Peptic ulcer | Medicina Clínica (English Edition)

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Double doses increase cure rates. **Pylera®: 1 tablet combines 140 mg bismuth subcitrate, 125 mg tetracycline hydrochloride and 125 mg metronidazole. ***Dosage schedule as described in the SmPC; data from the European H. pylori Registry suggest that the dose of 4 capsules every 8 h is most effective and well tolerated." ] ] ] "textoCompleto" => "DefinitionThe term peptic ulcer (PU) defines a characteristic lesion consisting of a solution of continuity of the proximal gastric and/or duodenal mucosa, although it can also develop in the oesophagus, small intestine, or in the ectopic gastric mucosa of Meckel's diverticulum. It may be a single lesion or multiple lesions and may extend beyond the muscularis mucosae into the submucosa. The size of the ulcer varies from 5 mm to several cm. Lesions measuring less than 5 mm and limited to the mucosa are considered erosions.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> Finally, stress ulcers are those that occur in the context of very severe organ diseases - usually in intensive care patients - and are associated with gastrointestinal bleeding.<a class="elsevierStyleCrossRef" href="#bib0010">2</a>EpidemiologyIt is estimated that about 5–10% of individuals will have a PU during their lifetime.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> The annual incidence ranges from 0.3 to 1.9 ‰. Most epidemiological studies in recent decades show a decrease in the incidence of PU complications,<a class="elsevierStyleCrossRef" href="#bib0020">4</a> especially in developed countries. In Europe, both hospital admissions and mortality from PU have been significantly reduced over the last 20 years.<a class="elsevierStyleCrossRefs" href="#bib0025">5,6</a> This decline has been attributed to a decrease in the prevalence of Helicobacter pylori (H. pylori) infection, the widespread use of antisecretory drugs, and a decrease in both smoking and the prescription of non-steroidal anti-inflammatory drugs (NSAIDs).<a class="elsevierStyleCrossRefs" href="#bib0035">7,8</a>Risk factors and pathophysiologyThe pathophysiology of PU is complex and multifactorial, being the result of an imbalance between aggressive gastric factors, such as acid and pepsin, and mucosal protective factors that act as a defensive barrier, such as mucus and bicarbonate. Thus, ulcer formation can be caused by both increased gastric acid secretion and dysfunction of the mucosal barrier.<a class="elsevierStyleCrossRef" href="#bib0005">1</a>The most important risk factors for PU are H. pylori infection and the use of NSAIDs and/or acetylsalicylic acid (ASA). More than 90% of duodenal ulcers and more than 70% of gastric ulcers are positive for H. pylori.<a class="elsevierStyleCrossRef" href="#bib0045">9</a>H. pylori infection and NSAID use independently elevate the risk of ulcer bleeding, increasing the risk 1.79-fold and 4.85-fold, respectively. Furthermore, synergy between the two factors has been observed.<a class="elsevierStyleCrossRefs" href="#bib0050">10,11</a>However, not all people with H. pylori infection and/or NSAID intake will develop PUs. This could be due to differences in H. pylori virulence, individual susceptibility and local inflammatory response to infection. In the case of NSAIDs, in addition to individual susceptibility, pharmacological characteristics will determine a significantly different ability to damage the gastroduodenal mucosa.Pathophysiology of H. pylori damageThe mechanism by which H. pylori causes PU is not exactly known. It is accepted that the pathophysiological mechanisms of duodenal ulcer and gastric ulcer are distinct and depend on the response to H. pylori infection.H. pylori colonises the gastric mucosa from the pylorus to the cardia. In patients with duodenal ulcer, inflammation of the pyloric antrum would be common, leading to increased gastrin production, which in turn stimulates acid secretion. On the other hand, the mucosa of the body - which secretes gastric acid - would be preserved and the acid hypersecretion that occurs would damage the duodenal mucosa.In patients with gastric ulcer, however, inflammation would also significantly affect the mucosa of the body, damaging the glands and decreasing acid secretion. Mucosal damage in this case is attributed to decreased protective factors.On the other hand, infection with H. pylori strains expressing virulence factors is associated with an increased risk of PU, with the expression of Cag A protein, which induces a strong local inflammatory response, and Vac A toxin, which causes vacuolar degeneration and ulceration, being the two most important factors.<a class="elsevierStyleCrossRefs" href="#bib0060">12,13</a>Pathophysiology of NSAID damageThe main ulcerogenic mechanism of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX), which in turn is the molecular mechanism of their anti-inflammatory action. This enzyme has two isoforms, COX-1 and COX-2. COX-1 inhibition - which is constitutive - decreases the synthesis of prostaglandins involved in gastrointestinal protection, reduces bicarbonate and mucus secretion and affects the integrity of the mucosal barrier. A second ulcerogenic mechanism of NSAIDs is direct damage to gastric mucosal cells by accumulation in the cytoplasm.All this favours the development of PU. COX-2 -which is inducible- develops in tissues in response to local inflammation and produces mediators of pain and inflammation. Inhibition of COX-2 is responsible for the beneficial effects of NSAIDs. Unlike non-selective NSAIDs that similarly inhibit both isoenzymes (COX-1 and COX-2), COXIBs inhibit COX-2 to a greater extent and are therefore less ulcerogenic.<a class="elsevierStyleCrossRef" href="#bib0070">14</a>A number of factors increase the risk of developing PU and its complications in patients receiving NSAIDs, usually due to decreased mucosal barrier efficacy. The main risk factors are age, smoking, the presence of comorbidities and the concomitant use of other drugs, which may influence the development of PU and its clinical course.<a class="elsevierStyleCrossRef" href="#bib0075">15</a>Clinical signs and symptomsThe usual clinical features consist of dyspepsia symptoms, often non-specific, such as epigastric pain or discomfort, commonly described as 'burning', sometimes with a feeling of painful hunger. Irradiation to the flanks or retrosternal area is rare. In duodenal ulcer, the pain occurs daily, developing 2−3 h after ingestion, wakes the patient early in the morning and is usually relieved after taking antacids or food. Radiation towards the back suggests a penetrating duodenal ulcer. In patients with gastric ulcer the pattern tends to be more atypical and irregular and many or all of these features may be missing.In most cases, peptic ulcer follows a chronic relapsing course with symptomatic flares lasting several weeks, often with a clear seasonal relationship (predominantly spring or autumn) followed by spontaneous remissions with symptom-free periods of months or years. Physical examination is usually normal, except for the occasional and completely non-specific epigastric tenderness. Most elderly patients with PU are asymptomatic or oligosymptomatic.<a class="elsevierStyleCrossRefs" href="#bib0070">14,16,17</a>Complications of peptic ulcer diseaseComplications include upper gastrointestinal bleeding (UGB), perforation, penetration and stenosis.Upper gastrointestinal bleedingIt is the most common complication of PU and the most common cause of non-varicose UGB, accounting for 40%–50% of cases. The most common presentation is in the form of haematemesis and/or melena, with or without abdominal pain. Up to 15% of cases may develop as rectal bleeding due to rapid transit of blood along the intestine, especially after major haemorrhages.<a class="elsevierStyleCrossRefs" href="#bib0005">1,3,18,19</a>Hospital admissions for UGB due to PU have decreased worldwide. In Spain, the incidence of hospitalisation per 100,000 person-years for non-varicose UGB decreased from 54.6 in 1996 to 25.8 in 2005. Given the lower incidence, overall mortality has decreased, although hospital mortality remains stable at around 5% of admissions.<a class="elsevierStyleCrossRef" href="#bib0095">19</a> The persistently high in-hospital mortality is probably due to the fact that UGB patients are now older and more often present with severe comorbidities, especially cardiovascular.<a class="elsevierStyleCrossRefs" href="#bib0100">20,21</a>Adequate treatment of UGB reduces mortality and is based on: (a) adequate treatment of haemodynamic status with early and non-aggressive crystalloid infusion, (b) a restrictive transfusion policy, (c) the use of high-dose intravenous PPI inhibitors, (d) early reintroduction of antiplatelet and/or antithrombotic therapy and (e) and performance of EGD within the first 24 h.In case of bleeding recurrence, a second endoscopic treatment is recommended. Arterial embolisation is reserved for cases of persistent bleeding after endoscopic treatment or a second recurrence after two endoscopic treatments. Although it depends on local availability and experience, embolisation is considered preferable to surgery because of its similar efficacy and lower morbidity and mortality. Surgery is therefore currently reserved for exceptional cases.<a class="elsevierStyleCrossRef" href="#bib0110">22</a>Perforation and penetrationPerforation is the PU complication with the highest mortality, up to 30% of cases, with duodenal perforation being more common than gastric perforation (60% vs. 40%), typically associated with NSAID treatment.<a class="elsevierStyleCrossRef" href="#bib0115">23</a> The triad of sudden abdominal pain, tachycardia and abdominal splinting as a sign of peritoneal irritation is characteristic: this is associated with the absence of peristalsis on physical examination and increased acute phase reactants on blood tests. In up to 15% of perforation cases, a plain chest X-ray in the standing position will not show subdiaphragmatic free air. In contrast, abdominal CT scan is much more sensitive (98%) and is considered the diagnostic technique of choice. Early diagnosis, haemodynamic resuscitation, antibiotic treatment and urgent surgical intervention are essential<a class="elsevierStyleCrossRef" href="#bib0120">24</a> to increase survival; thus, one of the factors most strongly associated with mortality is surgery delay.<a class="elsevierStyleCrossRef" href="#bib0125">25</a>Penetration is defined as invasion of the ulcer by erosion of the intestinal wall into an adjacent organ or anatomical structure, with no outflow of air or intestinal contents into the peritoneum. The pancreas is the most common location. Patients may notice changes in the characteristics of the pain, e.g., an increase in intensity that does not improve with food or medication, or back irradiation. Diagnosis is confirmed by abdominal CT scan and treatment is usually surgical.<a class="elsevierStyleCrossRef" href="#bib0130">26</a>StenosisDuodenal cap or pyloro-antral stenosis is the least common complication of PU, accounting for 5%. Until the 1970s, PU was the most common cause of gastric obstruction. Today, however, the main cause of stricture is antral neoplasm.<a class="elsevierStyleCrossRef" href="#bib0135">27</a> Symptomatology consists of nausea, vomiting, early satiety, anorexia and weight loss. Diagnosis is made by EGD and biopsy and initial treatment should be with high-dose intravenous PPIs. Unresponsive patients should be assessed for endoscopic dilatation. However, in patients with scarring fibrosis, endoscopic therapy may be ineffective. In these cases, direct surgery -pyloroplasty or gastro-jejunostomy- can either be chosen or reserved if dilatation fails.<a class="elsevierStyleCrossRef" href="#bib0140">28</a>DiagnosisPU symptoms are often non-specific and of low predictive value. The most common are dyspepsia symptoms (epigastric pain or burning, bloating or early satiety). In patients younger than 55 years, without warning signs for neoplasm and uninvestigated dyspepsia, as an alternative to EGD, a 'test and treat' strategy is recommended, which consists of performing a non-invasive test for H. pylori and in case of a positive result, implement treatment.<a class="elsevierStyleCrossRef" href="#bib0145">29</a> On the other hand, in patients older than 55 years or with warning signs or symptoms, it is recommended to perform a baseline EGD to exclude malignancy.<a class="elsevierStyleCrossRefs" href="#bib0150">30,31</a>EGD is the diagnostic test of choice, allowing diagnosis of PU and biopsies to rule out malignancy in the case of gastric ulcer (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). It also allows detection of H. pylori infection by histology, rapid urease test or molecular techniques, useful for further treatment planning.<elsevierMultimedia ident="fig0005"></elsevierMultimedia>Endoscopic data not only allow the diagnosis to be made, but also suggest whether the aetiology is benign or malignant. Duodenal ulcers are very rarely malignant and therefore do not routinely require biopsy. Gastric ulcers with inflammatory margins of regular appearance suggest a benign aetiology. In contrast, irregular or thickened margins and/or the presence of a mass raised towards the lumen suggest a malignant aetiology (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). Regardless of the endoscopic appearance, biopsies of the base and margins of any gastric ulcer should be performed.<a class="elsevierStyleCrossRef" href="#bib0160">32</a> Follow-up endoscopy is also recommended to check for healing and to rule out malignant aetiology, even if the previous biopsy is benign.<a class="elsevierStyleCrossRef" href="#bib0165">33</a>TreatmentInitially it will include PPIs at standard doses for 4 weeks in duodenal ulcer and for 8 weeks in gastric ulcer.In patients with H. pylori infection, the treatment of choice for PU is eradication therapy, based on a combination of several antibiotics active against H. pylori together with a PPI. The target cure rate should be at least 90%. According to the most recent consensus, the key points for the choice of eradication therapy are<a class="elsevierStyleCrossRefs" href="#bib0170">34,35</a>:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">-Use quadruple regimens. Triple therapies are not recommended because of their low efficacy in our setting.</li><li class="elsevierStyleListItem" id="lsti0010">-Extend the duration of treatment to 14 days.</li><li class="elsevierStyleListItem" id="lsti0015">-Use high doses of PPIs. Use of PPIs at double doses, every 12 h, increases cure rates.</li><li class="elsevierStyleListItem" id="lsti0020">-In salvage regimens, do not repeat antibiotics with high rates of secondary resistance such as clarithromycin or levofloxacin.</li></ul>As treatment of choice, a quadruple combination with bismuth using a PPI is recommended, associated with the combination of bismuth, tetracycline and metronidazole in a single capsule. This combination is well tolerated and achieves cure rates of over 90% with only 10 days of treatment. A second alternative is concomitant quadruple therapy without bismuth (PPI, clarithromycin, amoxicillin and metronidazole) for 14 days. If these first-line regimens fail to cure the infection, salvage treatment includes a quadruple regimen with levofloxacin (PPI, amoxicillin, levofloxacin and bismuth).<a class="elsevierStyleCrossRef" href="#bib0175">35</a> In penicillin-allergic patients, a quadruple regimen with bismuth and salvage therapy with a quadruple regimen of levofloxacin PPI, clarithromycin and bismuth is recommended. Failure of two treatment regimens makes it necessary to reconsider the indication for eradication therapy and to assess causes of non-adherence before proceeding with further lines of treatment.<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a> summarises the drugs, doses and duration of H. pylori eradication treatment recommended in our setting.<elsevierMultimedia ident="fig0010"></elsevierMultimedia>In patients with uncomplicated duodenal ulcer who do not require NSAIDs or ASA, it is not recommended to maintain antisecretory therapy after completion of H. pylori treatment. In contrast, in patients with gastric ulcer who do not require NSAIDs or ASA, it is recommended to maintain antisecretory therapy for four to eight weeks.<a class="elsevierStyleCrossRef" href="#bib0175">35</a>Treatment and prevention of NSAID-induced peptic ulcersIn patients with NSAID-induced PUs, duodenal ulcers heal after 4 weeks of treatment with a PPI and gastric ulcers heal after 6–8 weeks, even if anti-inflammatory treatment is maintained. PPIs reduce the risk of developing a peptic ulcer in patients receiving NSAIDs or ASA in both acute (OR 0.70, 95% CI 0.24–2.04) and chronic (OR 0.32, 95% CI 0.15−0.67) treatment.<a class="elsevierStyleCrossRef" href="#bib0180">36</a>PPIs are the treatment of choice for the prevention of PU in patients receiving NSAIDs, with PPIs being superior to placebo and anti-H2 agents and equally effective than misoprostol, although with better tolerance.<a class="elsevierStyleCrossRefs" href="#bib0185">37,38</a>The available data suggest that all PPIs provide equivalent, safe and effective prophylaxis. They are effective at standard doses (omeprazole 20 mg/day, lansoprazole 30 mg/day, pantoprazole 40 mg/day, rabeprazole 20 mg/day or esomeprazole 20 mg/day), with no evidence that higher doses are superior for either treatment or prevention of NSAID-induced gastroduodenal lesions.<a class="elsevierStyleCrossRef" href="#bib0190">38</a> Lower doses, which may decrease the efficacy of prevention, are also not recommended. Given its lower cost, omeprazole 20 mg is the PPI of choice. In patients with one or more risk factors for gastrointestinal bleeding, the benefits of PPI therapy -prevention of PU- far outweigh the risk of complications of these drugs. Although several studies have suggested an association between long-term PPI treatment and multiple pathologies such as bone fractures or Clostridium difficile infection, all of them are observational, the increased risk is very modest and many of the associations can be explained by the presence of confounding factors.<a class="elsevierStyleCrossRef" href="#bib0195">39</a> Moreover, no study has shown an increase in mortality associated with PPI use.<a class="elsevierStyleCrossRefs" href="#bib0200">40,41</a> Therefore, there is no justification for under-therapeutic doses, avoidance or discontinuation of these drugs in accepted indications.<a class="elsevierStyleCrossRef" href="#bib0210">42</a> That said, it is clear that we cannot completely rule out potential risks and that the drug should not be used if it is not indicated. Therefore, as with any medicine, it is important to carefully assess the benefits and risks before prescribing.On the other hand, it is important to define the gastrointestinal and cardiovascular risks of each patient (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>), which will allow us to select the appropriate NSAID (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). In this regard, COXIBs are associated with a lower risk of peptic complications compared to non-selective NSAIDs. Their risk of gastrointestinal complications is similar to that of the association of an NSAID with PPIs. However, the benefits of selective COX-2 inhibitors are reduced -in fact, they practically disappear- with the co-administration of low doses of ASA. In these cases, it would be necessary to associate a PPI to the COXIB to prevent PU. The association of NSAIDs and anticoagulants significantly increase the risk of bleeding; again, the risk is lower with COXIBs than with non-selective NSAIDs.<elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia>In patients at cardiovascular risk, it should first be assessed whether administration is strictly necessary. If it is, the minimum effective dose should be used for the shortest possible time. Finally, NSAIDs with the best cardiovascular safety profile should be used (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).<a class="elsevierStyleCrossRef" href="#bib0015">3</a>Eradication of H. pylori in patients on NSAID/ASA treatmentIt is highly controversial whether patients on chronic treatment with NSAIDs and/or ASA should be treated for H. pylori.There is some evidence in favour of eradication in patients who are about to start NSAID treatment (naive). Thus, a meta-analysis showed that both H. pylori infection and the use of non-selective NSAIDs are independent risk factors for the development of PU.<a class="elsevierStyleCrossRef" href="#bib0215">43</a> The approach will depend on whether patients are naïve or already on chronic NSAID therapy and whether or not they have a history of previous PU.<a class="elsevierStyleCrossRef" href="#bib0220">44</a> Thus, in naïve patients with no history of PU or complications, eradication of H. pylori significantly reduces the risk of PU and ulcer bleeding<a class="elsevierStyleCrossRefs" href="#bib0225">45,46</a> but not in those already on chronic NSAID therapy.<a class="elsevierStyleCrossRefs" href="#bib0235">47,48</a>In patients with a history of PU or complications, on chronic NSAID treatment, at least 2 randomised controlled trials (RCTs) show that chronic PPI treatment is superior to eradication<a class="elsevierStyleCrossRefs" href="#bib0245">49,50</a> and a third RCT concludes that there is no difference between eradication and PPI treatment.<a class="elsevierStyleCrossRef" href="#bib0255">51</a> In NSAID naïve patients, one RCT<a class="elsevierStyleCrossRef" href="#bib0260">52</a> shows that eradication is clearly superior to non-eradication in preventing PU during the six months following treatment (12.1% vs. 34%), although neither group received prophylactic PPI treatment in this study.Therefore, it is recommended to investigate and treat H. pylori in patients who are about to start NSAID therapy (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>). Eradication should be associated with prophylaxis whenever patients have any gastrointestinal risk factors (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). It is not recommended to investigate H. pylori in patients on chronic NSAID therapy, especially in those already receiving PPI prophylaxis. There are no studies showing that H. pylori eradication provides additional efficacy in reducing the risk of PU or its complications in this group of patients. On the other hand, this is a generally older group, with comorbidity and often polypharmacy. In this context, the risk of bleeding after temporarily stopping PPIs to assess H. pylori and the risk of adverse effects or interactions of eradication therapy are likely to outweigh the possible -and unproven- benefits of H. pylori eradication.<elsevierMultimedia ident="tbl0010"></elsevierMultimedia>In patients on chronic ASA treatment, H. pylori eradication has been shown to slightly reduce the risk of PU bleeding.<a class="elsevierStyleCrossRefs" href="#bib0265">53,54</a>However, a meta-analysis<a class="elsevierStyleCrossRef" href="#bib0275">55</a> showed that the evidence was not sufficient to conclude that H. pylori is a risk factor for UGB in patients receiving ASA. In addition, an epidemiological study<a class="elsevierStyleCrossRef" href="#bib0280">56</a> found neither additive nor potentiating effect between ASA and H. pylori infection in patients with PU. In an RCT in 250 high-risk patients -with a history of UGB for PU- and chronic ASA, Chan et al.<a class="elsevierStyleCrossRef" href="#bib0250">50</a> compared H. pylori eradication versus chronic PPI, with a 6-month follow-up. The rate of bleeding was low in both groups, 1.9% in patients receiving eradication treatment and 0.9% in patients with prophylactic PPI. The differences were not significant, probably due to the limited follow-up and the small number of patients.On the other hand, there is strong evidence<a class="elsevierStyleCrossRef" href="#bib0285">57</a> that the use of PPIs reduces the risk of PU and bleeding in patients on chronic treatment with NSAIDs or ASA. Therefore, treatment with PPIs is recommended in patients receiving ASA with gastrointestinal risk factors.On the other hand, it is not recommended to systematically investigate and treat H. pylori in patients receiving or about to receive ASA.Peptic ulcer in H. pylori-negative patients not taking NSAIDs/ASAWith the decreasing prevalence of H. pylori infection, some studies indicate an increased proportion of 'idiopathic' PU, i.e., H. pylori-negative and not associated with NSAIDs or ASA. However, there is an important limitation in these studies, and that is the fact that there is no objective method to assess ASA and NSAID intake. In the studies, this information is generally obtained during history-taking or from the medical records. In a study conducted in our setting, the prevalence of idiopathic PU was very low: only 1.6% of all duodenal ulcers and 4.1% of all gastric ulcers were negative for NSAIDs and H. pylori.<a class="elsevierStyleCrossRef" href="#bib0290">58</a>The diagnosis of NSAID- and H. pylori-negative PUs should be made only after careful exclusion of 'occult' NSAID use and/or a false negative diagnosis of H. pylori infection.In NSAIDs and H. pylori-negative PUs, the use of other drugs or toxins with ulcerogenic potential such as bisphosphonates, cocaine, radiotherapy or oral iron should be assessed. Other causes to rule out are atypical herpes virus or cytomegalovirus infections, other disorders such as Crohn's disease or malignant aetiology, especially in the case of duodenal ulcers where biopsies should not be performed. Lymphoma or Kaposi's sarcoma are very rare causes of ulceration and are usually related to a state of immunosuppression. Another rare cause is gastrinoma (Zollinger Ellison syndrome). In this case, patients usually have diarrhoea accompanying PU that responds to PPI treatment. PU due to gastrinoma is usually severe, multiple and often extends into the distal duodenum, although the typical gastrinoma symptoms may be masked by previous PPI use.<a class="elsevierStyleCrossRef" href="#bib0295">59</a>Future challengesImportant challenges remain in the treatment and prevention of PU. These include determining the best medication combination in NSAID/ASA users and, above all, addressing the increase in difficult-to-treat bleeding in patients with severe co-morbidity on anticoagulant therapy.Conflict of interestXavier Calvet has received lecture fees from Allergan. Pilar García-Iglesias and Isabel Laucirica declare no conflicts of interest in relation to this review." "textoCompletoSecciones" => array:1 [ "secciones" => array:17 [ 0 => array:3 [ "identificador" => "xres1975402" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1699048" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1975403" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1699049" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Definition" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Epidemiology" ] 6 => array:3 [ "identificador" => "sec0015" "titulo" => "Risk factors and pathophysiology" "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0020" "titulo" => "Pathophysiology of H. pylori damage" ] 1 => array:2 [ "identificador" => "sec0025" "titulo" => "Pathophysiology of NSAID damage" ] ] ] 7 => array:2 [ "identificador" => "sec0030" "titulo" => "Clinical signs and symptoms" ] 8 => array:3 [ "identificador" => "sec0035" "titulo" => "Complications of peptic ulcer disease" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0040" "titulo" => "Upper gastrointestinal bleeding" ] 1 => array:2 [ "identificador" => "sec0045" "titulo" => "Perforation and penetration" ] 2 => array:2 [ "identificador" => "sec0050" "titulo" => "Stenosis" ] ] ] 9 => array:2 [ "identificador" => "sec0055" "titulo" => "Diagnosis" ] 10 => array:2 [ "identificador" => "sec0060" "titulo" => "Treatment" ] 11 => array:2 [ "identificador" => "sec0065" "titulo" => "Treatment and prevention of NSAID-induced peptic ulcers" ] 12 => array:2 [ "identificador" => "sec0070" "titulo" => "Eradication of H. pylori in patients on NSAID/ASA treatment" ] 13 => array:2 [ "identificador" => "sec0075" "titulo" => "Peptic ulcer in H. pylori-negative patients not taking NSAIDs/ASA" ] 14 => array:2 [ "identificador" => "sec0080" "titulo" => "Future challenges" ] 15 => array:2 [ "identificador" => "sec0085" "titulo" => "Conflict of interest" ] 16 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2023-03-24" "fechaAceptado" => "2023-05-29" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1699048" "palabras" => array:6 [ 0 => "Peptic ulcer disease" 1 => "Helicobacter pylori" 2 => "Gastroprotection" 3 => "Non-steroidal anti-inflammatory drugs" 4 => "COX-2 selective inhibitors" 5 => "Upper gastrointestinal complications" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1699049" "palabras" => array:6 [ 0 => "Úlcera péptica" 1 => "Helicobacter pylori" 2 => "Gastroprotección" 3 => "Antiinflamatorios no esteroideos" 4 => "Inhibidores selectivos COX-2" 5 => "Complicaciones gastrointestinales" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "Peptic ulcer disease (PUD) is a frequent pathology; although the incidence has decreased in recent years, it continues to be an important cause of morbidity and mortality associated with high healthcare costs. The most important risk factors are Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID). Most patients with PUD remain asymptomatic, with dyspepsia being the most frequent and often characteristic symptom. It can also debut with complications such as upper gastrointestinal bleeding, perforation or stenosis. The diagnostic technique of choice is upper gastrointestinal endoscopy. Treatment with proton pump inhibitors (PPIs), eradication of H. pylori and avoiding the use of NSAIDs are the basis of treatment. However, prevention is the best strategy, it includes an adequate indication of PPIs, investigation and treatment of H. pylori, avoiding NSAIDs or using those that are less gastrolesive." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "La enfermedad ulcerosa péptica (UP) es una patología frecuente; aunque su incidencia ha disminuido en los últimos años, sigue siendo una causa importante de morbimortalidad asociada a un elevado gasto sanitario. Los factores de riesgo más importantes son la infección por Helicobacter pylori y el uso de antiinflamatorios no esteroideos (AINE). La mayoría de los pacientes con UP permanecen asintomáticos, siendo la clínica más frecuente la dispepsia, a menudo característica (dispepsia ulcerosa). También puede debutar con complicaciones como hemorragia digestiva alta, perforación o estenosis. La técnica diagnóstica de elección es la endoscopia digestiva alta. El tratamiento con inhibidores de la bomba de protones (IBP), la erradicación de H. pylori y evitar el consumo de AINE son la base del tratamiento. Sin embargo, la prevención es la mejor estrategia, incluye una adecuada indicación de IBP, la investigación y tratamiento de H. pylori, evitar los AINE o utilizar aquellos menos gastrolesivos." ] ] "multimedia" => array:5 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 982 "Ancho" => 1740 "Tamanyo" => 273533 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Endoscopic images of peptic ulcer. (A) Duodenal ulcer with fibrin base. (B) Gastric ulcer with haematin stain. (C) Duodenal ulcer with visible non-bleeding vessel. (D) Gastric ulcer secondary to gastric adenocarcinoma. (E) Duodenal ulcer with active bleeding. (F) Gastric ulcer with adherent clot." ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1489 "Ancho" => 2925 "Tamanyo" => 366901 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Eradication treatment of choice for Helicobacter pylori. *PPIs: proton pump inhibitors. Double doses increase cure rates. **Pylera®: 1 tablet combines 140 mg bismuth subcitrate, 125 mg tetracycline hydrochloride and 125 mg metronidazole. ***Dosage schedule as described in the SmPC; data from the European H. pylori Registry suggest that the dose of 4 capsules every 8 h is most effective and well tolerated." ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 784 "Ancho" => 1675 "Tamanyo" => 141384 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "Selection of anti-inflammatory and gastroprotective therapy according to digestive and cardiovascular risk. ASA, acetylsalicylic acid; NSAID, non-steroidal anti-inflammatory drug; PPI, proton pump inhibitor." ] ] 3 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0020" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "SSRIs, selective serotonin reuptake inhibitors." "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Gastrointestinal risk</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><1.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">No \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Moderate \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1.5−10 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1 or 2 of the following:Age over 65 yearsUncomplicated peptic ulcerationSevere comorbidityDrugs: glucocorticoids, SSRIs, clopidogrel \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">>10 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">More than 2 risk factors orComplicated peptic ulcerationConcomitant use of anticoagulants \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " colspan="3" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Cardiovascular risk</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">No \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-platelets in secondary cardiovascular prophylaxis \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab3287839.png" ] ] ] ] "descripcion" => array:1 [ "en" => "Gastrointestinal and cardiovascular risk stratification." ] ] 4 => array:8 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "ASA, acetylsalicylic acid; NSAID, non-steroidal anti-inflammatory drug; PPI, proton pump inhibitor." "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Drug \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Gastrointestinal risk \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Recommendation \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ASA</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Do not investigate or treat H. pylori \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Moderate/high \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Do not investigate or treat H. pylori. PPI \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">No previous NSAID (naive)</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Investigate and treat H. pylori. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Moderate/high \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">No evidence. PPI \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Chronic NSAID</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Do not investigate or treat H. pylori \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Moderate/high \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Do not investigate or treat H. pylori. PPI \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab3287840.png" ] ] ] ] "descripcion" => array:1 [ "en" => "Eradication of Helicobacter pylori in patients receiving ASA or NSAIDs." ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:59 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Peptic ulcer disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "P. Malfertheiner" 1 => "F.K. Chan" 2 => "K.E.L. McColl" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/S0140-6736(09)60938-7" "Revista" => array:6 [ "tituloSerie" => "Lancet." 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Peptic ulcer

Úlcera péptica

Isabel Lauciricaa, Pilar Garcia Iglesiasa, Xavier Calveta,b,

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xcalvet@tauli.cat

Corresponding author.

a Servei d’Aparell Digestiu, Parc Taulí Hospital Universitari, Institut d’Investigació i Innovació Parc Taulí (I3PT-CERCA), Departament de Medicina, Universitat Autònoma de Barcelona, Sabadell, Spain

b Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain

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however&#44; inflammation would also significantly affect the mucosa of the body&#44; damaging the glands and decreasing acid secretion&#46; Mucosal damage in this case is attributed to decreased protective factors&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">On the other hand&#44; infection with <span class="elsevierStyleItalic">H&#46; pylori</span> strains expressing virulence factors is associated with an increased risk of PU&#44; with the expression of Cag A protein&#44; which induces a strong local inflammatory response&#44; and Vac A toxin&#44; which causes vacuolar degeneration and ulceration&#44; being the two most important factors&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12&#44;13</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Pathophysiology of NSAID damage</span><p id="par0050" class="elsevierStylePara elsevierViewall">The main ulcerogenic mechanism of NSAIDs is the inhibition of the enzyme cyclooxygenase &#40;COX&#41;&#44; which in turn is the molecular mechanism of their anti-inflammatory action&#46; This enzyme has two isoforms&#44; COX-1 and COX-2&#46; COX-1 inhibition - which is constitutive - decreases the synthesis of prostaglandins involved in gastrointestinal protection&#44; reduces bicarbonate and mucus secretion and affects the integrity of the mucosal barrier&#46; A second ulcerogenic mechanism of NSAIDs is direct damage to gastric mucosal cells by accumulation in the cytoplasm&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">All this favours the development of PU&#46; COX-2 -which is inducible- develops in tissues in response to local inflammation and produces mediators of pain and inflammation&#46; Inhibition of COX-2 is responsible for the beneficial effects of NSAIDs&#46; Unlike non-selective NSAIDs that similarly inhibit both isoenzymes &#40;COX-1 and COX-2&#41;&#44; COXIBs inhibit COX-2 to a greater extent and are therefore less ulcerogenic&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">A number of factors increase the risk of developing PU and its complications in patients receiving NSAIDs&#44; usually due to decreased mucosal barrier efficacy&#46; The main risk factors are age&#44; smoking&#44; the presence of comorbidities and the concomitant use of other drugs&#44; which may influence the development of PU and its clinical course&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p></span></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Clinical signs and symptoms</span><p id="par0065" class="elsevierStylePara elsevierViewall">The usual clinical features consist of dyspepsia symptoms&#44; often non-specific&#44; such as epigastric pain or discomfort&#44; commonly described as &#39;burning&#39;&#44; sometimes with a feeling of painful hunger&#46; Irradiation to the flanks or retrosternal area is rare&#46; In duodenal ulcer&#44; the pain occurs daily&#44; developing 2&#8722;3&#8239;h after ingestion&#44; wakes the patient early in the morning and is usually relieved after taking antacids or food&#46; Radiation towards the back suggests a penetrating duodenal ulcer&#46; In patients with gastric ulcer the pattern tends to be more atypical and irregular and many or all of these features may be missing&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">In most cases&#44; peptic ulcer follows a chronic relapsing course with symptomatic flares lasting several weeks&#44; often with a clear seasonal relationship &#40;predominantly spring or autumn&#41; followed by spontaneous remissions with symptom-free periods of months or years&#46; Physical examination is usually normal&#44; except for the occasional and completely non-specific epigastric tenderness&#46; Most elderly patients with PU are asymptomatic or oligosymptomatic&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">14&#44;16&#44;17</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Complications of peptic ulcer disease</span><p id="par0075" class="elsevierStylePara elsevierViewall">Complications include upper gastrointestinal bleeding &#40;UGB&#41;&#44; perforation&#44; penetration and stenosis&#46;</p><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Upper gastrointestinal bleeding</span><p id="par0080" class="elsevierStylePara elsevierViewall">It is the most common complication of PU and the most common cause of non-varicose UGB&#44; accounting for 40&#37;&#8211;50&#37; of cases&#46; The most common presentation is in the form of haematemesis and&#47;or melena&#44; with or without abdominal pain&#46; Up to 15&#37; of cases may develop as rectal bleeding due to rapid transit of blood along the intestine&#44; especially after major haemorrhages&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3&#44;18&#44;19</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Hospital admissions for UGB due to PU have decreased worldwide&#46; In Spain&#44; the incidence of hospitalisation per 100&#44;000 person-years for non-varicose UGB decreased from 54&#46;6 in 1996 to 25&#46;8 in 2005&#46; Given the lower incidence&#44; overall mortality has decreased&#44; although hospital mortality remains stable at around 5&#37; of admissions&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> The persistently high in-hospital mortality is probably due to the fact that UGB patients are now older and more often present with severe comorbidities&#44; especially cardiovascular&#46;<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">20&#44;21</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Adequate treatment of UGB reduces mortality and is based on&#58; &#40;a&#41; adequate treatment of haemodynamic status with early and non-aggressive crystalloid infusion&#44; &#40;b&#41; a restrictive transfusion policy&#44; &#40;c&#41; the use of high-dose intravenous PPI inhibitors&#44; &#40;d&#41; early reintroduction of antiplatelet and&#47;or antithrombotic therapy and &#40;e&#41; and performance of EGD within the first 24&#8239;h&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">In case of bleeding recurrence&#44; a second endoscopic treatment is recommended&#46; Arterial embolisation is reserved for cases of persistent bleeding after endoscopic treatment or a second recurrence after two endoscopic treatments&#46; Although it depends on local availability and experience&#44; embolisation is considered preferable to surgery because of its similar efficacy and lower morbidity and mortality&#46; Surgery is therefore currently reserved for exceptional cases&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Perforation and penetration</span><p id="par0100" class="elsevierStylePara elsevierViewall">Perforation is the PU complication with the highest mortality&#44; up to 30&#37; of cases&#44; with duodenal perforation being more common than gastric perforation &#40;60&#37; vs&#46; 40&#37;&#41;&#44; typically associated with NSAID treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> The triad of sudden abdominal pain&#44; tachycardia and abdominal splinting as a sign of peritoneal irritation is characteristic&#58; this is associated with the absence of peristalsis on physical examination and increased acute phase reactants on blood tests&#46; In up to 15&#37; of perforation cases&#44; a plain chest X-ray in the standing position will not show subdiaphragmatic free air&#46; In contrast&#44; abdominal CT scan is much more sensitive &#40;98&#37;&#41; and is considered the diagnostic technique of choice&#46; Early diagnosis&#44; haemodynamic resuscitation&#44; antibiotic treatment and urgent surgical intervention are essential<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> to increase survival&#59; thus&#44; one of the factors most strongly associated with mortality is surgery delay&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">Penetration is defined as invasion of the ulcer by erosion of the intestinal wall into an adjacent organ or anatomical structure&#44; with no outflow of air or intestinal contents into the peritoneum&#46; The pancreas is the most common location&#46; Patients may notice changes in the characteristics of the pain&#44; e&#46;g&#46;&#44; an increase in intensity that does not improve with food or medication&#44; or back irradiation&#46; Diagnosis is confirmed by abdominal CT scan and treatment is usually surgical&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Stenosis</span><p id="par0110" class="elsevierStylePara elsevierViewall">Duodenal cap or pyloro-antral stenosis is the least common complication of PU&#44; accounting for 5&#37;&#46; Until the 1970s&#44; PU was the most common cause of gastric obstruction&#46; Today&#44; however&#44; the main cause of stricture is antral neoplasm&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Symptomatology consists of nausea&#44; vomiting&#44; early satiety&#44; anorexia and weight loss&#46; Diagnosis is made by EGD and biopsy and initial treatment should be with high-dose intravenous PPIs&#46; Unresponsive patients should be assessed for endoscopic dilatation&#46; However&#44; in patients with scarring fibrosis&#44; endoscopic therapy may be ineffective&#46; In these cases&#44; direct surgery -pyloroplasty or gastro-jejunostomy- can either be chosen or reserved if dilatation fails&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a></p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Diagnosis</span><p id="par0115" class="elsevierStylePara elsevierViewall">PU symptoms are often non-specific and of low predictive value&#46; The most common are dyspepsia symptoms &#40;epigastric pain or burning&#44; bloating or early satiety&#41;&#46; In patients younger than 55 years&#44; without warning signs for neoplasm and uninvestigated dyspepsia&#44; as an alternative to EGD&#44; a <span class="elsevierStyleItalic">&#39;test and treat&#39;</span> strategy is recommended&#44; which consists of performing a non-invasive test for <span class="elsevierStyleItalic">H&#46; pylori</span> and in case of a positive result&#44; implement treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> On the other hand&#44; in patients older than 55 years or with warning signs or symptoms&#44; it is recommended to perform a baseline EGD to exclude malignancy&#46;<a class="elsevierStyleCrossRefs" href="#bib0150"><span class="elsevierStyleSup">30&#44;31</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">EGD is the diagnostic test of choice&#44; allowing diagnosis of PU and biopsies to rule out malignancy in the case of gastric ulcer &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; It also allows detection of <span class="elsevierStyleItalic">H&#46; pylori</span> infection by histology&#44; rapid urease test or molecular techniques&#44; useful for further treatment planning&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0125" class="elsevierStylePara elsevierViewall">Endoscopic data not only allow the diagnosis to be made&#44; but also suggest whether the aetiology is benign or malignant&#46; Duodenal ulcers are very rarely malignant and therefore do not routinely require biopsy&#46; Gastric ulcers with inflammatory margins of regular appearance suggest a benign aetiology&#46; In contrast&#44; irregular or thickened margins and&#47;or the presence of a mass raised towards the lumen suggest a malignant aetiology &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Regardless of the endoscopic appearance&#44; biopsies of the base and margins of any gastric ulcer should be performed&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> Follow-up endoscopy is also recommended to check for healing and to rule out malignant aetiology&#44; even if the previous biopsy is benign&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Treatment</span><p id="par0130" class="elsevierStylePara elsevierViewall">Initially it will include PPIs at standard doses for 4 weeks in duodenal ulcer and for 8 weeks in gastric ulcer&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">In patients with <span class="elsevierStyleItalic">H&#46; pylori</span> infection&#44; the treatment of choice for PU is eradication therapy&#44; based on a combination of several antibiotics active against H<span class="elsevierStyleItalic">&#46; pylori</span> together with a PPI&#46; The target cure rate should be at least 90&#37;&#46; According to the most recent consensus&#44; the key points for the choice of eradication therapy are<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">34&#44;35</span></a>&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">-</span><p id="par0140" class="elsevierStylePara elsevierViewall">Use quadruple regimens&#46; Triple therapies are not recommended because of their low efficacy in our setting&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">-</span><p id="par0145" class="elsevierStylePara elsevierViewall">Extend the duration of treatment to 14 days&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">-</span><p id="par0150" class="elsevierStylePara elsevierViewall">Use high doses of PPIs&#46; Use of PPIs at double doses&#44; every 12&#8239;h&#44; increases cure rates&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">-</span><p id="par0155" class="elsevierStylePara elsevierViewall">In salvage regimens&#44; do not repeat antibiotics with high rates of secondary resistance such as clarithromycin or levofloxacin&#46;</p></li></ul></p><p id="par0160" class="elsevierStylePara elsevierViewall">As treatment of choice&#44; a quadruple combination with bismuth using a PPI is recommended&#44; associated with the combination of bismuth&#44; tetracycline and metronidazole in a single capsule&#46; This combination is well tolerated and achieves cure rates of over 90&#37; with only 10 days of treatment&#46; A second alternative is concomitant quadruple therapy without bismuth &#40;PPI&#44; clarithromycin&#44; amoxicillin and metronidazole&#41; for 14 days&#46; If these first-line regimens fail to cure the infection&#44; salvage treatment includes a quadruple regimen with levofloxacin &#40;PPI&#44; amoxicillin&#44; levofloxacin and bismuth&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> In penicillin-allergic patients&#44; a quadruple regimen with bismuth and salvage therapy with a quadruple regimen of levofloxacin PPI&#44; clarithromycin and bismuth is recommended&#46; Failure of two treatment regimens makes it necessary to reconsider the indication for eradication therapy and to assess causes of non-adherence before proceeding with further lines of treatment&#46;</p><p id="par0165" class="elsevierStylePara elsevierViewall"><a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a> summarises the drugs&#44; doses and duration of <span class="elsevierStyleItalic">H&#46; pylori</span> eradication treatment recommended in our setting&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0170" class="elsevierStylePara elsevierViewall">In patients with uncomplicated duodenal ulcer who do not require NSAIDs or ASA&#44; it is not recommended to maintain antisecretory therapy after completion of <span class="elsevierStyleItalic">H&#46; pylori</span> treatment&#46; In contrast&#44; in patients with gastric ulcer who do not require NSAIDs or ASA&#44; it is recommended to maintain antisecretory therapy for four to eight weeks&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Treatment and prevention of NSAID-induced peptic ulcers</span><p id="par0175" class="elsevierStylePara elsevierViewall">In patients with NSAID-induced PUs&#44; duodenal ulcers heal after 4 weeks of treatment with a PPI and gastric ulcers heal after 6&#8211;8 weeks&#44; even if anti-inflammatory treatment is maintained&#46; PPIs reduce the risk of developing a peptic ulcer in patients receiving NSAIDs or ASA in both acute &#40;OR 0&#46;70&#44; 95&#37; CI 0&#46;24&#8211;2&#46;04&#41; and chronic &#40;OR 0&#46;32&#44; 95&#37; CI 0&#46;15&#8722;0&#46;67&#41; treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a></p><p id="par0180" class="elsevierStylePara elsevierViewall">PPIs are the treatment of choice for the prevention of PU in patients receiving NSAIDs&#44; with PPIs being superior to placebo and anti-H2 agents and equally effective than misoprostol&#44; although with better tolerance&#46;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">37&#44;38</span></a></p><p id="par0185" class="elsevierStylePara elsevierViewall">The available data suggest that all PPIs provide equivalent&#44; safe and effective prophylaxis&#46; They are effective at standard doses &#40;omeprazole 20&#8239;mg&#47;day&#44; lansoprazole 30&#8239;mg&#47;day&#44; pantoprazole 40&#8239;mg&#47;day&#44; rabeprazole 20&#8239;mg&#47;day or esomeprazole 20&#8239;mg&#47;day&#41;&#44; with no evidence that higher doses are superior for either treatment or prevention of NSAID-induced gastroduodenal lesions&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> Lower doses&#44; which may decrease the efficacy of prevention&#44; are also not recommended&#46; Given its lower cost&#44; omeprazole 20&#8239;mg is the PPI of choice&#46; In patients with one or more risk factors for gastrointestinal bleeding&#44; the benefits of PPI therapy -prevention of PU- far outweigh the risk of complications of these drugs&#46; Although several studies have suggested an association between long-term PPI treatment and multiple pathologies such as bone fractures or <span class="elsevierStyleItalic">Clostridium difficile</span> infection&#44; all of them are observational&#44; the increased risk is very modest and many of the associations can be explained by the presence of confounding factors&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a> Moreover&#44; no study has shown an increase in mortality associated with PPI use&#46;<a class="elsevierStyleCrossRefs" href="#bib0200"><span class="elsevierStyleSup">40&#44;41</span></a> Therefore&#44; there is no justification for under-therapeutic doses&#44; avoidance or discontinuation of these drugs in accepted indications&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a> That said&#44; it is clear that we cannot completely rule out potential risks and that the drug should not be used if it is not indicated&#46; Therefore&#44; as with any medicine&#44; it is important to carefully assess the benefits and risks before prescribing&#46;</p><p id="par0190" class="elsevierStylePara elsevierViewall">On the other hand&#44; it is important to define the gastrointestinal and cardiovascular risks of each patient &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#44; which will allow us to select the appropriate NSAID &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46; In this regard&#44; COXIBs are associated with a lower risk of peptic complications compared to non-selective NSAIDs&#46; Their risk of gastrointestinal complications is similar to that of the association of an NSAID with PPIs&#46; However&#44; the benefits of selective COX-2 inhibitors are reduced -in fact&#44; they practically disappear- with the co-administration of low doses of ASA&#46; In these cases&#44; it would be necessary to associate a PPI to the COXIB to prevent PU&#46; The association of NSAIDs and anticoagulants significantly increase the risk of bleeding&#59; again&#44; the risk is lower with COXIBs than with non-selective NSAIDs&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0195" class="elsevierStylePara elsevierViewall">In patients at cardiovascular risk&#44; it should first be assessed whether administration is strictly necessary&#46; If it is&#44; the minimum effective dose should be used for the shortest possible time&#46; Finally&#44; NSAIDs with the best cardiovascular safety profile should be used &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Eradication of <span class="elsevierStyleItalic">H&#46; pylori</span> in patients on NSAID&#47;ASA treatment</span><p id="par0200" class="elsevierStylePara elsevierViewall">It is highly controversial whether patients on chronic treatment with NSAIDs and&#47;or ASA should be treated for <span class="elsevierStyleItalic">H&#46; pylori</span>&#46;</p><p id="par0205" class="elsevierStylePara elsevierViewall">There is some evidence in favour of eradication in patients who are about to start NSAID treatment &#40;<span class="elsevierStyleItalic">naive</span>&#41;&#46; Thus&#44; a meta-analysis showed that both <span class="elsevierStyleItalic">H&#46; pylori</span> infection and the use of non-selective NSAIDs are independent risk factors for the development of PU&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> The approach will depend on whether patients are <span class="elsevierStyleItalic">na&#239;ve</span> or already on chronic NSAID therapy and whether or not they have a history of previous PU&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a> Thus&#44; in <span class="elsevierStyleItalic">na&#239;ve</span> patients with no history of PU or complications&#44; eradication of <span class="elsevierStyleItalic">H&#46; pylori</span> significantly reduces the risk of PU and ulcer bleeding<a class="elsevierStyleCrossRefs" href="#bib0225"><span class="elsevierStyleSup">45&#44;46</span></a> but not in those already on chronic NSAID therapy&#46;<a class="elsevierStyleCrossRefs" href="#bib0235"><span class="elsevierStyleSup">47&#44;48</span></a></p><p id="par0210" class="elsevierStylePara elsevierViewall">In patients with a history of PU or complications&#44; on chronic NSAID treatment&#44; at least 2 randomised controlled trials &#40;RCTs&#41; show that chronic PPI treatment is superior to eradication<a class="elsevierStyleCrossRefs" href="#bib0245"><span class="elsevierStyleSup">49&#44;50</span></a> and a third RCT concludes that there is no difference between eradication and PPI treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> In NSAID <span class="elsevierStyleItalic">na&#239;ve</span> patients&#44; one RCT<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> shows that eradication is clearly superior to non-eradication in preventing PU during the six months following treatment &#40;12&#46;1&#37; vs&#46; 34&#37;&#41;&#44; although neither group received prophylactic PPI treatment in this study&#46;</p><p id="par0215" class="elsevierStylePara elsevierViewall">Therefore&#44; it is recommended to investigate and treat <span class="elsevierStyleItalic">H&#46; pylori</span> in patients who are about to start NSAID therapy &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46; Eradication should be associated with prophylaxis whenever patients have any gastrointestinal risk factors &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46; It is not recommended to investigate <span class="elsevierStyleItalic">H&#46; pylori</span> in patients on chronic NSAID therapy&#44; especially in those already receiving PPI prophylaxis&#46; There are no studies showing that <span class="elsevierStyleItalic">H&#46; pylori</span> eradication provides additional efficacy in reducing the risk of PU or its complications in this group of patients&#46; On the other hand&#44; this is a generally older group&#44; with comorbidity and often polypharmacy&#46; In this context&#44; the risk of bleeding after temporarily stopping PPIs to assess <span class="elsevierStyleItalic">H&#46; pylori</span> and the risk of adverse effects or interactions of eradication therapy are likely to outweigh the possible -and unproven- benefits of <span class="elsevierStyleItalic">H&#46; pylori</span> eradication&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0220" class="elsevierStylePara elsevierViewall">In patients on chronic ASA treatment&#44; <span class="elsevierStyleItalic">H&#46; pylori</span> eradication has been shown to slightly reduce the risk of PU bleeding&#46;<a class="elsevierStyleCrossRefs" href="#bib0265"><span class="elsevierStyleSup">53&#44;54</span></a></p><p id="par0225" class="elsevierStylePara elsevierViewall">However&#44; a meta-analysis<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> showed that the evidence was not sufficient to conclude that <span class="elsevierStyleItalic">H&#46; pylori</span> is a risk factor for UGB in patients receiving ASA&#46; In addition&#44; an epidemiological study<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> found neither additive nor potentiating effect between ASA and <span class="elsevierStyleItalic">H&#46; pylori</span> infection in patients with PU&#46; In an RCT in 250 high-risk patients -with a history of UGB for PU- and chronic ASA&#44; Chan et al&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> compared <span class="elsevierStyleItalic">H&#46; pylori</span> eradication versus chronic PPI&#44; with a 6-month follow-up&#46; The rate of bleeding was low in both groups&#44; 1&#46;9&#37; in patients receiving eradication treatment and 0&#46;9&#37; in patients with prophylactic PPI&#46; The differences were not significant&#44; probably due to the limited follow-up and the small number of patients&#46;</p><p id="par0230" class="elsevierStylePara elsevierViewall">On the other hand&#44; there is strong evidence<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> that the use of PPIs reduces the risk of PU and bleeding in patients on chronic treatment with NSAIDs or ASA&#46; Therefore&#44; treatment with PPIs is recommended in patients receiving ASA with gastrointestinal risk factors&#46;</p><p id="par0235" class="elsevierStylePara elsevierViewall">On the other hand&#44; it is not recommended to systematically investigate and treat <span class="elsevierStyleItalic">H&#46; pylori</span> in patients receiving or about to receive ASA&#46;</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Peptic ulcer in <span class="elsevierStyleItalic">H&#46; pylori-negative</span> patients not taking NSAIDs&#47;ASA</span><p id="par0240" class="elsevierStylePara elsevierViewall">With the decreasing prevalence of <span class="elsevierStyleItalic">H&#46; pylori</span> infection&#44; some studies indicate an increased proportion of &#39;idiopathic&#39; PU&#44; i&#46;e&#46;&#44; <span class="elsevierStyleItalic">H&#46; pylori-</span>negative and not associated with NSAIDs or ASA&#46; However&#44; there is an important limitation in these studies&#44; and that is the fact that there is no objective method to assess ASA and NSAID intake&#46; In the studies&#44; this information is generally obtained during history-taking or from the medical records&#46; In a study conducted in our setting&#44; the prevalence of idiopathic PU was very low&#58; only 1&#46;6&#37; of all duodenal ulcers and 4&#46;1&#37; of all gastric ulcers were negative for NSAIDs and <span class="elsevierStyleItalic">H&#46; pylori&#46;</span><a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a></p><p id="par0245" class="elsevierStylePara elsevierViewall">The diagnosis of NSAID- and <span class="elsevierStyleItalic">H&#46; pylori-negative</span> PUs should be made only after careful exclusion of &#39;occult&#39; NSAID use and&#47;or a false negative diagnosis of <span class="elsevierStyleItalic">H&#46; pylori</span> infection&#46;</p><p id="par0250" class="elsevierStylePara elsevierViewall">In NSAIDs and <span class="elsevierStyleItalic">H&#46; pylori-negative</span> PUs&#44; the use of other drugs or toxins with ulcerogenic potential such as bisphosphonates&#44; cocaine&#44; radiotherapy or oral iron should be assessed&#46; Other causes to rule out are atypical herpes virus or cytomegalovirus infections&#44; other disorders such as Crohn&#39;s disease or malignant aetiology&#44; especially in the case of duodenal ulcers where biopsies should not be performed&#46; Lymphoma or Kaposi&#39;s sarcoma are very rare causes of ulceration and are usually related to a state of immunosuppression&#46; Another rare cause is gastrinoma &#40;Zollinger Ellison syndrome&#41;&#46; In this case&#44; patients usually have diarrhoea accompanying PU that responds to PPI treatment&#46; PU due to gastrinoma is usually severe&#44; multiple and often extends into the distal duodenum&#44; although the typical gastrinoma symptoms may be masked by previous PPI use&#46;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a></p></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Future challenges</span><p id="par0255" class="elsevierStylePara elsevierViewall">Important challenges remain in the treatment and prevention of PU&#46; These include determining the best medication combination in NSAID&#47;ASA users and&#44; above all&#44; addressing the increase in difficult-to-treat bleeding in patients with severe co-morbidity on anticoagulant therapy&#46;</p></span><span id="sec0085" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Conflict of interest</span><p id="par0260" class="elsevierStylePara elsevierViewall">Xavier Calvet has received lecture fees from Allergan&#46; Pilar Garc&#237;a-Iglesias and Isabel Laucirica declare no conflicts of interest in relation to this review&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Peptic ulcer disease &#40;PUD&#41; is a frequent pathology&#59; although the incidence has decreased in recent years&#44; it continues to be an important cause of morbidity and mortality associated with high healthcare costs&#46; The most important risk factors are <span class="elsevierStyleItalic">Helicobacter pylori</span> infection and the use of non-steroidal anti-inflammatory drugs &#40;NSAID&#41;&#46; Most patients with PUD remain asymptomatic&#44; with dyspepsia being the most frequent and often characteristic symptom&#46; It can also debut with complications such as upper gastrointestinal bleeding&#44; perforation or stenosis&#46; The diagnostic technique of choice is upper gastrointestinal endoscopy&#46; Treatment with proton pump inhibitors &#40;PPIs&#41;&#44; eradication of <span class="elsevierStyleItalic">H&#46; pylori</span> and avoiding the use of NSAIDs are the basis of treatment&#46; However&#44; prevention is the best strategy&#44; it includes an adequate indication of PPIs&#44; investigation and treatment of <span class="elsevierStyleItalic">H&#46; pylori</span>&#44; avoiding NSAIDs or using those that are less gastrolesive&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">La enfermedad ulcerosa p&#233;ptica &#40;UP&#41; es una patolog&#237;a frecuente&#59; aunque su incidencia ha disminuido en los &#250;ltimos a&#241;os&#44; sigue siendo una causa importante de morbimortalidad asociada a un elevado gasto sanitario&#46; Los factores de riesgo m&#225;s importantes son la infecci&#243;n por <span class="elsevierStyleItalic">Helicobacter pylori</span> y el uso de antiinflamatorios no esteroideos &#40;AINE&#41;&#46; La mayor&#237;a de los pacientes con UP permanecen asintom&#225;ticos&#44; siendo la cl&#237;nica m&#225;s frecuente la dispepsia&#44; a menudo caracter&#237;stica &#40;dispepsia ulcerosa&#41;&#46; Tambi&#233;n puede debutar con complicaciones como hemorragia digestiva alta&#44; perforaci&#243;n o estenosis&#46; La t&#233;cnica diagn&#243;stica de elecci&#243;n es la endoscopia digestiva alta&#46; El tratamiento con inhibidores de la bomba de protones &#40;IBP&#41;&#44; la erradicaci&#243;n de <span class="elsevierStyleItalic">H&#46; pylori</span> y evitar el consumo de AINE son la base del tratamiento&#46; Sin embargo&#44; la prevenci&#243;n es la mejor estrategia&#44; incluye una adecuada indicaci&#243;n de IBP&#44; la investigaci&#243;n y tratamiento de <span class="elsevierStyleItalic">H&#46; pylori</span>&#44; evitar los AINE o utilizar aquellos menos gastrolesivos&#46;</p></span>"
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                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n
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                  \t\t\t\t">&#60;1&#46;5&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">1&#46;5&#8722;10&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">Moderate&#47;high&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">Do not investigate or treat <span class="elsevierStyleItalic">H&#46; pylori</span>&#46; PPI&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">Investigate and treat <span class="elsevierStyleItalic">H&#46; pylori</span>&#46;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">Moderate&#47;high&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">No evidence&#46; PPI&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " rowspan="2" align="left" valign="\n
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                  \t\t\t\t">Chronic NSAID</td><td class="td" title="\n
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                  \t\t\t\t">Low&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">Do not investigate or treat <span class="elsevierStyleItalic">H&#46; pylori</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">Moderate&#47;high&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">Do not investigate or treat <span class="elsevierStyleItalic">H&#46; pylori</span>&#46; PPI&nbsp;\t\t\t\t\t\t\n
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          "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Eradication of <span class="elsevierStyleItalic">Helicobacter pylori</span> in patients receiving ASA or NSAIDs&#46;</p>"
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Article information

ISSN: 23870206
Original language: English

DOI:10.1016/j.medcle.2023.05.015

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