Duodenal ulcer, can it be cured?

Treatment

Medical Care

Treatment of duodenal ulcers varies depending on the etiology and clinical presentation. The initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper GI hemorrhage. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention.

Although the therapeutic principles of these distinct clinical scenarios share some similarities, they differ sufficiently to warrant separate discussions. Age is an independent risk factor for the incidence and mortality from bleeding peptic ulcer, with the risk increasing in persons older than 65 years, and increasing further in those older than age 75 years.64 In one study, at least 2 risk factors (previous duodenal ulcer, H pylori infection, use of ASA/NSAID, and smoking) were present in two thirds of persons with acute gastroduodenal bleeding.65

The principles of management of bleeding peptic ulcers outlined below are equally applicable to both gastric and duodenal ulcers.

  • Medical management of bleeding duodenal ulcers
    • Urgent EGD is the treatment of choice in the setting of a bleeding duodenal ulcer for diagnostic and therapeutic reasons. Endoscopy provides an opportunity to visualize the ulcer, to determine the degree of active bleeding, and to attempt hemostasis by direct measures. Primary endoscopic hemostatic therapy (EHT) is successful in about 90% of patients; when this fails, transcatheter embolization may be useful.66 (See Surgical Care for a full discussion of endoscopic therapy.) Medical management usually serves as an adjunct to direct endoscopic therapy.
    • Risk factors to predict rebleeding following EHT for nonvariceal upper GI bleeding include failure to use a PPI after the procedure; endoscopically demonstrated bleeding, especially peptic ulcer bleeding; EHT monotherapy; post-EHT use of heparin; and bleeding in the patient with moderate or severe cirrhosis.67 Other predictors of rebleeding after EHT include pre-endoscopic hemodynamic instability, comorbid illness, active bleeding at endoscopy, large ulcer size, or posterior wall duodenal ulcer.68 These high risk persons might be considered for initial care in the ICU, and follow-up (“second look”) endoscopy, especially because many of these factors (advanced age, comorbidities, in-hospital bleeding, rebleeding, hypovolemic shock, need for surgery) are associated with hospital mortality.69
    • Acid suppression is the general pharmacologic principle of medical management of acute bleeding from a peptic ulcer. Reducing gastric acidity is believed to improve hemostasis primarily through the decreased activity of pepsin in the presence of a more alkaline environment. Pepsin is believed to antagonize the hemostatic process by degrading fibrin clots. By suppressing acid production and maintaining a pH above 6, pepsin becomes markedly less active.
    • Two classes of acid-suppressing medications currently in use are H2RAs and PPIs.70 Both classes are available in intravenous or oral preparations. Examples of H2RAs include ranitidine, cimetidine, famotidine, and nizatidine. Examples of PPIs include omeprazole, pantoprazole, lansoprazole, and rabeprazole.
    • There is a very good safety profile for PPIs, although attention must continue to be focused on adverse effects, especially with long-term and/or high-dose therapy, such as Clostridium difficile infection, community-acquired pneumonia, hip fracture, and vitamin B12 deficiency.71
    • Long-term use of PPIs are also associated with decreased absorption of some medications. PPIs impair gastric secretion of acid; thus, absorption of any medication that depends on gastric acidity, such as ketoconazole and iron salt, is impaired on long-term PPI therapy. In fact, achlorhydria (absence of intragastric acidity) may be associated with iron deficiency anemia, because the ferric form of iron must be converted to the ferrous form by gastric acid. Most iron absorbed is in the ferrous form.
    • H2RAs are an older class of medications, and their use in the setting of an actively bleeding duodenal ulcer has been largely superseded by the use of PPIs. Many gastroenterologists assert that intravenous PPI therapy maintains hemostasis more effectively than intravenous H2RA. Thus, intravenous H2RA no longer has a role in the management of bleeding peptic ulcers.72
    • Andriulli et al evaluated the use of high- versus low-dose PPIs after endoscopic hemostasis in patients with peptic ulcer bleeding.73 The primary end point was the in-hospital rebleeding rate (determined on repeat endoscopy). Patients with actively bleeding ulcers and those with nonbleeding visible vessel or adherent clot were treated with epinephrine injection and/or thermal coagulation, then randomized to receive an intensive regimen of 80-mg PPI bolus, followed by 8 mg/h as continuous infusion for 72 hours, or a standard regimen of a 40-mg PPI bolus daily, followed by saline infusion for 72 hours. After the infusion, all patients were given 20 mg PPI twice daily orally.73
    • Of 238 patients in the intensive PPI regimen group, bleeding recurred in 28 (11.8%); of 236 patients in the standard regimen group, bleeding recurred in 19 (8.1%) (P = 0.18).73 Most of the rebleeding episodes occurred during the initial 72-hour infusion. The duration of hospital stay was <5 days for 88 (37.0%) in the intensive regimen group and 111 patients (47.0%) in the standard group (P = 0.03), and there were fewer surgical interventions in the standard group (1) relative to the intensive regimen group (3). Five patients in each treatment group died.73 The investigators concluded that standard-dose PPIs infusion was as effective as a high-dose regimen in reducing the risk of recurrent bleeding following endoscopic hemostasis of bleeding ulcers.
    • Parenteral PPI is indicated after successful endoscopic therapy for ulcers with high-risk signs, such as active bleeding, visible vessels, and adherent clots. Parenteral PPI use before endoscopy is common practice. A Canadian database (RUGBE) indicated some benefit in decreasing rebleed rates.72 No randomized control trial provided evidence to support the use of parenteral PPI in this setting, but giving oral PPI both before and after EHT for those persons with peptic ulcers with signs of recent hemorrhage can be justified on the grounds of cost-effectiveness.22
    • Based on intragastric pH data, nonvomiting patients with bleeding ulcers may be treated with oral lansoprazole (120-mg bolus, followed by 30 mg every 3 h).2
    • When indicated, intravenous pantoprazole or omeprazole is administered as an 80-mg bolus followed by a continuous 8-mg/h infusion for 72 hours. This treatment is changed to oral PPI therapy after 72 hours if no rebleeding occurs.
    • Whether acid suppression improves therapeutic outcomes of peptic ulcers compared with placebo may be more important than the issues raised above. Many researchers have compared parenteral PPI therapy with placebo. Overall, the results demonstrate a shorter period bleeding and a decreased incidence of rebleeding with PPI therapy. Some studies have demonstrated a decreased need for emergency surgery and transfusion; however, evidence that parenteral PPI reduces mortality from ulcer bleeding is relatively recent.19
    • Concomitant H pylori infection in the setting of bleeding peptic ulcers should be eradicated, as this lowers the rate of rebleeding.74,75
  • Medical management of stable duodenal ulcers
    • Treatment of duodenal ulcers depends on the cause. Because the 2 most common causes are H pylori infection and NSAID use, the focus of this section is specific strategies aimed at treating duodenal ulcers in these settings.
    • H pylori infection: In general, patients with a documented duodenal ulcer who have H pylori infection should receive eradication therapy.76,77,78,79,80,81 Several studies have evaluated different regimens for H pylori eradication. In 1998, The American College of Gastroenterology (ACG) published practice guidelines for the management of H pylori infection (the 2007 guidelines can be found here82 ).83 The ACG guidelines recommended the following treatments83 :
      • Lansoprazole 30 mg PO bid or omeprazole 20 mg PO bid, plus amoxicillin 1000 mg PO bid and clarithromycin 500 mg PO bid for 14 days (Other PPIs may also be substituted.)
      • Lansoprazole 30 mg PO bid or omeprazole 20 mg PO bid, plus metronidazole 500 mg PO bid and clarithromycin 500 mg PO bid for 14 days
      • Ranitidine bismuth citrate 400 mg PO bid, plus clarithromycin 500 mg PO bid and amoxicillin 1000 mg PO bid or metronidazole 500 mg PO bid or tetracycline 500 mg PO bid for 14 days
      • Bismuth subsalicylate 525 mg PO qid, plus metronidazole 500 mg PO tid and tetracycline 500 mg PO qid and a PPI (eg, lansoprazole 30 mg PO [optimal dose] or omeprazole 20 mg PO [optimal dose]) for 14 days
      • Bismuth subsalicylate 525 mg PO qid, plus metronidazole 250 mg PO qid and tetracycline 500 mg PO qid and any H2RA for 14 days
      • These first-line treatments may fail in over 20% of H pylori –positive individuals, especially those with non-ulcer dyspepsia as compared with those with duodenal ulcers, and second- or third-line therapies may be necessary.84
      • Dyspepsia is more common in H pylori –positive than H pylori –negative persons, and treatment offers a small incremental symptom benefit.85
      • Size of the ulcer, the presence of associated atrophic gastritis, and successful eradication of associated H pylori are independent predictive factors for the healing of peptic ulcers.86 A 7-day treatment is adequate in those patients whose condition has not failed previous attempts at eradication.80,87
      • Spouses and H pylori –positive family members of H pylori –positive persons should be considered for testing and treatment of H pylori infection,88 since mother-to-child transmission may be a major route of H pylori infection.89
      • It is controversial whether new GERD and erosive esophagitis occur after eradication of H pylori in duodenal ulcer patients, but if they do occur, the inflammation is usually mild and short-lived, and maintenance therapy is usually not required.90
      • In a study by Liou et al, H pylori eradication rates were higher for a 7-day antibiotic regimen containing clarithromycin, amoxicillin, and lansoprazole (CAL) when used as first-line therapy compared with levofloxacin, amoxicillin, and lansoprazole (LAL).91 Additionally, CAL did not achieve a higher rate of eradication than LAL as second-line therapy; thus, consideration of the sequence of administering antibiotic regimens for H pylori is important.
    • Medical management of NSAID ulcers
      • Discontinuation of NSAIDs is paramount, if it is clinically feasible.
      • Treat H pylori infection if it is present. For patients who must continue with their NSAIDs, PPI maintenance is recommended to prevent recurrences even after eradication of H pylori.37,92
      • If NSAIDs must be continued, changing to a COX-2 selective inhibitor is an option. However, use of a traditional NSAID and once-daily PPI is comparable to a selective COX-2 inhibitor with respect to ulcer bleeding in patients with a history of peptic ulcer disease.39
      • In general, 6-8 weeks of therapy with a PPI is required for complete healing of a duodenal ulcer.

Surgical Care

Endoscopic intervention is the primary mode of treating bleeding ulcers. Surgical management of duodenal ulcers is generally reserved for refractory ulcers and bleeding ulcers that fail to respond to medical management.

  • Endoscopic therapy
    • Endoscopic therapeutic intervention is indicated for bleeding duodenal ulcers with high-risk signs (eg, active bleeding, visible vessels, adherent clots).
    • Several tools are available to the endoscopist to achieve hemostasis; these tools include bipolar cautery, use of a heater probe or hemoclips, argon plasma coagulation, and local injection of epinephrine and other agents.
      • Bipolar cautery and use of a heater probe both apply heat to the ulcer and cauterize the bleeding vessel. Hemoclip placement is a promising therapy but requires a skilled endoscopist and a lesion amenable to clip placement.
      • Injection with epinephrine achieves hemostasis through the vasoconstrictive effect of epinephrine. However, some physicians argue that it is effective mainly through the tamponade effect of local fluid injection. This is supported by the fact that injection of saline achieves comparable hemostasis.
      • Argon plasma coagulation uses heat to achieve hemostasis. One group compared argon plasma coagulation with heater probe and found no difference in the incidence of rebleeding or the need for surgical intervention.93
    • In ulcers with high-risk signs, endoscopic combination therapy with epinephrine injection and hemoclip placement is superior to injection alone.94
  • Urgent surgical management
    • The indications for urgent surgery include the following: (1) failure to achieve hemostasis endoscopically, (2) recurrent bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after 2 failed endoscopic attempts), and (3) perforation.
    • In general, 5% of bleeding ulcers eventually require operative management. Most emergent surgical procedures involve simple oversewing of the ulcer to achieve hemostasis.
  • Elective surgical management
    • The indications for elective surgical management include the following: (1) duodenal ulcer refractoriness to medical treatment, (2) patient intolerance to medications, and (3) patient noncompliance with medications.
    • With the advent of improved antisecretory therapy and with the discovery of H pylori, elective surgical management of duodenal ulcers has become much less common in areas where such treatment is readily available.
  • Elective surgical approaches
    • Vagotomy
      • Vagotomy involves resection of the vagus nerve, which eliminates the autonomic stimulation of the parietal cells. Historically, a truncal vagotomy was performed; however, this led to gastric atony and subsequent stasis in as many as 20% of patients. Currently, selective vagotomies are the procedures of choice.
      • Selective vagotomy preserves the celiac and hepatic branches of the vagus nerve, thus decreasing the incidence of gastric atony. However, a gastric drainage procedure (eg, pyloroplasty) remains an essential component of this surgical approach. Highly selective vagotomy results in denervation of the parietal cells but preserves nerves supplying the pyloroantral region.
      • The Billroth I and Billroth II procedures are the 2 types of truncal vagotomy and antrectomy. These surgical approaches carry a mortality rate of approximately 1% and are currently performed much less frequently.

Consultations

Surgical consultation is recommended for all patients with bleeding ulcers, especially those patients who are at high risk of significant bleeding. Such ulcers include those that are causing hemodynamic instability, those that are actively bleeding, and those that are showing a visible vessel on endoscopy.

Diet

Diet, Alcohol Consumption, and Smoking

A special diet is not indicated in patients with duodenal ulcers. It is common sense to avoid any food or beverages which on a person-by-person basis aggravate symptoms. Although the link between duodenal ulcers and alcohol use and smoking is inconclusive, moderation of alcohol intake and cessation of smoking may be recommended for other health reasons.

Medication

The goals of pharmacotherapy are to eradicate H pylori infection, to reduce morbidity, and to prevent complications in patients with duodenal ulcers.

Proton Pump Inhibitors (PPIs)

PPIs are inhibitors of the gastric H+/K+ -ATPase (proton pump) enzyme system, which catalyzes the exchange of H+ and K+.

Omeprazole (Prilosec)

Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Administer 30 min before sucralfate to prevent reduction in bioavailability.

Adult

H pylori eradication: 20 mg PO bid

Uncomplicated duodenal ulcer: 20 mg PO qd

Refractory duodenal ulcer: 40 mg PO qd

Pediatric

Not established

May decrease the effectiveness of itraconazole and ketoconazole; may increase the toxicity of warfarin (increased plasma levels of warfarin observed only with high doses)

Documented hypersensitivity

Pregnancy

C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Bioavailability may increase in elderly patients; adjust the dose in the presence of hepatic impairment, the half-life can increase up to 4-fold.

Pantoprazole (Protonix, Pantoloc)

Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Indicated for <8-wk treatment of erosive esophagitis associated with GERD. May consider additional 8-wk course if ulcer does not heal. Safety and efficacy for maintenance therapy (eg, >16 wk) not established.

Adult

40 mg PO qd

Pediatric

Not established

May decrease the effects of ketoconazole and iron salts

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Decrease the dose in the presence of hepatic impairment, half-life can increase 7- to 9-fold; no dose adjustment required in patents with renal impairment.

Lansoprazole (Prevacid)

Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Used for <4 wk to treat and relieve the symptoms of an active duodenal ulcer.

Adult

H pylori eradication: 30 mg PO qd

Maintenance: 15 mg PO qd

Pediatric

Not established

May decrease the effectiveness of ketoconazole and itraconazole; may increase theophylline clearance

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not to exceed 30 mg/d in the presence of liver impairment

Esomeprazole magnesium (Nexium)

Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells.

Adult

20-40 mg PO qd for 4-8 wk

Pediatric

Not established

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Symptomatic relief with PPIs may mask symptoms of gastric malignancy.

Antihistamine, H2 Blocker

H2 blocker antihistamine agents are used in the short-term treatment of an active duodenal ulcer and as prophylaxis in the long term.

Cimetidine (Tagamet)

Inhibits histamine at H2 receptors of gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Adult

800 mg PO hs or 600 mg PO bid or 300 mg PO qid; not to exceed 1200 mg/d

Pediatric

Neonate: 5-10 mg/kg/d PO/IV/IM divided q8-12h

Infant: 10-20 mg/kg/d PO/IV/IM divided q6-12h

>1 year: 20 mg/kg/d PO divided q4-6h

1-12 years: 20-25 mg/kg/d PO divided q4-6h

>12 years: Administer as in adults.

May increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Confusional states in elderly patients; may cause impotence and gynecomastia in young men; may increase the levels of many drugs; adjust dose or discontinue if renal function changes

Famotidine (Pepcid AC, Pepcid)

Competitively inhibits histamine at H2 receptors of gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Adult

Initial: 40 mg PO hs

Maintenance: 20 mg PO hs

Pediatric

Not established

May decrease the effectiveness of ketoconazole and itraconazole

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Consider adjusting dose or discontinuing treatment if renal function changes

Nizatidine (Axid)

Competitively inhibits histamine at H2 receptors of the gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Adult

Initial: 300 mg PO hs or 150 mg bid

Maintenance: 150 mg PO qhs

Pediatric

Not established

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Administer half the dose if CrCl is 20-50 mL/min; administer 150 mg PO qod if CrCl is <20 mL/min.

Ranitidine (Zantac)

Inhibits histamine stimulation of H2 receptors in gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.
Administer 30 min before sucralfate to prevent decrease in bioavailability.

Adult

300 mg PO qhs or 150 mg PO bid

Pediatric

<8 years: Not established

>8 years: 150 mg PO bid

May decrease the effectiveness of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with renal or liver impairment; administer half the dose if CrCl is <10 mL/min

Ranitidine bismuth citrate (Tritec, Pylorid)

Combination of ranitidine and bismuth citrate, compound with bactericidal effects against H pylori. Used in with clarithromycin, because drugs act synergistically against H pylori.

Adult

400 mg PO bid for 14 d for H pylori eradication; coadminister with clarithromycin 500 mg PO for 14 d

Pediatric

Not established

May decrease the effectiveness of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin; coadministration with anticoagulants may increase the risk of bleeding; may increase the toxicity of aspirin and hypoglycemics; decreases the effect of tetracyclines and uricosurics

Documented hypersensitivity; porphyria

Pregnancy

C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Darkening stool reported in 19% of patients; caution in patients with renal or liver impairment; not recommended if CrCl <25 mL/min

Antimicrobials

Antimicrobial agents exert an antibacterial effect on H pylori.

Amoxicillin (Amoxil, Trimox)

Semisynthetic penicillin antibiotic; interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Adult

1000 mg PO bid for H pylori eradication

Pediatric

<20 kg: 20 mg/kg/d PO q8h

>20 kg: 50 mg/kg/d PO q8h

May increase serum levels with probenecid; reduces efficacy of oral contraceptives

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in the presence of renal impairment; increase interval from q8h to q12h if CrCl is 10-50 mL/min; increase interval to q12-24h if CrCl is <10 mL/min.

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents.

Adult

500 mg PO bid for H pylori eradication

Pediatric

Not established

Cimetidine may increase toxicity; may increase the effects of anticoagulants; may increase the toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol

Documented hypersensitivity

Pregnancy

B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Decrease dose in patients with hepatic disease; monitor for seizures and peripheral neuropathy; transient eosinophilia and leukopenia observed.

Tetracycline (Sumycin)

Semisynthetic antibacterial agent derived from Streptomyces cultures. Effective against gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunit(s).

Adult

500 mg PO divided bid/qid

Pediatric

<8 years: Not recommended

>8 years: 25 mg/kg/d PO divided bid/qid

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease the effects of oral contraceptives, causing breakthrough bleeding and an increased risk of pregnancy; can increase the effects of anticoagulants

Documented hypersensitivity; severe renal or hepatic dysfunction

Pregnancy

D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in the presence of renal impairment; consider serum determinations of drug levels during prolonged therapy; the use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome (ie, nausea, vomiting, polyuria, hypophosphatemia, glycosuria, hypokalemia, acidosis) may occur with outdated tetracyclines; oral tablets may cause esophagitis.

Clarithromycin (Biaxin)

Macrolide antibiotic that inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, arresting RNA-dependent protein synthesis.

Adult

500 mg PO bid for 14 d for H pylori eradication

Pediatric

Not established

Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; effects may decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase the toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents; concurrent administration with astemizole (recalled from US market), terfenadine (recalled from US market), cisapride, or pimozide has been associated with prolonged QT intervals and predisposition to developing VT

Documented hypersensitivity

Pregnancy

C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer half the dose or increase the dosing interval if CrCl <30 mL/min; diarrhea may be a sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Antidiarrheal Agents

Antidiarrheal agents may have antisecretory and antimicrobial action.

Bismuth subsalicylate (Pepto-Bismol, Pink Bismuth, Bismatrol, Devrom)

Used in combination with antibiotics and H2RAs or PPIs to treat active duodenal ulcers associated with H pylori.

Adult

525 mg PO qid

Pediatric

Not established

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