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Daub, Discolouration, Pigmentation-Solar Lentigo

Published on: 7th August, 2019

Solar lentigo is defined as an alteration in cutaneous pigment deposition on account of exposure to ultraviolet radiation. Solar lentigo is a benign, pigmented lesion with a characteristic increment in the quantification of pigmented keratinocytes. It can manifest as a dark brown spot on the skin. The benign, pigmented spot or solar lentigo or multiple solar lentigines are preponderantly delineated in the sun exposed skin in a majority (> 90%) of Caucasians above 60 years of age although younger individuals and Asians can be implicated. Solar lentigines are induced by repetitive exposure to ultraviolet light with constituent mutagenic potential. Ultraviolet radiation can induce a localized proliferation of melanocytes with a subsequent accumulation of melanin within the keratinocytes. Individuals who are genetic carriers of one or two melanocortin-1- receptor (MC1R) gene or cogent variants demonstrate a 1.5 to twice the probability of developing solar lentigines [1,2].
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The blubbery protrusions: Lipoma arborescens

Published on: 15th December, 2020

OCLC Number/Unique Identifier: 8870468711

Preface Lipoma arborescens is an exceptional condition comprised of frond-like excrescences of mature adipose tissue. The condition was originally described by Albert Hoffa in 1904 with characteristic morphology of macroscopic, villous, frond- like excrescences recapitulating a tree-like appearance, as denominated by the term “arborescens” [1]. Lipoma arborescens is additionally designated as “diffuse articular lipomatosis”, “villous lipomatous proliferation of synovial membrane” or “diffuse lipoma of joint”. The essentially benign condition appears within large joints and typically exhibits adipose tissue infiltration of sub-synovial connective tissue. Synovial sheaths of tendons are infrequently incriminated [1,2].
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The coral crunch: Amyloidoma

Published on: 20th January, 2021

OCLC Number/Unique Identifier: 8895645427

Amyloidoma is an exceptional, progressive disorder demonstrating a characteristic accumulation of significant quantities of amyloid within soft tissues. Amyloidoma is additionally nomenclated as tumoural amyloidosis, nodular amyloid or localized amyloidosis. Furthermore, insulin-derived amyloidoma is referred to as insulin ball. Amyloid is a protein polymer configured of identical monomeric protein units wherein pathological variety is articulated from misfolded proteins. In excess > of twenty three subtypes of proteins can configure amyloid fibres in vivo. Extra-cellular or intra-cellular deposition of amyloid can modify normal organ function [1]. Amyloidosis is categorized into systemic and localized subtypes. Localized amyloidosis displays a localized mass effect and demonstrates a superior prognosis. Insulin-derived amyloidosis was initially documented by Storkel, et al. in 1983 who recognized accumulated insulin- amyloid fibrils in diabetic individuals subjected to continuous infusion of porcine insulin over a period of 5 weeks or more [1,2]. Amyloid nodules may be associated with systemic amyloidosis.
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