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Nexium (Esomeprazole) decreases the amount of acid produced in the stomach and is therefore used to treat symptoms of gastroesophageal reflux disease (GERD) and similar conditions.
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Combination therapy (with amoxicillin and clarithromycin) for eradication of H pylori in patients with duodenal ulcer 40 mg PO q Day for 10 days, PLUS Amoxicillin 1000 mg PO q12hr for 10 days, PLUS Clarithromycin 500 mg PO q12hr for 10 days IV indicated for risk reduction of rebleeding of gastric or duodenal ulcers following therapeutic endoscopy in adults 80 mg IV infused over 30 min, THEN continuous IV infusion of 8 mg/hr for total treatment duration of 72 hr Follow IV therapy with oral acid suppressive therapy Blood and lymphatic system disorders: Agranulocytosis, pancytopenia Blurred vision GI disorders: Pancreatitis, stomatitis, microscopic colitis Hepatobiliary disorders: Hepatic failure, hepatitis with or without jaundice Anaphylactic reaction/shock GI candidiasis Hypomagnesemia Musculoskeletal disorders: Muscular weakness, myalgia, bone fracture Nervous system disorders: Hepatic encephalopathy, taste disturbance Psychiatric disorders: Aggression, agitation, depression, hallucination Interstitial nephritis Gynecomastia Bronchospasm Skin and subcutaneous tissue disorders: Alopecia, erythema multiforme, hyperhidrosis, photosensitivity, Stevens-Johnson syndrome, toxic epidermal necrolysis (sometimes fatal fatal) PPIs are possibly associated with increased incidence of Clostridium difficile-associated diarrhea (CDAD); consider diagnosis of CDAD for patients taking PPIs who have diarrhea that does not improve PPIs may decrease the efficacy of clopidogrel by reducing the formation of the active metabolite Severe hepatic impairment Cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE) reported with PPIs; avoid using for longer than mediy indicated; discontinue if sns or symptoms consistent with CLE or SLE are observed and refer patient to specialist Relief of symptoms does not eliminate the possibility of a gastric malnancy Breastfeeding Therapy increases risk of Salmonella, Campylobacter, and other infections Contains enteric coated granules (acid labile); do not chew or crush; take 1 hr before meals Published observational studies suggest that PPI therapy may be associated with an increased risk for osteoporosis-related fractures of the hip, wrist, or spine; particularly with prolonged (1 yr), hh-dose therapy Decreased gastric acidity increases serum chromogranin A (Cg A) levels and may cause false-positive diagnostic results for neuroendocrine tumors; temporarily discontinue PPIs before assessing Cg A levels Hypomagnesemia may occur with prolonged use (ie, 1 yr; adverse effects may result and include tetany, arrhythmias, and seizures; in 25% of cases reviewed, magnesium supplementation alone did not improve low serum magnesium levels, and the PPI had to be discontinued Daily long-term use (e.g., longer than 3 years) may lead to malabsorption or a deficiency of cyanocobalamin Acute interstitial nephritis reported in patients taking proton pump inhibitors May elevate and/or prolong serum concentrations of methotrexate and/or its metabolite when administered oncomitantly with PPIs, possibly leading to toxicity; consider a temporary withdrawal of PPI therapy with hh dose methotrexate administration Bioavailability: PO: 89-90%; food decreases AUC by 33-53%; take 1 hr before meal Onset: 1-2 hr (gastric acid inhibition); within 4 wk (GERD) Duration (multiple dose): Gastric acid inhibition; PO: 17 hr Peak plasma time: PO: 1-1.6 hr Liver; extensively metabolized by hepatic P450 enzyme; major metabolic pathway is via CYP2C19; the rest is via CYP3A4 Metabolites: 5-hydroxyesomeprazole (inactive), esomeprazole sulfone (inactive), desmethyl-esomeprazole (activity unknown) Enzymes inhibited: CYP2C19 Slow metabolizers (3% of Caucasians and African-Americans) are deficient in CPY2C19 enzyme system; plasma concentration can be hher than in persons who have the enzyme Metabolites of esomeprazole lack antisecretory activity The major part of esomeprazole’s metabolism is dependent on the CYP2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites CYP2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15-20% of Asians lack CYP2C19 and are termed poor metabolizers At steady state, the ratio of AUC in poor metabolizers to AUC in the rest of the population (extensive metabolizers) is approximately 2 The above information is provided for general informational and educational purposes only.
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