Melanosis coli

The most common cause of melanosis coli is the extended use of laxatives, and commonly anthraquinone containing laxatives such as senna, aloe vera and other plant glycosides.[1] The anthranoid laxatives pass through the gastrointestinal tract unabsorbed until they reach the large intestine, where they are changed into their active forms. The resulting active compounds cause damage to the cells in the lining of the intestine and leads to apoptosis (a form of cell death). The damaged (apoptotic) cells appear as darkly pigmented bodies that may be taken up by scavenger cells known as macrophages. When enough cells have been damaged, the characteristic pigmentation of the bowel wall develops. The condition can develop after just a few months of laxative use.[2]

However, other causes are identified, including an increase in colonic epithelial apoptosis.[3] Endoscopically, the mucosa may show a brownish discoloration in a moiré pattern.

On biopsy, melanosis coli shows characteristic pigment-laden macrophages within the mucosa on PAS staining.[4]

The histologic differential diagnosis of mucosal pigmentation is: lipofuscin (melanosis coli), hemosiderin-laden macrophages, and melanin (rare).

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  Micrograph showing melanosis coli, which appears as brown pigmentation in the macrophages in the lamina propria.
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  Micrograph of melanosis coli. H&E stain.
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  Micrograph of melanosis coli. H&E stain.

No adverse effects or consequences of melanosis coli have been identified.[4]

The condition is unrelated to true melanoses, such as Peutz–Jeghers syndrome and smoker's melanosis.[5]

Peutz–Jeghers syndrome causes pigmentation of the skin and mucous surfaces with melanin, and polyps in the digestive tract.

Pseudomelanoses of other parts of the gastrointestinal tract have also been reported, and are of unclear relevance.[6]

Patients with colostomies can have melanosis involving the stoma, which is also of no significance.[7]