Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and acceptability of classical bismuth triple therapy may be limited by poor patient compliance and adverse effects. It is widely agreed that improved, simpler, and reliable therapies are needed to cure Helicobacter pylori infection and foster patient compliance. We evaluated the efficacy and side effects of a Bazzoli triple therapy substituting lansoprazole for omeprazole for H. pylori infection in active peptic ulcer in Korea (30 mg of lansoprazole, 250 mg of clarithromycin, and 400 mg of metronidazole, all twice daily). H. pylori status was evaluated by rapid urease test, histology, and culture at entry and four or more weeks after ending antimicrobial therapy. Fifty-eight patients (mean age: 43 years) with gastric (N = 30) or duodenal ulcer (N = 28) and H. pylori infection were studied. H. pylori was cured in 47 (81%, 95% CI = 69-90%). Mild side effects, including vomiting, diarrhea, and itching, were observed in four patients (7%). Compliance averaged 95%. Fifty-five ulcers (95%) were healed. Pretreatment pylorobulbar deformity was observed in 49 patients (85%), and in 43 (88%) the deformity disappeared after treatment. Pretreatment metronidazole and clarithromycin resistance was observed in 87% and 2% of patients, respectively. The cure rate of H. pylori infection was significantly higher in patients >50 years of age than those <50. Treatment with low-dose one-week lansoprazole, clarithromycin, and metronidazole resulted in a relatively low cure rate, but was well tolerated. Studies to define the optimal duration, dose, and dosing interval of this combination therapy in Korea are needed.
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PMID:One-week triple therapy with lansoprazole, clarithromycin, and metronidazole to cure Helicobacter pylori infection in peptic ulcer disease in Korea. 953 38

Since Helicobacter pylori (Hp) was first isolated in 1983, much work has been carried out on the pathogenic effects of this organism. Hp infection is common in humans and currently is the most important etiologic agent in the development of chronic active gastritis, gastric and duodenal ulcers, carcinoma and Malt-lymphoma of the stomach. Moreover Hp infection has also been associated with various extradigestive diseases. At present, a role of Hp infection in dyspepsia is discussed. Dyspepsia is defined by persistence of pain, burning or discomfort localised to the upper abdomen; some authors include in dyspepsia symptoms such as belching, bloating, alitosis, nausea, postprandial repletion, vomiting and regurgitation. In absence of any underlying pathologies, such as peptic ulcer, gastroesophageal reflux, pancreatitis, biliary tract disease or others, dyspepsia is defined as functional or idiopathic dyspepsia. Functional dyspepsia may be distinct in ulcer, reflux or dysmotility-like dyspepsia and unspecified dyspepsia. Hp infection is common in dyspeptic patients and a role of this bacterium has been postulated mostly in ulcer-like dyspepsia. Mechanisms by when Hp induces dyspeptic symptoms are uncertain; bacterial cytotoxins, phlogosis mediators, activity of chronic gastritis Helicobacter-related and host immune response probably play an important role in pathogenesis of functional dyspepsia. However, dyspepsia is not present only in infected patients; therefore other pathogenic factors may be implicated in expression of dyspeptic symptoms in uninfected subjects, such as gastric dysmotility, modifications of gastric output or altered visceral sensibility, psychological factors, gastroesophageal reflux and irritable bowel.
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PMID:[Dyspepsia and Helicobacter pylori]. 1036 46

Patients with a history of Billroth II gastrojejunostomy who present with a symptom complex of postprandial nausea, fullness, and bilious vomiting leading to relief should be suspected of having an afferent loop syndrome. Diagnosis depends on barium radiography and upper intestinal endoscopy. Surgical correction is the treatment. The current age of medical therapy has dramatically decreased the frequency and necessity of surgery for peptic ulcer disease. However, we should not forget the lessons of the past and fail to diagnose a patient who has a chronic complication of a previously common operation.
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PMID:A woman with abdominal pain and bilious vomiting. A very late aftermath of Billroth II gastrectomy. 1110 9

Dyspepsia refers to pain or discomfort centered in the upper abdomen. This symptom is remarkably common, with 1-year prevalence rates averaging 25% in the community. Symptoms suggestive of the irritable bowel syndrome and reflux disease frequently overlap but do not form part of the definition of dyspepsia. Electrical and other stimuli can cause similar or different symptoms in various patients, and even the site to which symptoms are referred varies considerably. Dyspeptic symptoms are therefore a relatively poor guide to the origin or nature of any "disturbances" in the gut. Identification of patients who require further investigation to rule out serious structural disease, such as peptic ulcer disease or cancer, is a key issue because unaided clinical diagnosis is unreliable. The use of an age threshold (typically 45 years) and the identification of alarm features, including weight loss, repeated vomiting, and signs of bleeding, seem to be valid on the basis of the limited evidence available. Dyspeptic symptoms fall into distinct subgroups resembling the perceived clinical entities of ulcer-like and dysmotility-like dyspepsia. Unfortunately, because of overlap with reflux symptoms and between the subgroups, the clinical significance of these groups remains highly questionable. A focus on symptom predominance may be more rewarding. Lack of validated outcome measures has hampered clinical studies and has led to the development of complex outcome measures that integrate and weigh different symptoms or other indirect indicators of outcome into a general score. Further testing and validation are in progress.
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PMID:Dyspepsia. 1134 16

Helicobacter pylori infection of the gastric mucosa can be found in approximately 50% of the world's population and is associated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer. To explore immunization as a strategy for preventing and treating H. pylori-associated disease, we assessed the safety and immunogenicity in healthy adults of a formalin-inactivated, oral H. pylori whole-cell (HWC) vaccine, administered with or without mutant Escherichia coli heat-labile toxin (LT(R192G)) as a mucosal adjuvant. In a dose-response study, 23 subjects with or without H. pylori infection were vaccinated with either 2.5 x 10(6) HWC, 2.5 x 10(8) HWC, or 2.5 x 10(10) HWC, plus 25 microg of LT(R192G). Thereafter, a randomized study was conducted in which 18 H. pylori-infected subjects were assigned, in a double-blind fashion, to receive either 2.5 x 10(10) HWC plus placebo-adjuvant, placebo-vaccine plus 25 microg of LT(R192G), placebo-vaccine plus placebo-adjuvant, or 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Diarrhea (six subjects), low-grade fever (five subjects), and vomiting (two subjects) were observed, usually after the first dose. Significant rises in geometric mean mucosal (fecal and salivary) anti-HWC immunoglobulin A antibodies occurred among H. pylori-infected and uninfected subjects following inoculation with 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Moreover, among H. pylori-negative volunteers, this regimen induced significant lymphoproliferative responses in 5 of 10 subjects and gamma interferon production responses to H. pylori sonicate in 7 of 10 subjects. There was no evidence that vaccination eradicated H. pylori in infected volunteers. These results suggest that it is possible to stimulate mucosal and systemic immune responses in humans to H. pylori antigens by using an HWC vaccine.
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PMID:Safety and immunogenicity of oral inactivated whole-cell Helicobacter pylori vaccine with adjuvant among volunteers with or without subclinical infection. 1134 17

Lansoprazole is an inhibitor of gastric acid secretion and also exhibits antibacterial activity against Helicobacter pylori in vitro. Current therapy for peptic ulcer disease focuses on the eradication of H. pylori infection with maintenance therapy indicated in those patients who are not cured of H. pylori and those with ulcers resistant to healing. Lansoprazole 30 mg combined with amoxicillin 1g, clarithromycin 250 or 500mg, or metronidazole 400 mg twice daily was associated with eradication rates ranging from 71 to 94%, and ulcer healing rates were generally >80% in well designed studies. In addition, it was as effective as omeprazole- or rabeprazole-based regimens which included these antimicrobial agents. Maintenance therapy with lansoprazole 30 mg/day was significantly more effective than either placebo or ranitidine in preventing ulcer relapse. Importantly, preliminary data suggest that lansoprazole-based eradication therapy is effective in children and the elderly. In the short-term treatment of patients with gastro-oesophageal reflux disease (GORD), lansoprazole 15, 30 or 60 mg/day was significantly more effective than placebo, ranitidine 300 mg/day or cisapride 40 mg/day and similar in efficacy to pantoprazole 40 mg/day in terms of healing of oesophagitis. Lansoprazole 30 mg/day, omeprazole 20 mg/day and pantoprazole 40 mg/day all provided similar symptom relief in these patients. In patients with healed oesophagitis. 12-month maintenance therapy with lansoprazole 15 or 30 mg/day prevented recurrence and was similar to or more effective than omeprazole 10 or 20 mg/day. Available data in patients with NSAID-related disorders or acid-related dyspepsia suggest that lansoprazole is effective in these patients in terms of the prevention of NSAID-related gastrointestinal complications, ulcer healing and symptom relief. Meta-analytic data and postmarketing surveillance in >30,000 patients indicate that lansoprazole is well tolerated both as monotherapy and in combination with antimicrobial agents. After lansoprazole monotherapy commonly reported adverse events included dose-dependent diarrhoea, nausea/vomiting, headache and abdominal pain. After short-term treatment in patients with peptic ulcer, GORD, dyspepsia and gastritis the incidence of adverse events associated with lansoprazole was generally < or = 5%. Similar adverse events were seen in long-term trials, although the incidence was generally higher (< or = 10%). When lansoprazole was administered in combination with amoxicillin, clarithromycin or metronidazole adverse events included diarrhoea, headache and taste disturbance. In conclusion, lansoprazole-based triple therapy is an effective treatment option for the eradication of H. pylori infection in patients with peptic ulcer disease. Preliminary data suggest it may have an important role in the management of this infection in children and the elderly. In the short-term management of GORD, lansoprazole monotherapy offers a more effective alternative to histamine H2-receptor antagonists and initial data indicate that it is an effective short-term treatment option in children and adolescents. In adults lansoprazole maintenance therapy is also an established treatment option for the long-term management of this chronic disease. Lansoprazole has a role in the treatment and prevention of NSAID-related ulcers and the treatment of acid-related dyspepsia; however, further studies are needed to confirm its place in these indications. Lansoprazole has emerged as a useful and well tolerated treatment option in the management of acid-related disorders.
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PMID:Lansoprazole: an update of its place in the management of acid-related disorders. 1169 67

We aimed to determine if changes in the patterns of upper gastrointestinal diseases at endoscopy have occurred over the past decade. Retrospectively, 917 consecutive patients were selected based on upper endoscopy between June 1 and August 31, in 1990 (n = 217), 1994 (n = 270), and 1998 (n = 430). Demographic, clinical, endoscopic, and histological information were extracted from the medical records on a standardized case record form. Over the eight-year period, follow-up of peptic ulcer (15%, 5%, and 5%, respectively, in 1990, 1994, and 1998, df = 2, P < 0.001), bleeding (22%, 14%, and 13%, P = 0.008), and nausea/vomiting (15%, 16%, and 10%, df = 2, P = 0.003) had become less frequent, but reflux (21%, 19%, and 34%, df = 2, P < 0.001) and dyspepsia (24%, 43%, and 32%, df = 2, P < 0.001) more frequent indications for upper endoscopy. The prevalence of peptic ulcer disease decreased (22%, 15%, and 13%, df = 2, P = 0.025), but the prevalence of reflux esophagitis increased significantly (29%, 30%, and 39%, df = 2, P = 0.010). The prevalence of both the use of nonsteroidal antiinflammatory drugs (NSAIDs) (18%, 20%, and 11%, respectively, in 1990, 1994, and 1998, df = 2, P = 0.004) and H. pylori infection (39% in 1994 and 30% in 1998, df = 1, P = 0.032) decreased. Overall, NSAID use was independently associated with gastric ulcers (OR = 2.39, 95% CI 1.21-4.73, chi2 = 6.31, df = 1, P = 0.012), but not esophagitis. H. pylori infection was independently associated with duodenal ulcers (OR = 4.74, 95% CI 2.30-9.77, chi2 = 17.8, df = 1, P < 0.001), histologically chronic (OR = 166.8, 95% CI 76.1-365.4, chi2 = 313.0, df = 1, P < 0.001) and active (OR = 30.1, 95% CI 17.0-53.5, chi2 = 189.7, df = 1, P < 0.001) gastritis and lymphoid aggregates (OR = 5.49, 95% CI 3.02-9.97, chi2 = 36.3, df = 1, P < 0.001). In conclusion, the prevalence of peptic ulcer disease appears to have been decreasing, whereas reflux esophagitis has been increasing over the past decade in Western Sydney. The decreased use of NSAIDs and decline of H. pylori infection have likely both contributed to the reduction of peptic ulcer disease, but the increase in reflux esophagitis remains to be fully explained.
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PMID:Reduction of peptic ulcer disease and Helicobacter pylori infection but increase of reflux esophagitis in Western Sydney between 1990 and 1998. 1176 65

In institutionalized adults with intellectual disability (ID), Helicobacter pylori infection occurs at approximately twice the rate it appears in the general population, and it may be responsible for the twofold higher rates of peptic ulcer disease and gastric cancer in this population. Medical, behavioural and additional environmental factors, as well as level of ID, may be related to the risk of infection with H. pylori. One hundred and sixty-eight adults with ID who were currently, had previously been or had never been institutionalized underwent a biopsychosocial evaluation. This included assessment of: level of ID using the Adaptive Behaviour Scale (ABS) Part I; levels of maladaptive behaviour using the ABS Part II; demographic, medical and environmental factors; as well as H. pylori tests using serology and faecal antigen. The overall rates of past or current infection with H. pylori in institutionalized and previously institutionalized participants were about twice that of the overall group of never-institutionalized participants, i.e. 87% and 79% compared to 44%, respectively (P < 0.001). The rates of H. pylori infection appeared to increase with age in the never-institutionalized group, but were consistently high across all ages in the other groups. The rate of infection was higher in those institutionalized for more than 5 years (95% versus 76%, P=0.02), in those with flatmates with excessive oral secretions (65% versus 21%, P < 0.001) or faecal incontinence (67% versus 27%, P < 0.001), and in those with more chronic illness and medications. All mean domain scores of the ABS Part I (Intellectual Disability) were significantly lower (indicating more severe ID) in the group currently infected with H. pylori compared to their non-infected counterparts. The majority of mean domain scores of the ABS Part II (Behaviour) were also worse, with half of these score differences reaching statistical significance in the currently infected group. The presence of alarm symptoms (e.g. vomiting, weight loss, haematemesis and melena), iron deficiency and body mass index were not significantly different in currently infected subjects. Adults with ID appear to be particularly at risk of infection with H. pylori. Environmental associations with infection include past or current institutionalization, a longer period of institutionalization, living with flatmates with excessive oral secretions and faecal incontinence. Medical associations include chronic disease and more medications, but not alarm symptoms or body mass index. Demographic associations may include increasing age in never-institutionalized adults, but no age effect in currently or previously institutionalized individuals. Psychosocial associations include more severe ID and maladaptive behaviour with current infection.
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PMID:Environmental, medical, behavioural and disability factors associated with Helicobacter pylori infection in adults with intellectual disability. 1185 56

The management of dementia patients encompasses pharmacologic, behavioral, and psychosocial intervention strategies. Before pharmacologic intervention is instituted, it is important that sources of excess disability and comorbidity be eliminated or reduced. Identification of comorbid medical and psychiatric conditions, such as depression and delirium, should be identified and appropriately treated. Providing caregivers with education, support, and practical advice is a critical component of the management of the demented patient. The current standard of care for pharmacologic management of the cognitive and functional disabilities of AD consists of the combination of a cholinesterase inhibitor and high-dose vitamin E. This standard is based on the results of large-scale, double-blind, placebo-controlled trials. Cholinesterase inhibitors are the only FDA-approved pharmacologic treatments for AD. Cholinesterase inhibitors have been shown to be effective in the treatment of the cognitive, behavioral, and functional deficits of AD. Large-scale placebo-controlled trials of tacrine, donepezil, rivastigmine, and galantamine have demonstrated moderate benefits in patients with mild to moderate AD. Donepezil, rivastigmine, and galantamine are the first-line choices in the treatment of AD because of their lack of hepatotoxicity, ease of administration, few significant drug-drug interactions, and mild to moderate side effects. There are few contraindications to the use of cholinesterase inhibitors. Known hypersensitivity to a specific drug or its derivatives is the only true contraindication. Cautious administration of cholinesterase inhibitors is advised in patients who have a previous history of allergy or adverse reactions to prior cholinesterase inhibitors, severe liver disease, preexisting bradycardia, peptic ulcer disease, current alcoholism, asthma, or chronic obstructive pulmonary disease. Nausea, vomiting, diarrhea, and anorexia are the most common side effects of cholinesterase inhibitors. These gastrointestinal side effects can be minimized by gradual dose increases, administration with food, adequate hydration, and judicious use of an antiemetic. Vitamin E has been demonstrated to slow the progression of AD in several small and one large placebo-controlled trials. Because of its low cost and safety, it is recommended in addition to a cholinesterase inhibitor for the treatment of AD. There are no FDA-approved treatments for DLB and VaD. One small placebo-controlled trial demonstrated that rivastigmine may be effective in the treatment of DLB. More large-scale placebo-controlled trials are needed to confirm the results of this study. Treatment of VaD focuses on the control, identification, and management of cerebrovascular disease and vascular risk factors. Although there are no peer-reviewed reports on the efficacy of cholinesterase inhibitors for VaD or mixed AD/VaD, early reports suggest that these agents may also be effective for mixed AD/VaD. The indications for the use of cholinesterase inhibitor drugs are eventually likely to broaden to include DLB, mixed AD/VaD, and AD in its more advanced stages.
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PMID:Pharmacologic treatments of dementia. 1217 Oct 61

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


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