Colonic melanosis was first reported in literature about 140 years ago by Cruveilhier, who described it in a patient with chronic diarrhea in which "the inner surface of the large intestine was black as" China ink ". Rudolf Virchow subsequently demonstrated the black pigment in the colon in an autopsy specimen and defined the condition "melanosis coli". Since then, the colon's melanosis has remained a medical curiosity.
Optical microscopy: histology, pigment-induced
macrophages in brown
Over the past fifty years, excellent publications have documented the evolution of the concepts of the etiology of melanosis by discussing the clinical observations of large numbers of patients. These and many other minor studies have contributed to what is the current concept of melanosis coli, namely that it is a benign condition in people who use catarrhs of the anthraquinone type, including the cascara sagrada, the senna, the aloe, rhubarb and frangula (constipation and its_cura). In almost all cases it is completely reversible. The age of the patients is different, but in general they are adults in old age. There are experimental clinical demonstrations that the use of anthraquinone cathartics in the presence of chronic fecal stasis is the cause of chronic melanosis. The shortest time needed for the appearance of melanosis coli in a patient who takes cascara preparation is four months and the longest is thirteen months (on average nine months).
In addition to cases of laxative abuse, melanosis appears in about half of patients with carcinoma of the large intestine. It is not sure how many
of these subjects took laxatives. However, the incidence of intestinal carcinoma
in patients with proven colonic melanosis is low and most authors deny that
there is a direct relationship. The melanin pigment can be distributed
throughout the body, but is observed above all in the cecum and in the rectum.
When melanosis is associated with a partially obstructing colon carcinoma, the
pigment is more intense in the site next to the tumor. Melanosis is specifically
linked to the abuse of laxatives and more intense above the anal sphincter and
less higher in the sigma.
A pigment similar to that of melanosis has been shown in the appendix, in the mesenteric lymph nodes in the terminal ileum and in the liver. A dark pigment similar to that of melanosis and which may be a lipofuscin was highlighted in the esophagus in association with esophagitis. The duodenum melanosis has been described as due to the accumulation of true melanin. The diagnosis of melanosis coli is usually performed in sigmoidoscopy. The color can vary from light brown to dark brown or black. The darker areas are divided into polyhedral squares with lighter colored stripes. Non-pigmented areas derive from a different degree of pigment deposition. The lymphoid submucous follicles are not pigmented and therefore appear as lighter areas on the dark surface. The mucous polyps of the areas of melanosis do not macroscopically contain the pigment and may have an intensely pink appearance in the dark background.
Colonoscopy: colonscopy appearance of the
colonic mucosa with melanotic pigment
Microscopic evaluation of a mucosal biopsy with colonic melanosis shows that
epithelial cells are normal. Occasionally the submucosa can be thickened and
edematous with large cells. The main finding consists of an increased number of
large mononuclear cells or macrophages in the lamina propria, many of which
contain the melanotic-black pigment. These macrophages are located mainly
between the crypts. The pigment cells can be microscopically highlighted even in
the absence of macroscopic melanosis. Four histological grades of melanosis have
been defined as Grade 1 variants, with only a few cells containing pigment
granules, up to grade 4, in which the pigmented cells are extended and are
located below the muscularis mucosae, lymphatic vessels and regional lymph nodes
. This classification has only a descriptive meaning. Recent attempts to
characterize the pigment of melanosis coli have only contributed to confirm that
the pigment exhibits the reactions of both melanin and lipofuscin. An origin
from degenerate mitochondria, endoplasmic reticulum and glycogen has been
suggested.
However, recent observations with an electron microscope have indicated that the
pigment can be derived from abnormal lysosomes. Special staining techniques have
demonstrated a normal enzymatic activity of the neurons in the submucosal plexus
in patients with colic melanosis. Therefore, it is probable that a broad
spectrum of colon alterations may be induced by anthraquinone laxatives, which
may lead to an accumulation of pigment or an altered neural function or both.
This group of laxatives can therefore lead to melanosis coli, an increase in fat
in the submucosa, atrophy of "smooth muscle and damage to intrinsic
innervation.When there is a predominance of these last two aspects, the function
of the large intestine is altered, as discussed elsewhere.The evidence of
melanosis coli on a patient must immediately pose the problem on the harmful use
of laxatives and symptoms of faecal stasis.In the absence of a history of abuse
of anthraquinone laxatives, the finding of melanosis coli it requires further
evaluation for the investigation of malignant neoplasm of the large intestine.