Histopathological Changes in the Gastrointestinal Tract Due to Medications

Abstract

In keeping with the stated goal of providing the surgical pathologist with tools to recognize abnormalities of the gastrointestinal (GI) tract due to drugs (AGIDS), in part II of this review we embark in a more organ-based description of AGIDS. Adequate space is given to the numerous adverse gastrointestinal effects of nonsteroidal anti-inflammatory drugs. Pill esophagitis, esophagitis dissecans, proton pump inhibitors' effects, diaphragm disease, and the recently described effects of drugs such as olmesartan, mycophenolate, and of compounds such as yttrium-90 are highlighted among several others. The inclusion of drug effects in the differential diagnosis of "conventional" diseases (such as gastric antral vascular ectasia, graft-versus-host disease, ischemic colitis, acute colitis, collagenous enteritis, inflammatory bowel disease) is underscored to avoid sometimes significant diagnostic pitfalls. We reiterate the message of the necessary collaboration between pathologist and clinician in the recognition of these entities to provide the best patient care.

Apoptotic enteropathy caused by antimetabolites and TNF-α antagonists

“…Interestingly, olmesartan, another antihypertensive drug of the same family, was previously shown to cause diarrhoea. However, olmesartan-related histological changes are characterised by sprue-like villous atrophy in the small intestine and lymphocytic and collagenous colitis in the colon,10 11 which differ from those observed in the patient described here. Moreover, losartan intake in this case was not temporally related to the patient's gastrointestinal symptoms.…”

Diagnosing Celiac Disease: Role of the Pathologists

“…Some drugs, such as nonsteroidal antiinflammatory drugs (NSAIDs) or proton pump inhibitors can cause increased IEL numbers, and some drugs are also capable of causing small intestinal villous atrophy (e.g. azathioprin, colchicine, ipilimumab, mycophenolate, NSAIDs, olmesartan) [40,41]. Tropical sprue is an endemic malabsorption syndrome with histology similar to CD, although total villous atrophy is rare and changes are equally prominent in the jejunum and ileum in addition to the duodenum [42].…”

The Ever-Changing Landscape of Drug-Induced Injury of the Lower Gastrointestinal Tract

“…8 The most common pattern is the one mimicking mild (grades 1-2) GVHD. 2 In both entities, the colonic mucosa shows increased apoptosis at the crypt bases, normal or mildly distorted crypt architecture, mild epithelial regenerative atypia, and occasional ''damaged crypts'' (dilated crypts with flattened epithelium and eosinophilic luminal debris; Figure 2, A and B). However, in MFA-associated colitis, the lamina propria shows significantly more eosinophils within the lamina propria compared with GVHD, but no significant increase in lymphocytes, plasma cells, neutrophils, or mast cells.…”

“…However, with the increased use of enteric-coated, slow-release preparations and enemas, lower GI tract involvement has become more common. In the colon, not only can NSAIDs cause direct mucosal injury, but they can also aggravate preexisting conditions (ie, diverticulitis, IBD) 2 and significantly increase the risk of injury by other concurrently administered medications. In the colon, NSAIDs cause toxicity mostly by inhibition of COX2 and reduced production of prostaglandins rather than contact irritation.…”

“…In these areas the mucosa shows architectural distortion and hamartoma-like changes, with a mixture of smooth muscle, nerves, ganglion cells, and blood vessels, and mild acute inflammation. 2 Diaphragm disease can progress to significant strictures and bowel obstruction, which may necessitate endoscopic or surgical intervention. Nonsteroidal anti-inflammatory drugs can also induce different patterns of colitis, including microscopic colitis (lymphocytic or collagenous), focal active colitis, IBD-like colitis, or ischemic colitis 2 (discussed in subsequent sections).…”