eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology
Esophagitis: Treatment & Medication
Updated: Mar 5, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- Symptomatic treatment may include antacids for mild reflux esophagitis or viral esophagitis in the immunocompetent host. Prone and elevated head positioning, feeding recommendations (eg, thickening formula, providing smaller and more frequent feedings, fasting for at least 2 h before sleeping in older children), and other conservative reflux measures may be used for mild gastroesophageal reflux (GER).
- Although gastroesophageal reflux disease (GERD) may be initially treated with histamine 2 (H2)–receptor antagonists, tachyphylaxis quickly develops. Proton pump inhibitors (PPIs) should be used when peptic esophagitis is diagnosed because the effect of PPI is more sustained and powerful.1 A recent study of healthy children reports that erosive esophagitis treated with adequate doses of PPIs has a low relapse rate and does not require maintenance with PPIs or H2-blocker therapy.2
- Infectious esophagitis requires the appropriate antiviral, antifungal, or antibiotic therapy based on the causative organism.
- For corrosive esophagitis with alkalis or acids, any continued exposure to the eye, mouth, and skin should be ceased and the area flushed with water. Airway, breathing, circulation, and the overall cardiorespiratory status should be addressed following any possible ingestion.
- Although large quantities of fluid (eg, water, milk) have often been given to dilute the corrosive agent, be aware that, if perforation has occurred, these fluids may extravasate, leading to mediastinitis. Large volumes of fluid may also induce vomiting, but a small amount of water or milk may wash away any residual agent from the mucosal surface.
- If alkaline or acidic fluids are given, an exothermic reaction can occur.
- Induced emesis or gastric lavage for GI decontamination is contraindicated and may exacerbate esophageal injury or lead to aspiration.
- Charcoal is not recommended.
- Endotracheal intubation or tracheostomy may be required if severe upper airway edema is present.
- Hospitalization for the administration of intravenous fluids and, possibly, tube feedings should probably occur for most children who have ingested a caustic agent.
- Broad-spectrum antibiotics may be used in severe cases to prevent secondary infection, and steroids may be used in an attempt to decrease stricture formation.
- The treatment of eosinophilic esophagitis is still widely debated.
- Evidence shows that food allergy is the most common cause of EE, and different approaches to removing the causative food antigens are available.
- Patch testing can help determine the allergen (most commonly milk, eggs, nuts, beef, wheat, fish, shellfish, corn, and soy).
- Selective elimination of implicated foods based on allergy testing, or, in certain cases, initiation of elemental diet is required.
- For 1-3 months, patients are placed on an exclusion diet or an elemental diet, and repeat endoscopies with biopsies are often necessary to determine both improvement and the time to start progressive reintroduction of foods.
- Elemental diet has higher success rate than testing-based elimination diet.3
- Other treatments, such as anti-inflammatory medications, mast cell stabilizers, and leukotriene receptor antagonists, have also been used.
- Oral corticosteroids were demonstrated to be effective in treating symptoms and normalizing the histology, but the disease recurs when these agents are discontinued.
- Since 1998, multiple studies demonstrated effectiveness of swallowed topical corticosteroids delivered from a metered dose inhaler in treating clinical symptoms and abnormal histology associated with eosinophilic esophagitis.4
- In this form of administration, patients should be instructed to administer the metered dose inhaler without using a spacer. The inhaler should be inserted into the mouth and sprayed with the lips sealed around the device; the powder should then be swallowed and not rinsed. The patient should not eat or drink for at least 30 minutes. The treatment course is usually between 6-8 weeks. However, similar to the effect seen with oral steroid treatment, the disease generally recurs upon discontinuation of treatment.
- The use of topical steroid for maintenance treatment has not been studied. The adverse effects in this form of treatment are thought to be significantly less compared with oral steroid because of the much smaller dose and the rapid metabolism by the liver with first-pass effect.
- Oral cromolyn sodium and other mast cell stabilizers have not been shown to be effective. Recent studies have demonstrated benefits from leukotriene-receptor antagonists in adults, and studies of monoclonal antibodies directed against IL-5 are ongoing.5
- Evidence shows that food allergy is the most common cause of EE, and different approaches to removing the causative food antigens are available.
Surgical Care
- For reflux esophagitis, consider Nissen fundoplication in severe cases unresponsive to aggressive medical management. With the availability of PPIs, the surgical indication is now restricted to less than 1% of all cases. Patients with associated delay in gastric emptying may require a pyloroplasty. A gastrostomy or jejunostomy tube may be placed to assist with feeding.
- For bacterial esophagitis, drainage of a paraesophageal abscess may be required.
- For corrosive esophagitis, surgical management of perforations and revisions may be required.
Consultations
- Consult a gastroenterologist, especially if endoscopy or biopsy is required for definitive diagnosis.
- For corrosive ingestions, always notify a local Poison Control Center. Their staff can help to identify problematic active ingredients and provide immediate management and monitoring guidelines. A gastroenterologist and, possibly, a surgeon need to be consulted. A significant number of patients have esophageal burns without oral burns.
Diet
- No dietary changes are required once proper medical treatment is successfully initiated. However, foods that exacerbate reflux or delay gastric emptying (eg, fats, fried foods, tomatoes, caffeine) should be restricted.
Medication
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 H2 receptors in gastric cells.
Ranitidine (Zantac)
Inhibits histamine stimulation of H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Adult
150 mg PO bid as maintenance; not to exceed 600 mg/d during treatment phase; alternatively, 50 mg/dose IV/IM q8h
Pediatric
2-8 mg/kg/d PO divided bid; not to exceed 300 mg/d
Alternatively, 1-4 mg/kg/d IV/IM divided tid; not to exceed 6 mg/kg/d or 150 mg/d
Inhibits CYP450 3A4 and 2D6; may decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Famotidine (Pepcid)
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Adult
20-40 mg PO bid for up to 12 wk; alternatively, 20 mg IV q12h
Pediatric
Neonates: 0.5 mg/kg PO qd
Infants and children <16 years: 0.5 mg/kg PO bid; not to exceed 40 mg bid; doses up to 2 mg/kg/d have been used in clinical studies
May decrease effects of ketoconazole and itraconazole (decreases bioavailability)
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose or discontinue with renal dysfunction
Prokinetic agents
These agents augment cholinergic activity and improve motility in the GI tract. However, no evidence-based efficacy in GERD is available.
Metoclopramide (Clopra, Maxolon, Reglan)
For patients with GER, may mildly increase resting pressure of the lower esophageal sphincter and increase rates of gastric emptying.
Adult
10-15 mg PO q6h, administer 30 min ac and hs
Pediatric
Infants and children: 0.3-0.5 mg/kg/d PO/IV/IM divided in 4 divided doses, administer 30 min ac and hs; doses up to 0.8 mg/kg/d may be used in patients with severe gastroesophageal reflux
May decrease GI absorption of cimetidine and digoxin; may increase cyclosporine absorption; opiate analgesics may increase metoclopramide toxicity in CNS; anticholinergic agents (eg, atropine, antihistamines) may antagonize effects
Documented hypersensitivity; pheochromocytoma; GI hemorrhage, obstruction, or perforation; history of seizure disorders
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in renal impairment; extrapyramidal symptoms, restlessness, agitation, sedation, headache, dizziness, leukopenia, rash, and diarrhea; only marginally effective as a prokinetic, and its adverse effects are common and may be serious
Proton pump inhibitors
These drugs inhibit the H+/K+/-ATPase pump in gastric parietal cells, thus inhibiting gastric acid secretion.
Omeprazole (Prilosec, Zegerid Oral Suspension)
Inhibits gastric acid secretion. Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATPase pump. Give with or before the first meal of the day.
Adult
Treatment: 20 mg PO qd for 4-8 wk
Maintenance: 20 mg PO qd
Pediatric
<2 years: 1 mg/kg/d PO qd or divided bid
≥2 years:
GERD or other acid-related disorders:
<20 kg: 10 mg PO qd
≥20 kg: Administer as in adults; doses as high as 3.3 mg/kg/day have been reported
Erosive esophagitis:
0.7 mg/kg/d PO initially; may increase dose, not to exceed 3.5 mg/kg/d or 80 mg/d
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Do not chew or crush cap; cap may be opened, and intact pellets may be administered in an acidic beverage; headache, dizziness, rash, GI disturbance, and cough
Lansoprazole (Prevacid)
Inhibits gastric acid secretion by specifically inhibiting H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells. Give with or before the first meal of the day.
Adult
Treatment: 30-60 mg PO qd for up to 8 wk; an additional 8 wk may be tried in those patients who failed to respond or for a recurrence of esophagitis
Maintenance: 15 mg PO qd
Pediatric
<10 kg: 7.5 mg PO qd for up to 12 wk
10-30 kg: 15 mg PO qd or bid for up to 12 wk
≥30 kg: 30 mg PO qd or bid for up to 12 wk
Cytochrome P450 isoenzyme CYP2C19 and CYP3A3/4 substrate; increases theophylline clearance mildly (10%); may increase warfarin effects; may interfere with the absorption of ketoconazole, ampicillin, iron salts, and digoxin; sucralfate delays and decreases lansoprazole absorption by 30%; cranberry juice significantly reduces gastric pH and may reduce effectiveness of PPIs
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Symptomatic response to therapy does not preclude the presence of gastric malignancy; use with caution in patients with liver disease, reduce dosage with severe impairment; Prevacid SoluTabs contain aspartame, which is metabolized to phenylalanine and must be used with caution in patients with phenylketonuria
Antifungal agents
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.
Fluconazole (Diflucan)
Fungistatic activity. Synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal CYP450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. May be preferred initial regimen for candidal esophagitis with fewer adverse effects.
Adult
200 mg PO once, then 100 mg PO qd
Pediatric
6 mg/kg PO once, then 3 mg/kg PO qd
CYP450 2C19 and 3A4 inhibitor; levels may increase with hydrochlorothiazide; fluconazole levels may decrease with chronic coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently
Documented hypersensitivity; cardiac dysrhythmias may occur with cisapride, terfenadine, or astemizole
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adjust dose for renal insufficiency; monitor closely if rashes develop and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) with underlying medical conditions (eg, AIDS, malignancy) and while taking multiple concomitant medications; not recommended for breastfeeding mothers
Ketoconazole (Nizoral)
Potential for development of resistance with ketoconazole. Fungistatic activity. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.
Adult
200 mg PO bid for 4 doses, then 200 mg PO qd
Pediatric
3.3-6.6 mg/kg/d PO qd
Inhibits CYP450 3A3/4 and 3A5-7; may increase levels of phenytoin, cyclosporine, digoxin, theophylline, corticosteroids, protease inhibitors, and warfarin; levels of ketoconazole may be decreased by phenobarbital, rifampin, and isoniazid; because gastric acidity is required for absorption, H2 antagonists, antacids, and omeprazole may decrease absorption
Documented hypersensitivity; fungal meningitis; cardiac dysrhythmias may occur when used with cisapride, terfenadine, or astemizole
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hepatotoxicity may occur; may reversibly decrease corticosteroid serum levels (adverse effects avoided with dose of 200-400 mg/d); administer antacid, anticholinergics, or H2 blockers at least 2 h after taking ketoconazole; GI disturbance, rash, pruritus, hepatotoxicity, headache, fever, and bone marrow suppression
Itraconazole (Sporanox)
Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome CYP450-dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Adult
200 mg PO/IV qd; not to exceed 400 mg/d
Pediatric
5-10 mg/kg/d PO/IV divided q12h
Antacids may reduce absorption of itraconazole; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; CYP450 3A4 inhibitor; may increase tacrolimus and cyclosporine plasma concentrations when high doses are used; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (lovastatin, simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death
May increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce itraconazole levels (phenytoin metabolism may be altered)
Documented hypersensitivity; cardiac dysrhythmias may occur when used with cisapride, terfenadine, or astemizole
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution with liver disease; phlebitis, rash, GI disturbance, fever, headache, fatigue, hepatotoxicity, and bone marrow suppression
Amphotericin B (Amphocin, Fungizone)
Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death.
Adult
0.25-1.5 mg/kg/d IV infused over 2-3 h
Pediatric
Administer as in adults
Antineoplastic agents may enhance potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; risk of renal toxicity is increased with cyclosporine
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor renal function, serum electrolytes such as magnesium and potassium, liver function, CBC count, and hemoglobin concentrations; resume therapy at lowest level (eg, 0.25 mg/kg) when therapy is interrupted for >7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in neutropenic patients receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion)
Corticosteroids
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, fibrosis, and, possibly, help decrease the incidence of stricture formation.
Methylprednisolone (Medrol, Solu-Medrol)
Decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.
Adult
20-60 mg/d PO/IV/IM divided q6-12h
Pediatric
1-2 mg/kg/d PO/IV/IM divided q6-12h
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Prednisone (Deltasone, Orasone)
Beneficial for allergic esophagitis that is unresponsive to antireflux therapy.
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Adult
20-60 mg/d PO for 4 wk for allergic esophagitis
Pediatric
1-2 mg/kg/d PO for 4 wk for allergic esophagitis
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI ulceration
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Fluticasone propionate (Flovent)
The HFA product is PO-inhaled corticosteroid and is available as 44, 110, and 220 mcg per actuation.
Adult
880-1760 mcg/d (4-8 actuations/d of 220 mcg per actuation) via PO inhalation divided 2-4 times/d
Pediatric
<4 years: Not established
440-880 mcg/d via PO inhalation divided 2-4 times/d
Coadministration with CYP450 3A4 isoenzyme inhibitors (eg, amprenavir, atazanavir, darunavir, delavirdine, fosamprenavir, indinavir, ketoconazole, nelfinavir, ritonavir, tipranavir) decreases fluticasone elimination and increases plasma fluticasone levels, case reports of iatrogenic Cushingoid symptoms have been reported
Documented hypersensitivity; bronchospasm, status asthmaticus, and other types of acute episodes of asthma
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Avoid using higher than recommended doses; suppression of HPA function, suppression of linear growth (ie, reduction of growth velocity), reduced bone mineral density, hypercorticism (Cushing syndrome), hyperglycemia, or glucosuria may occur; these adverse effects (as well as intracranial hypertension) may occur with topical use and have been reported in pediatric patients; use with extreme caution in patients with respiratory tuberculosis, untreated systemic infections, or ocular herpes simplex; use with caution and monitor patients closely with hepatic dysfunction
Eosinophilic conditions (eosinophilia, vasculitic rash, cardiac complications, worsening pulmonary symptoms, and/or neuropathy) may occur and are usually associated with withdrawal or decrease of PO corticosteroids after the initiation of fluticasone (PO inhalation); a causal relationship by fluticasone has not been established
Antiviral agents
These agents are used to treat infectious esophagitis. Patients with immunocompetency may not require specific antiviral therapy.
Acyclovir (Zovirax)
Prodrug activated by phosphorylation by virus-specific thymidine kinase that inhibits viral replication. Herpes virus thymidine kinase (TK), but not host cells 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.
Has affinity for viral thymidine kinase and once phosphorylated causes DNA chain termination when acted on by DNA polymerase. Inhibits activity of both HSV-1 and HSV-2. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h from rash onset. May prevent recurrent outbreaks. Early initiation of therapy is imperative. Used for HSV esophagitis.
Adult
250 mg/m2/d IV q8h for 7 d
Pediatric
<3 months: 20 mg/kg IV q8h for 14-21 d
3 months to 12 years: 10 mg/kg IV q8h for 7-14 d
>12 years: 5 mg/kg IV q8h for 7-14 d
Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in renal failure or when using nephrotoxic drugs
Foscarnet (Foscavir)
Organic analogue of inorganic pyrophosphate that inhibits replication of HSV, including CMV. Selectively inhibits at pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular polymerases. Unlike ganciclovir, does not require activation by a kinase and is active in vitro.
Adult
CMV:
Induction: 90 mg/kg IV q12h for 14-21 d
Maintenance: 90-120 mg/kg/d IV
HSV resistant to acyclovir:
40 mg/kg IV bid/tid until infection resolves
Adjust dose with renal impairment
Pediatric
Not established
Avoid administration with potentially nephrotoxic drugs (eg, aminoglycosides, amphotericin B, IV pentamidine) may increase nephrotoxicity (do not administer unless potential benefits outweigh risks); coadministration with IV pentamidine may cause hypocalcemia
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause decline in renal function; for correct dosing, obtain 24-h serum creatinine at baseline and continue to monitor (discontinue if serum creatinine <0.4 mL/min/kg); hydration may reduce nephrotoxicity
Carefully monitor electrolytes (eg, calcium, magnesium); assess for electrolyte and mineral level abnormalities if mild perioral numbness, paresthesias symptoms, or seizures; granulocytopenia and anemia may occur (regularly monitor CBC count)
Infuse foscarnet solutions into veins with adequate blood flow to avoid local irritation; to avoid toxicity do not administer by rapid or bolus IV injection
Ganciclovir (Cytovene)
Acyclic nucleoside analogue of 2'deoxyguanasine. 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. 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 only exerts its effect on replicating virus.
Adult
Induction: 5 mg/kg IV q12h for 14-21 d
Maintenance: 6 mg/kg IV 5 times/wk
Role of PO ganciclovir maintenance at doses of 1 g tid is uncertain
Adjust dose for renal impairment
Pediatric
Administer as in adults
Concomitant administration with cytotoxic drugs such as dapsone, vinblastine, doxorubicin, pentamidine, flucytosine, vincristine, amphotericin B, trimethoprim/sulfamethoxazole combinations or other nucleoside analogs may result in additive toxicity in bone marrow, spermatogonia, and germinal layers of skin and GI mucosa (coadminister only if potential benefits outweigh risks); coadministration with imipenem-cilastatin may cause generalized seizures (use only if potential benefits outweigh risks); serum creatinine may increase following concurrent use of ganciclovir with either cyclosporine or amphotericin B; in presence of probenecid, ganciclovir renal clearance is reduced; bioavailability may increase when didanosine is administered either 2 h prior to or simultaneously with ganciclovir; bioavailability of ganciclovir may decrease in presence of zidovudine, while bioavailability of zidovudine is increased in presence of ganciclovir
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause granulocytopenia, anemia, and thrombocytopenia; since PO is associated with higher rate of CMV retinitis progression, compared to IV formulation, use only when benefits outweigh risks (advanced HIV disease); half-life and plasma/serum concentrations may be increased as a result of reduced renal clearance; dosages >6 mg/kg IV may result in increased toxicity; rapid infusions may result in increased toxicity; initially, reconstituted IV solutions have a high pH (11); phlebitis or pain may occur at site of IV infusion despite further dilution in IV fluids; adequate hydration must accompany administration; photosensitization (photoallergy or phototoxicity) may occur
More on Esophagitis |
| Overview: Esophagitis |
| Differential Diagnoses & Workup: Esophagitis |
 Treatment & Medication: Esophagitis |
| Follow-up: Esophagitis |
| References |
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Further Reading
Keywords
esophagitis, inflammation of esophagus, esophagus inflammation, gastroesophageal reflux, GER, corrosive ingestion, reflux esophagitis, peptic esophagitis, corrosive esophagitis, caustic esophagitis, eosinophilic esophagitis, radiation esophagitis, Barrett esophagus, candidal esophagitis, Sandifer syndrome, gastroesophageal reflux disease, GERD, lower esophageal sphincter, LES, EE, esophagogastroduodenoscopy, EGD, pediatric esophagitis, acid reflux, food allergy, chemical esophagitis, infectious esophagitis, acid GER, nonacid GER, poison ingestion, household cleaner ingestion, accidental ingestion, herpes simplex virus, HSV, cytomegalovirus, CMV, allergic esophagitis, Nissen fundoplication, histamine 2–receptor antagonist, prokinetic agent, proton pump inhibitor
