Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 67-year-old patient has had exanthema in the lower right limb since 51 years ago (16 years old at onset), which underwent repeated remission and recurrence. At present, he has bilateral symmetrical widespread infiltrating exanthema and asymmetrical marked neuralhypertrophy, and has been diagnosed typical LLs (His father had the same disease). The exanthema recurred several years ago, and the patient is being treated for Hansen's disease. He had a dark brown flat elevation with a rough surface and the size of a small finger tip in his right abdominal skin for approximately 20 years. A biopsy was performed, and the specimen was fixed in 10% formalin and paraffin sections were prepared for histopathologic examination. A part of the specimen was processed forscanning electron microscopic examination. Seborrheic keratosis was diagnosed by H & E staining. Acid-fast (FITE) staining, immunohistochemical staining (keratin, S-100 protein, anti-PGL antibody and anti-BCG antibody) and scanning electron microscopy revealed the presence of bacteria (M. leprae) in the dermal foam cells, the matrix with a banded structure and the squamous epithelial cells which normally lack phagocytosis function. Compared to the basal cells of normal epidermis, the basal cells located adjacent to the dermis affected with seborrheic keratosis showed increased proliferation and more marked characteristics of a germinative cell. The degree of differentiation of the basal cells appeared regressed, and they probably possessed augmented phagocytic activity. The phagocytosed bacteria were probably carried by the epidermal cell cycle toward the surface layer. However, bacteria could not be found in the stratum corneum, probably due to an association with the lysosome.
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PMID:[Intraepidermal mass of M. leprae in a case of seborrheic keratosis due to Hansen's disease (LLs)]. 858 83

A clinical diagnosis of lentigo maligna at an early stage is often difficult even for experienced dermatologists. Differential diagnoses would include solar lentigo, early lesions of seborrheic keratosis, lichen planus-like keratosis, pigmented actinic keratosis and melanocytic nevus. Dermoscopy has been shown to have higher diagnostic accuracy, especially in the diagnosis of pigmented skin lesions, in the past two decades. To aim of the present study was to review the diagnostic key points on dermoscopy in the published work to differentiate lentigo maligna from other differential diagnoses and reassess these important features on dermoscopy for specificity by describing the findings in detail. Diagnostic key points for lentigo maligna/lentigo maligna melanoma on dermoscopy are asymmetrical pigmented follicular openings, rhomboidal structures, annular-granular structures and gray pseudo-network. Lentigo maligna, at first, seems to occur as asymmetrical pigmented follicular openings and/or annular-granular structures, then expand and develop into the rhomboidal structures. Annular-granular structures and gray pseudo-network seem to be observed also in regressive areas of solar lentigo/initial seborrheic keratosis, lichen planus-like keratosis and pigmented actinic keratosis. The four important criteria on dermoscopy for the diagnosis of lentigo maligna have been reviewed, and the former two criteria seem to be more specific, but it might be difficult to recognize these findings without misinterpretation. The latter two seem to be not so specific as they would also be demonstrated in other pigmented epidermal lesions, although the distribution of the structures in these disorders would be inclined to be more homogeneous than that of lentigo maligna.
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PMID:Key points in dermoscopic differentiation between lentigo maligna and solar lentigo. 2117 56