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Query: UMLS:C0042963 (vomiting)
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Functional (nonulcer) dyspepsia refers to upper abdominal pain or discomfort with or without symptoms of early satiety, nausea, or vomiting with no definable organic cause. The current Rome II criteria help to diagnose functional dyspepsia and avoid misdiagnosis of gastroesophageal reflux disease and irritable bowel syndrome as functional dyspepsia. Assessment of gastric emptying with scintigraphy or breath testing may be useful in identifying delayed gastric emptying in patients with dyspeptic symptoms and may be helpful in patient management. Electrogastrography is a noninvasive test that evaluates for gastric dysrhythmias. Satiety testing is being evaluated as an indirect test for impaired fundic relaxation and visceral hypersensitivity. The symptom response to Helicobacter pylori therapy in patients with functional dyspepsia and a negative endoscopy examination but a positive H. pylori test is marginal. Lifestyle modifications often are suggested for initial treatment of functional dyspepsia. Dietary changes such as frequent small meals, low-fat diet, and avoidance of certain aggravating foods may improve symptoms. Additional measures include cessation of smoking, avoiding excess alcohol intake, and minimizing coffee intake. Antacids and over-the-counter histamine type 2 receptor antagonists may be helpful as an "on-demand" therapy for intermittent symptoms. They are safe and relatively inexpensive. Different subgroups of functional dyspepsia are based on the predominant symptom and may help in choosing an appropriate drug to initiate therapy. If the predominant symptom is epigastric pain (ulcer-like functional dyspepsia), histamine-2 receptor antagonists or proton pump inhibitors are the initial treatment of choice. If fullness, bloating, early satiety or nausea is the predominant complaint (dysmotility-like functional dyspepsia), a prokinetic agent may help. Metoclopramide is the only available effective prokinetic agent at present. If metoclopramide is used, short-term treatment and discussion of possible side effects with the patient are advised. If there is no response to these initial treatments, switching therapy from proton pump inhibitor to prokinetic or vice versa can be tried. If these treatment options fail, patient re-evaluation for other disorders (including other functional bowel disorders) is advised. A low-dose tricyclic antidepressant at bedtime may be helpful for treatment of visceral hypersensitivity.
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PMID:Functional (Nonulcer) Dyspepsia. 1187 96

Proton pump inhibitors (PPI) are widely used for the treatment of peptic ulcer, but cases of anaphylactic reactions have rarely been described. We present a patient who experienced an episode of urticaria 30 minutes after oral intake of an omeprazole capsule. Skin prick tests to omeprazole, pantoprazole and lansoprazole were positive. Challenge test with lansoprazole was carried out and within 45 minutes the patient developed urticaria, facial edema, vomiting, and hypotension. Oral challenge with other imidazole derivatives (ketoconazole, cimetidine, metronidazole) were carried out with good tolerance. Serum tryptase levels determined 3 hours after the adverse reaction to lansoprazole were elevated. Specific IgE to PPI were not detected by an enzyme-linked immunosorbent assay technique. The clinical findings, positive skin prick test to PPI and elevated serum tryptase levels suggest that an IgE-mediated mechanism was implicated in the reactions to both omeprazole and lansoprazole. Skin prick tests may be a useful tool for detecting patients sensitized to PPI. An experimental protocol was used to detect specific IgE antibodies against PPI, which may explain RAST negativity. The previous findings suggest that cross-reactivity between PPI exists, but not with other imidazoles.
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PMID:Anaphylaxis to proton pump inhibitors. 1246 68

Functional dyspepsia is a clinical syndrome defined by chronic or recurrent pain or discomfort in the upper abdomen of unknown origin. Although generally accepted, investigators differently interpret this definition and clinical trials are often biased by inhomogeneous inclusion criteria. The poorly defined multifactorial pathogenesis of dyspeptic symptoms has hampered efforts to develop effective treatments. A general agreement exists on the irrelevant role played by Helicobacter pylori in the pathophysiology of functional dyspepsia. Gastric acid secretion is within normal limits in patients with functional dyspepsia but acid related symptoms may arise in a subgroup of them. Proton pump inhibitors appear to be effective in this subset of patients with dyspepsia. Non-painful dyspeptic symptoms are suggestive of underlying gastrointestinal motor disorders and such abnormalities can be demonstrated in a substantial proportion of patients. Postprandial fullness and vomiting have been associated with delayed gastric emptying of solids, and early satiety and weight loss to postcibal impaired accommodation of the gastric fundus. Prokinetics have been shown to exert beneficial effects, at least in some patients with dyspepsia. In contrast, drugs enhancing gastric fundus relaxation have been reported to improve symptoms, although conflicting results have also been published. An overdistended antrum may also generate symptoms, but its potential pathogenetic role and the effects of drugs on this abnormality have never been investigated formally. Visceral hypersensitivity plays a role in some dyspeptic patients and this abnormality is also a potential target for treatment. Both chemo- and mechanoreceptors can trigger hyperalgesic responses. Psychosocial abnormalities have been consistently found in functional digestive syndromes, including dyspepsia. Although useful in patients with irritable bowel syndromes (IBS), antidepressants have been only marginally explored in functional dyspepsia. Among the new potentially useful agents for the treatment of functional dyspepsia, serotonin 5-HT(4) receptor agonists have been shown to exert a prokinetic effect. Unlike motilides, 5-HT(4) receptor agonists do not appear to increase the gastric fundus tone and this may contribute to improve symptoms. 5-HT(3) receptor antagonists have been investigated mainly in the IBS and the few studies performed in functional dyspepsia have provided conflicting results. Also, kappa-opioid receptor agonists might be useful for functional digestive syndromes because of their antinociceptive effects, but available results in functional dyspepsia are scanty and inconclusive. Other receptors that represent potential clinical targets for antagonists include purinoceptors (i. e., P2X2/3 receptors), NMDA receptors (NR2B subtype), protease-activated receptor-2, the vanilloid receptor-1, tachykinin receptors (NK(1)/NK(2)) and cholecystokinin (CCK)(1) receptors.
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PMID:New developments in the treatment of functional dyspepsia. 1267 73

Gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease (GORD) have a higher prevalence among infants than among children or adults. This is linked to the immaturity of the oesophagus and stomach and the higher liquid intake of infants. Genetic factors could also be contributory in some families. Clinical symptoms in infants are mainly regurgitation and vomiting, which usually disappear between 1 and 3 years of age. Symptoms in children are similar to those in adults. Treatment in children depends on age and GORD severity. With GOR or mild GORD, particularly in infants, explanation and reassurance together with thickening of formula feed and lifestyle changes are usually effective. Prokinetics either have unproven efficacy (metoclopramide, domperidone) or have been withdrawn (cisapride). Chronic antacid therapy is not recommended. In moderate to severe GORD, histamine-2-receptor antagonists and particularly proton pump inhibitors (PPIs) are effective, especially when oesophagitis is present. PPIs, in particular omeprazole and lansoprazole, have proven efficacy in infants and children. They are well tolerated, with pharmacokinetics similar to those in adults. However, dosages should be adapted in neonates and children under 10 years old. Fundoplication should be avoided before 2 to 3 years of age if possible.
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PMID:Managing gastro-oesophageal reflux disease in children. 1500 29

It is estimated that by 2020, >16% of people in the United States will be > or =65 years of age and that nearly 20 million will be >85 years of age. Aging imparts a variety of physiologic changes in the oropharynx, esophagus, and stomach that increase the risk for esophageal and gastrointestinal disorders. Older individuals also tend to have a higher prevalence of comorbid factors, such as Helicobacter pylori infection, smoking, presence of other diseases, or use of medications (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs]) that increase their risk for acid-related disorders. Given these physiologic and comorbidity factors, the elderly are at higher risk for gastroesophageal reflux disease (GERD), pill-induced esophagitis, peptic ulcer disease, and complications related to the use of NSAIDs. Unfortunately, in the elderly patient with these disorders--even those with severe disease or complications--symptom presentation may be subtle or atypical, resulting in a delayed diagnosis. Endoscopy remains the "gold standard" for the identification of mucosal disease and should be performed in all patients with "new-onset" or persistent symptoms who are >45 years of age, as well as in individuals of any age who present with alarm symptoms, such as weight loss, vomiting, anemia, dysphagia, or evidence of gastrointestinal bleeding. In general, the treatment of older individuals with peptic ulcer or GERD and its complications is similar to that of younger individuals. Proton pump inhibitors are the mainstay of therapy for symptom relief, healing of erosive esophagitis, resolution of peptic ulceration, reduction of the risk for NSAID-induced mucosal damage, and prevention of disease recurrence.
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PMID:Aging, the gastrointestinal tract, and risk of acid-related disease. 1547 47

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

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

Idiopathic dyspepsia refers to pain and/or discomfort perceived in the epigastrium that is not secondary to organic, systemic, or metabolic diseases. Symptoms may overlap with those of gastroesophageal reflux disease and irritable bowel syndrome. Gastrointestinal motor disorders, hypersensitivity to mechanical or chemical stimuli, and psychosocial factors can act individually or in concert to induce the symptoms of dyspepsia. Accordingly, there is no single therapy, and treatment must be individualized. Eradication of Helicobacter pylori infection rarely achieves symptom improvement. Treatment of idiopathic dyspepsia should begin by reassuring the patient about the benign nature of the syndrome and educating them on the knowledge that has been achieved in recent years regarding potential causes of the syndrome. Both prokinetic and antisecretory drugs have been reported to improve dyspeptic symptoms, but results are not completely convincing. Although well-designed studies demonstrate superiority of proton pump inhibitors over placebo, it should be noted that patients with nonerosive gastroesophageal reflux disease were invariably included; when these patients are excluded, the benefit of antisecretory medications is questionable. We suggest that patients with idiopathic dyspepsia be initially treated according to the predominant symptom. Those with epigastric pain/burning should receive a trial with standard doses of proton pump inhibitors for 4 to 8 weeks, whereas prokinetic patients should be prescribed at recommended doses for similar periods of time to patients with nonpainful dyspeptic symptoms such as posprandial fullness, early satiety, nausea, or vomiting. Nonresponders may benefit from combination therapies or short trials with higher doses of drugs. Visceral analgesics and antidepressants can also be prescribed alone or in combinations with other therapeutic strategies. Recent studies demonstrate utility for psychologic therapy and hypnotherapy, although truly controlled studies are difficult in this area. Herbal medicines deserve further evaluation.
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PMID:Idiopathic Dyspepsia. 1576 39

Gastroesophageal Reflux disease (GERD) has a common clinical presentation of a burning discomfort in the retroesternal area, regurgitation and dysphagia. Yet, an estimated of 20 to 60 percent of patients with GERD have head and neck symptoms without any appreciable heartburn. Careful history and a meticulous physical exam can guide us to have a correct diagnosis and give adequate treatment. Other methods, such as gastroscopy and gastric pH monitoring, as well as other diagnostic studies can help us to confirm the diagnosis. Once we have the correct diagnosis stabilized, life style modification should be the first step in the management of GERD, aided with antacids, H2 receptors antagonists and/or Proton pump inhibitors. Family physicians should be aware that helping patients to understand the cause of their symptoms and reinforcing the life style modifications will bring better control of the disease and patients can have improvement of their symptoms leading to possible cure of the disease. Gastroesophageal Reflux Disease (GERD) is defined as the movement of gastric contents into the esophagus without presence of vomiting. It is frequently associated with heartburn, the sensation of burning discomfort in retrosternal area, that moves upward, toward the throat. GERD is a chronic, relapsing condition with associated morbidity and adverse impact on quality of life. The purpose of this article is to give an overall look at the clinical presentations of GERD with typical and atypical symptoms, the various presentations of this disease in all of the age groups, and to identify all of the aspects that contribute to the progression and solution of this problem.
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PMID:Typical and atypical presentations of gastroesophageal reflux disease and its management. 1580 87

Eosinophilic esophagitis (EE) is an increasingly recognized disease of the esophagus with distinct clinicopathologic features. Adult and pediatric patients experience upper intestinal symptoms including food impaction, vomiting, abdominal pain, or dysphagia. Histopathologic analysis of the distal and proximal esophageal mucosa demonstrates dense eosinophilic infiltration despite proton pump inhibition. Few studies document the long-term outcomes of EE but current evidence suggests that EE is a chronic condition that can sometimes lead to esophageal strictures. Although the incidence of this complication is not yet known, it has sparked significant interest in defining safe, effective treatments. Once a diagnosis of EE is made, patients should seek the consultation of the allergist in an effort to identify possible food sensitivities. This is particularly important because the etiologic agent(s) that drive the eosinophilia are likely different for each patient. If the allergic evaluation identifies a specific food, this food should be strictly avoided as a first-line treatment. If a food is not identified, an elemental formula should be used to induce a remission. If an elemental diet cannot be used, topical steroids are effective in inducing a remission. The side effects associated with long-term steroid administration limit their use as a maintenance medication. Given the lack of prognostic data, the use of systemic corticosteroids should be reserved for severe cases when dietary elimination or topical steroids are ineffective. Most importantly, patients should remain under the care of a physician so that long-term outcomes can be identified. To date, diet restriction has been identified as the only effective maintenance treatment, but montelukast and topical cromolyn may also offer benefit. Anti-interleukin-5 antibody represents an emerging form of targeted therapy.
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PMID:Treatment of eosinophilic esophagitis in children. 1616 5


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