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Drug-induced esophagitis

Article in Diseases of the Esophagus · May 2009

DOI: 10.1111/j.1442-2050.2009.00972.x · Source: PubMed

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Diseases of the Esophagus (2009) 22, 633–637
DOI: 10.1111/j.1442-2050.2009.00972.x

Review article

Drug-induced esophagitis

G. N. Zografos,1 D. Georgiadou,1 D. Thomas,2 G. Kaltsas,2 M. Digalakis3

1
Department of Sugery, Athens General Hospital, 2Endocrine Unit, Department of Pathophysiology, Medical
School, National and Kapodostrian University of Athens, Athens, and 3Department of Surgery, Asklipion
Hospital, Voula, Greece

SUMMARY. Drug-induced esophagitis is being recognized increasingly in the past few years. Since 1970 more
than 650 cases have been reported worldwide caused by 30 or more medications. We have reviewed these cases with
a view to classifying this disease based on underlying pathological mechanism. Drug-induced esophageal injury
tends to occur at the anatomical site of narrowing, with the middle third behind the left atrium predominating
(75.6%). The disease is broadly classified into two groups. The first group being transient and self-limiting as
exemplified by the tetracycline group induced injury (65.8%). The second is the persistent esophagitis group, often
with stricture, with two distinct entities: (i) patients on nonsteroidal anti-inflammatory agents whose injury is
aggravated by gastroesophageal reflux (21.8%) (reflux aggravated); and (ii) patients with potasium chloride and
quinidine sulphate induced injury (12.4%) (persistent drug injury). Severe esophageal injury has been reported in
some women taking biphosphonates as treatment for postmenopausal osteoporosis. Endoscopic findings in such
patients with esophageal injury generally suggested a chemical esophagitis, with erosions or ulcerations and
exudative inflammation accompanied by thickening of the esophageal wall. Most cases of medication-induced
esophageal injury heal without intervention within a few days. Thus, the most important aspect of therapy is to
make the correct diagnosis and then to avoid reinjury with the drug. When possible, potentially caustic oral
medications should be discontinued.
KEY WORDS: drugs, esophageal injury, esophagitis.

INTRODUCTION cefotiam hydrochloride, phenytoin, have been

Since 1970 at least 650 cases of esophageal injury
have been reported, caused by 30 different pills.
Many cases of drug-induced esophagitis (DIO)
remain unrecognized as most patients fully recover,
or after being reported they are not published. The
incidence of the disease was estimated to 3.9 per
100 000 population per year.1
A great variety of drugs are associated with esoph-
ageal injuries. Anti-inflammatory analgesics (ibupro-
fen, indomethacin, aspirin, naproxen), quinidine,
potassium chloride, emepronium bromide, doxycy-
cline, tetracycline, clindamycin, ideocyclin, oxytetral
ferrous sulphate, ascorbic acid, alprenolol chloride,
theophylline, mycophenolate mofetil, warfarin,
cyproterone acetate and ethinylestradiol, rifampin,
Address correspondence to: Dr Dimitrios Thomas, MD, PhD,
Endocrine Unit, Department of Pathophysiology, Medical
School, National and Kapodostrian University of Athens, Mikras
Asias 75, 15575, Athens, Greece. E-mail: thomasproge@endo.gr
© 2009 Copyright the Authors
Journal compilation © 2009, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus
reported as causative factors of DIO.2–10
EPIDEMIOLOGY
The mean age for the 650 patients reported was 41.5
years, with the youngest 9-year-old taking emephro-
nium bromide and the oldest an 89-year-old woman
who developed hypopharyngeal ulceration following
a ferrous sulphate treatment.11,12 Patients suffering
from esophageal injury caused by quinidine have a
mean age of 60 years whereas patients injured by oral
antibiotics have a mean age of 30 years.
Elderly patients are particularly at risk for DIO.
Compared with the general population, the older
patients consume more medications, are more likely
to have cardiac enlargement with concomitant com-
pression of the mid-esophagus. Esophageal motility
problems in the elderly are often related to coexisting
diabetes mellitus and autonomic neuropathy or
633
634 Diseases of the Esophagus

connective tissue disease.13 Also, saliva production
decreases with age, reducing esophageal lubrication
and increasing the likelihood that pills with an acid
pH remains longer in the esophagus.14
Most of patients with DIO are women (66.2%).
This predominance of females can be attributed to
female predominance among the subgroups receiving
emephronium bromide, potassium chloride tablets,
and biphosphonates for osteoporosis. Emepronium
bromide is an anticholinergetic drug utilized to
relieve urinary frequency. Many more females
suffering from urinary symptoms receive this drug.1
Similarly, potassium chloride tablets can cause
esophageal injury mainly in patients with rheumatic
heart disease more common in females.
PATHOGENESIS
Medications can induce esophageal abnormalities via
both systemic and local actions. Examples of systemic
effects include gastroesophageal reflux promoted by
smooth muscle relaxants, and medication-induced
compromise of the immune system, resulting in infec-
tious complications. In the following discussion, only
drugs that cause direct esophageal mucosal injury will
be discussed (Table 1).
The injury occurs at the anatomical sites of nar-
rowing of the esophagus or at sites of pathological
narrowing. The most common site of injury has been
near the level of the aortic arch (75.6%), an area
characterized by external compression from the arch
and by physiologic reduction of amplitude of the
esophageal peristaltic wave.1,15 The underlying dis-
eases as motility disorders and tumors might also be
expected to predispose to these complications.
The first group of medications that cause transient
and self-limiting esophageal injury includes doxy-
cycline, tetracycline, clindamycin, emepronium
bromide, ascorbic acid, and ferrous sulfate. These
medications have a low acid pH when dissolved in
solution, causing localized discrete ulcers that heal
after withdrawal of the drug and that are not associ-
ated with stricture formation.4
Emepronium bromide is a quaternary ammonium
anticholinergetic drug that blocks peripheral cholin-
ergic nerves and ganglionic transmission. It increases
bladder capacity, delays the first desire to void, and
decreases voiding pressure.16 More than 30 cases of
DIO from emepronium bromide have been described.
A hydrophilic swelling agent incorporated into eme-
pronium bromide tablets may be responsible for
excessive adherence of this tablet. This swelling agent
is intended to cause rapid disintegration of the tablet.
However, when ingested with only a small amount of
water, these tablets form a sticky mass that may
adhere to the esophageal wall.17,18 Emepronium
bromide can lower the pressure of the lower esoph-
ageal sphincter, promoting gastroesophageal reflux.19
However, as the drug-induced ulcers are more often
found in the middle or upper esophagus, it is likely
that a direct irritant effect is more significant.20
Eighty-two instances of DIO have been reported
to result from the tetracycline group. In most of these

Table 1 Pathophysiological characteristics of the direct esophageal mucosal injury caused by drugs

Esophageal
injury Drugs Pathophysiological mechanism Site of injury Complications

Transient/self- Doxycycline, tetracycline, Direct irritant effect (pH in Distal or mid-esophagus –

limiting clindamycin, ascorbic acid,
ferrous sulfate, warfarin
Emepronium bromide
Cyproterone acetate and
ethinylestradiol, rifampin,
cefotiam† hydrochloride
Biphosphonates
Persistent Quinidine and potassium
chloride
Nonsteroidal
anti-inflammatory agents
solution <5), ulcer
formation‡, resultant
esophagitis
Chemical esophagitis, erosions
or ulcerations, exudative
inflammation, thickening of
the esophageal wall.
Prolonged transit time of
medications, hyperosmotic
solutions (direct tissue
damage and ulcer
formation)(pH in solution:
6–7)
Disruption of the normal
cytoprotective barrier in the
mucosa of the esophagus,
aggravation of reflux
esophagitis, ulcer formation
(pH in solution: variable)
Middle or upper esophagus –
Upper, middle, distal –
esophagus
Distal esophagus Strictures (<1%),
hematemesis of
esophageal
hemorrhage (rare)
Mid-esophagus (compression Strictures (>60%) and
form aortic arch or left fistulas formation,
atrium) bleeding, deaths
Distal esophagus (acid-exposed Strictures (40–50%),
region related to hemorrhage
concomitant acid reflux)

†A case of cefotiam-induced esophagitis with mucosal dissection has been referred;9 ‡Emepronium bromide can lower the pressure of the
lower esophageal sphincter, promoting gastroesophageal reflux.
© 2009 Copyright the Authors
Journal compilation © 2009, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus

reports the antibiotics were taken immediately before
lying down to sleep. These drugs, when dissolved in
10 cc of distilled water, produce moderate to severe
injury when held in contact with the buccal
mucosal.21
Doxycycline, when held within the esophagus,
accumulates within the basal layer of squamous epi-
thelium, a possible mechanism for tissue damage pro-
duced by this or other pills.22,23
The second group is the ‘persistent esophagitis’
group, often related with stricture, and has two dis-
tinct entities. The first entity includes quinidine and
potassium chloride. The mucosal injury caused by
these medications is not entirely explained on the
basis of PH, given that these drugs have a near
neutral PH. Transit time of medications may be quite
prolonged even in normal persons. Patients with
esophageal abnormalities were more likely to have
prolonged transit of either tablets or capsules.
Four patients developed strictures attributed to
quinidine, but one patient was also taking potassium
chloride.24,25 Five esophagograms performed in
patients injured by quinidine have shown esophageal
irregularity and narrowing or intraluminal polypoid
filling defects, which in three cases were initially con-
fused with a malignancy.1
Potassium chloride has been implicated in several
cases of DIO. It has long been postulated as causing
small bowel ulceration, a result of local vascular
injury and thrombosis.26,27 This agent may also
produce hyperosmotic solutions capable of tissue
desiccation and damage.28 In all cases, concomitant
cardiomegaly or left atrial enlargement existed and
delayed the passage of potassium resulting in a high
local concentration. This was proved to be sufficient
for ulceration.29 Eleven of these patients had esoph-
ageal stricture at the level of compression of the
esophagus by the aortic arch or left atrium. Five
deaths were related to potassium-induced esophageal
injury. These patients developed fistulas from the
esophagus into the aorta or left atrium, perforation
into the mediastinum, bleeding ulcer, or inanition
related to the esophageal stricture.27,30,31 It is recom-
mended that oral potassium chloride supplements in
liquid form should be administered to patients with
cardiomegaly and disorders of esophageal motility.32
Severe esophageal injury has reported in some
patients (mostly women >50 years old) taking alendr-
onate as treatment for postmenopausal osteoporosis.
Endoscopic findings in the patients with esophageal
injury generally suggested a chemical esophagitis,
with erosions or ulcerations and exudative inflamma-
tion accompanied by thickening of the esophageal
wall (as showed by computed tomography and endo-
scopic ultrasonography), whereas bleeding was rare.33
One interesting aspect of the alendronate-induced
esophagitis is that the lesions described included
severe ulcerative esophagitis involving 10 cm or more
© 2009 Copyright the Authors
Journal compilation © 2009, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus
Drug-induced esophagitis 635
of the esophagus. These lesions are somewhat
unusual compared with those occurring in the typical
case of DIO. In most of the patients, esophageal com-
plications occur during the first month of alendronate
therapy. Of these patients, more than 50% either took
the alendronate without an adequate quantity of
water or failed to remain upright for 30 min or more
after taking the tablet. Esophagitis was more
common in patients with preexisting esophageal dis-
orders. Subsequent studies failed to prove the higher
incidence of esophageal injury for both daily34 and
weekly administration,35 mainly because of the fre-
quent follow-up visits and regular reminders to
patients regarding proper use of the medication.
Another bisphosphonate, risedronate, appears to
have minimal gastrointestinal toxicity. In a pooled
analysis of nine clinical trials that included 10 068
patients randomly assigned to receive risedronate
(5 mg/day) or placebo for up to 3 years; upper gas-
trointestinal tract adverse events were no different
between the two groups.36 Although risedronate
seems to be related with fewer gastric ulcers in endo-
scopical studies, however, it is not known if it is
superior to alendronate when given long-term for
prevention and treatment of osteoporosis.37 For most
of the commercially available biphosphonates, it has
been suggested that that a decrease in the frequency
of administration may lead to improvement of gas-
trointestinal tolerability, thus reducing the risk of
esophageal injury.38
The second entity includes nonsteroidal anti-
inflammatory agents. Forty-six cases of esophagitis
caused by ibuprofen, indomethacin, aspirin, benory-
late naproxen, and phenylbutazone have been
reported the last 10 years. Many of them have devel-
oped stricture and a few of them perforation or non-
fatal hemorrhage.1 Aspirin disrupts the normal
cytoprotective barrier in the mucosa of the stomach
and a similar process has been found to occur in the
esophagus.39 The nonsteroidal anti-inflammatory
drugs may exert their ulcerogenic effect by reducing
the cytoprotective action of the prostaglandins on the
gastric mucosa. A similar action in the esophagus
might contribute to mucosal damage and esophagi-
tis.3 Before dysphagia occurred, most of the patients
who were taking anti-inflammatory drugs had had
symptoms of gastroesophageal reflux. This advocates
that these drugs may aggravate reflux esophagitis and
so increase the risk of stricture formation. The per-
centage of stricture formation may be as high as
40–50%, and these patients are usually 10 years older
than patients without strictures, have longer duration
of heartburn symptoms, and are more likely to have
mucosal injury.40 Esophageal emptying is slow in the
elderly, resulting a prolonged exposure of the mucosa
to their irritant action. Nonsteroid anti-inflammatory
drugs should be prescribed with caution in the pres-
ence of symptomatic gastroesophageal reflux.41
636 Diseases of the Esophagus
CLINICAL PRESENTATION
The clinical presentation of patients with DIO is
usually retrosternal pain or heartburn (60%),
odynophagia (50%), and dysphagia (40%).2,19 Less
common symptoms are hematemesis, abdominal
pain, low-grade fever and weight loss.4,31,42,43,44 The
onset of the symptoms occurs from a few hours to 1
month after ingestion of the drug. In the vast major-
ity of cases and in those uncomplicated by stricture,
symptoms resolved usually within 7 to 10 days, but in
some patients symptoms persist for many weeks after
the drug has been discontinued.43
DIAGNOSIS
The diagnosis of the DIO is usually suspected by the
clinical history alone. The differential diagnosis is
between foreign body, esophageal carcinoma, or con-
ditions where the diagnosis of acquired immune defi-
ciency syndrome could be entertained. A normal
barium esophagram is the usual finding in uncompli-
cated drug-induced esophageal injury. However, a
more sensitive double contrast technique may detect
ulcers in most of the cases.1 Quinidine, potassium
chloride, alprenolol chloride, ferrous sulfate can
cause lesions detectable on single-contrast barium
meal.4,45
Flexible fiberoptic endoscopy is more sensitive
than the barium swallow in establishing a diagnosis
of DIO. Typical endoscopic findings in the esophagus
include erythema, erosions, ulcers (in some cases
‘kissing’ ulcers have been reported), esophageal ulcer
with bleeding, and esophageal strictures.46 This type
of esophagitis often produce superficial ulceration
and areas of erythema and friability2 that are difficult
to detect with the standard barium swallow. Recent
reports suggest the air contrast barium swallow in
detecting minor mucosal abnormalities.47,48
The discreteness of the ulcerations and the typical
clinical setting limit the differential diagnosis.
Herpetic esophagitis or ulcerations arising in associa-
tion with Barrett’s epithelium could give a similar
appearance.2
THERAPY AND PROGNOSIS
Most cases of DIO are self-limited and resolve
without complications. Thus, the most important
aspect of therapy is to make the correct diagnosis and
then to avoid reinjury with the drug. When possible,
potentially caustic oral medications should be discon-
tinued. Antacids, histamine H-2 receptor blockers,
proton pump inhibitors, sucralfate, and even local
anesthetic agents are often prescribed, but their value
is unsubstantiated. For the patient who is unable to
Journal compilation © 2009, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus
eat or drink because of the severe odynophagia, a
temporary period of parenteral hydration or alimen-
tation may be required. If strictures develop, patients
must undergo esophageal dilatation. Surgical man-
agement is necessary only if complications occur. Pre-
vention of esophagitis is the best treatment of this
disease. Patients should be advised to take their medi-
cation with sufficient amount of water and to have
enough time before recumbency. Additionally, liquid
forms of drugs must be preferred mainly for elderly
patients with cardiomegaly or motility disorders.
Nonsteroidal anti-inflammatory agents should be
used with caution in patients with symptoms of gas-
troesophageal reflux.
References
1 Kikendall J W, Arnold G F, Oyewole M A, Fleischer D,
Johnson L F. Pill-induced esophageal injury. Case reports and
review of the medical literature. Dig Dis Sci 1983; 28: 174–82.
2 Bott S, Prakash C, McCallum R W. Medication-induced
esophageal injury: survey of the literature. Am J Gastroenterol
1987; 82: 758–63.
3 Heller J R, Fellows I W, Ogilvie A L, Atkinson M. Non-
steroidal anti-inflammatory drugs and benign oesophageal
stricture. BMJ 1982; 285: 167–8.
4 Collins F J, Matthews H R, Baker S E, Strakova J M. Drug-
induced oesophageal injury. BMJ 1979; 1: 1673–6.
5 Parfitt J R, Jayakumar S, Driman D K. Mycophenolate
mofetil-related gastrointestinal mucosal injury: variable injury
patterns, including graft-versus-host disease-like changes. Am J
Surg Pathol 2008; 1367–72.
6 Loft D E, Stubington S, Clark C, Rees W D W. Oesophageal
ulcer caused by warfarin. Postgrad Med J 1989; 65: 258–9.
7 Gulsen M T, Buyukberber N M, Karaca M, Kadayifci A.
Cypoterone acetate and ethinylestradiol-induced pill oesoph-
agitis. A case report. Int J Clin Pract Suppl 2005; 147: 79–
81.
8 Smith S J, Lee A J, Maddix D S, Chow A W. Pill-induced
esophagitis caused by oral rifampin. Ann Pharmacother 1999;
33: 27–31.
9 Adachi W, Watanabe H, Yasawa K et al. A case of pill-induced
esophagitis with mucosal dissection. Diagn Ther Endosc 1998;
4: 149–53.
10 Bonavina L, Demeester T R, McChesney R, Schwizer W,
Albertucci M, Bailey R T. Drug induced esophageal strictures.
Ann Surg 1987; 206: 173–83.
11 Hughes R. Drug-induced oesophageal injury. BMJ 1979; 2:
132.
12 Abbarah T R, Fredell J E, Ellenz G B. Ulceration by oral
ferrous sulfate. JAMA 1976; 236: 2320.
13 Mittal R K, Siskind B N, Hongo M, Flye M W, McCallum
R W. Dysphagia aortica. Clinical, radiological and manometric
findings. Dig Dis Sci 1986; 31: 379–84.
14 Helm J F, Dodds W J, Pelc L R, Palmer D W, Hogan W J,
Teeter B C. Effect of esophageal emptying and saliva on clear-
ance of acid from the esophagus. N Engl J Med 1984; 310:
284–8.
15 Humphries T J, Castell D O. Pressure profile of esophageal
peristalsis in normal humans as measured by direct intraesoph-
ageal transducers. Am J Dig Dis 1977; 22: 641–5.
16 Fellows I W, Atkinson M, Ogilvie A L. Oesophageal stricture
associated with emepronium bromide therapy. BMJ 1982; 58:
43–4.
17 Pilbrant A. Ulceration due to emepronium bromide tablets.
Lancet 1977; 1: 749.
18 Lauder A D. Cetiprin and oesophageal ulceration. BMJ 1979;
2: 211.
19 Parfitt J R, Driman D K. Pathological effects of drugs on the
gastrointestinal tract: a review. Hum Pathol 2007; 38: 527–36.
© 2009 Copyright the Authors

20 Hongo M, Traube M, McCallum R W. Comparison of effects
of nifedipine, propantheline bromide and the combination on
esophageal motor function in normal volunteers. Dig Dis Sci
1984; 29: 300–4.
21 Crowson T D, Lionel H H, Ferrante W A. Oesophageal ulcers
associated with tetracycline therapy. JAMA 1976; 235: 2747–8.
22 Leong R W, Chan F K. Drug-induced side effects affecting the
gastrointestinal tract. Expert Opin Drug Saf 2006; 5: 585–92.
23 Fraser G M, Odes H S, Krugliak P. Severe localised esophagitis
due to doxycycline. Endoscopy 1987; 19: 86.
24 Teplick J G, Teplick S K, Ominsky S H, Haskin M E. Esoph-
agitis caused by oral medication. Radiology 1980; 134: 23–5.
25 Lambert J R, Newman A. Ulceration and stricture of the
esophagus due to oral potassium chloride therapy. Am J Gas-
troenterol 1980; 73: 508–11.
26 Allen A C, Boley S J, Schultz L, Schwartz S. Potassium-
induced lesions of the small bowel. JAMA 1965; 193: 1001–6.
27 Rosental T, Adar R, Militianu J, Deutsch V. Esophageal ulcer-
ation and oral potassium chloride ingestion. Chest 1974; 65:
463–5.
28 Carlborg B. Biverkningar vid accidental losning av lakemedel I
esofagus ah bronker. Lakartidningen 1976; 73: 4201–4.
29 Evans K T, Roberts G M. Where do all the tablets go? Lancet
1976; 4: 1237–9.
30 Geagea A, Cellier C. Scope of drug-induced, infectious and
allergic esophageal injury. Curr Opin Gastroenterol 2008; 24:
496–501.
31 McCall A J. Slow-K ulceration of oesophagus with aneurysmal
left atrium. BMJ 1975; 3: 230–1.
32 Peters J L. Benign oesophageal stricture following oral potas-
sium chloride therapy. Br J Surg 1976; 63: 698–9.
33 de Groen P C, Lubbe D F, Hirsch L J et al. Esophagitis asso-
ciated with the use of alendronate. N Engl J Med 1996; 335:
1016–21.
34 Black D M, Cummings S R, Karpf D B et al. Randomised trial
of effect of alendronate on risk of fracture in women with
existing vertebral fractures. Lancet 1996; 348: 1535–41.
35 Lanza F, Sahba B, Schwartz H et al. The upper GI safety and
tolerability of oral alendronate at a dose of 70 milligrams once
weekly: a placebo-controlled endoscopy study. Am J Gastro-
enterol 2002; 97: 58–64.
© 2009 Copyright the Authors
Journal compilation © 2009, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus
Drug-induced esophagitis 637
36 Taggart H, Bolognese M A, Lindsay R et al. Upper gas-
trointestinal tract safety of risedronate: a pooled anaylysis of 9
clincial trials. Mayo Clin Proc 2002; 77: 262–70.
37 Lanza F L, Hunt R H, Thomson A B, Provenja J M, Blank
M A. Endoscopic comparison of esophageal and gastroduode-
nal effects of risedronate and alendronate in postmenopausal
women. Gastroenterology 2000; 119: 631–8.
38 Strampel W, Emkey R, Civitelli R. Safety considerations with
biphosphonates for the treatment of osteoporosis. Drug Saf
2007; 30: 755–63.
39 Safaie-Shirazi S S, Zike W L, Brubacher M, DenBesten L.
Effect of aspirin alcohol and pepsin on mucosal permeability of
esophageal mucosa. Surg Forum 1974; 25: 335–7.
40 Kim S L, Hunter J G, Wo J M, Dvis L P, Waring J P. NSAIDs,
aspirin and esophageal strictures: are over-the-counter media-
tions harmful to the esophagus? J Clin Gastroenterol 1999; 29:
32–4.
41 Netzer P, Gschossmann J M, Staumann A, Sendesky A,
Weiman R, Schoepfer A M. Corticosteroid-dependent eosino-
philic oesophagitis: azathioprine and 6-mercaptopurine can
induce and maintain long-term remission. Eur J Gastroenterol
Hepatol 2007: 865–9.
42 Williams J G. Drug-induced oesophageal injury. BMJ 1979; 2:
273.
43 Parfitt J R, Jayakumar S, Driman D K. Mycophenolate
mofetil-related gastrointestinal mucosal injury: variable injury
patterns, including graft-versus-host disease-like changes. Am J
Surg Pathol 2008; 32: 1367–72.
44 Jaspersen D. Drug-induced oesophageal disorders: pathogen-
esis, incidence, prevention and management. Drug Saf 2000;
22: 237–49.
45 Howie A D, Strachan R W. Slow release potassium chloride
treatment. BMJ 1975; 2: 176.
46 Abid S, Mumtaz K, Jafri W et al. Pill-induced esophageal
injury: endoscopic features and clinical outcome. Endoscopy
2005; 37: 740–4.
47 Amendola M A, Spera T D. Doxycycline induced esophagitis.
JAMA 1985; 253: 1009–11.
48 Creteur V, Laufer I, Kressel H Y et al. Drug-induced esoph-
agitis detected by double-contrast radiography. Radiology
1983; 147: 365–8.