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To evaluate the efficacy of furazolidone-containing regimens in eradicating H. pylori.
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At one month post-antibiotic therapy, we have observed lymphoma responses in 7 of 32 patients (21.9%). Two additional patients had objective response during followup (28.1% overall response). The median treatment free survival for antibiotic responders is 69.9 months and for non-responders, 30.6 months (p = 0.019).
We studied the action on acid secretion of lansoprazole compared with famotidine by 24-h intragastric pH monitoring, evaluated its clinical effects prospectively, and assessed the importance of acid inhibition in gastric ulcer patients. Twenty symptomatic patients with active gastric ulcers diagnosed by endoscopy were assigned to a lansoprazole (LAN) group (lansoprazole 30 mg q.d., n = 10) or a famotidine (FAM) group (famotidine 20 mg b.i.d., n = 10). There were no differences between the groups in pretreatment pH profiles or background factors such as age, sex, smoking, previous ulcer therapy, ulcer site, or Helicobacter pylori infection. The FAM group showed a continuous increase in intragastric pH during the night, with low pH values except for a transient increase associated with food intake during the day. However, the LAN group showed a more neutral pH throughout the day, with pH-3 holding time ratios of 99.0% for 24 h, 98.3% at night, and 99.8% during the day, compared with 68.0, 76.5, and 59.4%, respectively, in the FAM group. The healing rate was also higher in the LAN group. We conclude that inhibition of gastric acidity is important in ulcer therapy and that lansoprazole is superior to famotidine in promoting ulcer healing.
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The effects of lansoprazole given intravenously on indomethacin-induced gastric bleeding and mucosal lesions were investigated in rats in comparison with those of omeprazole, famotidine and ranitidine. Lansoprazole inhibited gastric bleeding induced by indomethacin with an ID50 value of 0.29 mg/kg. Omeprazole and famotidine significantly inhibited gastric bleeding, but ranitidine provided negligible inhibition. A correlation was found between the inhibitory action of lansoprazole on gastric bleeding, and acid secretion, and its inhibitory action on gastric bleeding was almost completely abolished by adding 50 mM-HCl to the gastric perfusate, suggesting that lansoprazole's inhibitory action on gastric bleeding was mainly due to its antisecretory action. Lansoprazole inhibited the development of gastric lesions induced by indomethacin with an ID50 value of 0.10 mg/kg, whereas histamine H2-receptor antagonists did not display a potent inhibitory effect. ID50 values for omeprazole, famotidine and ranitidine were 0.69, 2.58 and 24.6 mg/kg, respectively. These results indicate that lansoprazole has a potent inhibitory action on indomethacin-induced gastric bleeding and mucosal lesions and that it is useful in the treatment of acute gastric mucosal lesions.
A miscellaneous therapy, based on the combination of multiple medications in high doses for 2 weeks, and with gastric pH elevation, is a highly effective treatment as a first-line therapy for the eradication of H. pylori.
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The groups of patients given 400 and 800 mg/day clarithromycin for H pylori eradication therapy showed 39% (from 2.20 +/- 1.29 to 1.35 +/- 0.88 mL/min [day 0 versus 7, mean +/- SD]; P <.05) and 68% (2.40 +/- 1.22 to 0.76 +/- 0.51 mL/min; P <.05) reductions in CL(cortisol-->6beta-hydroxycortisol), respectively. In contrast, the control subjects given lansoprazole and amoxicillin without clarithromycin showed no significant changes in CL(cortisol-->6beta-hydroxycortisol). The urinary 6beta-hydroxycortisol/cortisol ratio also decreased significantly (P <.05) in the patient groups but not in the control subjects. The mean 3-hour plasma lansoprazole levels elevated in proportion to the doses of clarithromycin: 385 +/- 338 ng/mL for the control subjects, 696 +/- 797 ng/mL for the H pylori-positive patients given 400 mg/day clarithromycin, and 947 +/- 806 ng/mL for the H pylori-positive patients given 800 mg/day clarithromycin (P <.05 versus the control subjects). No significant differences were observed among the groups in the mean plasma ratios of 5-hydroxylansoprazole or lansoprazole sulfone to lansoprazole.
After oesophageal manometric and pH-metric evaluation and detailed information 55 patients asked to undergo laparoscopic antireflux surgery while 75 chose a medical treatment regimen based on lansoprazole. Treatment efficacy was assessed by ambulatory oesophageal pH-monitoring.
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Gastro-oesophageal reflux disease is a very common disorder. Treatment intends to relieve symptoms, prevent complications and recurrence of the disease. The initial approach in a patient with heartburn alone is to begin a therapeutic trial with antacids sucralfate, a prokinetic agent, a histamine-receptor antagonist or a low dose of a proton pump inhibitor. If the therapeutic trial fails, dysphagia or atypical symptoms are present, therapy depends on diagnostic findings. In mild and moderate disease, acute treatment consists of 20 to 40 mg of a proton pump inhibitor (omeprazole, lansoprazole or pantoprazole) and maintenance treatment of low dose omeprazole (10 mg). In severe disease a higher dose is administered, 40 to 80 mg of omeprazole, lansoprazole or pantoprazole for acute treatment and 20 mg of omeprazole for maintenance treatment. Maintenance treatment is adjusted to symptoms and in the case of severe disease also to endoscopic findings.
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Esomeprazole showed non-inferiority and safety in a 7 day-triple therapy for eradication of H. pylori compared with lansoprazole.
There has been a rapid increase in proton pump inhibitor (PPI) prescribing in recent years, and controlling the cost and improving the quality of prescribing is an issue of concern to many GPS:
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In the studies reviewed, dexlansoprazole was well tolerated and effective in the healing and maintenance of EE, and in the treatment of nonerosive reflux disease. However, most of the available evidence involved comparisons with placebo, making it difficult to draw meaningful conclusions about the place of dexlansoprazole among PPIs. More head-to-head comparative trials with other PPIs are needed to determine whether the unique formulation of dexlansoprazole translates into a clinically meaningful improvement in outcomes.
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Adverse events occurred relatively infrequently in all three cohorts. There were only small absolute differences in event rates between the three drugs, although these data suggest the hypothesis that lansoprazole is associated with more frequent occurrence of diarrhoea, particularly in the elderly.
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A literature search was conducted through PubMed (up to December 2009), International Pharmaceutical Abstracts (1970-December 2009), and The Cochrane Library (up to December 2009) using combinations of the following key search terms: proton pump inhibitor, GERD, infant, children, pediatric, omeprazole, rabeprazole, lansoprazole, esomeprazole, and pantoprazole. Reference citations from identified articles were also reviewed.
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To examine retrospectively the effect of proton pump inhibitors (PPIs) on thyrotropin (thyroid-stimulating hormone or TSH) values in patients with hypothyroidism and normal TSH levels receiving levothyroxine (LT4) replacement therapy.
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One hundred one patients with H pylori infection were included in the study. Patients were randomised to receive triple therapy comprising of lansoprazole 30 mg, amoxycillin 1 g, clarithromycin 500 mg, all b.d. (LAC), or quadruple therapy comprising of lansoprazole 30 mg b.d., metronidazole 500 mg t.d.s., bismuth subcitrate 240 mg b.d., and tetracycline chloride 500 mg q.d.s. (LMBT). Cure was defined as a negative (13)C urea breath test 2 mo after treatment.
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168 dyspepsia patients with H. pylori infection were randomized to receive a 5-day course of either LCM, LAC or CALM, and a 13C-urea breath test was performed after 4 weeks to assess eradication.
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Triple therapy for 1 week with lansoprazole as the antisecretory agent seems to be as effective as is reported for omeprazole-based regimens.
To conduct a systematic review of evidence supporting the efficacy and safety profiles of nonsteroidal anti-inflammatory drugs (NSAIDs) introduced in the last decade for the treatment of patients with osteoarthritis (OA), including their analgesic effects, ability to improve function, and adverse event profiles relative to current standards of care.
Barrett's esophagus (BE) is a change in the cellular structure of the lower esophagus believed by many to be caused by frequent acid exposure. The condition is troublesome because of a tendency toward cell proliferation, dysplastic transformation, and cancerous changes within the lesions. It is speculated that the pronounced increase in esophageal adenocarcinoma during the past 25 years may be attributable to acid reflux and associated BE. Strict acid control may cause lesion regression in these patients. However, pH monitoring to confirm adequate acid control is essential, and more than 1 drug may be needed to achieve adequate acid control and manage many patients. More research is needed to determine whether aggressive acid control reduces the dysplasia and cancer risk associated with BE.
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Proton pump inhibitors (PPIs) are widely prescribed as first-line therapy for the treatment of acid-related diseases, such as peptic ulcers and gastro-esophageal reflux disease, and for the eradication of Helicobacter pylori. However, the therapeutic efficacy of conventional PPIs is considered limited because: (1) they are unstable under acidic conditions and require an enteric-coated formulation in clinical use; (2) they show high interindividual variability in pharmacokinetics due to genetic polymorphisms of cytochrome P450 (CYP) 2C19 metabolism; (3) they have a relatively slow onset of pharmacological action and may require several doses to achieve optimal acid suppression and symptom relief; and (4) they often do not provide stable suppression of gastric acid secretion over 24 h. Vonoprazan fumarate (TAK-438, hereinafter referred to as "vonoprazan") is a new potassium-competitive acid blocker (P-CAB) developed to resolve the above limitations of conventional PPIs. Various physicochemical data have shown that vonoprazan has a high solubility and stability over a broad pH range in aqueous conditions. In addition, vonoprazan has a more potent and longer-lasting acid suppression effect than the conventional PPI, lansoprazole. Preclinical pharmacokinetic studies have shown that vonoprazan is accumulated and retained in the stomach for more than 24 h, even after it is eliminated from the plasma. From these findings, we propose that vonoprazan, which possesses a novel mode of action, can improve on the outcomes seen with conventional PPI-based treatments for acid-related diseases.