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Esophagitis Medication

  • Author: Deepika Devuni, MBBS; Chief Editor: BS Anand, MD  more...
 
Updated: Nov 12, 2015
 

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.[57]

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.

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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.

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Gastrointestinal Protective 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. These drugs are also useful 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.

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Proton Pump Inhibitors

Class Summary

These agents inhibit gastric acid secretion by inhibiting the H+/K+ -ATPase enzyme system in the 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.

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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.

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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.

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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.

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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.

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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.

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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 causes variable alterations in antibody production.

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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 the 2 strands of helical DNA and subsequent interference with replication.

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Contributor Information and Disclosures
Author

Deepika Devuni, MBBS Resident Physician, Department of Internal Medicine, University Of Connecticut School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

John W Birk, MD, FACG Associate Professor of Medicine, Director, Gastroenterology and Hepatology Fellowship Program, University of Connecticut School of Medicine; Chief, Division of Gastroenterology, University of Connecticut Health Center

John W Birk, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Sajid Ansari, MD Consulting Staff, Department of Gastroenterology, St Anthony's Medical Center

Sajid Ansari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and Missouri State Medical Association

Disclosure: Nothing to disclose.

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chin Hung Chung, MBBS, FRCS(Glasg), FHKAM(Surgery) Chief of Service, Department of Accident and Emergency, North District Hospital, Hong Kong

Chin Hung Chung, MBBS, FRCS(Glasg), FHKAM(Surgery) is a member of the following medical societies: American College of Surgeons and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chun-hing Ludwig Tsoi MB, ChB, MPH, MRCP, FRCS(Edin), Senior Medical Officer, Accident and Emergency Department, Tseng Kwan O Hospital, Hong Kong; Chairman, Committee on Training, Hong Kong St John Ambulance

Chun-hing Ludwig Tsoi is a member of the following medical societies: Royal College of Physicians of the United Kingdom and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

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Esophagitis. Location of fungal and viral infections in ulcers.
Peptic esophagitis. A rapid urease test (RUT) was performed on the esophageal biopsy sample. The result was positive for Helicobacter pylori.
Corrosive esophagitis. This is a vinegar-induced esophageal burn. The patient had a fish bone in her throat. She ingested vinegar in an attempt to dissolve the fish bone but to no avail; this led to corrosive esophagitis.
Infectious esophagitis. Candida esophagitis. Double-contrast esophagram shows linear plaquelike lesions in the esophagus, with normal intervening mucosa.
Infectious esophagitis. Two examples of advanced Candida esophagitis demonstrate a shaggy esophagus. In both images, the double-contrast esophagram shows a grossly irregular esophageal contour due to innumerable plaques and pseudomembranes, with the trapping of barium between lesions. Patients with this fulminant form of esophageal candidiasis are almost always found to have acquired immunodeficiency syndrome (AIDS).
Infectious esophagitis. Candida esophagitis with a foamy esophagus. This patient has a dilated esophagus with beaklike narrowing (arrow) at the gastroesophageal junction as a result of long-standing achalasia. Innumerable tiny bubbles are layering out in the barium column due to infection by the yeast form of candidiasis.
Infectious esophagitis. Herpes esophagitis. Double-contrast esophagram shows small, discrete ulcers (arrows) in the mid esophagus on a normal background mucosa. Note the radiolucent mounds of edema surrounding the ulcers. In the appropriate clinical setting, this appearance is highly suggestive of herpes esophagitis, since ulceration in candidiasis almost always occurs on a background of diffuse plaque formation.
Infectious esophagitis. Cytomegalovirus esophagitis in a patient with acquired immunodeficiency syndrome (AIDS). Double-contrast esophagram shows a large, flat ulcer in profile (large arrows) in the mid esophagus with a cluster of small satellite ulcers (small arrows). Because HIV esophagitis may produce identical radiographic findings, endoscopy is required to confirm the presence of cytomegalovirus before patients are treated.
Infectious esophagitis. Two examples of giant human immunodeficiency virus (HIV) esophageal ulcers (arrows) in patients with acquired immunodeficiency syndrome (AIDS). In A, the ulcer is seen in profile, whereas in B, the ulcer is seen en face. Endoscopy is required to exclude cytomegalovirus as the cause of this finding before treating patients.
 
 
 
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