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Decreasing prevalence combined with increasing eradication of Helicobacter pylori infection in the United States has not resulted in fewer hospital admissions for peptic ulcer disease-related complications
Abstract
Helicobacter pylori infection is a major cause of peptic ulcer disease, but the prevalence of this infection has been decreasing steadily. Additionally, eradication of H. pylori decreases ulcer recurrence and prevents ulcer complications such as bleeding.
To examine whether the decreased prevalence of H. pylori and increased use of eradication regimens have affected the prevalence of peptic ulcer disease-related hospitalizations.
We chose to study a period between 1996 and 2005. The number of gastric and duodenal ulcers as primary or secondary hospital discharge diagnoses per year for the 10-year span was collected from five large US hospitals. Collected data were analysed using Spearman correlation.
No statistically significant trend was observed in the number of gastric or duodenal ulcers listed as primary or secondary discharge diagnoses at any of the five healthcare centres.
Despite a decreasing prevalence of H. pylori and the increasing use of successful H. pylori eradication regimens, the prevalence of peptic ulcer disease and its complications has not changed. In the US other aetiologies, including non-steroidal anti-inflammatory drugs, may be playing a larger role than once thought.
... In the US, HP infection mainly affects older adults (~50% of those aged >60 years compared to 20% of those aged <40 years), particularly those with low economic resources. 40,41 However, other factors that may influence peptic ulcer risk in infected subjects are the amount of gastric acid production, the presence of gastric metaplasia in the duodenal bulb, smoking, and genetic factors. 1,8,29,38 The most common ulcer-associated symptoms are nausea, epigastric discomfort, and ulcer pain. ...
... [43][44][45] Nevertheless, compared to infection with a cagA-negative strain, infection with a cagA-positive strain may increase the risk of cancer by ~2-3 times. 1,39,40 In this investigation, the prevalence of HP infection associated with GI cancer was 2.4%, 2.0%, 4.6%, 1.9%, and 6.5% for the white, black, Hispanic, API, and NA/AN populations, respectively. However, the prevalence of GI cancer in patients with HP infection varies across studies. ...
Background
In the US, neither the prevalence nor the gastrointestinal (GI) diagnosis/symptoms associated with Helicobacter pylori (HP) have been examined in different racial/ethnic groups.
Aim
To determine the racial/ethnic differences in HP infection associated with GI diagnoses/symptoms using the Cerner Health Facts® database.
Methods
This cross-sectional study collected data during the period of 2000–2015 from the following ethnic/racial groups: 8,236,317 white, 2,085,389 black, 426,622 Hispanic, 293,156 Asian Pacific/Islander (APIs), and 89,179 Native American/Alaskan Native (NA/AN) patients aged 21–65 years old; the data were then analyzed. The primary dependent variable was a diagnosis of HP (ICD-9-Clinical Modification/ICD-10 classification). SAS version 9.4 was used for the statistical analysis. The statistical analysis was performed on 11,130,663 patients with GI symptoms, and of these, 152,086 patients were positive for the infection.
Results
Hispanics and NA/ANs had the highest prevalence of HP associated with upper GI symptoms/diagnosis. Nevertheless, blacks and APIs presented the highest relative risk (RR) of HP associated with dyspepsia (RR [95% CI] =11.2 [10.7–11.9] and 14.2 [12.8–15.6]), peptic ulcer (RR =13.8 [13.3–14.5] and 10.7 [9.3–12.3]), and atrophic gastritis (RR =9 [8.5–9.6] and 7.4 [6.4–8.5]), respectively. In all racial/ethnic groups, HP was also associated with inflammatory bowel diseases, liver diseases, and celiac diseases.
Conclusion
Black and API populations had the highest risk of HP associated with upper GI symptoms/diagnosis. Black patients also had the highest risk for HP associated with GI cancer.
... Uncomplicated PUD has a lower incidence because of the effective eradication regimens for H. pylori; however, an increasing incidence of the complications related to PUD has been observed [17]. Most of these complications have been attributed to the frequent use of NSAIDs in the US [18]. The most common complication encountered in our study was hemorrhage (84%) mostly in the gastric region (54%). ...
... A study suggested that smoking was more common in winters [27]. Other less obvious contributing factors may be due to the presence of concomitant diseases such as Crohn's disease, Zollinger-Ellison syndrome [18]. Alcohol and caffeine consumption may also contribute, but their association with the seasons is weakly linked and requires further studies. ...
Background
Peptic ulcer disease (PUD) is a major public health burden significantly impacting the cost of hospitalization in the United States (US). We examined the trends, characteristics, complications, cost, and seasonality of PUD-related hospitalizations from 2000 to 2011.
Methods
With the use of the Nationwide Inpatient Sample from 2000 through 2011, we identified PUD-related hospitalizations using the International Classification of Diseases (ICD-9), 9th Revision, and the Clinical Modification code 531.00 to 534.91 as the principal discharge diagnosis. The total number of hospitalizations for each calendar month of the year were added over a 12-year period, and this number was divided by the number of days in that particular month to obtain the mean hospitalizations per day for each month.
Results
The study found that 351,921 hospitalizations with the primary discharge diagnosis of peptic ulcer disease (PUD) occurred in the US between 2000 and 2011. This number dropped significantly from 49,524 to 17,499 between 2000 and 2011, and the rate of PUD-related mortality decreased from 4.3% to 3.1%. The mean age of the study population was 66.2 ± 17.4 years; 52.3% were males, and 56.8% were white. The number of hospitalizations in the US peaked in the spring season (916/day), and reached a nadir in the fall season (861/day). The mean cost of PUD hospitalization increased significantly from $11,755 in 2001 to $13,803 in 2011 (relative increase of 17%; p <0.001).
Conclusion
The incidence of PUD and its mortality has decreased significantly in the last decade, but its economic burden on the healthcare system remains high. A seasonal pattern of PUD hospitalization showed a peak in PUD-related admissions in the spring season and a trough in the fall season.
... Peptic ulcer (PU), as a common disease, has been decreasing according to the recent reports with the treatment of Helicobacter pylori (H.pylori) eradication [1] . Nevertheless, this decreasing prevalence has "not resulted fewer hospital admissions for peptic ulcer disease-related complication" [2] . Duodenal ulcer (DU), as the most common form of this disease, is still prevalent with a high incidence and frequently in China [3,4] . ...
... The free ends of the electrodes were brought subcutaneously to the back of the neck where the skin and muscle were opened for 0.5 cm [27] . Some rats were randomly made models that duodenal bulb was contacted by glass tube covered with 50% ethylic acid and others were contacted instead of normal saline for 30 s before electrodes were implanted [2] . After the operation, they were individually housed with free access to water after a day and food after 2 days. ...
AIM: To investigate effects of Saussurea lappa (S.lappa) on rat chronic duodenal ulcer induced by ethylic acid and the underlying mechanisms.
METHODS: Wistar rat chronic duodenal ulcer was patterned according to Okabe model while two pairs of bipolar stainless steel electrodes were implanted onto the serosal layer of gastrointestinal tract. Then, the rats were treated with water, Omeprazole, diverse-dose S.lappa for 10 days. Gastrointestinal motility, intestine propulsion and duodenal ulcer crater were detected. Expressions of cholecystokinin and motilin in duodenum were detected by immunohistochemistry (IHC). Motilin serum level was measured with enzyme-linked immunosorbent assay (ELISA).
RESULT：Duodenal ulcer group rats had obvious disorders of gastrointestinal motility and brain-gut peptide secretion, including gastrointestinal myoelectric activity inhibition, migrating myoelectric complex (MMC) interruption, intestinal propulsion slowdown, cholecystokinin and motilin secretion decrease. Similarity to Omeprazole, S.lappa accelerated the coalescence of ethylic acid–induced duodenal ulcer significantly (p<0.01, vs model group), but no obvious dose-dependent effect was found. S.lappa also improved gastrointestinal myoelectric activity and accelerated intestinal propulsion. Furthermore, S.lappa could increase the expression levels of cholecystokinin and motilin in duodenum and increase motilin level in serum.
CONCLUSION：S.lappa can accelerate the coalescence of chronic duodenal ulcer, and increase gastrointestinal myoelectric activity and the expression of cholecystokinin and motilin in duodenum.
... The trend of upper gastrointestinal bleeding (UGIB) has been on a gradual decline recently. [1][2][3] However, UGIB remains a frequent symptom that prompts visits to the emergency room. Advancements in endoscopic hemostatic procedures, use of proton pump inhibitors, and eradication therapy of Helicobacter pylori infection have considerably improved the treatment of UGIB. ...
... Also in peptic ulcer patients, ulcer recurrences as well as ulcer bleeding and rebleeding rates are rare following successful eradication of H. pylori, which can be achieved in over 90% of patients with peptic ulcer [17,18]. However, despite a decreasing incidence of H. pylori infection and the widespread use of successful H. pylori eradication regimens, peptic ulcer disease remains the most common cause of AUGIB [19]. Guo et al in a previously published study on the reduction in peptic ulcer disease-related hospitalizations from 2005 to 2014 in USA found that the rate of decline decreased from -7.2% per year before 2008 to -2.1% per year after 2008 [20]. ...
Background:
Acute upper gastrointestinal bleeding (AUGIB) remains a common medical emergency with considerable morbidity and mortality. The aim of this study was to describe the patient characteristics, diagnoses and clinical outcomes of patients presenting with AUGIB nowadays and compare these with those of patients 15 years ago.
Methods:
This was a single-center survey of adults (> 16 years) presenting with AUGIB to a tertiary hospital. Data from 401 patients presenting with AUGIB in a tertiary hospital between January 1, 2019 and December 31, 2020 were analyzed and compared with data from 434 patients presenting with AUGIB at the same hospital between January 1, 2004 and December 31, 2005.
Results:
Nowadays, patients were older, mean age was 69.5 (± 15.4) vs. 66.2 (± 16.0) years, they had more frequently coexisting diseases (83.5% vs. 72.8%), especially cardiovascular diseases (62.3% vs. 52.5%), and more individuals were inpatients at onset of bleeding (8.2% vs. 4.1%). In addition, more patients were under anticoagulants (18.5% vs. 6.2%), but less were under acetylsalicylic acid ± clopidogrel (36.9% vs. 33.9%). Carlson Comorbidity Index was higher nowadays (5.6 ± 6.4 vs. 3.4 ± 2.3). Moreover, a peptic ulcer was less frequently found as the cause of bleeding (38.4% vs. 56.9%), while more often nowadays endoscopy was negative (12.7% vs. 3.5%). In patients with peptic ulcer, active bleeding on endoscopy was less frequent (7.1% vs. 14.2%). Also, bleeding spots requiring hemostasis were less common on endoscopy (39.6% vs. 49.4%) and more patients were without spots of recent bleeding (49.4% vs. 38.9%). Finally, the rate of rebleeding statistically decreased (7.8% vs. 4.2%), while overall mortality remained relatively unchanged (5.0% vs. 6.2%).
Conclusions:
AUGIB episodes nowadays are less severe with less peptic ulcer bleeding, but the patients are older and with more comorbidities.
... 5,6 Despite this, the incidence of PUD is increasing in the elderly population, mainly due to increasing use of NSAIDs or aspirin. 7 In addition, gastric mucosal defense mechanism in the elderly might be damaged and vulnerable to injury caused by NSAIDs or aspirin use, resulting in increased mortality due to complications of PUD. 8,9 Therefore, a strategy to reduce complications of PUD is very important. ...
See "Risk Factors for the Presence of Symptoms in Peptic Ulcer Disease" by Sang Pyo Lee, In-Kyung Sung, Jeong Hwan Kim, et al., on page 578-584.
... Stomach ulcers are common and afflict millions of individuals annually (www.mayoclinic.com) [1] . Like many gastrointestinal (GI) disorders, stomach ulcers cause significant pain, a hallmark feature of many ailments affecting visceral organs. ...
AIM
To evaluate whether non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastropathy is a clinically predictive model of referred visceral hypersensitivity.
METHODS
Gastric ulcer pain was induced by the oral administration of indomethacin to male, CD1 mice (n = 10/group) and then assessed by measuring referred abdominal hypersensitivity to tactile application. A diverse range of pharmacological mechanisms contributing to the pain were subsequently investigated. These mechanisms included: transient receptor potential (TRP), sodium and acid-sensing ion channels (ASICs) as well as opioid receptors and guanylate cyclase C (GC-C).
RESULTS
Results showed that two opioids and a GC-C agonist, morphine, asimadoline and linaclotide, respectively, the TRP antagonists, AMG9810 and HC-030031 and the sodium channel blocker, carbamazepine, elicited a dose- and/or time-dependent attenuation of referred visceral hypersensitivity, while the ASIC blocker, amiloride, was ineffective at all doses tested.
CONCLUSION
Together, these findings implicate opioid receptors, GC-C, and sodium and TRP channel activation as possible mechanisms associated with visceral hypersensitivity. More importantly, these findings also validate NSAID-induced gastropathy as a sensitive and clinically predictive mouse model suitable for assessing novel molecules with potential pain-attenuating properties.
... pylori) infection and improvement of peptic ulcer treatment such as proton pump inhibitors (PPIs) or eradication therapies for H. pylori resulted in reduction of the incidence of uncomplicated peptic ulcer disease in recent decades [1][2][3] . However, several studies have shown controversial results showing constant incidence of complicated peptic ulcer disease [4][5][6][7] , which may be due to multifactorial risk factors including the increased consumption of non-steroidal anti-inflammatory drugs (NSAIDs) or acetylsalicylic acid (ASA), especially in elderly patients with multiple comorbidities, smoking habits, or unknown etiologies [8,9] . Previous studies evaluated the epidemiologic characteristics and associated risk factors of perforated peptic ulcer (PPU) and demonstrated increasing incidence of PPU by age [7][8][9][10][11][12][13][14][15] . ...
AIM
To elucidate the epidemiological characteristics and associated risk factors of perforated peptic ulcer (PPU).
METHODS
We retrospectively reviewed medical records of patients who were diagnosed with benign PPU from 2010 through 2015 at 6 Hallym university-affiliated hospitals.
RESULTS
A total of 396 patients were identified with postoperative complication rate of 9.1% and mortality rate of 0.8%. Among 174 (43.9%) patients who were examined for Helicobacter pylori (H. pylori) infection, 78 (44.8%) patients were positive for H. pylori infection, 21 (12.1%) were on non-steroidal anti-inflammatory drugs (NSAIDs) therapy, and 80 (46%) patients were neither infected of H. pylori nor treated by any kinds of NSAIDs. Multivariate analysis indicated that older age (OR = 1.09, 95%CI: 1.04-1.16) and comorbidity (OR = 4.11, 95%CI: 1.03-16.48) were risk factors for NSAID-associated PPU compared with non-H. pylori, non-NSAID associated PPU and older age (OR = 1.04, 95%CI: 1.02-1.07) and alcohol consumption (OR = 2.08, 95%CI: 1.05-4.13) were risk factors for non-H. pylori, non-NSAID associated PPU compared with solely H. pylori positive PPU.
CONCLUSION
Elderly patients with comorbidities are associated with NSAIDs-associated PPU. Non-H. pylori, non-NSAID peptic ulcer is important etiology of PPU and alcohol consumption is associated risk factor.
... Exact mechanism is unclear, and role of local inflammation and cytokines, such as tumor necrosis factor alpha and interleukin-1-beta have been implicated. Furthermore, Hp infection enhances the acid suppression by PPI therapy [17][18][19]. These interesting finding coupled with our result supports previous speculation that Hp infection may even be protective against development of GERD [20]. ...
Abstract
Background: Helicobacter pylori (Hp) infection has previously been thought to account for nearly all chronic gastritis. However, recent studies have suggested that Hp-negative gastritis is common and increasing in prevalence in the United States. The etiology and associated risk factors for Hp-negative gastritis remain uncertain.
Objective: Our primary aims were to: 1) Assess the prevalence of Hp-negative gastritis and 2) Characterize differences and similarities in associated demographics, clinical features, risk factors and medical co-morbidities between Hp-negative and Hp-positive gastritis.
Methods: We performed a retrospective study of 131 consecutive patients who were referred for EGD for upper gastrointestinal symptoms at a single tertiary care center from 7/2012-7/2013. Referral symptoms comprised dysphagia, abdominal pain, nausea, vomiting, iron deficiency anemia, bloating, belching, or Barrett’s esophagus surveillance. All 131 cases had biopsies at this institution, and clinical, demographic, and laboratory data were compared between individuals with Hp-negative and Hp-positive gastritis.
Results: Among all patients surveyed, 50 (38.2%) had gastritis present on biopsy, of which 39 (78.0%) were Hp- negative and 11 (22.0%) were Hp-positive. Among Hp-negative gastritis patients, 61.5% had chronic chemical gastritis, while 33.2% had chronic inactive gastritis and 5.1% had chronic active gastritis. Among Hp-positive patients, 100% had chronic active gastritis. The distribution of Hp-negative vs. Hp-positive gastritis differed (p = 0.016): antrum only (76.9% vs. 36.0%), corpus (10.3% vs. 36.0%), antrum and corpus (12.8% vs. 27.0%). Racial distribution differed significantly between Hp-negative (61.5% Caucasian, 20.5% African American, 18.0% other races) and Hp-positive (0% Caucasian, 72.7% African-American, and 27.3% other races) patients (p < 0.001). The presence of medical co-morbidities was significantly associated with Hp-negative gastritis vs. Hp-positive gastritis: 82.1% vs. 18.2% (p < 0.001). GERD was the most common medical co-morbidity noted, being present in 66.7% of Hp-negative patients in contrast to only 9.1% of Hp-positive gastritis (p = 0.001). There were no significant differences between Hp-negative and Hp-positive patients in predominant symptoms, primary referral indication, age, gender, prior Hp infection, tobacco, alcohol, PPI, NSAID, or antibiotic usage.
Conclusions: Hp-negative gastritis is a common entity that comprised the majority of consecutive gastritis cases in our study. It was significantly associated with the presence of medical co-morbidities, particularly GERD, and Caucasian race. Hp-negative gastritis also appears to have an anatomic predilection for the antrum. No association with referral symptoms, PPI use, NSAID use, or other risk factors was identified. Large-scale prospective studies are needed to further delineate the natural history, etiology, risk factors, pathogenesis, and clinical relevance of this increasingly common disease entity.
... In a very recently published study reporting data from a 20% stratified sample of all hospitalizations in the US, the number of hospitalizations for PUD decreased from 222,601 in 1993 to 156,108 in 2006 (rates per 100,000 inhabitants not given) (Wang 2010). However, in another study from the US no significant trend was found in number of duodenal and gastric ulcers as discharge diagnoses at five large hospitals between 1996 and 2005 (Manuel 2007). ...
... The increasing use of NSAIDs is considered to be an important underlying cause. Many studies have confirmed that current UGI bleeding in patients can be attributed to NSAID usage [122][123][124][125][126]. One study from the United States found that admission for PUD-related complications has not decreased despite decreasing Hp prevalence and increasing Hp eradication [127], and the authors proposed that this could be due to NSAID use. Meanwhile, Hp eradication can decrease the long-term incidence of recurrent ulcer bleeding in low-dose aspirin users [128]. ...
Upper gastrointestinal (UGI) bleeding is the most frequently encountered complication of peptic ulcer disease. Helicobacter pylori (Hp) infection and nonsteroidal anti-inflammatory drug (NSAID) administration are two independent risk factors for UGI bleeding. Therefore, testing for and diagnosing Hp infection are essential for every patient with UGI hemorrhage. The presence of the infection is usually underestimated in cases of bleeding peptic ulcers. A rapid urease test (RUT), with or without histology, is usually the first test performed during endoscopy. If the initial diagnostic test is negative, a delayed (13)C-urea breath test (UBT) or serology should be performed. Once an infection is diagnosed, antibiotic treatment is advocated. Sufficient evidence supports the concept that Hp infection eradication can heal the ulcer and reduce the likelihood of rebleeding. With increased awareness of the effects of Hp infection, the etiologies of bleeding peptic ulcers have shifted to NSAID use, old age, and disease comorbidity.
... However, H. pylori does not explain all incident cases of ulcer [8], as the bacterium is present in many individuals who do not develop ulcer and is not present in all who do develop the disease. Furthermore, although the prevalence of H. pylori is decreasing and eradication therapies for the bacterium are more common, the population prevalence of ulcer complications has remained unaffected [9]. These findings suggest that a multifactorial model of the causation of ulcer may be more useful than a singular causal pathway in understanding the development of the disease [6]. ...
Objective
Previous epidemiologic studies have documented a link between anxiety disorders and ulcer among adults. Few studies have examined these associations over time and little is understood about the pathways underlying these relationships.
Method
Data were drawn from n = 2,101 adult participants in the Midlife Development in the United States (MIDUS) I and II. Data on ulcer diagnoses were collected through self-report: among participants in the current sample, 38 reported ulcer at Waves 1 and 2 (prevalent ulcer) and 18 reported ulcer at Wave 2 but not at Wave 1 (incident ulcer). Panic attacks and generalized anxiety disorder at Wave 1 (1994) were examined in relation to prevalent (past 12-month) and incident ulcer approximately ten years later at Wave 2 (2005).
Results
Anxiety disorders at Wave 1 were associated with increased prevalence of ulcer (OR = 4.1, 95% CI = 2.0 – 8.4), increased risk of incident ulcer at Wave 2 (OR = 4.1, 95% CI = 1.4 – 11.7), and increased risk of treated ulcer at Wave 2 (OR = 4.7, 95% CI = 2.3 – 9.9) compared with those without anxiety.
Conclusions
In this large population sample of adults anxiety disorders were associated with an increased risk of ulcer over a 10-year period. These relationships do not appear to be explained by confounding or mediation by a wide range of factors. Future studies should address potential mechanisms underlying the relationship between anxiety and ulcer.
... It has been observed that the prevalence of PUD did not change in concomitance with the regimes of H. pylori eradication in the countries with low prevalence of the infection (6) . The increase in the rate of eradication of the bacterium in the USA did not result in reduction of the rates of hospital admissions related to complications from PUD (41) . ...
Objectives:
To review some aspects of the etiopathogenesis of peptic ulcerous disease especially on the basis of studies on its correlation with Helicobacter pylori (H. pylori).
Methods:
A search was made in the data bases MEDLINE, LILACS and PubMed, and in Brazilian and foreign books, referring to the incidence and prevalence of infection by H. pylori and of peptic ulcerous disease in various populations of different countries.
Results:
It was observed that the prevalence of H. pylori infection is similar in individuals with peptic ulcerous disease and the general population. There are differences between countries with respect to the prevalence of infection and of gastric or duodenal peptic ulcers. In many countries the prevalence of infection by H. pylori shows stability while the prevalence of peptic ulcerous disease is declining. The prevalence of peptic ulcerous disease without H. pylori infection varies between 20% and 56% in occidental countries.
Discussion:
The observations might be suggestive of H. pylori being only one more factor to be summed together with other aggressive components in the genesis of peptic ulcerous disease. We would therewith be returning to the classic concept that peptic gastric and duodenal ulcers have multifactorial etiology and would result from imbalance between aggressive and defensive factors. The focus of studies should be enriched with the identification of the defensive factors and of other aggressive factors besides the well known H. pylori and non-steroidal anti-inflammatory drugs, since these two aggressors do not exhaust the full causal spectrum.
... It is likely attributable to reduction in smoking prevalence, earlier diagnoses and treatment of hypertension and diabetes, and general improvements of the lifestyle. While the incidence rates of asthma and ulcer decreased significantly in our study, results of other studies varied from trend stabilisation to their decrease [17][18][19][20]. These studies were performed in the general population or among children and young adults but not among elderly, thus making it difficult to compare with our results. ...
Objectives:
time trends of age-adjusted incidence rates of 19 ageing-related diseases were evaluated for 1992-2005 period with the National Long Term Care Survey and the Surveillance, Epidemiology and End RESULTS Registry data both linked to Medicare data (NLTCS-Medicare and SEER-Medicare, respectively).
Methods:
the rates were calculated using individual medical histories (34,077 individuals from NLTCS-Medicare and 199,418 from SEER-Medicare) reconstructed using information on diagnoses coded in Medicare data, dates of medical services/procedures and Medicare enrolment/disenrolment.
Results:
increases of incidence rates were dramatic for renal disease [the average annual percent change (APC) is 8.56%, 95% CI = 7.62, 9.50%], goiter (APC = 6.67%, 95% CI = 5, 90, 7, 44%), melanoma (APC = 6.15%, 95% CI = 4.31, 8.02%) and Alzheimer's disease (APC = 3.96%, 95% CI = 2.67, 5.26%), and less prominent for diabetes and lung cancer. Decreases of incidence rates were remarkable for angina pectoris (APC = -6.17%, 95% CI = -6.96, -5.38%); chronic obstructive pulmonary disease (APC = -5.14%, 95% CI = -6.78,-3.47%), and ulcer (APC = -5.82%, 95% CI = -6.77,-4.86%) and less dramatic for carcinomas of colon and prostate, stroke, hip fracture and asthma. Incidence rates of female breast carcinoma, myocardial infarction, Parkinson's disease and rheumatoid arthritis were almost stable. For most diseases, an excellent agreement was observed for incidence rates between NLTCS-Medicare and SEER-Medicare. A sensitivity analysis proved the stability of the evaluated time trends.
Conclusion:
time trends of the incidence of diseases common in the US elderly population were evaluated. The results show dramatic increase in incidence rates of melanoma, goiter, chronic renal and Alzheimer's disease in 1992-2005. Besides specifying widely recognised time trends on age-associated diseases, new information was obtained for trends of asthma, ulcer and goiter among the older adults in the USA.
... Several interesting data came from other studies outside Europe. Decreased prevalence of H. pylori was also found for instance in the United States [43,44] , China [45,46] , Japan [47] , South Korea [48] and Singapore [49] . After fifteen years, the prevalence of H. pylori infection among both children and adults in China remained significantly higher in areas with a high incidence of gastric cancer compared with that in areas with a low incidence of gastric cancer. ...
To study possible decrease in prevalence of Helicobacter pylori (H. pylori) infection in the Czech Republic within a 10-year period.
A total of 22 centres entered the study. The catchment areas of these centres covered cities and towns with more than 20 000 inhabitants, smaller towns (≤ 20 000 inhabitants) with surrounding villages and rural areas, and were spread over the whole country, corresponding well to the geographical distribution of the Czech population. A total of 1 837 subjects (aged 5-98 years) took part in the study, randomly selected out of 38 147 people from the general population. H. pylori infection was investigated by means of a (13)C-urea breath test. Breath samples in duplicates were analysed using isotope ratio mass spectrometry. The cut-off point was 3.5. Social and demographic characteristics were based on data from self-completed questionnaires.
The overall prevalence of H. pylori infection was 23.5% (430/1826), and 4.8% (20/420) in children aged 15 or less. There was no statistically significant difference in prevalence between males (24.3%; 208/857) and females (22.9%, 222/969, P = 0.494). H. pylori infection was strongly associated with higher age, among subjects aged 55+ years, prevalence of H. pylori infection was 39.8% (252/633, P < 0.001). The highest prevalence of H. pylori infection was found among persons aged 55-64 years (43.9%, 97/221) and 75+ years (37.9%, 58/153). Among study subjects aged 15+ years, prevalence of H. pylori infection was significantly increased in those with lowest education (odds risk 3.19, 95% CI 1.87-5.47). Compared to never married (14.1%), the prevalence of H. pylori infection was statistically significantly higher among married (35.4%, 246/694, P < 0.001), divorced (36.8%, 49/133, P < 0.001) and widowed study subjects (40.2%, 45/112, P < 0.001), both in minimally and fully adjusted analysis. There was no significant difference in the prevalence of H. pylori infection between married and widowed subjects (35.4%, 246/694 vs 40.2%, 45/112, P = 0.389). There was little variation in smoking prevalence across categories of smoking and there was no evidence of an increased risk of H. pylori infection among current or past smokers in our data (odds risk 1.04 with 95% CI 0.78-1.40 for current smokers; odds ratio 0.83 with 95% CI 0.60-1.16 for former smokers). The current prevalence of H. pylori in 2011 was significantly lower compared to the prevalence reported from identical geographical areas in 2001 (23.5% vs 41.7%, P < 0.001).
The overall prevalence of H. pylori infection in the general population has fallen substantially in the Czech Republic over the past 10 years.
... The analysis of endoscopic findings associated with gastric and duodenal ulcers ( Table 3), showed that antral erosive gastritis was the most frequent endoscopic finding and the in Northeastern Brazil (92% in subjects 46-60 years) (19,20) ; the prevalence of peptic ulcers has not changed in countries with a low prevalence of H. pylori infection due to eradication regimens (13) . ...
In spite of Helicobacter pylori infection being the etiological cause of peptic ulcer and its high prevalence in Brazil, the prevalence of peptic ulcer disease has been poorly studied.
To verify the peptic ulcer disease prevalence in patients of a tertiary care hospital.
Diagnostic findings from 1,478 consecutive endoscopies were correlated with the urease test results for H. pylori infection diagnosis and demographic data in a total of 3,779 endoscopies performed in 2005. The mean age of the patients was 51.14 ± 16.46, being 613 (41.5%) men.
Peptic ulcer was diagnosed in 494 (33.4%) patients with a mean age of 54.86 ± 14.53, 205 (52%) were men, being 391 (26.5%) duodenal ulcer and 103 (7%) gastric ulcer. Normal endoscopy was found in 272 (18.4%) patients with a mean age of 38.4 ± 15.22, being 49 (18%) men. The comparison of peptic ulcer group with the patients that had normal endoscopy revealed that H. pylori infection [P = 0.005; OR = 1.70; 95% CI = 1.17-2.47], male gender [P<0.0001; OR = 5.53; 95%CI = 3.67-8.34] and older age [P<0.0001; OR = 1.08; 95%CI = 1.06-1.09] increased the risk of peptic ulcers. The overall H. pylori prevalence was 53% (786).
Prevalence of duodenal ulcer is high in a Brazilian population that had H. pylori infection associated with older age and male gender as important determinants to gastrointestinal diseases outcome. Future prospective studies should confirm these findings.
... Despite advances in H. pylori-related basic and clinical research, duodenal ulcers remain the most prevalent form of ''peptic ulcer'' with major public health and economic effects [1]. Part of the problem is the increasing proportion of H. pylori-negative duodenal ulcers, which has reached 20-30% in clinical studies [2,3], and the fact that ''increasing eradication of H. pylori infection in the US has not resulted in fewer hospital admissions for peptic ulcer disease-related complications,'' for example hemorrhage and perforations [4]. These data also emphasize the role of other etiologic factors such as stress, non-steroidal antiinflammatory drugs (NSAID), and other chemicals in ulcer pathogenesis [5,6] and the need for more mechanistic studies related to duodenal ulceration. ...
Despite recent advances and better understanding of the etiology and the pathogenesis of gastrointestinal ulcer diseases, e.g., duodenal ulcer, the molecular events leading to ulcer development, delayed healing, and recurrence remain poorly elucidated.
After we found that duodenal ulcers did not heal despite increased levels of vascular endothelial growth factor (VEGF), we tested the hypothesis that an imbalance in angiogenic VEGF and anti-angiogenic endostatin and angiostatin might be important in the development and delayed healing of experimental duodenal ulcers.
Levels of VEGF, endostatin, and angiostatin, and the expression and activity of related matrix metalloproteinases (MMP) 2 and 9 were measured in scrapings of rat proximal duodenal mucosa in the early and late stages of chemically induced duodenal ulceration. Furthermore, animals were treated with recombinant endostatin and MMP 2 inhibitor to test the relationship between MMP2 and endostatin and their involvement in healing of experimental duodenal ulcers.
A concurrent increase of duodenal VEGF, endostatin, and angiostatin was noted during duodenal ulceration. Endostatin treatment aggravated duodenal ulcer. Levels of MMP2, but not MMP9, were increased. Inhibition of MMP2 reduced levels of endostatin and angiostatin, and attenuated duodenal ulcers.
Increased levels of endostatin and angiostatin induced by MMP2 delayed healing of duodenal ulcers despite concurrently increased VEGF. Thus, an inappropriate angiogenic response or "angiogenic imbalance" may be an important new mechanism in ulcer development and impaired healing.
... Several interesting data came from other studies outside Europe. Decreased prevalence of H. pylori was also found for instance in the United States [43,44] , China [45,46] , Japan [47] , South Korea [48] and Singapore [49] . After fifteen years, the prevalence of H. pylori infection among both children and adults in China remained significantly higher in areas with a high incidence of gastric cancer compared with that in areas with a low incidence of gastric cancer. ...
Helicobacter pylori (Hp) is the most common chronic bacterial infection in humans. Hp has been demonstrated worldwide and in individuals of all ages. The overall prevalence of Hp infection has fallen dramatically in the Czech Republic over recent 15 years (from 70% in 1993 to 35% in 2006). This decrease can be explained mostly by the relatively favourable and improving socioeconomic conditions after the fall of communist regime. However, it is necessary to consider also the fundamental determinants of "modern times" that could cause gradual disappearing of Hp from the human "microbiome".
... 1,2,4,5 After the introduction of H pylori eradication therapy to prevent ulcers and bleeding, the primary cause of peptic ulcer bleeding has become drug exposure, especially NSAIDs, in Western countries. 17 H pylori infection was common in Taiwan, with a high prevalence of 54.4%. 11 However, after the introduction of H pylori eradication, peptic ulcer related events such as bleeding and perforation have decreased dramatically. ...
Helicobacter pylori infection and drugs are the two major risk factors for peptic ulcer bleeding. The role of these two factors may change with changes in the prevalence of H pylori and use of NSAIDs. This study aimed to determine the cause, endoscopic features, and outcome of peptic ulcer bleeding in a community hospital in southern Taiwan.
Patients who received esophagogastroduodenoscopy on arrival at the emergency department and were found to have actively bleeding ulcers or ulcers with stigmata of recent hemorrhage were included. H pylori infection was documented by the rapid urease test, histology, and/or C-13 urease breath test. Medication history, comorbidities, requirement for endoscopic therapy, blood transfusion, hospitalization days, and rebleeding rates were analyzed.
A total of 204 patients were enrolled with a mean age of 64.8 ± 15.2 years, with 58.3% of the subjects being female. There were 62 patients (30.4%) with H pylori infection only, 40 patients (19.6%) with drug use only, 67 patients (32.8%) with H pylori infection and drug use, and 37 patients (17.2%) without H pylori or drug use. A total of 107 patients (52.5%) were found to have had drug exposure. Drug exposure had an odds ratio (OR) of 2.34 [95% Confidence Interval (CI) = 1.30-4.20] for gastric ulcer bleeding and H pylori had an OR of 2.64 (95% CI = 1.17-5.97) for combined gastric and duodenal ulcer bleeding. The mean hospitalization period was 5.7 ± 4.0 days and the overall re-bleeding rate was 4.0%. The H pylori negative and drug negative subjects needed more endoscopic therapy (p < 0.05).
Drug use, especially NSAIDs, aspirin, and clopidogrel has become an important cause of peptic ulcer bleeding in southern Taiwan.
... After bleeding, perforation is the second most common complication requiring emergent operative intervention in peptic ulcer disease [60,61] . Helicobacter pylori infection is the most common cause of gastric and duodenal ulcers. ...
ABSTRACT: Intra-abdominal infection (IAI) is an important cause of morbidity and mortality. It is the second most commonly identified cause of severe sepsis in the intensive care unit and it has been associated with a high mortality rate. Most IAI are the result of inflammation and perforations of the gastrointestinal tract, such as appendicitis, peptic ulcer disease, and diverticulitis. Successful treatment of IAI is based on early and appropriate source recognition, containment and antimicrobial coverage. We will review the pathophysiology of IAI and provide clinical guidelines for its management.
Functional dyspepsia (FD) is categorized into postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). FD is 1.36–2.71 times more common in women than in men in the studies of outpatient clinic, and women demonstrated a higher prevalence in large-scale studies of health checkup participants. Usually, the rate of Helicobacter pylori (H. pylori) infection is significantly higher among males than females after the age of 16. The prevalence of atrophic gastritis and intestinal metaplasia is also higher in males than in females. Furthermore, duodenal and gastric ulcers were twice as common among males as females. However, the incidence of nonsteroidal anti-inflammatory drug (NSAID)-induced gastric ulcers has recently increased among females who take NSAIDs more than males, resulting in gastric ulcers becoming relatively more prevalent and attenuating sex/gender differences. The Lauren classification categorizes gastric cancer (GC) into two types: the intestinal-type and the diffuse-type. A higher prevalence of GC in males than in females can be observed throughout the world, but younger patients with GC are more likely to be female, have the diffuse and undifferentiated types, and present with advanced GC (AGC). Older patients with GC are more likely to be male, have the intestinal-type, and present with simultaneous tumors. A multivariate analysis of the risk factors of diffuse-type GC found that female sex, age under 50, family history of GC, and smoking were independent risk factors. In females, the diffuse-type accounts for most cases before menopause, but the proportion of the intestinal-type becomes similar to that in males 20 years after menopause, indicating that female sex hormones suppress the incidence of intestinal-type GC. Interestingly, the risk of cardiac GC is associated with obesity. This elevated cardiac GC risk related to obesity being greater in males than in females with the following reasons: First, increased concentrations of female hormones in obese females might have a protective effect against GC. Second, different prevalence of cardiac GC precursors such as Barrett’s esophagus is higher in males than in females. Meanwhile, being underweight increases the risk of noncardiac GC, especially in females mainly in Asian countries.
The incidence and prevalence of peptic ulcer have been decreasing with the advancement of medical management and low prevalence of Helicobacter pylori (H. pylori) infection. However, complications of peptic ulcer are still common, and admission rate has not been decreasing with the wide use of nonsteroidal anti-inflammatory drugs (NSAIDs) and antiplatelet agents. H. pylori and NSAIDs are the most common and important etiologies of peptic ulcer. Early diagnosis with endoscopic and radiologic examinations is important for the prevention of complications. Similar endoscopic features with peptic ulcer can be seen with malignancy and should be excluded for the differential diagnosis. Elimination of causative factors and proton pump inhibitor (PPI)-based medications are main treatment strategies. Potassium competitive acid blocker, which inhibits gastric H+-K+-ATPase is expected to partially supplement the unmet clinical needs of PPI and showed a noninferior efficacy compared to PPI for the treatment of gastric ulcers and the prevention of peptic ulcers in NSAID users. High-risk factors of NSAID-induced peptic ulcer and its complications include old age, a history of peptic ulcer, administration of high-dose NSAIDs, and coadministration of aspirin, antiplatelet agent, anticoagulants or steroid. Patients with long-term NSAID or low-dose aspirin therapy are recommended testing for, and treatment of H. pylori infection to prevent peptic ulcer and its complications. These patients with high-risk factors are also recommended to receive low-dose PPIs to prevent peptic ulcer and its complications. The risk of cardiovascular diseases should be considered in high-risk patients who are taking NSAIDs, and these patients with low-risk of cardiovascular diseases are recommended to administrate cyclooxygenase-2 inhibitor as NSAID. The clinical characteristics of idiopathic or non-H. pylori, non-NSAID ulcer need more investigation.
Helicobacter pylori (H. pylori) infection is associated with an increased risk of cardiovascular diseases (CVD), with variable prevalence rates worldwide. The pathogen contributes to CVD through mechanisms such as inflammation, lipid metabolism dysregulation, and enhanced platelet aggregation, which are linked to atherosclerosis development. Treatment typically involves antibiotics and proton pump inhibitors, and may confer additional cardiovascular benefits by addressing the bacterium's systemic effects. Future research should focus on the long-term impact of H. pylori eradication on CVD risk and outcomes, potentially informing prevention strategies. This review underscores the necessity for a comprehensive understanding of H. pylori's implications for cardiovascular health.
Duodenal and gastric ulcers were twice as common among males than females, and duodenal ulcers were more common than gastric ulcers. However, the incidence of gastric ulcers has recently increased among females, resulting in gastric ulcers becoming relatively more prevalent and attenuating sex/gender differences. Important causes of peptic ulcers are Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drug (NSAID) use. As the prevalence of H. pylori rapidly decreased in recent years, it was expected that peptic ulcers would become less common. Indeed, the prevalence of gastric and duodenal ulcers did decrease in 2011 and 2016–2018 health check-up center studies. However, in a multicenter, tertiary hospital study, the prevalence of duodenal ulcers decreased slightly, while the prevalence of gastric ulcers increased. This result is interpreted as a consequence of the increased use of aspirin or other NSAIDs among the aging population. NSAID use, including aspirin, impacts the incidence of gastric ulcers more than it does the incidence of duodenal ulcers. In contrast, duodenal ulcers are more influenced by H. pylori infection than gastric ulcers. As complications of peptic ulcers, bleeding and perforation are more common in males than in females mainly because the female sex hormone estrogen increases the expression of tight junction proteins that seal the gap between cells, reduce mucosal permeability, and stimulate the excretion of bicarbonate ion in the duodenal mucosa.KeywordsPeptic ulcerSexGenderGastric ulcerDuodenal ulcer
Helicobacter pylori
NSAID
Background and Aim
Several scoring systems for predicting outcomes in patients with non-variceal upper gastrointestinal bleeding (NVUGIB) have recently been devised, but not sufficiently validated. We compared the predictive accuracy of several scoring systems and assessed the usefulness of new scoring systems.
Methods
The medical records of 1048 patients with NVUGIB were reviewed to collect demographic, clinical, laboratory, and endoscopic data. The areas under the receiver operating characteristic curve (AUROC) were calculated for the ABC, new Japanese scoring system, Progetto Nazionale Emorrhagia Digestiva (PNED), and other scores to compare their predictive accuracy for 30-day mortality, therapeutic intervention, rebleeding, and prolonged hospital stay (≥ 10 days). Outcome predictors were identified by multivariate analysis.
Results
The ABC, new Japanese scoring system, and PNED score best predicted 30-day mortality (AUROC 0.907), need for therapeutic intervention (AUROC 0.707), and rebleeding (AUROC 0.874), respectively (all P < 0.001). The ABC and PNED scores were similarly better at predicting prolonged hospital stay (ABC AUROC: 0.765; PNED, AUROC: 0.790; both P < 0.001). Thirty-day mortality was related to sex, systolic blood pressure (SBP), syncope, estimated glomerular filtration rate (eGFR), albumin, heart failure, disseminated malignancy, chronic obstructive pulmonary disorder (COPD), and liver cirrhosis. Sex, age, SBP, hematemesis, blood urea nitrogen, and eGFR independently predicted the need for therapeutic intervention. Sex, SBP, pulse, albumin level, heart failure, disseminated malignancy, and COPD predicted rebleeding.
Conclusion
The outcomes of patients with NVUGIB were better predicted by newly developed than by old scoring systems.
Nonsteroidal anti-inflammatory drugs (NSAID) are some of the most commonly prescribed medications in clinical practice. The long-term use of NSAIDs is one of the main causes of peptic ulcers and the increased risk of upper gastrointestinal tract complications, such as perforation and bleeding. Thus, the prevention of NSAID-induced peptic ulcers is an important clinical issue. Previous studies have evaluated various strategies for preventing ulcers in patients requiring prolonged NSAID use. The Korean clinical practice guidelines have been published recently based on the evidence of the currently available data. This review describes the strategies for the prevention of peptic ulcers due to NSAID. An assessment of the risk factors for peptic ulcers from NSAID is recommended to identify patients who should be considered for primary prophylaxis. The risk of NSAID-induced peptic ulcers can be reduced by the concomitant use of proton pump inhibitors (PPI), misoprostol, and histamine-2 receptor antagonists. Selective cyclooxygenase-2 inhibitors can be used with caution due to concerns regarding cardiovascular toxicity. Attempts should
be made to use the lowest dose and shortest duration of the NSAID.
Gastroduodenal disease (GDD) was initially thought to be uncommon in Africa.
Amongst others, lack of access to optimal health infrastructure and suspicion of
conventional medicine resulted in the reported prevalence of GDD being
significantly lower than that in other areas of the world. Following the increasing
availability of flexible upper gastro-intestinal endoscopy, it has now become
apparent that GDD, especially peptic ulcer disease (PUD), is prevalent across the
continent of Africa. Recognised risk factors for gastric cancer (GCA) include
Helicobater pylori (H. pylori), diet, Epstein-Barr virus infection and industrialchemical exposure, while those for PUD are H. pylori, non-steroidal antiinflammatory
drug (NSAID)-use, smoking and alcohol consumption. Of these, H.
pylori is generally accepted to be causally related to the development of atrophic
gastritis (AG), intestinal metaplasia (IM), PUD and distal GCA. Here, we perform
a systematic review of the patterns of GDD across Africa obtained with
endoscopy, and complement the analysis with new data obtained on premalignant
gastric his-topathological lesions in Accra, Ghana which was
compared with previous data from Maputo, Mozambique. As there is a general
lack of structured cohort studies in Africa, we also considered endoscopy-based
hospital or tertiary centre studies of symptomatic individuals. In Africa, there is
considerable heterogeneity in the prevalence of PUD with no clear geographical
patterns. Furthermore, there are differences in PUD within-country despite
universally endemic H. pylori infection. PUD is not uncommon in Africa. Most of
the African tertiary-centre studies had higher prevalence of PUD when compared
with similar studies in western countries. An additional intriguing observation is
a recent, ongoing decline in PUD in some African countries where H. pylori
infection is still high. One possible reason for the high, sustained prevalence of
PUD may be the significant use of NSAIDs in local or over-the-counter
preparations. The prevalence of AG and IM, were similar or modestly higher
over rates in western countries but lower than those seen in Asia. . In our new
data, sampling of 136 patients in Accra detected evidence of pre-malignant
lesions (AG and/or IM) in 20 individuals (14.7%). Likewise, the prevalence of
pre-malignant lesions, in a sample of 109 patients from Maputo, were 8.3% AG
and 8.3% IM. While H. pylori is endemic in Africa, the observed prevalence for
GCA is rather low. However, cancer data is drawn from country cancer registries
that are not comprehensive due to considerable variation in the availability of
efficient local cancer reporting systems, diagnostic health facilities and expertise.
Validation of cases and their source as well as specificity of outcome definitions
are not explicit in most studies further contributing to uncertainty about the
precise incidence rates of GCA on the continent. We conclude that evidence is
still lacking to support (or not) the African enigma theory due to inconsistencies
in the data that indicate a particularly low incidence of GDD in African countries.
Gastroduodenal disease (GDD) was initially thought to be uncommon in Africa. Amongst others, lack of access to optimal health infrastructure and suspicion of conventional medicine resulted in the reported prevalence of GDD being significantly lower than that in other areas of the world. Following the increasing availability of flexible upper gastro-intestinal endoscopy, it has now become apparent that GDD, especially peptic ulcer disease (PUD), is prevalent across the continent of Africa. Recognised risk factors for gastric cancer (GCA) include Helicobater pylori (H. pylori), diet, Epstein-Barr virus infection and industrial chemical exposure, while those for PUD are H. pylori, non-steroidal anti-inflammatory drug (NSAID)-use, smoking and alcohol consumption. Of these, H. pylori is generally accepted to be causally related to the development of atrophic gastritis (AG), intestinal metaplasia (IM), PUD and distal GCA. Here, we perform a systematic review of the patterns of GDD across Africa obtained with endoscopy, and complement the analysis with new data obtained on pre-malignant gastric his-topathological lesions in Accra, Ghana which was compared with previous data from Maputo, Mozambique. As there is a general lack of structured cohort studies in Africa, we also considered endoscopy-based hospital or tertiary centre studies of symptomatic individuals. In Africa, there is considerable heterogeneity in the prevalence of PUD with no clear geographical patterns. Furthermore, there are differences in PUD within-country despite universally endemic H. pylori infection. PUD is not uncommon in Africa. Most of the African tertiary-centre studies had higher prevalence of PUD when compared with similar studies in western countries. An additional intriguing observation is a recent, ongoing decline in PUD in some African countries where H. pylori infection is still high. One possible reason for the high, sustained prevalence of PUD may be the significant use of NSAIDs in local or over-the-counter preparations. The prevalence of AG and IM, were similar or modestly higher over rates in western countries but lower than those seen in Asia. . In our new data, sampling of 136 patients in Accra detected evidence of pre-malignant lesions (AG and/or IM) in 20 individuals (14.7%). Likewise, the prevalence of pre-malignant lesions, in a sample of 109 patients from Maputo, were 8.3% AG and 8.3% IM. While H. pylori is endemic in Africa, the observed prevalence for GCA is rather low. However, cancer data is drawn from country cancer registries that are not comprehensive due to considerable variation in the availability of efficient local cancer reporting systems, diagnostic health facilities and expertise. Validation of cases and their source as well as specificity of outcome definitions are not explicit in most studies further contributing to uncertainty about the precise incidence rates of GCA on the continent. We conclude that evidence is still lacking to support (or not) the African enigma theory due to inconsistencies in the data that indicate a particularly low incidence of GDD in African countries.
Upper gastrointestinal bleeding (UGIB) develops in the oesophagus, stomach or duodenum and has an incidence of 47/100,000. Lower GIB (LGIB) develops in the small bowel, colon or anorectum and has an incidence of 33/100,000. Where the incidence of UGIB has fallen, driven by helicobacter pylori eradication and the use of proton pump inhibitors, the incidence of LGIB may be increasing. Interventions such as early endoscopy, risk assessment and national guidelines have improved clinical outcomes but have had limited impact on the economic burden of GIB. Previously LGIB was thought to be less severe than UGIB, but contemporary data suggest that patients with LGIB tend to have a longer length of hospital stay and may be at higher risk of death or re-bleeding.
Peptic ulcers diseases (PUD) were thought to be caused by a variety of cofactors such as smoking, stress, and nonsteroidal anti‐inflammatory drugs (NSAIDs) including aspirin. This chapter presents the evidence for the etiological role of Helicobacter pylori in PUD. It considers the prevalence of H. pylori in both duodenal and gastric ulcer patients. The chapter demonstrates the temporal relationship between infection with H. pylori and the development of duodenal ulcer. The clinically relevant evidence for the role of H. pylori comes from intervention trials in which H. pylori was eradicated and recurrence of ulcer disease markedly reduced. The highest risk for ulcer perforation was identified in a cohort of men born between 1900 and 1920. There are only two recommended first‐line empiric therapies: non‐bismuth quadruple therapy, bismuth quadruple therapy for H. pylori eradication. The potent acid suppressive drugs are potent acid suppressing agents that effectively heal duodenal and gastric ulcers and provide prompt symptom relief.
Peptic ulcer disease – chiefly gastric and duodenal ulcers – remains of global importance to human health. The majority of peptic ulcers are caused by Helicobacter pylori (Hp) infection or nonsteroidal anti-inflammatory drug (NSAID) use, including aspirin. However non-Hp, non-NSAID ulcers are becoming more common. Healthcare practitioners from different countries face different diagnostic and therapeutic challenges, at both the patient and population level. These arise from the changing epidemiology of the major causes, differences in Hp antibiotic resistance, and other temporal and geographical trends. Fundamental considerations in management are however constant: firstly treatment to achieve ulcer healing; and secondly the identification and management of specific causes – particularly eradication therapy for Hp and preventative strategies for drug-induced ulcers.
This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the benefits and harms of medical versus surgical treatment for people with recurrent or refractory peptic ulcer.
Despite decreasing Helicobacter pylori prevalence, the prevalence of peptic ulcer disease is increasing in the aged population, mainly due to increasing use of NSAIDs to manage pain and inflammation. In addition, low dose aspirin is employed as an anti-coagulant for those who have suffered or are at high risk of ischemic stroke and cardiovascular disease. However, NSAIDs and aspirin are injurious to mucosa of stomach and duodenum. NSAID-induced inhibition of mucosal prostaglandin synthesis is thought to be a major mechanism of gastrointestinal mucosal injury. The proportion of elderly has increased rapidly in Korea, with the proportion over 65 years old expected to be 24.3% in 2030. In this higher-risk population, the strategy to reduce the incidence of NSAID-related peptic ulcers and complications such as bleeding, obstruction and perforation is very important. Proton pump inhibitors (PPIs) with cyclooxygenase-2 inhibitor can be used for reducing the risk of NSAID-related ulcers and upper gastrointestinal (GI) complications. However, continuous use of PPI has several problems. In addition, NSAID-related problems in the lower GI tract have increased, in contrast to the decrease of NSAID-related upper GI disease. The aim of this review is to provide an evidence-based knowledge regarding the mechanism, complications of treatment, and prevention strategies for NSAID- or aspirin-related peptic ulcer disease in Korea.
Although the global prevalence of peptic ulcer disease (PUD) is decreasing, PUD is still one of the most common upper gastrointestinal diseases in the world due to Helicobacter pylori infection and increased use of non-steroidal anti-inflammatory drugs. In Korea, the prevalence of H. pylori infection is also declining, but it is still the major cause of PUD. The outcomes of H. pylori infection are caused by imbalances between bacterial virulence factors, host factors, and environmental influences. In this review, we describe the prevalence trends of H. pylori infection in Korea, the mechanism of H. pylori infection-related PUD, and treatment strategies.
The incidence and prevalence of peptic ulcer have been decreasing with the advancement of medical management and low prevalence of Helicobacter pylori (H. pylori) infection. However, complications of peptic ulcer are still common, and admission rate has not been decreasing with the wide use of nonsteroidal anti-inflammatory drugs (NSAIDs) and antiplatelet agents. H. pylori and NSAIDs are the most common and important etiologies of peptic ulcer. Early diagnosis with endoscopic and radiologic examinations is important for the prevention of complications. Similar endoscopic features with peptic ulcer can be seen with malignancy and should be excluded for the differential diagnosis. Elimination of causative factors and proton pump inhibitor -based medications are main treatment strategies. The clinical characteristics of idiopathic or non-H. pylori, non-NSAID ulcer need more investigation.
Background:
Refractory peptic ulcers are ulcers in the stomach or duodenum that do not heal after eight to 12 weeks of medical treatment or those that are associated with complications despite medical treatment. Recurrent peptic ulcers are peptic ulcers that recur after healing of the ulcer. Given the number of deaths due to peptic ulcer-related complications and the long-term complications of medical treatment (increased incidence of fracture), it is unclear whether medical or surgical intervention is the better treatment option in people with recurrent or refractory peptic ulcers.
Objectives:
To assess the benefits and harms of medical versus surgical treatment for people with recurrent or refractory peptic ulcer.
Search methods:
We searched the specialised register of the Cochrane Upper GI and Pancreatic Diseases group, the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE, EMBASE, Science Citation Index Expanded, and trials registers until September 2015 to identify randomised trials and non-randomised studies, using search strategies. We also searched the references of included studies to identify further studies.
Selection criteria:
We considered randomised controlled trials and non-randomised studies comparing medical treatment with surgical treatment in people with refractory or recurrent peptic ulcer, irrespective of language, blinding, or publication status for inclusion in the review.
Data collection and analysis:
Two review authors independently identified trials and extracted data. We planned to calculate the risk ratio, mean difference, standardised mean difference, or hazard ratio with 95% confidence intervals using both fixed-effect and random-effects models with Review Manager 5 based on intention-to-treat analysis.
Main results:
We included only one non-randomised study published 30 years ago in the review. This study included 77 participants who had gastric ulcer and in whom medical therapy (histamine H2 receptor blockers, antacids, and diet) had failed after an average duration of treatment of 29 months. The authors do not state whether these were recurrent or refractory ulcers. It appears that the participants did not have previous complications such as bleeding or perforation. Of the 77 included participants, 37 participants continued to have medical therapy while 40 participants received surgical therapy (antrectomy with or without vagotomy; subtotal gastrectomy with or without vagotomy; vagotomy; pyloroplasty and suture of the ulcer; suture or closure of ulcer without vagotomy or excision of the ulcer; proximal gastric or parietal cell vagotomy alone; suture or closure of the ulcer with proximal gastric or parietal cell vagotomy). Whether to use medical or surgical treatment was determined by participant's or treating physician's preference.The study authors reported that two participants in the medical treatment group (2 out of 37; 5.4%) had gastric cancer, which was identified by repeated biopsy. They did not report the proportion of participants who had gastric cancer in the surgical treatment group. They also did not report the implications of the delayed diagnosis of gastric cancer in the medical treatment group. They did not report any other outcomes of interest for this review (that is health-related quality of life (using any validated scale), adverse events and serious adverse events, peptic ulcer bleeding, peptic ulcer perforation, abdominal pain, and long-term mortality).
Authors' conclusions:
We found no studies that provide the relative benefits and harms of medical versus surgical treatment for recurrent or refractory peptic ulcers. Studies that evaluate the natural history of recurrent and refractory peptic ulcers are urgently required to determine whether randomised controlled trials comparing medical versus surgical management in patients with recurrent or refractory peptic ulcers or both are necessary. Such studies will also provide information for the design of such randomised controlled trials. A minimum follow-up of two to three years will allow the calculation of the incidence of complications and gastric cancer (in gastric ulcers only) in recurrent and refractory peptic ulcers. In addition to complications related to treatment and disease, health-related quality of life and loss of productivity should also be measured.
Helicobacter pylori is among the most common bacterial pathogens, but it has not yet been conquered. It is related to various gastrointestinal diseases, including chronic gastritis, peptic ulcer, gastric marginal zone B cell lymphoma, and gastric cancer. The association between Helicobacter pylori infection and functional dyspepsia or gastroesophageal reflux disease is not clear. Numerous factors determine disease course and outcome, such as bacterial virulence, genotype, host immunity, and environmental factors. The eradication of Helicobacter pylori in associated gastrointestinal diseases is important for the treatment and prevention of recurrent or severe outcomes, especially in Korea where gastric cancer is prevalent.
Although there have been reports showing a decreasing trend in the global prevalence of peptic ulcer diseases (PUD), PUD is still one of the most common upper gastrointestinal diseases. Helicobacter pylori is a major cause of PUD and the prevalence of H. pylori infection has been reported to be declining in Korea. However the use of ulcerogenic drugs such as non-steroidal anti-inflammatory drugs and aspirin has been reported to be increasing in Korea. The purpose of this review was to investigate how these changing trends affect the prevalence of PUD in Korea. In this review, we identified the risk factors for PUD and assessed the prevalence of PUD in Korea according to different time trends.
Despite the improvement of medical managements of peptic ulcer and decline of Helicobacter pylori infection, complications of peptic ulcer are still prevalent in clinical practice. This is because of the increased use of ulcerogenic medications such as aspirin or non-steroidal anti-inflammatory drug (NSAID) in elderly patients. Peptic ulcer complications include bleeding, perforation, penetration and gastric outlet obstruction. These complications need to be managed by multidisciplinary approaches such as combination of endoscopic treatment, radiologic embolization, or surgical treatments. In addition to using proton pump inhibitors, H. pylori eradication and discontinuing ulcerogenic medications are essential in the prevention of recurrence. Although uncommon, non-H. pylori, non-NSAID ulcers should be suspected as a potential cause in recurrent cases of peptic ulcer complications.
The characteristics of peptic ulcer disease (PUD) are changing.
To evaluate time trends in the incidence of PUD and its complications in hospitalised patients at the beginning of the 21st century, drug therapies in out-patient care as a risk factor for recurrent PUD, and medication used by PUD patients compared with the background population.
In this retrospective epidemiologic cohort study, data from the years 2000-2008 came from The Hospital District of Helsinki and Uusimaa, and the Finnish Care Register. All hospitalised adult patients with PUD in the capital region of Finland were included. The data were linked with nationwide Prescription Register of the Finnish Social Insurance Institution allowing detailed individual medicine purchase data.
A total of 9951 peptic ulcers were detected among 8146 individual patients during the study period. The mean annual incidence of all peptic ulcers decreased from 121/100 000 (95% CI: 117-125) in 2000-2002, to 79 (95% CI: 76-82) in 2006-2008 [Incidence rate ratio = 0.62 (95% CI: 0.58-0.64), P < 0.001 after age and sex adjustment]. Decrease in incidence was seen in all age groups and in both sexes. The overall rate of severe complications of PUD was reduced. One-year cumulative incidence of recurrent ulcers was 13%. Use of several drugs was associated with increased risk for recurrence. The purchases of various drugs were more common among PUD patients compared with background population.
Both the incidence and complication rates have markedly decreased during the study period. Recurrent peptic ulcer disease was associated with polypharmacy.
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that directly upregulates VEGF, Ref-1, p21, and anti-apoptotic genes such as Bcl-xL. In this study, we hypothesized that STAT3 signaling is activated and provides a critical protective role that is required for enterocyte survival during the early phases of cysteamine-induced duodenal ulcers.
We studied the effect of inhibition of STAT3 activity on cysteamine-induced duodenal ulcers in rats and egr-1 knockout mice using STAT3/DNA binding assay, immunohistochemistry, immunoblot, and quantitative reverse transcriptase PCR analyses.
We found that G-quartet oligodeoxynucleotides T40214, a specific inhibitor of STAT3/DNA binding, aggravated cysteamine-induced duodenal ulcers in rats 2.8-fold (p < 0.05). In the pre-ulcerogenic stage, cysteamine induced STAT3 tyrosine phosphorylation, its translocation to nuclei, an increased expression and nuclear translocation of importin α and β in the rat duodenal mucosa. Cysteamine enhanced the binding of STAT3 to its DNA consensus sequences at 6, 12, and 24 h after cysteamine by 1.5-, 1.8-, and 3.5-fold, respectively, and activated the expression of STAT3 target genes such as VEGF, Bcl-xL, Ref-1, and STAT3-induced feedback inhibitor, a suppressor of cytokine signaling 3. We also demonstrated that egr-1 knockout mice, which are more susceptible to cysteamine-induced duodenal ulcers, had lower levels of STAT3 expression, its phosphorylation, expression of importin α or β, and STAT3/DNA binding than wild-type mice in response to cysteamine.
Thus, STAT3 represents an important new molecular mechanism in experimental duodenal ulceration.
Epidemiology of peptic ulcer disease (PUD) in India differs from that in the West. It may have undergone a change with recent improvement in hygiene and availability of potent antisecretory and ulcerogenic drugs. We therefore tried to assess time-trends in the frequency of PUD over the past two decades.
Records of patients with uninvestigated dyspepsia and no alarm symptoms who had undergone upper gastrointestinal endoscopy at our institution during the years 1988 (n = 2,358), 1992 (n = 2,240), 1996 (n = 5,261), 2000 (n = 7,051), 2004 (n = 5,767) and 2008 (n = 7,539) were retrospectively reviewed. The frequencies of duodenal and gastric ulcer disease in these groups were compared.
Of the 30,216 patients (age:41.7±12.7 years, 34 % females) during the six study periods, 2,360 (7.8 %) had PUD. The frequencies of both duodenal ulcer and gastric ulcer showed a decline from 1988 to 2008, i.e. from 12 % to 2.9 % and 4.5 % to 2.7 %, respectively (p-value <0.001 for trend for each). The decline was more marked for duodenal ulcer, and the ratio of duodenal to gastric ulcer declined from 2.7 in 1988 to 1.1 in 2008.
The epidemiology of PUD in India may have changed in the past two decades with the incidence of duodenal ulcer declining more rapidly than that of gastric ulcer.
Peptic ulcer disease (PUD) is due mostly to the widespread use of low-dose aspirin and nonsteroidal anti-inflammator drugs. It occurs mostly in older patients and those with comorbidities. Pain awakening the patient from sleep between 12 and 3 a.m. affects two-thirds of duodenal ulcer patients and one-third of gastric ulcer patients. Older adults (>80 years old) with PUD often do not present with abdominal pain; instead, epigastric pain, nausea and vomiting are among their most common presenting symptoms.
Common gastrointestinal diseases often exhibit geographic, cultural, and gender variations. Diseases previously less common in certain areas of the world have shown a recent increase in prevalence. Industrialization has traditionally been noted as a major cause for this epidemiologic evolution. However, environmental factors such as diet, hygiene, and exposure to infections may play a major role. Moreover, the way one disease presents in a certain location may vary significantly from the way it manifests in another culture or location. This article discusses global variations of inflammatory bowel disease, Helicobacter pylori, irritable bowel disease, fecal incontinence, hepatitis B, and hepatocellular cancer.
Peptic ulcer bleeding is the most common cause of acute bleeding in the upper GI tract. The incidence of peptic ulcer bleeding has slowly decreased and endoscopic treatment options have improved; nevertheless, it remains a very common condition with a 7-15% mortality. Acidic environments have a negative effect on hemostasis. Therefore, acid inhibitors have been applied in the adjuvant treatment of peptic ulcer bleeding, both in preventing rebleeding and in treating the underlying cause. This requires profound acid suppressive therapy aiming for a rapid onset of effect and a persistent intragastric pH above 6. This can only be achieved by proton pump inhibitors (PPIs). Esomeprazole is the S-isomer of omeprazole, and the first PPI to consist of only the active isomer. A number of studies have compared esomeprazole with other PPIs, demonstrating a faster and more persistent increase in intragastric pH with the use of esomeprazole than with other agents. Continuous high-dose intravenous treatment with esomeprazole decreases rebleeding, surgery, transfusion rates and hospital days in peptic ulcer bleeding.
Infection with Helicobacter pylori increases the risk for peptic ulcer disease (PUD) and its complications. To determine whether hospitalization rates for PUD have declined since antimicrobial drugs to eradicate H. pylori became available, we examined 1998-2005 hospitalization records (using the Nationwide Inpatient Sample) in which the primary discharge diagnosis was PUD. Hospitalizations for which the diagnosis was H. pylori infection were also considered. The age-adjusted hospitalization rate for PUD decreased 21% from 71.1/100,000 population (95% confidence interval [CI] 68.9-73.4) in 1998 to 56.5/100,000 in 2005 (95% CI 54.6-58.3). The hospitalization rate for PUD was highest for adults > or =65 years of age and was higher for men than for women. The age-adjusted rate was lowest for whites and declined for all racial/ethnic groups, except Hispanics. The age-adjusted H. pylori hospitalization rate also decreased. The decrease in PUD hospitalization rates suggests that the incidence of complications caused by H. pylori infection has declined.
Corticotropin-releasing factor (CRF) plays a major role in controlling the body's response to stress. Because painful conditions are inherently stressful, we hypothesize that CRF may act via CRF-1 receptors to contribute to the pain experience. Studies were designed to investigate whether blocking CRF-1 receptors with selective antagonists or reducing their expression with CRF-Saporin, would attenuate ulcer, inflammatory- and neuropathic-like pain. Five experimental designs were undertaken. In experiment 1, ulcer pain was induced in mice following oral administration of indomethacin, while in experiments 2 and 3, inflammatory pain was induced in rats with either carrageenan or FCA, respectively. For these studies, animals were dosed with CP-154,526 (3, 10, 30 mg/kg) and NBI 27914 (1-30 mg/kg) 1 h prior to the assessment of tactile, thermal or mechanical hypersensitivity, respectively. In experiment 4, neuropathic pain was induced. Twenty-one days following spinal nerve ligation (SNL), animals received CRF-Saporin or control. Three weeks later tactile allodynia was assessed. Similarly, in experiment 5, a separate set of rats received CRF-Saporin or control. Twenty-one days later, mechanical hyperalgesia was assessed following intraplantar carrageenan. Results from the antagonist studies showed that CP-154,526 and NBI 27914 either fully or partially reversed the referred ulcer pain with minimal effective doses (MED) equal to 3 and 10 mg/kg, respectively. Similarly, both NBI 27914 and CP-154,526 reversed the thermal and mechanical hypersensitivity elicited by carrageenan and FCA with MEDs </= 5 and 10 mg/kg, respectively. Findings from the two CRF-Saporin studies determined that pre-treatment with this toxin significantly attenuated SNL- and carrageenan-induced tactile hypersensitivity. Together, these findings suggest that CRF-1 receptors mediate pain and implicate CRF in this regard.
Peptic ulcers are caused by acidic stomach juices damaging the lining of the stomach (gastric ulcer) or upper small intestine (duodenal ulcer). This causes pain, indigestion and sometimes bleeding. Bleeding in the gut can be life-threatening. Several treatments aim to heal the ulcer and prevent future bleeding. These include acid-suppressing drugs and antibiotics to treat Helicobacter pylori, a bacterium that causes most peptic ulcers. The review found that, for people who have had a bleeding peptic ulcer caused by Helicobacter pylori, treatment with antibiotics more effectively prevents gastrointestinal re-bleeding than acid-suppressing drugs. Antibiotics when Helicobacter pylori infection is present are also cheaper and more convenient than long-term acid-suppressing drugs.
OBJECTIVE: Published studies have estimated the rate of Helicobacter pylori (H. pylori) infection in patients with duodenal ulcer disease to be as high as 95%; the majority of remaining duodenal ulcers have been attributed to the use of ulcerogenic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs). We aimed to assess the H. pylori prevalence rates of U.S. duodenal ulcer patients in large, well-controlled studies.
Several studies of Helicobacter pylori infection have examined identification of new infections and loss of existing infections over time. These studies bring additional information to the many studies on prevalence that have been performed across the world. Direct evidence of the major routes of transmission is still lacking, however. Apart from studies of transmission, the influence of H. pylori infection on upper gastrointestinal diseases is undergoing reappraisal. This article updates previous reviews and focuses on information made available in the last few years, mostly in the second half of the 1990s, regarding the epidemiology of H. pylori.
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Gastroduodenal intolerance is one of the major factors limiting the use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAID) in patients with arthritic conditions. We evaluated the endoscopic appearance of the gastroduodenal mucosa in 65 patients (63 men and two women) taking regular daily doses of NSAIDs over a long period for osteoarthritis or rheumatoid arthritis. Eight different drugs (indomethacin, ibuprofen, naproxen, sulindac, piroxicam, aspirin, salsalate, and tolmetin) had been taken continuously for at least 6 wk. Seven patients took two different NSAIDs. No other drug known to damage the mucosa was used. Twenty-one patients (32%) had an endoscopically completely normal stomach and duodenum, and 44 (68%) had evidence of injury (mucosal hemorrhage 44.6%, erosions 53.8%, both mucosal hemorrhage and erosions 34%). Ten patients had ulcers detected (seven gastric, two pyloric channel, one duodenal bulb) for a point prevalence of 15.4%. Ulcers were found in patients taking naproxen, indomethacin, tolmetin, sulindac, and ibuprofen, either alone, or in combination with aspirin. Dyspeptic symptoms were present in 19% of those with completely normal endoscopy and in only 9% of those with abnormal endoscopic findings. Only three of the 10 patients with ulcer had dyspeptic symptoms. There was no significant difference between drugs in tendency to cause gastroduodenal injury. We confirm that fairly severe gastroduodenal injury occurs in asymptomatic patients with rheumatoid and osteoarthritis, and that symptoms do not predict the presence of damage.
Published studies have estimated the rate of Helicobacter pylori (H. pylori) infection in patients with duodenal ulcer disease to be as high as 95%; the majority of remaining duodenal ulcers have been attributed to the use of ulcerogenic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs). We aimed to assess the H. pylori prevalence rates of U.S. duodenal ulcer patients in large, well-controlled studies.
More than 2900 patients with endoscopically diagnosed non-NSAID duodenal ulcers were enrolled in a series of six placebo-controlled, double-blind studies conducted in the United States that assessed H. pylori using a combination of tests. Patients were considered infected with H. pylori only if culture growth was observed, or both histological and CLOtest results were positive. Patients were considered uninfected if the results of at least two tests were negative. Patients with missing test results, results of only a single test, or conflicting test results were not evaluable for H. pylori assessment.
Of the 2394 endoscopically diagnosed evaluable duodenal ulcer patients, 73% (1737) were confirmed infected with H. pylori at study entry.
The results of six carefully designed and controlled studies suggest that an assumed H. pylori infection rate of approximately 95% may overestimate the actual rate of H. pylori infection in duodenal ulcer patients in the United States. Although H. pylori infection is an important factor in the etiology of noniatrogenic duodenal ulcer disease, other factors may predominate in some patients and should not be overlooked in determining an appropriate course of treatment. The empiric use of antibiotic therapy for ulcer patients without confirmation of the presence of H. pylori cannot be recommended.
Background:
Peptic ulcer disease is the cause for dyspepsia in about 10% of patients. 95% of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of H pylori reduces the relapse rate of ulcers but the magnitude of this effect is uncertain.
Objectives:
The primary outcomes were the proportion of peptic ulcers healed initially and proportion of patients free from relapse following successful healing. Eradication therapy was compared to placebo or pharmacological therapies in H. pylori positive patients. Secondary aims included symptom relief and adverse effects.
Search strategy:
Searches were conducted on the Cochrane Central register of Controlled Trials - CENTRAL (which includes the Cochrane Upper Gastrointestinal and Pancreatic Diseases Group Trials Register) on The Cochrane Library (Issue 3 2002) MEDLINE (1966 to July 2002) and EMBASE (1980 to July 2002). Reference lists from trials selected by electronic searching were handsearched to identify further relevant trials. Published abstracts from conference proceedings from the United European Gastroenterology Week (published in Gut) and Digestive Disease Week (published in Gastroenterology) were handsearched. The search was updated in September 2003, November 2004 and November 2005. Members of the Cochrane UGPD Group, and experts in the field were contacted and asked to provide details of outstanding clinical trials and any relevant unpublished materials
Selection criteria:
Randomised controlled trials of short and long-term treatment of peptic ulcer disease in H. pylori positive adults were analysed. Patients received at least one week of H pylori eradication compared with ulcer healing drug, placebo or not treatment. Trials were included if they reported assessment from 2 weeks onwards.
Data collection and analysis:
Data were collected on ulcer healing, recurrence, relief of symptoms and adverse effects.
Main results:
63 trials were eligible. Data extraction was not possible in 7 trials, and 56 trials were included. In duodenal ulcer healing, eradication therapy was superior to ulcer healing drug (UHD) (34 trials, 3910 patients, relative risk [RR] of ulcer persisting = 0.66; 95% confidence interval [CI] = 0.58, 0.76) and no treatment (2 trials, 207 patients, RR = 0.37; 95% CI 0.26, 0.53). In gastric ulcer healing, no significant differences were detected between eradication therapy and UHD (14 trials, 1572 patients, RR = 1.25; 95% CI = 0.88, 1.76). In preventing duodenal ulcer recurrence no significant differences were detected between eradication therapy and maintenance therapy with UHD (4 trials, 319 patients, relative risk [RR] of ulcer recurring = 0.73; 95% CI = 0.42, 1.25), but eradication therapy was superior to no treatment (27 trials 2509 patients, RR = 0.20; 95% CI = 0.15, 0.26). In preventing gastric ulcer recurrence, eradication therapy was superior to no treatment (11 trials, 1104 patients, RR = 0.29; 95% CI 0.20, 0.42).
Authors' conclusions:
A 1 to 2 weeks course of H. pylori eradication therapy is an effective treatment for H. pylori positive peptic ulcer disease.
Despite reports of decreasing hospitalizations and mortality due to peptic ulcer, it is unclear whether the incidence has truly declined over time.
To investigate time trends in the incidence of and in hospital admission rates for peptic ulcer in the Netherlands.
The nationwide registry of pathology reports (PALGA) and the national registry of hospital admissions (Landelijke Medische Registratie) were used. Standardized morbidity ratios were calculated to assess the magnitude of the changes.
The age-adjusted incidence of gastric ulcer halved for both men (standardized morbidity ratio 0.48; CI 0.46-0.49) and women (standardized morbidity ratio 0.49; CI 0.47-0.51). Although the number of gastric biopsies obtained at endoscopy increased, the proportion with a diagnosis of peptic ulcer decreased by more than 50% (standardized morbidity ratio 0.47; CI 0.46-0.49). The admission rate for peptic ulcer more than halved between 1980 and 2003. In contrast, admission rates for complicated ulcers barely changed and slightly increased among women.
The incidence of histopathologically confirmed gastric ulcer halved between 1992 and 2003 in the Netherlands. As the number of gastric biopsies increased in this period, a true decrease is likely. Hospital admissions for peptic ulcer declined dramatically between 1980 and 2003, but remained unchanged or slightly increased for complicated ulcers.