Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lansoprazole is a proton pump inhibitor widely prescribed for gastroesophageal reflux and benign peptic ulcer disease. According to the manufacturer's package insert (TAP Pharmaceuticals, Lake Forest, IL, USA), the most common side-effects are diarrhea, headache and abdominal pain, which occur in approximately 3% of patients and are reversible with drug discontinuation. An unusual case of microscopic colitis is reported in a previously asymptomatic patient who developed new-onset diarrhea after initiation of lansoprazole. The case is reviewed and possible mechanisms of diarrhea secondary to proton pump inhibitors are discussed.
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PMID:Diarrhea associated with lansoprazole. 1270 56

Despite advances in medical management, gastrointestinal bleeding remains a substantial cause of morbidity and mortality. At risk are patients with history of the event, those taking nonsteroidal antiinflammatory agents, and those with active peptic ulcer disease. Endoscopy may be performed for diagnosis and treatment. Antisecretory therapy may be employed to control gastric acid secretion, treat active peptic ulcer disease, and control symptoms such as diarrhea and abdominal pain. Options for antisecretory therapy include histamine2-receptor antagonists (H2RAs) that target the histamine pathway, and proton pump inhibitors (PPIs) that target the final step in acid secretion. The H2RAs generally are ineffective at reaching a target pH of 6 in patients with gastrointestinal bleeding because of tachyphylaxis. The PPIs are more effective and do not lead to tachyphylaxis. With the availability of an intravenous PPI, pantoprazole, options for managing hospitalized patients with gastrointestinal bleeding are expanding.
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PMID:Treating patients with acute gastrointestinal bleeding or rebleeding. 1458 62

H pylori infection is highly prevalent in asymptomatic children and it varies between countries and often within a country as well. Initial infection probably occurs at an early age and prevalence increases with age. Ethnic and racial factors, socio-economic status and living conditions affect the prevalence of infection. Long term population based studies are needed to identify the exact prevalence and clinical significance in Indian children. There is strong evidence for an association between H pylori infection and antral gastritis and duodenal ulcer disease in children, but it's association with recurrent abdominal pain needs further evaluation. Diagnostic tests for H pylori are based either on direct demonstration of the organism or indirectly by detecting a by-product (of the urease reaction) or by demonstrating antibodies. Histopathological identification of H pylori in [table: see text] antral biopsy specimen is by far the best method and is currently regarded as gold standard. Serological tests detecting IgG and IgA are possible tools for diagnosis but have many drawbacks. They may be useful for population surveys where invasive tests are not feasible. These tests should be standardized for the population for which they are going to be used. Urea breath test is a highly sensitive non-invasive test for H pylori infection and can be used even in a field setting. Urea Breath test needs to be standardized in tropical countries with high rates of dental colonization and duodenal microbial contamination. Newer diagnostic tests for H pylori infection are emerging but most have not been validated in various populations. Routine testing for H pylori is not indicated in children or adults. The decision to perform a diagnostic test has often to be linked with a therapeutic proposal. The only condition for which H pylori treatment is indicated is duodenal ulcer which is very uncommon in children. Treatment for RAP or even dyspepsia is not warranted on clinical grounds. There are several treatment regimens available, but it appears that at least three drugs including two antibiotics and a proton pump inhibitor are required for satisfactory eradication. In developing countries where the prevalence of infection is very high, well-planned double blind cross-over studies are needed before an evidence based answer can be provided for an optimal therapeutic strategy.
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PMID:Helicobacter pylori infection in children: a review. 1497 81

Helicobacter pylori (H. pylori) is among the most common bacterial infections in humans. In 1982, H. pylori was discovered by Marshal and Warren, demonstrating an association between H. pylori and ulcer disease. H. pylori is a gram-negative, S-shaped rod that produces enzymes like urease, catalase and oxidase. The mechanism of acquisition and transmission of H. pylori is unclear, although the most likely mode of transmission is fecal-oral and oral-oral. The mode of transmission is supported by studies that demonstrate viable H. pylori organisms can be cultured from the stool or vomitus of infected patients. Risk factors such as minimal education and low socio-economic status during childhood affect the prevalence. Children infected with H. pylori develop histologic chronic active gastritis despite the fact that they are generally asymptomatic. A small percentage of these children will go on to develop peptic ulcer disease, and even gastric cancer. In contrast, the association of abdominal pain and H. pylori infection remains controversial. In the year 2000, the North American Society of Pediatric Gastroenterology guidelines on H. pylori reported that there is no evidence demonstrating a link between H. pylori-associated gastritis and abdominal pain, except in rare cases in which gastric or duodenal ulcer disease is present. Currently, treatment with a combination of two antimicrobial agents in conjunction with a proton pump inhibitor (PPI) continues to be recommended for the treatment of H. pylori associated peptic ulcer disease.
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PMID:Treatment of Helicobacter pylori in Pediatrics. 1534 11

Atazanavir is the first once-daily protease inhibitor for the treatment of human immunodeficiency virus type 1 infection and should be used only in combination therapy, as part of a highly active antiretroviral therapy (HAART) regimen. In addition to being the most potent protease inhibitor in vitro, atazanavir has a distinct cross-resistance profile that does not confer resistance to other protease inhibitors. However, resistance to other protease inhibitors often confers clinically relevant resistance to atazanavir. Currently, atazanavir is not a preferred protease inhibitor for initial HAART regimens. In treatment-naive patients, atazanavir can be given as 400 mg/day. However, atazanavir should be pharmacologically boosted with ritonavir in treatment-experienced patients or when coadministered with either tenofovir or efavirenz. Patients who receive atazanavir experience similar rates of adverse events compared with patients receiving comparator regimens. An exception is an increased risk of asymptomatic hyperbilirubinemia, which is due to competitive inhibition of uridine diphosphate-glucuronosyltransferase 1A1. Although hyperbilirubinemia is a common adverse drug reaction of atazanavir therapy (22-47%), fewer than 2% of patients discontinue atazanavir therapy because of this adverse effect. Common adverse effects reported with atazanavir include infection, nausea, vomiting, diarrhea, abdominal pain, headache, peripheral neuropathy, and rash. Of significance, fewer abnormalities have been observed in plasma lipid profiles in patients treated with atazanavir compared with other protease inhibitor-containing regimens. As with other protease inhibitors, atazanavir is also a substrate and moderate inhibitor of the cytochrome P450 (CYP) system, in particular CYP3A4 and CYP2C9. Clinically significant drug interactions include (but are not limited to) antacids, proton pump inhibitors, histamine type 2 receptor antagonists, tenofovir, diltiazem, irinotecan, simvastatin, lovastatin, St. John's wort, and warfarin. We conclude that atazanavir is a distinctively characteristic protease inhibitor owing to its in vitro potency, once-daily dosing, distinct initial resistance pattern, and infrequent association with metabolic abnormalities.
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PMID:Atazanavir for the treatment of human immunodeficiency virus infection. 1558 41

The proton pump inhibitors (PPIs) are a relatively new class of agents used for the treatment of acid-related disorders, including peptic ulcer diseases, reflux oesophagitis and Zollinger-Ellison syndrome, and in enhancing antibiotic therapy in the eradication of Helicobacter pylori in patients with peptic ulcer disease. The PPIs are the most potent gastric acid-suppressing agents currently in clinical use. According to the recent basic study, PPIs may act not only as potent acid suppressants, but also as anti-inflammatory or pro-regenerative agents. On the other hand, in the clinical field, general practitioners still tend to prescribe PPIs for unlicensed indications, such as non-ulcer dyspepsia and nonspecific abdominal pain. This article reviews the novel pharmacological action other than acid secretion and the diverse clinical usage of PPIs, in order to seek possible extensions of the use of this unique agent.
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PMID:Novel effects other than antisecretory action and off-label use of proton pump inhibitors. 1570 83

Helicobacter pylori infection causes gastritis and peptic ulcers and is associated with the development of gastric cancer. Approximately 50% of the world population is infected with H pylori , with the highest prevalence rates in developing countries. In the vast majority of individuals, infection is acquired during childhood with those of low socioeconomic means and having infected family members being at highest risk for early childhood acquisition. Definitive routes of transmission of the infection are unclear, with evidence suggesting oral-oral, gastric-oral, and fecal-oral routes. If untreated, H pylori infection is lifelong. Although clinical disease typically occurs decades after initial infection acquisition, children infected with H pylori may have gastritis, ulcers, mucosal-associated lymphoid type lymphoma, and, rarely, gastric atrophy with/without intestinal metaplasia (ie, both precursor lesions for gastric cancer). Controversy persists regarding testing for and treating H pylori , if found, in the large number of children who present with recurrent abdominal pain. Because young children (ie, younger than 5 years of age) who are treated and cured of their H pylori infection may be at risk for reinfection, the current recommendations do not recommend treatment unless an ulcer or gastric atrophy is present. However, despite the lack of clinical evidence, the trend is to more aggressively screen children for the presence of H pylori and to treat those children who are found to have the infection. H pylori infection can be eradicated by antimicrobial therapy plus a proton pump inhibitor, but no treatment regimen is 100% effective. Multiple drugs, frequent dosing, and length of treatment often contribute to poor patient compliance, and antibiotic eradication therapy is associated with increasing drug resistance.
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PMID:Helicobacter pylori infection: detection, investigation, and management. 1575 99

Gastroesophageal reflux disease (GERD) presents in different ways in children, most commonly with vomiting, or with esophageal symptoms such as regurgitation, heartburn, or dysphagia. Extraesophageal symptoms and signs also frequently occur. Less well recognized is that abdominal pain is a relatively common mode of presentation. Although abdominal pain is common in school-aged children, GERD and other acid-related disorders such as peptic ulcer disease are relatively uncommon causes of such. A careful history will usually determine whether an acid-related disorder is in the differential diagnosis of abdominal pain. Early detection and treatment of GERD in children may prevent, attenuate, or heal complications such as failure to thrive or feeding refusal as well as pulmonary, ear-nose-and-throat disorders, erosive esophagitis, and peptic stricture. In children with persistent or severe symptoms and/or complications of GERD such as erosive esophagitis, the major treatment options are pharmacologic management with acid-suppressing medication, specifically proton pump inhibitors (PPIs), or antireflux surgery. For many patients, PPI treatment offers advantages over surgery. When given in adequate doses, PPIs can safely effect relief of GERD symptoms and healing of esophagitis in children. Antireflux surgery may work well in selected patients, but it carries significant risk of morbidity, including high failure rates, even in the short term. Some postoperative studies report that more than 60% of patients are back on medical treatment with proton pump inhibitors for recurrence of GERD symptoms, and a similar percentage have new symptoms that were not present before surgery. Death is uncommon but does occur and is an unacceptable risk in an otherwise healthy, low-risk individual. Laparoscopic surgery may have some disadvantages compared with open surgery, including a higher rate of redo operations. Studies show that many children undergo surgery for unclear indications, often with few preoperative diagnostic studies. The availability of highly effective medical therapy, together with more careful selection of patients for surgery, may result in better patient outcomes, with much lower operative rates.
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PMID:Decisions in diagnosing and managing chronic gastroesophageal reflux disease in children. 1575

A 41-year-old man presented with severe gastric ulceration 3 mo after beginning treatment with atorvastatin 20 mg once daily for hypercholesterolemia. The patient was not taking any ulcerogenic drugs and had no evidence of Helicobacter pylori infection. Proton pump inhibitor therapy was initiated and atorvastatin was replaced by simvastatin with complete resolution of gastrointestinal symptoms. To our knowledge, this is the first report of atorvastatin-induced gastric ulceration, which should be looked for in patients who develop abdominal pain while on this drug.
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PMID:Atorvastatin-induced severe gastric ulceration: a case report. 1591 10

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented. The clinical issues addressed and recommendations made were: population-based screening for H. pylori in asymptomatic children to prevent gastric cancer is not warranted; testing for H. pylori in children should be considered if there is a family history of gastric cancer; the goal of diagnostic interventions should be to determine the cause of presenting gastrointestinal symptoms and not the presence of H. pylori infection; recurrent abdominal pain of childhood is not an indication to test for H. pylori infection; H. pylori testing is not required in patients with newly diagnosed gastroesophageal reflux disease; H. pylori testing may be considered before the use of long-term proton pump inhibitor therapy; testing for H. pylori infection should be considered in children with refractory iron deficiency anemia when no other cause has been found; when investigation of pediatric patients with persistent or severe upper abdominal symptoms is indicated, upper endoscopy with biopsy is the investigation of choice; the 13C-urea breath test is currently the best noninvasive diagnostic test for H. pylori infection in children; there is currently insufficient evidence to recommend stool antigen tests as acceptable diagnostic tools for H. pylori infection; serological antibody tests are not recommended as diagnostic tools for H. pylori infection in children; first-line therapy for H. pylori infection in children is a twice-daily, triple-drug regimen comprised of a proton pump inhibitor plus two antibiotics (clarithromycin plus amoxicillin or metronidazole); the optimal treatment period for H. pylori infection in children is 14 days; and H. pylori culture and antibiotic sensitivity testing should be made available to monitor population antibiotic resistance and manage treatment failures.
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PMID:Canadian Helicobacter Study Group Consensus Conference: Update on the approach to Helicobacter pylori infection in children and adolescents--an evidence-based evaluation. 1601 Mar


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