Drug-induced injury of the gastrointestinal tract is increasingly
common but generally under-recognized. Within the esophagus, abnormalities are
commonly referred to as “nonspecific pill esophagitis”,
characterized by erosions, ulcers or occasionally strictures. Alendronate,
doxycycline, and potassium chloride have been identified as potential causes
[1].
A 63-year-old man who was on long-term calcineurin inhibitor
(cyclosporine) therapy due to heart transplantation 12 years earlier, presented
with retrosternal pain, odynophagia, and dysphagia. Laboratory tests were
unremarkable. The oral cavity was normal on inspection. Endoscopy disclosed
multiple glassy polyps measuring up to 5 mm in diameter within the
esophagus ([Fig. 1 a]), of which three were
removed by snare polypectomy.
Fig. 1 Calcineurin inhibitor
therapy-associated polyps. a Multiple glassy polyps are
detected within the esophagus. b Endoscopic ultrasound
shows thickening and splitting of the submucosal layer.
Endoscopic ultrasound showed thickening and splitting of the
submucosal layer ([Fig. 1 b]). Histology
revealed massive subepithelial matrix accumulation with edema, fibrosis, and
patchy mixed inflammatory infiltrate ([Fig. 2]).
Fig. 2 Histology of calcineurin
inhibitor therapy-associated polyps. Hematoxylin and eosin-stained section
shows massive subepithelial matrix accumulation with edema, fibrosis, and
patchy mixed inflammatory infiltrate.
Cyclosporine was changed to tacrolimus, and the patient was put on
symptomatic therapy with sucralfate. At control endoscopy 6 months later, the
number and size of the polyps had markedly decreased and the patient was
asymptomatic ([Fig. 3]).
Fig. 3 After 6 months and a
change from cyclosporine to tacrolimus, control endoscopy shows marked
regression in the number and size of esophageal polyps.
Gingival overgrowth represents a well recognized side effect of
long-term calcineurin inhibitor therapy, occurring in up to 70 %
of transplant patients [2]
[3]. The
pathogenesis is complex, and several mechanisms have been proposed to explain
increased production of matrix and/or collagen, which is accompanied by reduced
activity of matrix metalloproteinases [4]. Less
frequently, calcineurin inhibitor therapy-associated inflammatory polyps
originate from nongingival tissues of the oral cavity, for example the tongue
or the buccal mucosa [4].
The presented case is the first to show calcineurin inhibitor
therapy-associated inflammatory polyps within the esophagus. Therapy is mainly
symptomatic. If dose reduction is not feasible in a transplant patient,
substitution with tacrolimus may be considered which, similar to cyclosporine,
can alter fibroblast metabolism, albeit to a lesser extent. In patients
suffering from autoimmune disease change to an immunosuppressant other than a
calcineurin inhibitor is recommended.
Endoscopy_UCTN_Code_CCL_1AB_2AC_3AB
