- Author: Deepika Devuni, MBBS; Chief Editor: BS Anand, MD more...
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.
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
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 competitively inhibits histamine at the H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Cimetidine inhibits histamine at H2 receptors of gastric parietal cells, decreasing 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 concentrations.
Gastrointestinal Protective Agents
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 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
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 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 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 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 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 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 are topical or systemic agents used to treat fungal infections.
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 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 is a synthetic triazole fungistatic agent. It is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 alpha demethylation.
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 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 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.
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 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 is a synthetic purine nucleoside analog that stops replication of viral DNA. It is used to treat HSV esophagitis.
Foscarnet is an organic analog of inorganic pyrophosphate that inhibits replication of HSV and CMV. It is used to treat acyclovir-resistant cases.
Ganciclovir is an acyclic nucleoside analog that inhibits replication of herpes viruses. It is active against CMV and HSV.
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 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 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 decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Leukotriene inhibitors can be used to treat eosinophilic esophagitis. Examples of leukotriene inhibitors include montelukast and zafirlukast.
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 selectively prevents the action of leukotrienes released by mast cells and eosinophils.
Mast Cell Stabilizers
Mast cell stabilizers such as cromolyn may be used for eosinophilic esophagitis.
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.
Immunosuppressive agents such as cyclosporine and azathioprine may be used for graft versus host disease esophagitis.
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 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.
Alkylating agents include nitrogen mustards such as chlorambucil. These agents can be used in the treatment of Behçet disease esophagitis.
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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