RESUMEN
Amelanotic melanoma (AM) is one of the great masqueraders in dermatology. It is a very difficult clinical diagnosis to make because these tumors are devoid of pigment and other clues of melanoma. They are commonly misdiagnosed clinically as other benign and malignant conditions. We present a new case of AM in an 84-year-old woman with a history of non-melanoma skin cancer. She had a thin pink plaque that was initially misdiagnosed as a basal cell carcinoma. We also discuss dermoscopy and its valuable role to improve diagnostic accuracy. A review of dermoscopic features that favor and oppose the clinical diagnosis of AM is discussed. Even with dermoscopy, it is still important to have a high index of suspicion and a low threshold to biopsy when the clinical diagnosis is unclear.
J Drugs Dermatol. 2017;16(11):1164-1165.
.Asunto(s)
Melanoma Amelanótico/diagnóstico , Neoplasias Cutáneas/diagnóstico , Anciano de 80 o más Años , Dermoscopía , Diagnóstico Diferencial , Femenino , Humanos , Melanoma Amelanótico/cirugía , Neoplasias Cutáneas/cirugíaRESUMEN
Glial cells that express the NG2 proteoglycan (NG2(+) cells) are considered to be oligodendrocyte progenitors (OPCs) in the central nervous system (CNS), based on their ability to give rise to mature oligodendrocytes in vitro. To understand how dysmyelinated conditions influence OPC proliferation and differentiation, we studied proliferation and differentiation of NG2(+) OPCs in vivo in the shiverer mutant (shi), which do not form compact myelin due to a deletion in the myelin basic protein gene. Acute bromodeoxyuridine (BrdU) labeling studies revealed a 4- to 6-fold increase in NG2(+) cell proliferation in shi spinal cord between postnatal day18 (P18) and P60, and most BrdU(+) cells were NG2(+) after P18. The increased proliferation was accompanied by a 2-fold increase in the number of OPCs and oligodendrocytes. Survival studies following a single injection of BrdU at P18 revealed a decline in the number of BrdU(+)/NG2(+) cells with a concomitant increase in the number of BrdU(+) oligodendrocytes over time, suggesting that the proliferated NG2(+) cells had differentiated into oligodendrocytes. BrdU(+) oligodendrocytes were generated over a longer period of time in shi spinal cord and persisted longer in shi than in wild type spinal cord. These findings suggest that new oligodendrocytes continue to be generated in the dysmyelinated shi spinal cord by enhanced proliferation and differentiation of NG2(+) oligodendrocyte progenitor cells.