eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Peptic Ulcer Disease: Treatment & Medication

Author: Mutaz I Sultan, MBChB, Instructor and Fellow, Department of Pediatrics, Division of Gastroenterology and Nutrition, Medical College of Wisconsin, Children's Hospital
Coauthor(s): B UK Li, MD, Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin; Ameesh Shah, MD, Assistant Professor of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital
Contributor Information and Disclosures

Updated: Nov 5, 2009

Treatment

Medical Care

In children with peptic ulcer disease (PUD) who appear to be well, in whom examination findings are normal and symptoms are mild, evaluation may be conducted on an outpatient basis.

  • The eradication of H pylori relies on a multidrug regimen.6 Triple therapy is considered to be the standard treatment for children, including a proton pump inhibitor combined with 2 antibiotics.7 This regimen has been shown to be very effective in eradicating H pylori from the stomach. The current recommendation is treatment with amoxicillin, clarithromycin, and a proton pump inhibitor for 2 weeks.
  • Non-H pylori peptic ulcer disease is effectively treated with acid suppression; however, prospective studies are lacking. Complete healing and resolution of symptoms requires appropriate therapy for underlying etiology, as in Crohn disease.
  • Proton pump inhibitors are increasingly used in the pediatric population, especially in children with gastroesophageal reflux disease (GERD), than before. Proton pump inhibitors provide consistent gastric pH control, and patients do not develop tachyphylaxis with repeated dosing.
  • A recent study in hospitalized adult patients revealed no significant difference among various proton pump inhibitors given through different routes (intravenous [IV] vs oral [PO]) on raising intragastric pH levels above 6 for 72 hours after successful endoscopic hemostasis in patients with a bleeding peptic ulcer.8 In addition standard-dose proton pump inhibitor infusion was as effective as a high-dose regimen in reducing the risk of recurrent bleeding.9
    • The risk of adverse effects appear to be minimal with long-term administration. The number of gastrin-secreting cells (G cells) increases, as does the ratio of G cells to D cells. The clinical significance of this effect is unknown. Long-term studies have demonstrated hypergastrinemia and enterochromaffinlike cell hyperplasia in children receiving continuous proton pump inhibitor therapy, but this has not affected histologic findings or caused an increase risk for carcinoid formation.10
    • Small gastric polyps may develop in some patients during proton pump inhibitor maintenance therapy. These polyps usually develop in the gastric corpus and are hyperplastic or benign fundic gland cysts.
    • Rebound acid hypersecretion arises from the trophic effects of the proton pump inhibitor–induced hypergastrinemia; 44% of previously asymptomatic subjects experienced clinically significant heartburn, acid reflux, or dyspepsia after discontinuing a 2-month course of esomeprazole at 40 mg/d compared with 15% after placebo.11
  • Sucralfate is an aluminum salt of sulfated sucrose, which, in the presence of acid pH, forms a complex, pastelike substance that adheres to the damaged mucosal area. It forms a protective coating that acts as a barrier between the lining and gastric acid, pepsin, and bile salts.
  • Misoprostol is a synthetic prostaglandin E1 analog with gastric antisecretory and cytoprotective properties. It is effective in adults for the prophylaxis and treatment of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy. Studies on the benefits of misoprostol administration in children are limited.
  • Optimal management of severe or refractory peptic ulcer disease requires a multidisciplinary team approach, using primary care providers, gastroenterologists, and general surgeons. Medical management has become the cornerstone of therapy. Identification and eradication of recurrent H pylori infection can heal ulceration and also prevent recurrence. Severe, intractable, or recurrent peptic ulcer disease with associated complications mandates a careful evaluation to determine potential etiologies like gastrinomas or Crohn disease.12

Surgical Care

Surgical intervention is required in a small percentage of infants and in children with complications of peptic ulcer disease that include perforation, obstruction, intractable pain, and bleeding unresponsive to medical or endoscopic therapy.

  • A bleeding ulcer can be treated with a simple plication or oversewing of the bleeding source. A more definitive procedure, such as vagotomy and pyloroplasty, may be required.
  • In patients with stress ulcers related to brain injury or burns, the procedure of choice may be pyloroplasty and antrectomy.
  • Total gastrectomy is rarely performed to treat multiple gastric ulcers in pediatric patients.
  • For perforation, repair is performed by using a simple closure or oversewing.
  • Gastric-outlet obstruction is surgically relieved with vagotomy and pyloroplasty or gastroenterostomy.

Consultations

  • Gastroenterologist
  • Radiologist
  • Surgeon

Diet

  • Recommend abstinence from all caffeine and alcohol.
  • In hospitalized children, milk feedings raise gastric pH and prevent GI bleeding.
  • Normal intake of milk is not a known risk factor for peptic ulcer disease. Several peptides and hormones found in bovine and human milk may be responsible for the reduction in gastric acidity.

Activity

  • Allow common sense to dictate appropriate activity restrictions in children with chronic symptoms.
  • Cessation of smoking should be recommended.

Medication

Medications used in patients with peptic ulcer disease (PUD) reduce gastric acidity and serve to eradicate H pylori infection. Proton pump inhibitors, which work at the final common pathway for gastric acid secretion, are the most potent acid inhibitors.

Histamine H2-receptor antagonists

Receptors for histamine are located on the acid-producing parietal cells. Blocking histamine action suppresses gastric acid secretion.


Ranitidine (Zantac)

H2 antagonist studied most often in children. H2 antagonists competitively inhibit histamine at H2 receptors of gastric parietal cells, lowering gastric acid secretion. Course of therapy tried for 8 wks, by which time most ulcers heal. Because H2 antagonists have no antibacterial effect, symptoms caused by H pylori infection may persist or recur. Pediatric preparations are syr 15 mg/mL; tab 75, 150, or 300 mg; and effervescent granules 150 mg.

Adult

150 mg/dose PO bid or 300 mg/dose PO qhs
Alternative: 50 mg/dose IV/IM q6-8h

Pediatric

Neonates: 2-4 mg/kg/d PO divided q8-12h or 2 mg/kg/d IV divided q6-8h
Infants and children: 6-9 mg/kg/d PO divided q8-12h or 2-4 mg/kg/d IV divided q6-8h
Continuous infusion: Administer daily IV dose over 24 h

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

Pregnancy

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

Precautions

Adjust dose in renal failure; avoid in liver disease; may cause malaise, headache, insomnia, sedation, and arthralgias

Proton pump inhibitors

Proton pump inhibitors are more potent acid inhibitors than H2-receptor antagonists. This class of drugs blocks gastric acid secretion at the proton pump (ie, hydrogen/potassium adenosine triphosphatase [H+/K+ ATPase] of the gastric parietal cell), which is the final common pathway of secretion. Proton pump inhibitors are recommended as a part of the drug regimen for symptomatic H pylori infection. Proton pump inhibitor therapy alone does not eradicate H pylori infection, but it does have bacteriostatic activity against H pylori.


Omeprazole (Prilosec, Zegerid)

Used in PUD, alone or in combination with antimicrobials to eradicate H pylori. Inhibits gastric acid secretion. Ulcers may heal more rapidly than with H2 antagonists. Best administered just before first meal of day. Enteric-coated granules in caps ensure appropriate bioavailability. In children unable to swallow intact caps, open and mix granules in acidic substance (eg, apple sauce, apple juice). Granules preferred to less bioavailable susp. Preparations include SR caps 10 or 20 mg or oral susp 20 or 40-mg unit-dose powder packets for immediate dispersal in water.

Adult

20 mg/d PO for 4-8 wk

Pediatric

0.6-0.7 mg/kg/d PO initially, may increase to 0.6-0.7 mg/kg/dose PO bid; reported effective dose range 0.7-3.3 mg/kg/d

Increases half-life of diazepam, phenytoin, and warfarin (because of its metabolism); may decrease absorption of itraconazole, ketoconazole, iron salts, and ampicillin esters; clarithromycin may increase bioavailability

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

May cause headaches, nausea, diarrhea, and vomiting

Antacids

These agents neutralize gastric acid and may be of benefit in children with peptic ulcer disease. Medication compliance may be a problem because of the requirement for frequent dosing.


Aluminum and magnesium hydroxide (Mylanta, Maalox)

Neutralizes gastric acids, raises stomach pH, and helps to provide pain relief. Antacids may be used in multidrug regimens to eradicate H pylori.
Mylanta: Each 5 mL contains 200 mg AlOH, 200 mg MgOH, and 20 mg simethicone
Maalox: Each 5 mL contains 225 mg AlOH and 200 mg MgOH
Mylanta or Maalox chewable tabs: 200 mg AlOH and MgOH

Adult

15-45 mL PO q3-6h or q1-3h pc and hs

Pediatric

5-15 mL PO q3-6h or q1-3h pc and hs
Alternative: 1-2 chewable tab PO q1-3h pc and hs

Reduces efficacy of fluoroquinolones, corticosteroids, benzodiazepines, and phenothiazines; aluminum and magnesium potentiate effects of valproic acid, sulfonylureas, quinidine, and levodopa

Documented hypersensitivity; hyperphosphatemia, hypokalemia, or renal failure

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

Use aluminum-containing antacids with caution in recent massive upper-GI hemorrhage

Antibiotics

Multidrug regimens have been studied in the eradication of H pylori infection. All regimens contain 1-2 antimicrobials and agents that neutralize acid or inhibit acid secretion.


Amoxicillin (Amoxil, Trimox)

Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Adult

250-500 mg/dose PO tid; not to exceed 2-3 g/d

Pediatric

50 mg/kg/d PO divided bid; not to exceed 2-3 g/d

Reduces the efficacy of PO contraceptives

Pregnancy

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

Precautions

Adjust dose in renal impairment; may enhance chance of candidiasis


Clarithromycin (Biaxin)

Macrolide antibiotic with antimicrobial spectrum similar to that of erythromycin but more stable in acid environment and has fewer adverse GI effects. Prescribed in 1- and 2-wk regimens for H pylori infection.

Adult

500 mg PO tid for 2 wk (with omeprazole) or 500 mg PO bid for 2 wk (with omeprazole and metronidazole or with ranitidine and tetracycline)

Pediatric

7.5 mg/kg PO bid for 2 wk (with omeprazole and metronidazole or with omeprazole only) or for 10 d (with amoxicillin and omeprazole)

CYP450 3A4 inhibitor; toxicity increases with coadministration of fluconazole and pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG-CoA–reductase inhibitors; 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

Documented hypersensitivity; coadministration of pimozide

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

GI agents

These agents protect the GI lining. They are effective in treating peptic ulcers and preventing relapse.


Sucralfate (Carafate)

Forms viscous adhesive substance that protects GI lining against pepsin, peptic acid, and bile salts. For short-term management of ulcers. Available as tabs or oral susp 1 g/10 mL.

Adult

1 g PO qid

Pediatric

Not established; 40-80 mg/kg/d PO divided q6h have been used

May decrease effects (by decreasing bioavailability) of H2 antagonists (eg, ranitidine), ketoconazole, ciprofloxacin, tetracycline, phenytoin, warfarin, quinidine, theophylline, and norfloxacin

Pregnancy

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

Precautions

Caution in renal failure and conditions that impair excretion of absorbed aluminum

More on Peptic Ulcer Disease

Overview: Peptic Ulcer Disease
Differential Diagnoses & Workup: Peptic Ulcer Disease
Treatment & Medication: Peptic Ulcer Disease
Follow-up: Peptic Ulcer Disease
Multimedia: Peptic Ulcer Disease
References

References

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Further Reading

Keywords

peptic ulcer disease, PUD, primary ulcer, secondary ulcer, stress ulcer, peptic ulcer, gastric disease, stomach ulcer, intestinal ulcer, ulceration, infection, mucosal ischemia, treatment, diagnosis

Contributor Information and Disclosures

Author

Mutaz I Sultan, MBChB, Instructor and Fellow, Department of Pediatrics, Division of Gastroenterology and Nutrition, Medical College of Wisconsin, Children's Hospital
Mutaz I Sultan, MBChB is a member of the following medical societies: American Gastroenterological Association and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition
Disclosure: Nothing to disclose.

Coauthor(s)

B UK Li, MD, Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin
B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Ameesh Shah, MD, Assistant Professor of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital
Ameesh Shah, MD is a member of the following medical societies: North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Medical Editor

Chris A Liacouras, MD, Director of Pediatric Endoscopy, Department of Pediatrics, Division of Gastroenterology and Nutrition, Associate Professor, Children's Hospital of Philadelphia and University of Pennsylvania
Chris A Liacouras, MD is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

B UK Li, MD, Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin
B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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