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At least 847 records · Page 47Linked to original sources
PubMed2003

A study of 124 Indian patients with lichen planus pigmentosus.

Lichen planus pigmentosus is a fairly common disorder of pigmentation in Indians, but reports comprising a sizeable number of patients are lacking in the literature. We now describe the clinical and epidemiological features and histopathological findings for 124 lichen planus pigmentosus patients. A retrospective analysis of medical records of patients attending our centre during the past 12 years was undertaken. Of the 124 patients (56 male, 68 female), the majority (48.4%) had the disease for 6 months to 3 years. The face and neck were the commonest sites affected with pigmentation varying from slate grey to brownish-black. The pattern of pigmentation was mostly diffuse (77.4%), followed by reticular (9.7%), blotchy (7.3%) and perifollicular (5.6%). Lichen planus was noted in 19 patients with typical histopathological changes of the disorder. Lichen planus pigmentosus, a distinct clinical entity commonly encountered in the Indian population, should be considered in the spectrum of lichenoid disorders as a variant of lichen planus.

Adolescent↗
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↗
PubMed1985

Trisomy 14 mosaicism with t(14;15)(q11;p11) in offspring of a balanced translocation carrier mother.

A 2-year-old girl with growth and developmental retardation, minor facial anomalies, asymmetry of face and body, tetralogy of Fallot, and reticular hyperpigmentation of the skin was found to have mosaic trisomy 14 involving a t(14;15)(q11;p11). The patient showed mosaicism for 46,XX cell line, apparently resulting from a break of the translocation chromosome and a subsequent loss of 14q. The mother has a balanced translocation t(14;15)(q11;p11). Inherited trisomy 14 has not been reported previously.

Abnormalities, Multiple↗