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GI Path Online

Drug related lesions of the Gastrointestinal Tract

  Dr Sampurna Roy MD      





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- Most common site of drug injury - Mid esophagus.

- Drugs dissolve & release caustic agents that can cause local damage.

- Pills tend to stick at parts of anatomic narrowing.

- Certain conditions may cause additional narrowing of the esophagus - (heart disease with left atrial enlargement, aortic aneurysms, enlarged thyroid, and enlarged lymph nodes ).

- Adverse effects of drugs is also a problem in dysmotility disorders & in the elderly.


Ulcers : ( pin point lesions to large circumferential ulcers)

- Strictures : due to potassium chloride, iron & quinidine.

- Slowing of gastric emptying results in acid reflux and reflux esophagitis.



NSAIDs damage the stomach by:

i)  Direct local toxicity to the mucosa 

ii) By inhibition of prostaglandin synthesis 
Erosions and ulcers related are  common.

Site: Antrum , body and  along the greater curvature.
Gastric lesions related to NSAIDs:
 Acute hemorrhagic gastritis, erosions, ulcers, and chemical gastritis.

Acute hemorrhagic gastritis:

Damaged surface epithelium, edema &hemorrhage of lamina propria and little inflammation.

Chemical gastritis:

Foveolar hyperplasia producing corkscrew appearance with villiform configuration. 

(Visit: Chronic Gastritis ; Helicobacter pylori  associated ( Type B) Gastritis ;

Autoimmune Gastritis  (Type A); 

Reactive /Reflux/ Chemical Gastritis (Type C) ; )

Prepyloric gastric ulcers : often multiple. Features of reactive gastritis in the adjacent mucosa. 

Antral ulceration produce cicatrizing submucosal fibrosis and prepyloric diaphragms.  

Iron is locally corrosive and is associated with erosions, ulcers, and almost infarct-like necrosis of the gastric mucosa. 

Fundic gland polyps : In patients using proton pump inhibitors like omeprazole.  Endoscopically : small bubble like polyps in the body and fundic mucosa.

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Small Intestine: 

Drug induced lesions in the small intestine:

Non-specific ulceration: (rule out Crohn's disease).

Ileal ulcers may be:

(i) Single or multiple aphthoid and punched out ulcers. 

(ii) Deeper ulceration with stricture formation.

(iii) Widespread erosion with pseudomembrane formation. 

Histologically :

Surface consists of a layer of neutrophils, deep to which is fibrinoid necrosis, granulation tissue formation and fibrotic reaction.

Perforation: Ileal ulcers may undergo perforation.

Stricture formation and diaphragm disease : NSAID induced ulcers may lead to stricture formation.

Diaphragm disease : Associated  with slow release NSAIDs and piroxicam.

Common in the distal ileum,  proximal colon and jejunum. 

Gross: Composed of multiple thin concentric luminal protrusions of fibrotic mucosa and submucosa blocking the lumen with  a small central opening.

Histologically : composed of mucosal folds with superficial ulceration , chronic  inflammation, vascular prominence and submucosal vertical fibrosis.

(Differential Diagnosis:

Absence of transmural inflammation and serosal changes rules out Crohn's disease).

Malabsorption:  NSAIDs have been associated with "NSAID enteropathy" (low grade GI blood loss, protein loss, ileal dysfunction and malabsorption with changes in intestinal permeability and inflammation).

Other drugs associated with malabsorption : Neomycin, progestational steroids and colchicine.

Mefenamic Acid Toxicity:

Hyperplastic crypts, partial villous atrophy, prominent enterocyte vacuolation, no increase in intraepithelial lymphocytes and little increase in inflammation in the lamina propria.

Progestational steroid- villous atrophy with hypoplastic crypts.

Neomycin- Mild villous atrophy.

Colchicine toxicity.

Duodenum, Jejunum and Stomach :

Increased numbers of metaphase mitoses, epithelial pseudo stratification and loss of polarity, and  increase in the proliferation zone (shown by Ki67 staining).

With therapeutic levels of colchicine - villous atrophy / hyperplasic crypt pattern with increased mitotic figures of the jejunal mucosa.

Collagenous Colitis and Lymphocytic Colitis  

Pseudomembranous Colitis


Drug induced damage in the colon :

1. Adverse effect on pre-existing disease:-

NSAIDs  associated with complications to diverticular disease :

GI hemorrhage, perforation, and fistulous tract formation.

Responsible for exacerbating preexisting inflammatory bowel disease (IBD). Analgesics may bring about relapse of ulcerative colitis.

Immunosuppressive drugs in IBD may provoke opportunistic infection.

(Example: Cytomegalo virus.)

2. Cause de novo disease:

- Ulceration & perforation:

Solitary, non- specific ulcers, usually present in the caecum following use of NSAIDs - (oxyphen butazone, diclofenac, ibuprofen), in the distal colon (naproxen,aspirin and phenylbutazone) and anorectal region (indomethacin).

- Stricures and diaphragm disease :

NSAIDs: Toxic megacolon - 

Methotrexate therapy.

- Mucosal necrosis:  

Kayexalate (sodium polystyrene sulfonate) in sorbitol.

Induce necrosis of the GIT.

Administered orally or by enema in the treatment of hyperkalemia.

Resected, long segments of  colon and rectum may be necrotic.

Ischaemic colitis: Associated with drugs that predispose to thrombosis (oral contraceptives, estrogen) and drugs that cause vasoconstriction (cocaine, amphetamines).

Histologically, characterized by damaged epithelium, decreased mucin and small shrunken crypts, dense pink lamina propria and relatively little inflammation.

Endoscopy may give rise to mucosal damage in colon.

Glutaraldehyde (to cleanse and sterilize endoscopes) may produce colitis with ischaemic features.

Indian ink and methylene blue (mark areas of colorectal mucosa during endoscopy) may produce ischaemia.

Acute "self limited" colitis associated with a number of drugs - diclofenac, naproxen, and carbamazepine.

Acute colitis is characterized by neutrophils in the lamina propria and epithelium associated with reactive epithelial changes but with minimal chronic inflammation or crypt distortion.

(Differential diagnosis: Inflammatory bowel disease ).



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Further reading:

TABLE:  Summary of histological features of drug related lesions of the large intestine

TABLE:  List of drugs related GI lesions

TABLE:  Summary of histological features of drug related lesions of the small intestine



Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)






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