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4.
Pediatr Dermatol ; 36(3): 393-394, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30811653

RESUMO

Dermoscopic findings in umbilical granuloma are vascular polymorphism comprised of linear irregular and arborizing vessels with structureless areas distributed over a milky-red background. The increase of angiogenesis and neovascularization is represented by the linear irregular and arborizing vessels. Structureless areas over an irregularly milky-red background are originated by the proliferation of vascular endothelial cells and fibroblasts, with capillary and granulation tissue formation.


Assuntos
Dermoscopia , Granuloma/patologia , Dermatopatias/patologia , Umbigo , Anti-Infecciosos Locais/uso terapêutico , Feminino , Granuloma/tratamento farmacológico , Humanos , Lactente , Nitrato de Prata/uso terapêutico , Dermatopatias/tratamento farmacológico
5.
Indian J Dermatol Venereol Leprol ; 84(3): 263-268, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29595184

RESUMO

Androgenetic alopecia is the most common form of progressive hair loss in humans. A genetic predisposition and hormonal status are considered as major risk factors for this condition. Several recent advances in molecular biology and genetics have increased our understanding of the mechanisms of hair loss in androgenetic alopecia. We review these advances and examine the trends in the genetic and molecular aspects of androgenetic alopecia.


Assuntos
Alopecia/genética , Alopecia/metabolismo , Epigênese Genética/fisiologia , Predisposição Genética para Doença/genética , Folículo Piloso/metabolismo , Alopecia/terapia , Epigênese Genética/efeitos dos fármacos , Finasterida/administração & dosagem , Estudo de Associação Genômica Ampla/métodos , Cabelo/efeitos dos fármacos , Cabelo/crescimento & desenvolvimento , Cabelo/metabolismo , Folículo Piloso/efeitos dos fármacos , Folículo Piloso/crescimento & desenvolvimento , Humanos , Minoxidil/administração & dosagem , Receptores Androgênicos/genética , Receptores Androgênicos/metabolismo
6.
Arch Med Res ; 47(3): 172-9, 2016 04.
Artigo em Inglês | MEDLINE | ID: mdl-27373815

RESUMO

BACKGROUND AND AIMS: FLT3-ITD mutations in acute myeloid leukemia (AML) are associated with a poor prognosis. In Latin America, little epidemiological data exist about these mutations and their influence on clinical evolution and prognosis. Standardization and well-established clinical correlation make FLT3 mutational analysis by molecular methods an invaluable tool to decide among treatment options and to determine AML prognosis. METHODS: We assessed the prevalence of FLT3-ITD mutations in 138 patients with AML at four hematology referral centers from Mexico and Colombia. Molecular methods based on polymerase chain reaction (PCR) were employed for determining FLT3-ITD status. RESULTS: Mutations were present in 28 patients indicating a prevalence of 20.28%. Median age was 47 years (5-96). The FLT3 mutation positive group was older, had higher WBC and hemoglobin values and lower platelet counts but without statistical significance. A not previously described mutation in the FLT3 gene was found in one patient involving a nucleotide exchange of timine for cytosine at the 66608 position. A high mortality was found in the FLT3-mutated group, 67.8 vs. 42.72% in the non-mutated group and median survival was 4.9 months vs. 20.4 months, p = 0.009. A mutated FLT3 did not confer poor prognosis to those with M3 AML. The mutated FLT3 population had poor overall survival (OS) despite hematoprogenitor stem cell transplantation (HSCT). CONCLUSION: Prevalence of FLT3-ITD mutation in AML was present in a proportion comparable to other populations and, when present, was associated with a very poor prognosis.


Assuntos
Leucemia Mieloide Aguda/enzimologia , Tirosina Quinase 3 Semelhante a fms/metabolismo , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Pré-Escolar , Análise Mutacional de DNA , Feminino , Humanos , Leucemia Mieloide Aguda/diagnóstico , Masculino , México , Pessoa de Meia-Idade , Mutação , Prognóstico , Adulto Jovem , Tirosina Quinase 3 Semelhante a fms/genética
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