Gene/Protein Disease Symptom Drug Enzyme Compound
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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We sought to determine whether orally consumed broccoli sprouts could eradicate Helicobacter pylori infection in infected human volunteers. Helicobacter pylori-positive patients were identified by stool antigen testing or gastric biopsies. Patients consumed broccoli sprouts (14, 28, or 56 g) twice daily for 7 days. We performed stool antigen testing immediately following the completion of treatment (day 8) and at day 35. Urea breath testing was performed on those patients who remained negative at day 35. Patients completed pre- and posttreatment questionnaires regarding symptoms (abdominal discomfort--pain, nausea, bloating), recent medications, and palatability. Nine patients completed the course of treatment and began follow-up testing. Seven of nine (78%) patients were stool antigen negative immediately after the completion of therapy and six remained negative at day 35. Urea breath testing was completed on six patients. Two patients were negative, two positive, and two indeterminate. Endoscopic gastric biopsies were obtained from one patient with an indeterminate breath test and the tissue was negative for H. pylori by immunohistochemical staining. Of the five patients who provided information on pre- and posttreatment symptoms, two reported improvement, one no change, and one reported worsening. Six patients rated the taste of broccoli sprouts from okay to very good; one patient stated they were "not good." Consumption of oral broccoli sprouts was temporally associated with eradication of H. pylori infection in three of nine patients. Most patients found broccoli sprouts palatable. Further studies are needed to determine the optimal dose of broccoli sprouts and whether concomitant proton pump inhibitors or antibiotics might augment the effectiveness.
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PMID:Oral broccoli sprouts for the treatment of Helicobacter pylori infection: a preliminary report. 1538 26

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 (GER) is a common episode in pediatric patients with severe motor and intellectual disabilities (SMID) and occasionally leads to a severe clinical state accompanied with nausea, hematemesis, melena, wheezing, pneumonia, anemia and/or failure to thrive. We report here a case of a 14-year-old male with Lennox syndrome who had been treated with a histamine H2 blocker intravenously or via a nasogastric tube for repeated gastric hemorrhage due to severe GER. Since his gastric hemorrhage became resistant to the H2 blocker, we decided to replace it with a proton pump inhibitor (PPI). Although lansoprazole can be decapsulated for administration via a nasogastric tube, it tends to block fine tubes. The acid-sensitive drug omeprazole, another oral PPI, is commercially available as enteric-coated tablets. Therefore, we pulverized the tablets and administered omeprazole, mixed with a small amount of antacid, via a nasogastric tube. The patient's gastric hemorrhage was dramatically improved. Thus, administration of pulverized omeprazole concomitantly with antacid via a fine nasogastric tube may provide a novel approach for the treatment of chronic GER in pediatric patients with SMID.
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PMID:Treatment of gastric hemorrhage by pulverized omeprazole and antacid--concomitant administration via a nasogastric tube. 1559 25

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

Omeprazole is a proton pump inhibitor which reduces both basal and stimulated gastric acid secretion by inhibiting the parietal cell enzyme H(+)-K(+)-adenosine triphosphatase. Typical adverse effects of proton pump inhibitors are nausea, diarrhea, constipation and endocrinologic abnormalities such as gynecomastia. Cutaneous side effects are rare but may include contact dermatitis, lichenoid eruption, leukocytoclastic vasculitis or toxic epidermal necrolysis; anaphylaxis is rare. We identified omeprazole as the causative agent by oral challenge test in a patient who had developed anaphylaxis while taking several drugs.
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PMID:[Anaphylaxis caused by omeprazole]. 1639 10

Dyspepsia comprises a broad spectrum of predominantly upper abdominal symptoms, such as pain, indigestion, nausea, early satiety and bloating. While these symptoms are highly prevalent, in less than 50% of patients presenting with dyspepsia, structural lesions or biochemical abnormalities are found that explain the symptoms when routine clinical tests are used. In patients without structural lesions the diagnosis of functional dyspepsia is justified. Exclusion of life-threatening disorders as the cause of symptoms and reassurance of the patient as well as proper explanation of the diagnosis and its underlying disease mechanisms (i.e. symptoms are due to a sensitive gut) is crucial and can be considered as an essential element of treatment. Since there is a remarkable comorbidity of anxiety and depression, psychosomatic interventions might be necessary in selected patients. Based on controlled clinical trials few drugs, such as proton pump inhibitors, prokinetics, tricyclic antidepressants, simethicone and selected herbal preparations have been found to be effective for treatment of functional dyspepsia. Effects of H. pylori eradication, even though strongly advocated, are most likely due to undiagnosed peptic ulcer disease in a very small group of patients. While there is currently no therapy that cures functional dyspepsia, the therapeutic target is to control symptoms.
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PMID:[Functional dyspepsia - diagnosis of desperation?]. 1676 73

With the ever-growing armamentarium of pharmacological agents, the gastrointestinal drug-induced side effects of dyspepsia, nausea, vomiting, diarrhoea and constipation are increasingly seen. They are often self-limiting and without serious sequelae, but of greater concern is drug-induced mucosal ulceration that can manifest as gastrointestinal haemorrhage, stricture and perforation. These complications are mainly attributable to NSAIDs and aspirin, which can injure the mucosa anywhere along the gastrointestinal tract. These iatrogenic serious side effects can be reduced with co-prescription of a proton pump inhibitor, substitution of a COX-2 inhibitor and eradication of Helicobacter pylori when the bacterium is present. Other recognised gastrointestinal complications include small intestinal diaphragm, microscopic colitis, a range of hepatotoxic effects and pancreatitis. The introduction of new classes of drugs has resulted in new adverse effects that require consideration in patients presenting with gastroenterological symptoms. These include pill oesophagitis from bisphosphonates and ischaemic colitis relating to serotonin antagonists. Here, the authors review the literature on drug-induced complications of the gastrointestinal tract and present the pertinent management issues relevant to clinical practice.
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PMID:Drug-induced side effects affecting the gastrointestinal tract. 1677 95

This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management. Duodenogastric reflux (DGR) consists of retrograde passage of alkaline duodenal contents into the stomach; it may occur due to antroduodenal motility disorder (primary DGR) or may arise following surgical alteration of gastoduodenal anatomy or because of biliary pathology (secondary DGR). Pathologic DGR may generate symptoms of epigastric pain, nausea, and bilious vomiting. In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma. The treatment of DGR is difficult, non-specific, and relatively ineffective in controlling symptoms. Proton pump inhibitors decrease the upstream effects of DGR on the esophagus by decreasing the volume of secretions; promotility agents diminish gastric exposure to duodenal secretions by improving gastric emptying. In patients with severe reflux resistant to medical therapy, a duodenal diversion operation such as the duodenal switch procedure may be indicated.
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PMID:[Duodenogastric and gastroesophageal bile reflux]. 1728 81

The authors present the case of a 43-year-old women who underwent a laparoscopic gastric bypass in 2003 for morbid obesity. They report that 2 years later, she had maintained significant weight loss, but had developed acute abdominal pain, followed by nausea and emesis. In the emergency room, she had diffuse tenderness, tachycardia, and leukocytosis. After initial resuscitation, a computed tomography was performed, which showed free air above the liver and thickened small bowel loops. She was brought emergently to the operating room for laparoscopy. At surgery, turbid fluid and inflamed small bowel loops were seen. A perforated marginal ulcer was discovered in the Roux limb, approximately 2 cm distal to the gastrojejunal anastomosis. The perforation was oversewn primarily and patched with omentum. The repair was tested by intraoperative endoscopy. A gastrostomy tube also was placed within the gastric remnant for enteral access. The patient did extremely well postoperatively, and had an uneventful postoperative course. She was discharged on postoperative day 4. The gastrostomy tube was removed at 1 month, and at this writing, she remains well since surgery. An upper endoscopy at 2 months was completely normal, and the Helicobacter pylori test results were negative. The gastric pouch had not significantly enlarged since initial surgery, as indicated by both endoscopy and barium study. Marginal ulcer is reported to be 0.6% to 16% after laparoscopic gastric bypass. Etiologies include gastrogastric fistula, excessively large gastric pouch containing antral mucosa, H. pylori infection, nonsteroidal antiinflammatory use, and smoking. Unfortunately, none of these applied to the reported patient. Because her exact etiology remains unknown, she at this writing continues to receive proton pump inhibitor therapy.
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PMID:Multimedia article. Laparoscopic repair of a perforated marginal ulcer 2 years after gastric bypass. 1770 79

Non ulcer dyspepsia is one of the most common problems encountered in primary care practice. The underlying pathophysiology of non ulcer dyspepsia is not fully understood, but it is known that this condition is associated with H. pylori infection and motility disorder. The presenting abdominal symptoms are non specific: they include bloating, belching, flatulence, excessive fullness after eating and nausea. Psychological condition such as anxiety, depression and stress do play a role in the recurrence of symptoms. Upper GI endoscopy is necessary in patients who presents with alarm symptoms suggestive of possible underlying organic condition before one makes the diagnosis of non ulcer dyspepsia. Pharmacological therapy using H2 receptor antagonist and proton pump inhibitors are effective for symptom relief. Patient's education and supportive care should be part of the management strategy in recurrent chronic dyspepsia.
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PMID:Understanding non ulcer dyspepsia. 1894 14


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