Pediatric Esophagitis Medication
- Author: Gayle H Diamond, MD; Chief Editor: Carmen Cuffari, MD more...
Depending on the etiology of the esophagitis, medications directed at treating gastroesophageal reflux (GER), treating or preventing infection, and decreasing inflammation may be required.
Histamine (H2)-receptor antagonists
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 inhibits histamine stimulation of H2 receptors in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Famotidine competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
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.
For patients with GER, metoclopramide may mildly increase resting pressure of the lower esophageal sphincter and increase rates of gastric emptying.
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.
Proton pump inhibitors
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 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 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.
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 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 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.
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 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 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.
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.
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 decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability.
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.
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.
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.
These agents are used to treat infectious esophagitis. Immunocompetent patients may not require specific antiviral therapy.
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 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 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.
Jensen ET, Kappelman MD, Kim HP, Ringel-Kulka T, Dellon ES. Early Life Exposures as Risk Factors Forpediatric Eosinophilic Esophagitis: A Pilot and Feasibility Study. J Pediatr Gastroenterol Nutr. 2013 Mar 19. [Medline].
Homan M, Orel R, Liacouras C. Caustic ingestion: a possible cause of eosinophilic esophagitis?. Pediatrics. 2013 Apr. 131(4):e1284-7. [Medline].
Al-Hussaini A, Al-Idressi E, Al-Zahrani M. The role of allergy evaluation in children with eosinophilic esophagitis. J Gastroenterol. 2013 Jan 11. [Medline].
[Guideline] Furuta GT, Liacouras CA, Collins MH, et al. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007 Oct. 133(4):1342-63. [Medline].
Liacouras CA, Ruchelli E. Eosinophilic esophagitis. Curr Opin Pediatr. 2004 Oct. 16(5):560-6. [Medline].
Noel RJ, Tipnis NA. Eosinophilic esophagitis -- a mimic of GERD. Int J Pediatr Otorhinolaryngol. 2006 Jul. 70(7):1147-53. [Medline].
Freedberg DE, Lamousé-Smith ES, Lightdale JR, Jin Z, Yang YX, Abrams JA. Use of Acid Suppression Medication is Associated With Risk for C. difficile Infection in Infants and Children: A Population-based Study. Clin Infect Dis. 2015 Sep 15. 61 (6):912-7. [Medline].
Cohen S, Bueno de Mesquita M, Mimouni FB. Adverse effects reported in the use of gastroesophageal reflux disease treatments in children: a 10 years literature review. Br J Clin Pharmacol. 2015 Aug. 80 (2):200-8. [Medline].
Terrin G, Passariello A, De Curtis M, Manguso F, Salvia G, Lega L, et al. Ranitidine is associated with infections, necrotizing enterocolitis, and fatal outcome in newborns. Pediatrics. 2012 Jan. 129 (1):e40-5. [Medline].
Spergel JM, Brown-Whitehorn TF, Cianferoni A, Shuker M, Wang ML, Verma R, et al. Identification of causative foods in children with eosinophilic esophagitis treated with an elimination diet. J Allergy Clin Immunol. 2012 Aug. 130 (2):461-7.e5. [Medline].
Esophageal reflux. Walker WA, Goulet O, Kleinman RE, et al, eds. Pediatric Gastrointestinal Disease. 4th ed. Lewiston, NY: BC Decker; 2004. 400-24.
Ruchelli ED, Liacouras CA. Esophageal disorders in childhood. Russo P, Ruchelli E, Piccoli DA, eds. Pathology of Pediatric Gastrointestinal and Liver Disease. New York, NY: Springer-Verlag; 2004. 37-46.
Committee on Infectious Diseases. Candidiasis. 2006 Red Book: Report of the Committee on Infectious Diseases. American Academy of Pediatrics; 2006. 242-6.
Committee on Infectious Diseases. Cytomegalovirus infection. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 273-7.
Committee on Infectious Diseases. Antifungal drugs for systemic fungal infection. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 774-6.
Committee on Infectious Diseases. Antiviral drugs for non-human immunodeficiency virus infections. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 785-9.
Committee on Infectious Diseases. Herpes simplex. In: 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 361-71.
Rodrigues F, Brandao N, Duque V, et al. Herpes simplex virus esophagitis in immunocompetent children. J Pediatr Gastroenterol Nutr. 2004 Nov. 39(5):560-3. [Medline].
Henderson CJ, Abonia JP, King EC, Putnam PE, Collins MH, Franciosi JP, et al. Comparative dietary therapy effectiveness in remission of pediatric eosinophilic esophagitis. J Allergy Clin Immunol. 2012 Jun. 129 (6):1570-8. [Medline].
Assa'ad AH, Gupta SK, Collins MH, Thomson M, Heath AT, Smith DA, et al. An antibody against IL-5 reduces numbers of esophageal intraepithelial eosinophils in children with eosinophilic esophagitis. Gastroenterology. 2011 Nov. 141 (5):1593-604. [Medline].
Xinias I, Maris T, Mavroudi A, Panteliadis C, Vandenplas Y. Helicobacter pylori infection has no impact on manometric and pH-metric findings in adolescents and young adults with gastroesophageal reflux and antral gastritis: eradication results to no significant clinical improvement. Pediatr Rep. 2013 Feb 5. 5(1):e3. [Medline].
Ramakrishnan JB. The role of food allergy in otolaryngology disorders. Curr Opin Otolaryngol Head Neck Surg. 2010 Feb 17. [Medline].
Papadopoulou A, Koletzko S, Heuschkel R, et al. Management guidelines of eosinophilic esophagitis in childhood. J Pediatr Gastroenterol Nutr. 2014 Jan. 58 (1):107-18. [Medline].
Straumann A, Conus S, Degen L, Felder S, Kummer M, Engel H, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology. 2010 Nov. 139 (5):1526-37, 1537.e1. [Medline].
Rodrigues M, D'Amico MF, Patiño FR, Barbieri D, Damião AO, Sipahy AM. Clinical manifestations, treatment, and outcomes of children and adolescents with eosinophilic esophagitis. J Pediatr (Rio J). 2013 Mar-Apr. 89(2):197-203. [Medline].
Haddad I, Kierkus J, Tron E, Ulmer A, Hu P, Silber S, et al. Maintenance of efficacy and safety of rabeprazole in children with endoscopically proven GERD. J Pediatr Gastroenterol Nutr. 2014 Apr. 58 (4):510-7. [Medline].
Vandenplas Y, Badriul H, Verghote M, Hauser B, Kaufman L. Oesophageal pH monitoring and reflux oesophagitis in irritable infants. Eur J Pediatr. 2004 Jun. 163(6):300-4. [Medline].
Gold BD. Gastroesophageal reflux disease: could intervention in childhood reduce the risk of later complications?. Am J Med. 2004 Sep 6. 117 Suppl 5A:23S-29S. [Medline].
Boccia G, Manguso F, Miele E et el. Maintenance therapy for erosive esophagitis in children after healing by Omeprazole: is it advisable?. Am J Gastroenterol. Jun 2007. 102(6):1291-7. [Medline].
Dellon ES. Epidemiology of eosinophilic esophagitis. Gastroenterol Clin North Am. 2014 Jun. 43 (2):201-18. [Medline].
Cianferoni A, Spergel J. Eosinophilic Esophagitis: A Comprehensive Review. Clin Rev Allergy Immunol. 2015 Jul 22. [Medline].
Kim KY, Jang JY, Kim JW, Shim JJ, Lee CK, Dong SH, et al. Acid suppression therapy as a risk factor for Candida esophagitis. Dig Dis Sci. 2013 May. 58 (5):1282-6. [Medline].
Daniell HW. Acid suppressing therapy as a risk factor for Candida esophagitis. Dis Esophagus. 2015 Apr 1. [Medline].
Gupta SK, Vitanza JM, Collins MH. Efficacy and safety of oral budesonide suspension in pediatric patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2015 Jan. 13 (1):66-76.e3. [Medline].
Spergel JM. Eosinophilic esophagitis in adults and children: evidence for a food allergy component in many patients. Curr Opin Allergy Clin Immunol. June 2007. 7(3):274-8. [Medline].
Dutt P, Shukla JS, Ventateshaiah SU, Mariswamy SJ, Mattner J, Shukla A, et al. Allergen-induced interleukin-18 promotes experimental eosinophilic oesophagitis in mice. Immunol Cell Biol. 2015 Nov. 93 (10):914. [Medline].
Liacouras CA, Wenner WJ, Brown K, Ruchelli E. Primary eosinophilic esophagitis in children: successful treatment with oral corticosteroids. J Pediatr Gastroenterol Nutr. 1998 Apr. 26(4):380-5. [Medline].
Blanchard C. Molecular pathogenesis of eosinophilic esophagitis. Curr Opin Gastroenterol. 2015 Jul. 31 (4):321-7. [Medline].
Zhang S, Wu X, Yu S. Prostaglandin D2 receptor D-type prostanoid receptor 2 mediates eosinophil trafficking into the esophagus. Dis Esophagus. 2014 Aug. 27 (6):601-6. [Medline].
Mavi P, Niranjan R, Dutt P, Zaidi A, Shukla JS, Korfhagen T, et al. Allergen-induced resistin-like molecule-α promotes esophageal epithelial cell hyperplasia in eosinophilic esophagitis. Am J Physiol Gastrointest Liver Physiol. 2014 Sep 1. 307 (5):G499-507. [Medline].
Noel RJ, Rothenberg ME. Eosinophilic esophagitis. Curr Opin Pediatr. Dec 2005. 17(6):690-4. [Medline].
Dellon ES, Kim HP, Sperry SL, Rybnicek DA, Woosley JT, Shaheen NJ. A phenotypic analysis shows that eosinophilic esophagitis is a progressive fibrostenotic disease. Gastrointest Endosc. 2014 Apr. 79 (4):577-85.e4. [Medline].
Chan SK, Mahmoudi M. Eosinophilic esophagitis. Compr Ther. 2009 Fall-Winter. 35(3-4):160-6. [Medline].