Esophagitis Medication
- Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC; Chief Editor: Julian Katz, MD more...
Medication Summary
Medications used to treat esophagitis vary depending on the etiology. Treatment goals for reflux esophagitis include pain relief, decreased acid production, decreased acid reflux, and protection of the esophageal mucosa. Multiple pharmacologic agents are available, including histamine-2 receptor antagonists, proton pump inhibitors (PPIs), gastroprokinetic agents, and protective agents.[46]
Therapy for infectious esophagitis is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications. The choice of the therapeutic agent depends on the severity of infection and the degree of host defense impairment.
Histamine-2 Receptor Antagonists
Class Summary
These agents decrease gastric acid production by blocking histamine-2 (H2) receptors in gastric cells. Some authorities recommend using larger doses than those used for peptic ulcer disease.
Ranitidine hydrochloride (Zantac, Zantac 75, Zantac 150)
Ranitidine hydrochloride competitively inhibits histamine at the H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Cimetidine (Tagamet HB 200)
Cimetidine inhibits histamine at H2 receptors of gastric parietal cells, decreasing gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Famotidine (Pepcid, Pepcid AC)
Famotidine competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.
Gastrointestinal Agents
Class Summary
These medications coat the ulcerated surfaces and are used mainly for peptic ulcer disease. They may be used as a second agent with an H2 antagonist and in radiation esophagitis.
Sucralfate (Carafate)
Sucralfate binds to positively charged proteins in exudates and forms a viscous, adhesive substance that protects the gastrointestinal lining against pepsin, peptic acid, and bile salts. It is used for short-term duodenal ulcer management.
Proton Pump Inhibitors
Class Summary
These agents inhibit gastric acid secretion by inhibiting the H+/K+ -ATPase enzyme system in gastric parietal cells. Products such as pantoprazole, lansoprazole, esomeprazole, and rabeprazole have been approved by the FDA and are at least as effective as the time-honored omeprazole.
Omeprazole (Prilosec)
Omeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump. It is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. It may be used up to 8 weeks to treat all grades of erosive esophagitis.
Lansoprazole (Prevacid, Prevacid SoluTab)
Lansoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump. It is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. It may be used up to 8 weeks to treat all grades of erosive esophagitis.
Esomeprazole (Nexium, Nexium I.V.)
Esomeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump. It is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. It may be used up to 8 weeks to treat all grades of erosive esophagitis.
Rabeprazole (Aciphex)
Rabeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump. It is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. It may be used up to 8 weeks to treat all grades of erosive esophagitis.
Pantoprazole (Protonix)
Pantoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump. It is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers. It may be used up to 8 weeks to treat all grades of erosive esophagitis.
Antifungal Agents
Class Summary
Antifungal agents are topical or systemic agents used to treat fungal infections.
Clotrimazole
Clotrimazole is a nonabsorbable imidazole. It is a broad-spectrum synthetic antifungal agent that inhibits the growth of yeasts by altering cell membrane permeability.
Nystatin
Nystatin is a nonabsorbable polyene antifungal agent obtained from Streptomyces noursei. It binds to sterols in the cell membrane of susceptible fungi, with a resulting change in membrane permeability, allowing leakage of intracellular components. It is indicated for the treatment of oral candidiasis.
Fluconazole (Diflucan)
Fluconazole is a synthetic triazole fungistatic agent. It is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 alpha demethylation.
Amphotericin B deoxycholate
Conventional amphotericin B binds to sterols in the cell membrane and alters permeability. It is used in patients with granulocytopenia. The oral route is infrequently used and has no advantage over oral clotrimazole or nystatin.
Anidulafungin (Eraxis)
Anidulafungin is an antifungal agent of the echinocandin class. It inhibits synthesis of 1,3-beta-D-glucan, an essential component of fungal cell walls. It is indicated to treat esophageal candidiasis, candidemia, and other forms of candidal infections (eg, intra-abdominal abscesses, peritonitis).
Itraconazole (Sporanox, Sporanox PulsePak)
Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Flucytosine (Ancobon)
Although the exact mode of action is unknown, it is proposed that flucytosine acts directly on fungal organisms by competitive inhibition of purine and pyrimidine uptake and indirectly by intracellular metabolism, where it is converted to 5-fluorouracil after penetrating fungal cells. It inhibits RNA and protein synthesis. It is active against Candida and Cryptococcus species and generally is used in combination with amphotericin B.
Antiviral Agents
Class Summary
Antiviral agents are used to treat herpes simplex virus (HSV) or cytomegalovirus (CMV) infections. In addition to the drugs listed below, famciclovir (Famvir), a prodrug of the antiviral agent penciclovir, which is not currently recommended for treatment, may replace acyclovir in prophylaxis and treatment.
Acyclovir (Zovirax)
Acyclovir is a synthetic purine nucleoside analog that stops replication of viral DNA. It is used to treat HSV esophagitis.
Foscarnet (Foscavir)
Foscarnet is an organic analog of inorganic pyrophosphate that inhibits replication of HSV and CMV. It is used to treat acyclovir-resistant cases.
Ganciclovir (Cytovene)
Ganciclovir is an acyclic nucleoside analog that inhibits replication of herpes viruses. It is active against CMV and HSV.
Famciclovir (Famvir)
Famciclovir is goes through biotransformation to active penciclovir. Penciclovir has inhibitory activity against varicella-zoster virus (VZV) and herpes simplex virus types 1 and 2. It may be used for herpes and VZV esophagitis.
Corticosteroids
Class Summary
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli. Corticosteroids may be used in various conditions such as eosinophilic esophagitis, Behçet disease esophagitis, inflammatory disease esophagitis, or HIV esophagitis.
Prednisone
Prednisone is administered in immunosuppressive doses, which may vary based on the underlying disease process. The dose is usually slowly tapered over weeks to months. An equivalent dose of methylprednisolone (Solu-Medrol) may be used instead of prednisone.
Methylprednisolone (Medrol, Solu-Medrol)
Methylprednisolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Leukotriene Inhibitors
Class Summary
Leukotriene inhibitors can be used to treat eosinophilic esophagitis. Examples of leukotriene inhibitors include montelukast and zafirlukast.
Montelukast (Singulair)
Montelukast inhibits effects by the leukotriene receptor, which has been associated with asthma, including airway edema, smooth muscle contraction, and cellular activity associated with the symptoms.
Zafirlukast (Accolate)
Zafirlukast selectively prevents the action of leukotrienes released by mast cells and eosinophils.
Mast Cell Stabilizers
Class Summary
Mast cell stabilizers such as cromolyn may be used for eosinophilic esophagitis.
Cromolyn sodium
Cromolyn inhibits the release of histamine, leukotrienes, and other mediators from sensitized mast cells exposed to specific antigens. It has no intrinsic anti-inflammatory, antihistamine, or vasoconstrictive effects.
Immunosuppressives
Class Summary
Immunosuppressive agents such as cyclosporine and azathioprine may be used for graft versus host disease esophagitis.
Cyclosporine (Neoral, Sandimmune)
Cyclosporine is an 11-amino acid cyclic peptide and natural product of fungi. It acts on T-cell replication and activity. It is a specific modulator of T-cell function and an agent that depresses cell-mediated immune responses by inhibiting helper T-cell function. Preferential and reversible inhibition of T lymphocytes in the G0 or G1 phase of cell cycle is suggested. It binds to cyclophilin, an intracellular protein, which, in turn, prevents the formation of interleukin 2 and the subsequent recruitment of activated T cells.
Azathioprine (Imuran)
Azathioprine is an imidazolyl derivative of 6-mercaptopurine. Many of the biological effects are similar to those of the parent compound. Both compounds are eliminated rapidly from the blood and are oxidized or methylated in erythrocytes and the liver. No azathioprine or mercaptopurine is detectable in urine 8 hours after the drug is taken. It antagonizes purine metabolism and inhibits the synthesis of DNA, RNA, and proteins. It works primarily on T cells and suppresses hypersensitivities of the cell-mediated type; it also and causes variable alterations in antibody production.
Alkylating Agents
Class Summary
Alkylating agents include nitrogen mustards such as chlorambucil. These agents can be used in the treatment of Behçet disease esophagitis.
Chlorambucil (Leukeran)
Chlorambucil is a bifunctional, slow-acting aromatic nitrogen mustard derivative that interferes with DNA replication, transcription, and nucleic acid function by alkylation. It alkylates and cross-links strands of DNA. Alkylation takes place through the formation of the highly reactive ethylenimonium radical. The probable mode of action involves cross-linkage of the ethylenimonium derivative between 2 strands of helical DNA and subsequent interference with replication.
Lowe RC, Wolfe MM. The pharmacological management of gastroesophageal reflux disease. Minerva Gastroenterol Dietol. Sep 2004;50(3):227-37. [Medline].
Rothenberg ME. Biology and treatment of eosinophilic esophagitis. Gastroenterology. Oct 2009;137(4):1238-49. [Medline].
Winstead NS, Bulat R. Pill Esophagitis. Curr Treat Options Gastroenterol. Feb 2004;7(1):71-76. [Medline].
Liacouras CA, Ruchelli E. Eosinophilic esophagitis. Curr Opin Pediatr. Oct 2004;16(5):560-6. [Medline].
Mann NS, Leung JW. Pathogenesis of esophageal rings in eosinophilic esophagitis. Med Hypotheses. 2005;64(3):520-3. [Medline].
Bradley J, Movsas B. Radiation esophagitis: Predictive factors and preventive strategies. Semin Radiat Oncol. Oct 2004;14(4):280-6. [Medline].
Quarto G, Sivero L, Somma P, De Rosa G, Mosella F, Nunziata G, et al. A case of infectious esophagitis caused by human papilloma virus. Minerva Gastroenterol Dietol. Sep 2008;54(3):317-21. [Medline].
Haron E, Vartivarian S, Anaissie E, Dekmezian R, Bodey GP. Primary Candida pneumonia. Experience at a large cancer center and review of the literature. Medicine (Baltimore). May 1993;72(3):137-42. [Medline].
Levine MS, Macones AJ Jr, Laufer I. Candida esophagitis: accuracy of radiographic diagnosis. Radiology. Mar 1985;154(3):581-7. [Medline].
Walsh TJ, Hamilton SR, Belitsos N. Esophageal candidiasis. Managing an increasingly prevalent infection. Postgrad Med. Aug 1988;84(2):193-6, 201-5. [Medline].
Kliemann DA, Pasqualotto AC, Falavigna M, Giaretta T, Severo LC. Candida esophagitis: species distribution and risk factors for infection. Rev Inst Med Trop Sao Paulo. Sep-Oct 2008;50(5):261-3. [Medline].
Vidal AP, Pannain VL, Bottino AM. [Esophagitis in patients with acquired human immunodeficiency syndrome: an histological and immunohistochemistry study]. Arq Gastroenterol. Oct-Dec 2007;44(4):309-14. [Medline].
Bianchi Porro G, Parente F, Cernuschi M. The diagnosis of esophageal candidiasis in patients with acquired immune deficiency syndrome: is endoscopy always necessary?. Am J Gastroenterol. Feb 1989;84(2):143-6. [Medline].
Sam JW, Levine MS, Rubesin SE, Laufer I. The "foamy" esophagus: a radiographic sign of Candida esophagitis. AJR Am J Roentgenol. Apr 2000;174(4):999-1002. [Medline].
Prasad GA, Alexander JA, Schleck CD, Zinsmeister AR, Smyrk TC, Elias RM, et al. Epidemiology of eosinophilic esophagitis over three decades in Olmsted County, Minnesota. Clin Gastroenterol Hepatol. Oct 2009;7(10):1055-61. [Medline].
Nurko S, Rosen R, Furuta GT. Esophageal dysmotility in children with eosinophilic esophagitis: a study using prolonged esophageal manometry. Am J Gastroenterol. Dec 2009;104(12):3050-7. [Medline].
McColl KE. Review article: Helicobacter pylori and gastro-oesophageal reflux disease--the European perspective. Aliment Pharmacol Ther. Dec 2004;20 Suppl 8:36-9. [Medline].
Chen LI, Chang JM, Kuo MC, Hwang SJ, Chen HC. Combined herpes viral and candidal esophagitis in a CAPD patient: case report and review of literature. Am J Med Sci. Mar 2007;333(3):191-3. [Medline].
DeGaeta L, Levine MS, Guglielmi GE, Raffensperger EC, Laufer I. Herpes esophagitis in an otherwise healthy patient. AJR Am J Roentgenol. Jun 1985;144(6):1205-6. [Medline].
Levine MS, Laufer I, Kressel HY, Friedman HM. Herpes esophagitis. AJR Am J Roentgenol. May 1981;136(5):863-6. [Medline].
Levine MS, Loevner LA, Saul SH, Rubesin SE, Herlinger H, Laufer I. Herpes esophagitis: sensitivity of double-contrast esophagography. AJR Am J Roentgenol. Jul 1988;151(1):57-62. [Medline].
Shortsleeve MJ, Levine MS. Herpes esophagitis in otherwise healthy patients: clinical and radiographic findings. Radiology. Mar 1992;182(3):859-61. [Medline].
Borowitz SM. Diagnosis: herpes simplex esophagitis. Clin Pediatr (Phila). Jul 2007;46(6):557-9. [Medline].
Geagea A, Cellier C. Scope of drug-induced, infectious and allergic esophageal injury. Curr Opin Gastroenterol. Jul 2008;24(4):496-501. [Medline].
Baroco AL, Oldfield EC. Gastrointestinal cytomegalovirus disease in the immunocompromised patient. Curr Gastroenterol Rep. Aug 2008;10(4):409-16. [Medline].
Buckner FS, Pomeroy C. Cytomegalovirus disease of the gastrointestinal tract in patients without AIDS. Clin Infect Dis. Oct 1993;17(4):644-56. [Medline].
Bonacini M, Young T, Laine L. Histopathology of human immunodeficiency virus-associated esophageal disease. Am J Gastroenterol. Apr 1993;88(4):549-51. [Medline].
Bonacini M, Young T, Laine L. The causes of esophageal symptoms in human immunodeficiency virus infection. A prospective study of 110 patients. Arch Intern Med. Aug 1991;151(8):1567-72. [Medline].
Calore EE, Cavaliere JM, Perez NM, Campos Sales PS, Warnke KO. Esophageal ulcers in AIDS. Pathologica. Apr 1997;89(2):155-8. [Medline].
Edwards P, Wodak A, Cooper DA, Thompson IL, Penny R. The gastrointestinal manifestations of AIDS. Aust N Z J Med. Apr 1990;20(2):141-8. [Medline].
Levine MS, Loercher G, Katzka DA, Herlinger H, Rubesin SE, Laufer I. Giant, human immunodeficiency virus-related ulcers in the esophagus. Radiology. Aug 1991;180(2):323-6. [Medline].
Levine MS, Woldenberg R, Herlinger H, Laufer I. Opportunistic esophagitis in AIDS: radiographic diagnosis. Radiology. Dec 1987;165(3):815-20. [Medline].
Raufman JP. Infectious esophagitis in AIDS: what have we learned in the last decade?. Am J Gastroenterol. Nov 1995;90(11):1914-5. [Medline].
Sor S, Levine MS, Kowalski TE, Laufer I, Rubesin SE, Herlinger H. Giant ulcers of the esophagus in patients with human immunodeficiency virus: clinical, radiographic, and pathologic findings. Radiology. Feb 1995;194(2):447-51. [Medline].
Villanueva JL, Torre-Cisneros J, Jurado R, Villar A, Montero M, López F, et al. Leishmania esophagitis in an AIDS patient: an unusual form of visceral leishmaniasis. Am J Gastroenterol. Feb 1994;89(2):273-5. [Medline].
Yangco BG, Kenyon VS. Epidemiology and infectious complications of human immunodeficiency virus antibody positive patients. Adv Exp Med Biol. 1993;335:235-40. [Medline].
Mimidis K, Papadopoulos V, Margaritis V, Thomopoulos K, Gatopoulou A, Nikolopoulou V, et al. Predisposing factors and clinical symptoms in HIV-negative patients with Candida oesophagitis: are they always present?. Int J Clin Pract. Feb 2005;59(2):210-3. [Medline].
Dellon ES, Gibbs WB, Fritchie KJ, Rubinas TC, Wilson LA, Woosley JT, et al. Clinical, endoscopic, and histologic findings distinguish eosinophilic esophagitis from gastroesophageal reflux disease. Clin Gastroenterol Hepatol. Dec 2009;7(12):1305-13; quiz 1261. [Medline]. [Full Text].
DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. Jan 2005;100(1):190-200. [Medline].
Amaro R, Poniecka AW, Goldberg RI. Herpes esophagitis. Gastrointest Endosc. Jan 2000;51(1):68. [Medline].
Howden CW, Hornung CA. A systematic review of the association between Barrett's esophagus and colon neoplasms. Am J Gastroenterol. Oct 1995;90(10):1814-9. [Medline].
Nonevski IT, Downs-Kelly E, Falk GW. Eosinophilic esophagitis: an increasingly recognized cause of dysphagia, food impaction, and refractory heartburn. Cleve Clin J Med. Sep 2008;75(9):623-6, 629-33. [Medline].
Wilheim AB, Miranda-Filho Dde B, Nogueira RA, Rêgo RS, Lima Kde M, Pereira LM. The resistance to fluconazole in patients with esophageal candidiasis. Arq Gastroenterol. Jan-Mar 2009;46(1):32-7. [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. Nov 2010;139(5):1526-37, 1537.e1. [Medline].
Agency for Healthcare Research and Quality. Comparative Effectiveness of Management Strategies for Gastroesophageal Reflux Disease. AHRQ: Agency for Healthcare Research and Quality. Available at http://effectivehealthcare.ahrq.gov/healthInfo.cfm?infotype=rr&ProcessID=1&DocID=42. Accessed January 30, 2009.
Donnellan C, Sharma N, Preston C, Moayyedi P. Medical treatments for the maintenance therapy of reflux oesophagitis and endoscopic negative reflux disease. Cochrane Database Syst Rev. Apr 18 2005;CD003245. [Medline].
Malfertheiner P, Lind T, Willich S, Vieth M, Jaspersen D, Labenz J, et al. Prognostic influence of Barrett's oesophagus and Helicobacter pylori infection on healing of erosive gastro-oesophageal reflux disease (GORD) and symptom resolution in non-erosive GORD: report from the ProGORD study. Gut. Jun 2005;54(6):746-51. [Medline]. [Full Text].
Medical Economics Staff. Physicians' Desk Reference. 55th ed. Medical Economics Company: Montvale, NJ; 2001.

