COLITIS

Eosinophilic colitis is characterised by eosinophilic infiltration of the wall of the colon. Isolated involvement of the colon is rare, with the upper gastrointestinal tract typically involved as well. Diagnosis depends on the exclusion of secondary causes of eosinophilia such as parasitic infection, inflammatory bowel disease (IBD) and food allergy or drug sensitivities (common with carbmazepine, clozapine, NSAIDS, rifampicin, and tacrolimus)[1,2] Isolated involvement of the colon is rare.

The exact cause of eosinophilic colitis remains elusive. Most will have a history of atopia 75% having either eczema or asthma[1]. eosinophilic major basic protein is often raised [5], and it is likely that this condition is mediated by allergen specific T cells

CLINICAL FEATURES

Eosinophilic colitis has a bimodal pattern with peaks occurring in the neonatal period and during young adulthood[1]. The clinical presentation depends on the extent of infiltration of the bowel wall. If there is only mucosal disease then the presentation is typically of malabsorption with bloody diarrhoea. If the infiltration is deeper, and of a more chronic duration, this leads to thickening of the entire bowel wall and can cause narrowing (stenosis) of the bowel with obstructive symptoms (colicky crampy pain) [1,3,5].

DIAGNOSIS

The features that support a diagnosis of eosinophilic colitis include:

Peripheral eosinophilia – with a raided eosinophil count on blood testing.

Eosinophilic infiltration of the colon – at least 20 eosinophils per high powered field.

DIARRHOEA OR OBSTRUCTIVE BOWEL FEATURES

X-ray or CT may show circumferential bowel wall thickening [1].

Colonoscopy typically shows patchy areas of mucosal oedema, erythema and lymphonodular hyperplasia [1,2].

MANAGEMENT

Corticosteroids (prednisone) over 2 weeks are effective in over 90% of cases. Relapse after steroid treatment is common, and maintenance therapy with steroid-sparing agents such as anti-histamines (i.e. ketotifen), the leukotriene inhibitors (e.g. montelukast) may help [1].

REFERENCES

1. Okpara N, Aswad B, Baffy G. Eosinophilic colitis. World Journal of Gastroenterology. 2009;15(24):2975-2979.
2. Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol. 2004;113:11-28.
3. Velchuru VR, Khan AB, Hellquist HB et al.Eosinophilic colitis. J Gastrointestinal Surg.2007;11:1373-1375.
4. Persic M, Stimac T, Stimac D et al.Eosinophilic Colitis:A Rare Entity. Journal of Pediatric Gastroenterology and Nutrition. 2001;32:325-326.
5. Prussin C, Gonsalves N. Eosinophilic gastroenteritis. Up to Date. Sep 2010.

Microscopic colitis includes both collagenous and lymphocytic colitis – so named because of their normal macroscopic appearance at colonoscopy. Both are characterised histologically by the presence of an increased number of intra-epithelial lymphocytes. Collagenous colitis is also distinct from other forms of colitis due to the presence of a thickened collagen band in the subepithelium [1,2,3].

The cause of Microscopic Colitis is unknown, although and immune mechanism is likely. There have been multiple associations, and these include:

CLINICAL FEATURES

Eosinophilic colitis has a bimodal pattern with peaks occurring in the neonatal period and during young adulthood[1]. The clinical presentation depends on the extent of infiltration of the bowel wall. If there is only mucosal disease then the presentation is typically of malabsorption with bloody diarrhoea. If the infiltration is deeper, and of a more chronic duration, this leads to thickening of the entire bowel wall and can cause narrowing (stenosis) of the bowel with obstructive symptoms (colicky crampy pain) [1,3,5].

• Medications –Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) – such as asprin, are much more commonly ingested in individuals with microscopic colitis, with some improvement typical with cessation of NSAIDS [1,4]. Antidepressants including selective serotonin re-uptake inhibitors (SSRIs) cholesterol lowering statin drugs, and acid lowering proton pump inhibitors (PPIs) all have an association with microscopic colitis [1,4].
• Infection –It has been proposed that bacterial toxins from previous infection may be a factor.
• Bile acid malabsorption – this is based on an observed improvement in colitis with the use of bile-binders such as cholestyramine [1,4].
• Autoimmune disorders – microscopic colitis is more common in patients with other auto-immune disorders such as eczema and celiac disease [4].

CLINICAL FEATURES

Microscopic colitis is more common in females. This is particularly the case with collagenous colitis, with a 4:1 female to male ratio. The incidence of these conditions is rare ranging from 0.5 to 5% per 100,000

for Collagenous colitis and 3 to 5% per 100,000 Lymphocytic colitis [1,5]. It occurs more commonly in late adulthood, with a peak age of onset in the 6th and 7th decade.

Typically, microscopic colitis presents with the passage of frequent non-bloodied watery stools per day.

DIAGNOSIS

Blood tests that may be elevated include ESR/CRP. Auto-antibodies such as ANCA, anti-nuclear and anti-mitochondrial anti-bodies are elevated in approximately 50% of patients [1]. Faecal calprotectin levels are elevated in patients with active microscopic colitis [1].

COLONOSCOPY

The diagnosis of microscopic colitis is based upon performing colonoscopy which allows biopsy of the often normal appearing colon. This allows for microscopic (histopathological) examination. Histological changes are more pronounced in the proximal colon and so biopsies should be taken from the right colon.

Microcytic colitis typically is associated with a predominance of intra-epithelial lymphocytes (≥20 intraepithelial lymphocytes per 100 epithelial cells). Collagenous colitis also has a thickened subepithelial collagen band (≥10μm) [3].

TREATMENT

Microscopic colitis is often self-limiting, with many cases resolving spontaneously. However, relapse is reported in 30-60%[1]. There has been no documented increased risk of colorectal cancer or inflammatory bowel disease in patients with microscopic colitis.

Medications such as those listed above, should be ceased to determine if they are causative factors. Once infection has been excluded, troublesome diarrhoea can be treated with loperamide. Budesonide (9mg daily for 6 weeks) causes cure in almost 90% of patients compared with 50% without treatment [5].

REFERENCES

1. Dietrich C. Lymphocytic and collagenous colitis. Up to Date. Sep 2010.
2. Jaskiewicz MD. Microscopic colitis in routine colonoscopies. Digestive diseases and sciences. 2006;51(2):241-244.
3. Liszka L. Histopathological diagnosis of microscopic colitis. Journal of Gastroenterology and Hepatology. 2006;21:792-797.
4. Datta I. Microscopic colitis:a review for the surgical endoscopist. Canadian Journal of Surgery. 2009;52(5):167-72.
5. Chande N. Interventions for treating lymphocytic colitis. The Cochrane Database of Systematic Reviews. Vol 3 2008.