and serious postoperative morbidity (especially in smokers). Empiric therapy and the use of diagnoses such as nonulcer dyspepsia invite additional hazards. Once diagnosed and adequately treated, ulcers in the elderly behave similarly to those in younger subjects matched for risk factors, and they respond well to treatment. In high-risk elderly patients without previous or active ulcer disease, misoprostol may be used to prevent gastric ulcers; other benefits of the drug await clarification. In those with previous or active ulcer disease, H2-antagonists given long-term in higher doses appear preferable. Side effects of antiulcer drugs are rarely serious and are easily managed by dose reductions or changes in products. The major benefits to the management of ulcers in the elderly come from increased vigilance on the part of physicians.     

Helicobacter pylori, non-steroidal anti-inflammatory drugs and smoking in risk pattern of gastroduodenal ulcers

BACKGROUND: Helicobacter pylori, NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. METHODS: 5967 dyspeptic patients underwent 13C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. RESULTS: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. CONCLUSIONS: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Should we eradicate Helicobacter pylori infection in patients receiving nonsteroidal anti-inflammatory drugs or low-dose aspirin?

Whether Helicobacter pylori infection alters the risk of ulcer disease in patients receiving nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin is one of the most controversial topics in peptic ulcer research. This is an important management issue, particularly in countries where peptic ulcer disease is common and the prevalence of H. pylori infection is high. Current evidence shows that H. pylori infection increases the ulcer risk associated with NSAIDs or low-dose aspirin. Eradication of H. pylori reduces the subsequent risk of endoscopic and complicated ulcers in patients who are about to start long-term NSAIDs. Among patients with H. pylori infection and a history of ulcer bleeding who continue to use low-dose aspirin, 1 week of eradication therapy prevents recurrent ulcer bleeding. Failure of eradication and concomitant use of NSAIDs, however, account for most cases of recurrent bleeding with low-dose aspirin. The apparent protective effect of H. pylori in long-term NSAIDs users reported in some studies was actually the weeding out of susceptible patients who were intolerant to NSAIDs. There is no convincing evidence that eradication of H. pylori has any clinically important adverse effect on the healing and prevention of ulcers in NSAIDs users.     

Helicobacter pylori,Non-steroidal Anti-inflammatory Drugs and Smoking in Risk Pattern of Gastroduodenal Ulcers

Background: Helicobacter pylori , NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. Methods: 5967 dyspeptic patients underwent 13 C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. Results: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. Conclusions: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Peptic ulcer bleeding: interaction between non-steroidal anti-inflammatory drugs, Helicobacter pylori infection, and the ABO blood group system

BACKGROUND: Helicobacter pylori infection is found in almost all patients with an uncomplicated ulcer. Non-steroidal anti-inflammatory drug (NSAID) use is the main risk factor for bleeding peptic ulcer. In the older literature ABO blood groups were mentioned as a risk factor. There is continuing uncertainty about the interaction between these risk factors and the development of peptic ulcer bleeding. We therefore determined the separate and combined effect of NSAIDs, H. pylori infection, and the ABO blood group system in patients with a bleeding peptic ulcer. METHODS: The prevalence of NSAID use, H. pylori infection, and blood group O was determined in 227 patients who were admitted with a bleeding gastric or duodenal ulcer between 1990 and 1997. These results were compared with the expected frequency of these risk factors in the Dutch population. RESULTS: NSAID use was reported in 48.2% of the patients with a bleeding peptic ulcer. The H. pylori prevalence was 62.0%, whereas blood group O was present in 49.3% of the patients. NSAID use was the strongest risk factor for hemorrhage caused by a peptic ulcer (relative risk, 8.4), whereas the relative risk associated with H. pylori infection and blood group O was 1.5 and 1.2, respectively. With univariate analysis NSAID use and H. pylori infection seemed to be separate risk factors and did not really potentiate each other's effect. Moreover, blood group O did not potentiate the strong effect of NSAIDs. CONCLUSION: H. pylori infection may add only a little to the important risk of NSAID use in the development of bleeding peptic ulcers.     

Relationship between non-steroidal anti-inflammatory drug use and Helicobacter pylori infection in bleeding or uncomplicated peptic ulcers: A case-control study

BACKGROUND AND AIMS: Non-steroidal anti-inflammatory drug (NSAID) use has been closely associated with an increased risk of bleeding peptic ulcers, while the prevalence of Helicobacter pylori infection has been reported to be lower in bleeding ulcers than in non-bleeding ones. However, whether an interaction exists between NSAID use and H. pylori infection has not clearly been elucidated yet. The aims of this study were to determine the frequency of NSAID use and H. pylori infection, to predict risk factors in bleeding peptic ulcers and to determine whether NSAID use and H. pylori infection interact with each other. METHODS: Ninety-six patients with bleeding ulcer were included in the study. The control group consisted of 106 patients with non-bleeding ulcer. Data were analyzed by using the chi-squared test, Fisher's exact test and logistic regression analysis with or without interaction term (H. pylori by NSAID). RESULTS: Non-steroidal anti-inflammatory drug use was significantly more common in patients with bleeding ulcers than in controls (79.2 vs 38.7%, unadjusted odds ratio (OR): 6.02, 95% confidence interval (CI): 3.21-11.29). The frequency of the H. pylori infection was significantly lower in patients with bleeding ulcers than in controls (66.7 vs 89.6%, unadjusted OR: 0.23, 95% CI: 0.10-0.49). In the logistic regression analysis with the interaction term, male sex (adjusted OR: 3.70, 95% CI: 1.65-8.29), multiplicity of ulcers (adjusted OR: 4.10, 95% CI: 1.02-16.45) and NSAID use (adjusted OR: 33.87, 95% CI: 4.36-262.97) were independent risk factors for bleeding ulcers. There was a negative interaction between H. pylori and NSAID use (adjusted OR: 0.09, 95% CI: 0.01-0.83). CONCLUSIONS: The negative interaction between the two variables suggests that the presence of H. pylori is associated with a lower risk of bleeding in ulcer patients taking NSAIDs.     

Preventing hospital-acquired pressure ulcers: a point prevalence study

The deleterious effects of mechanical forces on the development of pressure ulcers have been recognized for many years. A cross-sectional study was conducted to ascertain the effect of implementing a new support surface on the development of pressure ulcers in one acute care facility. Two pressure ulcer prevalence studies were conducted using the Pressure Ulcer Prevalence Audit Data Collection Tool. To ascertain whether ulcers were facility-acquired, a retrospective chart review was completed for all patients with pressure ulcers. Following completion of the first audit, only the support surface used for at-risk patients was changed. The second audit was conducted 3 months after the new support surface was implemented. Pressure ulcer prevalence was 8.3% in June 1999 and 7.8% in October 2000; whereas, the prevalence of nosocomial pressure ulcers was 5.5% in 1999 and 3.1% in October 2000. Despite the inherent limitations of this study design, the results suggest that use of the new support surfaces for at-risk patients has lowered the prevalence of nosocomial pressure ulcers in this facility.     

Epidemiology of peptic ulcer disease

In the United States about four million people have active peptic ulcers and about 350,000 new cases are diagnosed each year. Four times as many duodenal ulcers as gastric ulcers are diagnosed. Approximately 3000 deaths per year in the United States are due to duodenal ulcer and 3000 to gastric ulcer. There has been a marked decrease in reported hospitalization and mortality rates for peptic ulcer in the United States. Changes in criteria for selecting the underlying cause of death might account for some of the apparent decrease in ulcer mortality rates. Hospitalization rates for duodenal ulcers decreased nearly 50 per cent from 1970 to 1978, but hospitalization rates for gastric ulcers did not decrease. Although this decrease in hospitalization rates may reflect a decrease in duodenal ulcer disease incidence, it appears that changes in coding practices, hospitalization criteria, and diagnostic procedures have contributed to the reported declines in peptic ulcer hospitalization and mortality rates. There is no good evidence to support the popular belief that peptic ulcer is most common in the spring and autumn. The most consistent pattern appears to be low ulcer rates in the summer. There is strong evidence that cigarette smoking, regular use of aspirin, and prolonged use of steroids are associated with the development of peptic ulcer. There is some evidence that coffee and aspirin substitutes may affect ulcers, but most studies do not implicate alcohol, food, or psychological stress as causes of ulcer disease. Genetic factors play a role in both duodenal and gastric ulcer. The first-degree relatives of patients with duodenal ulcer have a two- to threefold increase in risk of getting duodenal ulcer and relatives of gastric ulcer patients have a similarly increased risk of getting a gastric ulcer. About half of the patients with duodenal ulcer have elevated plasma pepsinogen I. A small increase in risk of duodenal ulcer is found in persons with blood group O and in subjects who fail to secrete blood group antigens into the saliva. In most Western countries, morbidity from duodenal ulcer is more common than from gastric ulcer, even though deaths from gastric ulcer exceed or equal those from duodenal ulcer. In Japan, both morbidity and mortality are higher for gastric ulcer than for duodenal ulcer.     

Gastroprotective therapy and risk of gastrointestinal ulcers: risk reduction by COX-2 therapy

OBJECTIVE: Proton pump inhibitors (PPI) and misoprostol decrease the risk of development of nonsteroidal antiinflammatory drug induced gastric ulcers and aid healing of upper gastrointestinal (GI) ulcers. H2 receptor antagonists (H2RA) are less effective for this task, but are widely used by patients and physicians for the treatment of GI symptoms and duodenal ulcers. Sucralfate is a weaker agent that is sometimes used for prophylaxis or treatment of upper GI ulcers. We investigated the effect of GI drugs and selective and nonselective NSAID on the incidence of GI ulcer development in a cohort of patients immediately after the release of celecoxib and rofecoxib to investigate the effect of confounding by indication when effective GI agents and cyclooxygenase 2 (COX-2)-specific inhibitors are prescribed to a high risk population. METHODS: During a 6 month period of observation 8547 NSAID users were evaluated by mailed questionnaire concerning NSAID drug use and ulcer development. In the first half of 1999, patients took 12,177 separate NSAID courses. GI therapy that followed the development of upper GI ulcers was excluded from analysis. Ulcer reports were confirmed by followup validation. RESULTS: GI drugs were used concomitantly in this population by 42% of patients using an NSAID. GI drugs were associated with an increased risk of ulcer. But this risk was confined to PPI (OR 4.1, 95% CI 2.95, 5.69), and not to other GI drugs. Overall, patients using nonselective NSAID compared to those taking COX-2-specific inhibitors had an increased risk of upper GI ulcers (OR 2.12, 95% CI 1.43, 3.34). Patients taking nonselective NSAID plus PPI were also at increased risk for upper GI ulcers compared to those taking nonselective NSAID alone (OR 5.09. 95% CI 3.88, 6.67). Similarly, the risk of upper GI ulcers was increased in the nonselective NSAID plus PPI group (OR 3.83, 95% CI 2.32, 6.31) compared to the COX-2 plus PPI group. CONCLUSION: PPI use, but not other GI drug use, is a marker for increased susceptibility to ulcers among NSAID users. This risk of upper GI ulcers is increased in PPI users regardless of which NSAID is used (nonselective or COX-2-specific inhibitor). Although COX-2 use is associated with greater risk factors for upper GI ulcers due to channeling bias, COX-2 users have significantly fewer ulcers than equivalent nonselective NSAID users regardless of concomitant PPI utilization.     

Who needs prophylaxis of nonsteroidal anti-inflammatory drug-induced ulcers and what is optimal prophylaxis?

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used successfully by many patients for the treatment of the signs and symptoms of arthritis, and other painful and inflammatory disorders. However, traditional nonselective NSAIDs that inhibit COX-1 and COX-2 lead to a state of propensity for gastric and duodenal ulcer disease and ulcer complications. The point prevalence of endoscopic ulcers ranges from 14 to 44% of patients using NSAIDs. Moreover, it is estimated that 1.46-1.90% of chronic NSAID users develop serious upper gastrointestinal (UGI) toxicity annually, most notably UGI bleeding, gastric/duodenal obstruction or ulcer perforation. In the USA, it has been estimated that 107,000 hospitalisations and 16,500 deaths occur annually related to the use of nonselective NSAIDs. Because these ulcer complications are often not heralded by chronic symptoms of dyspepsia, symptoms alone are not sufficient to guide long-term management of NSAID-related toxicity. Instead, prophylactic and preventive therapies are recommended in patients at above-average and high risk. Epidemiological data have identified that patients with a past history of ulcer disease, past history of UGI bleeding, greater age, concomitant corticosteroid use, and those who use higher doses and multiple NSAIDs fall into this category. Other risk factors of lesser importance have also been identified. A controversial issue remains regarding the possible increased risk of NSAID-associated ulcers and ulcer complications in patients who are infected with Helicobacter pylori. Prophylactic therapies have been evaluated primarily in randomised clinical trials, with the rate of endoscopic ulcers as the primary endpoint. It is assumed, but not proven, that these endoscopic ulcer rates are surrogate markers for gastrointestinal toxicity and are predictive of the rate of significant UGI adverse events. In the only outcomes trial to date, it was reported that misoprostol (200 microg 4 times daily) caused an approximately 50% reduction in serious UGI adverse events in a large 6-month trial involving rheumatoid arthritis patients. In parallel, this approximates the 50% reduction of endoscopic ulcers seen in randomised controlled trials using misoprostol. While H2 receptor antagonists are ineffective agents at traditional doses, proton pump inhibitors have been clearly shown to reduce the rate of endoscopic ulcers in several trials. In fact, the efficacy approximates to the efficacy seen with misoprostol. Beyond efficacy and in practical terms, the choice of optimal prophylaxis should take into consideration patient compliance, patient satisfaction, side-effects and cost.     

Diabetic foot ulcers: a quality of life issue

Foot ulcers are a serious complication of diabetes mellitus that are associated with adverse sequelae and high costs. In addition, such foot ulcers have a significant impact on quality of life (QoL). For example, the loss of mobility associated with foot ulcers affects patients' ability to perform simple, everyday tasks and to participate in leisure activities. These and other consequences of foot ulcers often lead to depression and poor QoL. Notably, several studies have shown that patients with diabetes mellitus and foot ulcers were more depressed and had poorer QoL than those who had no diabetic complications. Given the detrimental effect foot ulcers have on patients, it is essential that these foot ulcers are prevented or treated more effectively than at present. Evidence suggests that many foot ulcers can be prevented by using intensive interventions and adopting a multidisciplinary approach to treatment. In addition, preventative strategies may become more effective if new research into how patients with diabetes experience and interpret their health threats (e.g. diagnosis ‘loss of sensation’ or a foot ulcer episode) is taken into account. With regard to treatment, new options should enable ulcers to heal more quickly than with standard therapies. One area of interest is the use of growth factors. For example, recombinant platelet‐derived growth factor, in addition to good ulcer care, has been shown to improve the number of ulcers that heal and healing times significantly compared with good ulcer care alone. Other potential new treatments include the use of skin substitutes. In summary, improved preventative measures and wound treatment should reduce the potential for patients with diabetes mellitus to experience impaired QoL caused by foot ulcers. Copyright © 2001 John Wiley & Sons, Ltd.     

Epidemiology and treatment of gastroduodenal lesions caused by non-steroidal anti-inflammatory agents

The most common serious adverse reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) are those affecting the gastro-intestinal tract. There is epidemiologic evidence that NSAIDs use is associated with the development of gastric ulcer and with upper gastrointestinal bleeding and perforation of both duodenal and gastric ulcers. The individual risk is low but given the widespread use of NSAIDs, the number of cases is large with appreciable morbidity and mortality. The main risk factors are age above 65, previous ulcer history and treatment with several NSAIDs. Prophylactic therapy is justified in high risk patients. Synthetic prostaglandin misoprostol has been shown to reduce significantly the frequency of gastric ulcer in patients on NSAIDs. By contrast, H2 receptor blockade with ranitidine has been demonstrated to prevent duodenal but not gastric ulcers. Gastric and duodenal ulcers associated with NSAIDs appear to heal on H2 receptors antagonists and prostaglandins even if NSAIDs are continued. However, large gastric ulcer may heal slowly over 8 to 12 weeks. The place of omeprazole remains to be determined.     

Management of NSAID-associated peptic ulcer disease

Non-steroidal anti-inflammatory drug (NSAID) use increases the risk of gastrointestinal complications such as ulcers or bleeding. The presence of factors like advanced age, history of peptic ulcer, Helicobacter pylori infection and the use of anticoagulants or antiplatelet agents increase this risk further. COX-2 inhibitors and antisecretory drugs, particularly proton pump inhibitors, help to minimize the risk of gastrointestinal complications in high-risk patients. This review presents a practical approach to the prevention and treatment of NSAID-associated peptic ulcer disease and examines the new advances in the rational use of NSAIDs.     

Peptic ulcer at the end of the 20th century: biological and psychological risk factors.

The prevailing concept of peptic ulcer etiology has swung over entirely in just a few years from the psychological to the infectious, yet the rich literature documenting an association between psychosocial factors and ulcer is not invalidated by the discovery of Helicobacter pylori. Physical and psychological stressors interact to induce ulcers in animal models, concrete life difficulties and subjective distress predict the development of ulcers in prospective cohorts, shared catastrophes such as war and earthquakes lead to surges in hospitalizations for complicated ulcers, and stress or anxiety can worsen ulcer course. Many known ulcer risk factors, including smoking, nonsteroidal anti-inflammatory drug use, heavy drinking, loss of sleep and skipping breakfast, can increase under stress; the association of low socioeconomic status with ulcer is also accounted for in part by psychosocial factors. Among possible physiological mechanisms, stress may induce gastric hypersecretion, reduce acid buffering in the stomach and the duodenum, impair gastroduodenal blood flow, and affect healing or inflammation through psychoneuroimmunological mechanisms. Psychosocial factors seem to be particularly prominent among idiopathic or complicated ulcers, but they are probably operative in run of the mill H pylori disease as well, either through additive effects or by facilitating the spread of the organism across the pylorus, while gastrointestinal damage by nonsteroidal anti-inflammatory drugs can also be potentiated by stress. Although the clinical importance of peptic ulcer is fading along with the millennium, due to secular trends and new therapies, it remains worthy of study as a splendid example of the biopsychosocial model.     

Peptic Ulcer Bleeding: Interaction between Non-Steroidal Anti-Inflammatory Drugs,Helicobacter pylori Infection,and the ABO Blood Group System

Background: Helicobacter pylori infection is found in almost all patients with an uncomplicated ulcer. Non-steroidal anti-inflammatory drug (NSAID) use is the main risk factor for bleeding peptic ulcer. In the older literature ABO blood groups were mentioned as a risk factor. There is continuing uncertainty about the interaction between these risk factors and the development of peptic ulcer bleeding. We therefore determined the separate and combined effect of NSAIDs, H. pylori infection, and the ABO blood group system in patients with a bleeding peptic ulcer. Methods: The prevalence of NSAID use, H. pylori infection, and blood group O was determined in 227 patients who were admitted with a bleeding gastric or duodenal ulcer between 1990 and 1997. These results were compared with the expected frequency of these risk factors in the Dutch population. Results: NSAID use was reported in 48.2% of the patients with a bleeding peptic ulcer. The H. pylori prevalence was 62.0%, whereas blood group O was present in 49.3% of the patients. NSAID use was the strongest risk factor for hemorrhage caused by a peptic ulcer (relative risk, 8.4), whereas the relative risk associated with H. pylori infection and blood group O was 1.5 and 1.2, respectively. With univariate analysis NSAID use and H. pylori infection seemed to be separate risk factors and did not really potentiate each other's effect. Moreover, blood group O did not potentiate the strong effect of NSAIDs. Conclusion: H. pylori infection may add only a little to the important risk of NSAID use in the development of bleeding peptic ulcers.     

Upper gastrointestinal complications induced by anti-platelet agents

Low-dose aspirin and thienopyridine are associated with gastrointestinal (GI) complications such as petechiae, erosion, ulcer, bleeding, and perforation. The incidence of GI bleeding in aspirin study groups was 0.82 % in the hypertension optimal treatment (HOT) study and 0.76 % in the primary prevention project (PPP) study. On the other hand, the incidence of GI bleeding by endoscopic evaluation was higher than in an observational study. In a study of 187 patients receiving low-dose aspirin for prevention of cardiovascular disease, the prevalence of endoscopically detected GI ulcers was 11 % (95 % CI 6.3–15.1 %). Several risk factors for GI bleeding (history of peptic ulcer or GI bleeding, high aspirin dose, concomitant use of non-steroidal anti-inflammatory drugs and anti-platelet agents, advanced age and Helicobacter pylori infection) were reported for patients receiving aspirin. Prevention strategies for GI complications induced by anti-platelet agents are treatment with proton pump inhibitors, histamine-2 receptor antagonists, prostaglandin analogs, prostaglandin inducers and H. pylori eradication therapy. Further investigation is necessary to identify the strategies which are suitable for Japan.     

Pressure ulcers among patients admitted to home care

CONTEXT: Pressure ulcers are an understudied problem in home care. OBJECTIVE: To determine the prevalence of pressure ulcers among patients admitted to home care services, describe the demographic and health characteristics associated with pressure ulcers in this setting, and identify the percentage of these patients at risk for developing pressure ulcers. DESIGN: Cross-sectional survey of patients on admission to home care agencies. SETTING: Forty-one home care agencies in 14 states. PATIENTS: A consecutive sample of 3,048 patients admitted March 1 through April 30, 1996 (86% of all admissions). Subjects had a mean age of 75 years; 63% were female and 85% white. MAIN OUTCOME MEASURES: Demographic, social, and clinical characteristics, functional status (Katz activities of daily living scale and Lawton instrumental activities of daily living scale), mental status (Katzman Short Memory-Orientation-Concentration test), pressure ulcer risk (Braden Scale), pressure ulcer status (Bates-Jensen Pressure Ulcer Status Tool), and a checklist of pressure-reducing devices and wound care products being used. RESULTS: In the total sample of 3,048 patients, 9.12% had pressure injuries: 37.4% had more than one ulcer and 14.0% had three or more ulcers. Considering the worst ulcer for each subject, 40.3% had Stage II and 27% had Stage III or IV injuries. Characteristics associated with pressure ulcers included recent institutional discharge, functional impairment, incontinence, and having had a previous ulcer. About 30% of subjects were at risk for new pressure ulcers. Pressure-relieving devices and other wound care strategies appeared to be underutilized and often indiscriminately applied. CONCLUSIONS: There is substantial need for pressure ulcer prevention and treatment in home care settings.