Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperpigmentation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMed1982

Fanconi's anemia. Tumor-like warts, hyperpigmentation associated with deranged keratinocytes, and depressed cell-mediated immunity.

A 27-year-old man had had Fanconi's anemia (FA) for 20 years. The patient had pancytopenia, retarded growth, hypogonadism, and chromosomal aberrations. He had freckle-like and darker pigmented macules scattered on his chest, shoulders, upper part of the back, and hips, with interspersed, hypopigmented areas. Biopsy specimens taken from both the hyperpigmented and hypopigmented spots showed a derangement of keratinocytes and nuclear abnormalities, more notable on sun-exposed skin sites. The patient also had numerous tumor-like, recalcitrant, viral warts. Immunologic studies showed normal humoral immunity, but there was evidence of depressed cell-mediated immunity. We speculate that the chromosomal aberrations, the depressed cell-mediated immunity, and the increased frequency of malignant neoplasms known to occur in patients with FA also reflect changes related to an increased susceptibility to viral infections.

Adult↗
PubMed2001

Hyperpigmentation in the Silkie fowl correlates with abnormal migration of fate-restricted melanoblasts and loss of environmental barrier molecules.

In most homeothermic vertebrates, pigment cells are confined to the skin. Recent studies show that the fate-restricted melanoblast (pigment cell precursor) is the only neural crest lineage that can exploit the dorsolateral path between the ectoderm and somite into the dermis, thereby excluding neurons and glial cells from the skin. This does not explain why melanoblasts do not generally migrate ventrally into the region where neurons and glial cell derivatives of the neural crest differentiate, or why melanoblasts do not escape from the dorsolateral path once they have arrived at this destination. To answer these questions we have studied melanogenesis in the Silkie fowl, which is a naturally occurring chicken mutant in which pigment cells occupy most connective tissues, thereby giving them a dramatic blue-black cast. By using markers for neural crest cells (HNK-1) and melanoblasts (Smyth line serum), we have documented the development of the Silkie pigment pattern. The initial dispersal of melanoblasts is the same in the Silkie fowl as in Lightbrown Leghorn (LBL), White Leghorn (WLH), and quail embryos. However, by stage 22, when all ventral neural crest cell migration has ceased in the WLH, melanoblasts in the Silkie embryo continue to migrate between the neural tube and somites to occupy the sclerotome. This late ventral migration was confirmed by filling the lumen of the neural tube with DiI at stage 19 and observing the embryos at stage 26. No DiI-labeled cells were observed in the sclerotome of LBL embryos, whereas in the Silkie embryos DiI-filled cells were found as far ventral as the mesentery. In addition to this extensive ventral migration, we also observed considerable migration of melanoblasts from the distal end of the dorsolateral space into the somatic mesoderm (the future parietal peritoneum), and into the more medioventral regions where they accumulated around the dorsal aorta and the kidney. The ability of melanoblasts in the Silkie embryos to migrate ventrally along the neural tube and medially from the dorsolateral space is correlated with a lack of peanut agglutinin (PNA) -binding barrier tissues, which are present in the LBL embryo. The abnormal pattern of melanoblast migration in the Silkie embryo is further exaggerated by the fact that the melanoblasts continue to divide, as evidenced by BrdU incorporation (but the rate of incorporation is not greater than seen in the LBL). Results from heterospecific grafting studies and cell cultures of WLH and Silkie neural crest cells support the notion that the Silkie phenotype is brought about by an environmental difference rather than a neural crest-specific defect. We conclude that melanoblasts are normally constrained to migrate only in the dorsolateral path, and once in that path they generally do not escape it. We further conclude that the barriers that normally restrain melanoblast migration in the chicken are not present in the Silkie fowl. We are now actively investigating the nature of this barrier molecule to complete our understanding of melanoblast migration and patterning.

Animals↗
PubMed1978

Hyperpigmentation after bleomycin therapy. Ultrastructural study.

Pigmentation in a Causasian male, resulting from bleomycin therapy for Hodgkin's disease, has been studied ultrastructurally. The melanocytes, though present in normal numbers, showed several abnormalities; the endoplasmic reticulum and the Golgi apparatus were were well developed and the mitochondria were enlarged. Lipid inclusions in the endoplasmic reticulum and numerous autophagocytic vacuoles, some containing lipids were observed. Transfer of melanosomes to keratinocytes appeared to be increased. The melanosomes, which measured less than 0.55 mu were dispersed in the cytoplasm and did not form complexes, as has been observed with nitrogen mustard. The increase of melanocytic activity and the disturbance of melanosome transfer are discussed.

Adult↗