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Pediatric Esophagitis Medication

  • Author: Gayle H Diamond, MD; Chief Editor: Carmen Cuffari, MD  more...
 
Updated: Dec 11, 2015
 

Medication Summary

Depending on the etiology of the esophagitis, medications directed at treating gastroesophageal reflux (GER), treating or preventing infection, and decreasing inflammation may be required.

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Histamine (H2)-receptor antagonists

Class Summary

These agents decrease the secretion and volume of gastric acid by competitively blocking histamine-2 (H2) receptors in gastric cells. Gastroesophageal reflux disease (GERD) may be initially treated with H2 -receptor antagonists; however, tachyphylaxis may quickly develop.

Ranitidine (Zantac)

 

Ranitidine inhibits histamine stimulation of H2 receptors in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)

 

Famotidine competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Cimetidine (Tagamet HB)

 

Nizatidine (Axid)

 
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Prokinetic Agents

Class Summary

These agents augment cholinergic activity and improve motility in the gastrointestinal (GI) tract. However, no evidence-based efficacy in gastroesophageal reflux disease (GERD) is available.

Metoclopramide (Maxolon, Reglan)

 

For patients with GER, metoclopramide may mildly increase resting pressure of the lower esophageal sphincter and increase rates of gastric emptying.

Erythromycin base (E.E.S, Ery-Tab)

 

Erythromycin is a macrolide antibiotic that duplicates the action of motilin and is responsible for the migrating motor complex activity, by binding to and activating motilin receptors. Intravenous administration of this drug enhances the emptying rate of both liquids and solids. The effect can be seen with oral erythromycin. Substitution of the enteric-coated form may be tolerated better by the patient.

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Proton pump inhibitors

Class Summary

These drugs inhibit the H+/K+/-ATPase pump in gastric parietal cells, thus inhibiting gastric acid secretion. Proton pump inhibitors (PPIs) should be used when reflux esophagitis is diagnosed because the effect of PPIs is more sustained and powerful.

Omeprazole (Prilosec, Zegerid Oral Suspension)

 

Omeprazole inhibits gastric acid secretion. It decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATPase pump. Give this agent with or before the first meal of the day.

Lansoprazole (Prevacid)

 

Lansoprazole inhibits gastric acid secretion by specifically inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells. Give this agent with or before the first meal of the day.

Pantoprazole (Protonix)

 

Rabeprazole (Aciphex, Aciphex Sprinkle)

 

Esomeprazole (Nexium, Nexium 24HR)

 

Dexlansoprazole (Dexilant, Kapidex)

 
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Antifungal agents

Class Summary

Appropriate use of these agents depends on the severity of the candidal esophagitis and the host’s age and immune status. One of several antifungal agents may be required for treatment. Nystatin or clotrimazole troches may be adequate for immunocompetent hosts.

Clotrimazole

 

Clotrimazole is a broad-spectrum synthetic antifungal agent that inhibits growth of yeasts by altering cell membrane permeability. Therapy is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications.

Fluconazole (Diflucan)

 

Fluconazole has fungistatic activity. It is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P450 (CYP450) and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. It may be the preferred initial regimen for candidal esophagitis, with fewer adverse effects.

Ketoconazole (Nizoral)

 

There is potential for development of resistance with ketoconazole. It has fungistatic activity. It is an imidazole broad-spectrum antifungal agent; it inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

Itraconazole (Sporanox)

 

Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting CYP450-dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Amphotericin B (Amphocin, Fungizone)

 

Amphotericin B is produced by a strain of Streptomyces nodosus; it can be fungistatic or fungicidal. It binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death.

Nystatin

 

Nonabsorbable polyene antifungal agent obtained from Streptomyces noursei. Binds to sterols in cell membrane of susceptible fungi, with resulting change in membrane permeability allowing leakage of intracellular components. Indicated for treatment of PO candidiasis.

Therapy is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications.

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Corticosteroids

Class Summary

The use of corticosteroids is controversial, but they may be helpful in patients with severe caustic esophageal mucosal injury (second- or third-degree burns) to decrease inflammation, edema, and fibrosis and, possibly, to help decrease the incidence of stricture formation.

Methylprednisolone (Medrol, Solu-Medrol)

 

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability.

Prednisone (Deltasone, Orasone)

 

Prednisone is beneficial for allergic esophagitis that is unresponsive to antireflux therapy. It may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Fluticasone inhaled (Flovent)

 

The HFA product is an oral-inhaled corticosteroid and is available as 44, 110, and 220 mcg per actuation. Several studies have demonstrated the effectiveness of swallowed topical corticosteroids delivered from a metered-dose inhaler in treating clinical symptoms and abnormal histology associated with eosinophilic esophagitis.

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

 

Studies are showing effectiveness of the swallowed topical steroid mixed with sucralose in treating abnormal histology associated with eosinophilic esophagitis. It is available in a 0.5 mg/2 mL dosage. 

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Antiviral agents

Class Summary

These agents are used to treat infectious esophagitis. Immunocompetent patients may not require specific antiviral therapy.

Acyclovir (Zovirax)

 

Acyclovir is a prodrug activated by phosphorylation by virus-specific thymidine kinase that inhibits viral replication. Herpes virus thymidine kinase (TK), but not host cell TK, uses acyclovir as a purine nucleoside, converting it into acyclovir monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate form into diphosphate and triphosphate analogues that inhibit viral DNA replication.

Acyclovir has affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted on by DNA polymerase. It inhibits activity of both herpes simplex virus (HSV)-1 and HSV-2. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 hours from rash onset. It may prevent recurrent outbreaks. Early initiation of therapy is imperative. Acyclovir is used for HSV esophagitis.

Foscarnet (Foscavir)

 

Foscarnet is an organic analogue of inorganic pyrophosphate that inhibits replication of HSV, including cytomegalovirus (CMV). It selectively inhibits at pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular polymerases. Unlike ganciclovir, foscarnet does not require activation by a kinase and is active in vitro.

Ganciclovir (Cytovene)

 

Ganciclovir is an acyclic nucleoside analogue of 2'deoxyguanasine. It phosphorylates first to monophosphate form by CMV-encoded protein kinase homologue, then to diphosphate and triphosphate forms by cellular kinases, allowing for a 100-fold greater concentration of ganciclovir in CMV-infected cells, possibly due to preferential phosphorylation of ganciclovir in virus-infected cells.

Ganciclovir is thought to inhibit CMV replication by competitive inhibition of viral DNA polymerases and by incorporating itself into viral DNA, causing termination of viral DNA elongation. Like acyclovir, ganciclovir is virostatic and exerts its effect on replicating virus only.

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Contributor Information and Disclosures
Author

Gayle H Diamond, MD Assistant Professor, Department of Pediatrics, Children’s Hospital of Philadelphia

Disclosure: Nothing to disclose.

Coauthor(s)

Maria Rebello Mascarenhas, MBBS Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Children's Hospital of Philadelphia

Maria Rebello Mascarenhas, MBBS is a member of the following medical societies: American Gastroenterological Association, American Society for Parenteral and Enteral Nutrition, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Stefano Guandalini, MD Founder and Medical Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Received consulting fee from AbbVie for consulting.

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, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching. for: Abbott Nutritional, Abbvie, speakers' bureau.

Additional Contributors

Marianne V Augustine, MD Fellow, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia

Marianne V Augustine, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Acknowledgements

Andrew S Chu, MD Medical Director, CHOP Connection at Grand View Hospital, Children's Hospital of Philadelphia; Clinical Assistant Professor, Division of General Pediatrics, Department of Pediatrics, University of Pennsylvania School of Medicine

Andrew S Chu, MD is a member of the following medical societies: American Academy of Pediatrics and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Vera De Matos, MD Fellow in Pediatric Gastroenterology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine

Vera De Matos is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Jayant Deodhar, MD Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India

Disclosure: Nothing to disclose.

Jessica Wen, MD Clinical Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital of Philadelphia

Jessica Wen, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American Medical Association, and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

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