This is dark pigment staining of the colonic wall is known as melanosis coli, the term initially established by Dr. Rudolf Virchow in 1870. While the name has persisted it has long been recognized that the pigment staining is not due to increased melanin deposits as initially thought but instead due to lipofuscin, a cellular degradation product. The lipofuscin is found in histiocytes or macrophages and is thought to represent degradation products from cells undergoing apoptosis. The association between melanosis coli and the use of cathartics that contain the active ingredient, anthraquinone, has been established. In laboratory settings, anthraquinones causes apoptosis of guinea pig enterocytes leading to lipofuscin accumulation. The pigment accumulation is documented to be reversible if intake of the offending agent is avoided. Melanosis typically is most intense in the cecum and diminishes in intensity down the length of the colon. Characteristically, the terminal ileum is devoid of any pigment uptake as seen here.
OK so why this pattern. What can we learn about melanosis by looking closely at this endoscopic picture? First on low power, we can identify lymphoid aggregates and see that they are devoid of any lipofuskin pigment. On high power, we again can see that these lymphoid aggregates are free of pigment but are in fact surrounded by pigment laden histiocytes which crowd around the periphery. Back again to low power view, we can clearly see that the pigment is located entirely in the lamina propria sparing the pits as well as the lymphoid aggregates. Thus returning to the endoscopic picture, we now understand that the pigment-free areas here are the lymphoid aggregates and that the surrounding brown halo is comprised of pigmented laden histiocytes. Furthermore, with magnification, we appreciate this geographic pattern of white dots which we known are the epithelial pits. The brown staining around the pits represents the pigment laden histiocytes in the surrounding lamina propria.
This second example demonstrates even more intense pigment accumulation in the colon. Here the cecal epithelium is so pigment congested, that it is difficult for the endoscope processor to generate adequate illumination. This polypoid structure stands out due to the absence of pigment. Because it is suspected of being a polyp it is removed by cold snare cautery and sent for pathologic examination. Pathology demonstrated this to be comprised of prominent fibro-adipose tissue of the submucosa lined by attenuated mucosa. Prominence of fibro-adipose in the submucosa can be seen as a normal finding in the right colon.
Unanswered questions remain about this common and commonly ignored finding. Why is the small bowel completely spared of pigment? Does everyone who consumes these anthracene containing laxatives develop the congestion of lipofuscin or this a consequence of some metabolic or enzymatic defect? And finally, what is the relationship between these lymphoid aggregates and their halo of congested histiocytes; who attracts who?
Peter B. Kelsey, M.D., Harvard Medical School, Massachusetts General Hospital
Mari Mino-Kenudson, M.D., Harvard Medical School, Massachusetts General Hospital