The pigment of melanosis coli: a lectin histochemical study.

BACKGROUND: The compositional nature of the pigment of melanosis coli is essentially unknown. Previous histochemical studies suggested that this pigment has certain similarities with lipofuscin (i.e., age-dependent pigment) and ceroids (i.e., pathologically derived pigments) and that it may contain, therefore, polymerized glycolipids and glycoproteins. However, the saccharide composition of this pigment was never explored by lectin histochemical procedures, which was the main object of this study. METHODS: Colonoscopic biopsy specimens from eight patients with melanosis coli and from three normal control subjects were studied by fluorescent microscopy and by standard and lectin histochemistry. The number of apoptoses in the lining colonic epithelium was also evaluated histologically. RESULTS: Apoptotic bodies were significantly more numerous in patients with melanosis coil than in control subjects. The pigment that accumulates in macrophages of the lamina propia showed autofluorescence, sudanophilia, acid-fastness, and positiveness to PAS and Schmorl's reactions, all of which are common to lipofuscin and ceroids, plus an intense argentaffin reaction abolished by bleaching, indicative of a melanic substance. Lectin histochemistry showed, in decreasing order of frequency, the presence of alpha-D-mannose, sialic acid, beta-D-galactose (lactose), gal-beta-(1-3)acetyl-galactosamine, alpha-D-galactose, and alpha-L-fucose, but no terminal alpha-D-acetyl-galactosaminyl residues. CONCLUSIONS: The significant increase of apoptotic bodies in the lining colonic epithelium indicated that this type of cell death is not due to the natural programmed cell renewal, but to the action of laxatives. Because the autofluorescent pigment of melanosis coli contains melanin (as well as glycoconjugates) and is not dependent on age but on the use of anthranoid laxatives, it should be categorized as a "melanized ceroid." The lectin affinities of this pigment indicated that it contains a substantial number of saccharide residues almost similar to those found in the ceroid pigment of human aortic atheromas. These findings and considerations on the metabolism and pharmacokinetics of anthranoids suggested that the apoptotic epithelial cells, rather than the laxatives, may be the source of the pigment saccharides, whereas the precursors of the melanic substance may be derived from the anthranoids.

Lectin histochemistry of lipofuscin and certain ceroid pigments.

Little is known at present about the saccharide components of lipofuscin (age pigment) and ceroid pigments in situ. The purpose of this study was, therefore, to study in detail the lectin reactivities of lipofuscin in neurons and cardiac myocytes of old humans and rats. In addition, those of diverse ceroid pigments found in human aortic atheromas, in the livers of choline-deficient rats, in the uteri of vitamin E-deficient rats and in the crushed epididymal fat pad of rats, are included. Cryostat and deparaffinized sections from all these tissues were either extracted with a solvent mixture of chloroform-methanol-water (10:10:3, v/v) and incubated with 7 different biotinylated lectins or left untreated. Delipidation was done in order to study whether it was possible to discriminate between the saccharide moieties of glycolipids and glycoproteins of lipofuscin and ceroid pigments in situ. Other similarly treated sections were used to study the autofluorescence, sudanophilia, acid-fastness and reactivity to PAS. The frequency and intensity of lectin binding and standard histochemical properties of all the pigments were evaluated semi-quantitatively and blind. The results indicated that mannose was in general the most consistently detected sugar residue in lipofuscin granules of humans and rats, and that this pigment may also contain acetylglucosamine, acetylgalactosamine, sialic acid, galactose and fucose. However, notable differences were found not only in the lipofuscin saccharide components of different cell types of humans and rats, but also in those in the same type of cells in both species. Although mannose was not detected in the hepatic ceroid of choline-deficient rats, this saccharide moiety was almost always present in the other ceroid pigments. Each of the ceroids also contained other types of saccharides although the frequency of the latter varied between different ceroid pigments. While lipofuscin and each of the ceroid pigments showed somewhat different lectin binding patterns, the variability in the frequency of reactivity to lectins suggests that these patterns may not be permanent but transient. In this sense, it appears that lectin histochemistry may not allow these pigments to be differentiated. Furthermore, the extractive procedures used in this study did not enable us to determine whether the saccharides detected in the pigments in situ corresponded to glycolipids or glycoproteins.

Clofazimine crystals and ceroid bodies in nerve: a case report

Clofazimina in one of the most widely used in leprosy bacause of its anti-bacteriostatic and anti-inflammatory activit deposition of clofaznine has been reported in various organs and body tissues, however, the authors think the deposition of clofazinime crystals in nerve tissue, as fas as we know has never been reported.

Hermansky-Pudlak syndrome: case report and clinicopathologic review.

The Hermansky-Pudlak syndrome is an autosomal recessive disorder consisting of the triad of albinism, a bleeding diathesis, and ceroid deposition within the reticuloendothelial system. In this study of a patient with Hermansky-Pudlak syndrome, we demonstrate the presence of ceroid within dermal macrophages. Electron microscopic studies suggest that melanosomes may be a substrate for the formation of ceroid in the skin. A review of the clinical and pathophysiologic features of this disorder is presented.

Reliability of absent platelet dense bodies as a diagnostic criterion for Hermansky-Pudlak syndrome.

The clinical, pigmentary, and ceroid storage manifestations of the Hermansky-Pudlak syndrome (HPS) triad of albinism, hemorrhagic diathesis, and ceroid storage disease are variable. Therefore, a rapid and accurate method of diagnosing HPS is needed. Platelets of 66 albinos were examined by electron microscopy for the presence or absence of dense bodies. Results show that patients reexamined over a period of 1 year had consistent findings. Those lacking dense bodies (15) when first examined also lacked dense bodies when reexamined a year later, and they had evidence of ceroid storage. Those with dense bodies when first examined (8) also had dense bodies when reexamined, did not have evidence of storage disease, and had types of albinism other than HPS. Of 20 propositi lacking dense bodies, all 32 albino relatives also lacked dense bodies, while 6 albino relatives of 6 propositi with dense bodies also had dense bodies in their platelets. The evidence supports the concept that HPS is a distinct genetic and biochemical disease in which the components of the triad are the result of a single genetic defect, either a point mutation or a small deletion. Comparison of whole mount preparations with thin section preparations of 13 albinos shows that whole mount preparations are an accurate and rapid method for diagnosing HPS. The most consistent diagnostic feature of HPS is lack of platelet dense bodies.

Hermansky-Pudlak syndrome. Pulmonary manifestations of a ceroid storage disorder.

The Hermansky-Pudlak syndrome is a form of oculocutaneous albinism, characterized by a qualitative platelet defect and deposition of ceroid-like material throughout the reticuloendothelial system. During a 16 month period five patients with Hermansky-Pudlak syndrome presented with symptoms, chest films and pulmonary function studies consistent with restrictive pulmonary disease. In two patients, lung biopsies revealed diffuse interstitial fibrosis. However, light and electron microscopy demonstrated ceroid-like material within alveolar macrophages. In addition, two patients presented with inflammatory bowel disease with deposition of ceroid-like material in the colon. This disorder appears to be more common than is currently recognized and should be considered in the differential diagnosis of diffuse interstitial pulmonary disease and inflammatory bowel disease. A relationship between the deposition of ceroid-like material and pulmonary fibrosis is discussed in light of recent research concerning inflammatory processes. In view of the serious pulmonary, gastrointestinal and hematologic consequences of this syndrome, there is a need for genetic counseling of these patients.