As anomalias vasculares (AVs) incluem um grupo de lesões distintas, como as más formações congênitas e os tumores vasculares benignos ou malignos. Estas lesões podem apresentar características clínicas e histopatológicas semelhantes, ocasionando equívocos diagnósticos e terapêuticos. Uma investigação precisa e o uso de terminologia adequada são fundamentais para as decisões do profissional responsável pelo acompanhamento da evolução de uma AV. A isoforma 1 da proteína humana transportadora de glicose (GLUT1) tem sido proposta como uma ferramenta auxiliar para o estabelecimento de diagnóstico diferencial entre AVs, uma vez que representa um marcador sensível e específico para a identificação de hemangiomas da infância de qualquer órgão. Este estudo objetiva fazer uma revisão da literatura acerca desta proteína como ferramenta eficaz na identificação e no possível diagnóstico diferencial entre as diversas AVs.

Vascular anomalies (VAs) include a group of distinct lesions, such as vascular system congenital malformations, as well as benign and malignant vascular tumors. These lesions may present similar clinical and histopathological features, leading to mistaken diagnoses and incorrect treatment choices. It is important that professionals responsible for monitoring the development of VAs conduct precise investigations and use the appropriate terminology. The human glucose transporter protein isoform 1 (GLUT1) has been proposed as a tool to aid in differential diagnosis between different VAs, given that it is a sensitive and specific marker for identification of infantile hemangiomas (HIs) in any organ. This article presents a review of the literature on this protein as an effective tool for identification and possible differential diagnosis between several VAs.

The aim of this study was to assess the effect of different remineralizing agents on enamel microhardness (KHN) and surface topography after an erosive challenge. Forty-eight human enamel specimens (4 × 4 mm) were randomly assigned to 4 groups: control (no treatment), fluoride varnish, calcium nanophosphate paste and casein phosphopeptide-amorphous calcium phosphate paste (CPP-ACP). Both pastes were applied for 5 minutes, and fluoride varnish, for 24 h. Four daily erosive cycles of 5 minutes of immersion in a cola drink and 2 h in artificial saliva were conducted for 5 days. KHN readings were performed at baseline and after 5 days. The percentage of enamel hardness change (%KHN) was obtained after erosion. The surface topography was evaluated by atomic force microscopy (AFM). The data were tested using ANOVA, Tukey's and paired-T tests (p < 0.05). After an erosive challenge, there was no statistically significant difference between the control (96.8 ± 11.4 KHN / 72.4 ± 3.0 %KHN) and the varnish (91.7 ± 14.1 KHN / 73.4 ± 5.5 %KHN) groups. The nanophosphate group showed lower enamel hardness loss (187.2 ± 27.9 / 49.0 ± 7.9 %KHN), compared with the CPP-ACP group (141.8 ± 16.5 / 60.6 ± 4.0 %KHN), and both were statistically different from the varnish and the control groups. AFM images showed a rough surface for the control and the varnish groups, a non-homogeneous layer with globular irregularities for CPP-ACP, and a thick homogeneous layer for the nanophosphate group. None of the agents provided protection against the development of erosion; however, nanophosphate paste was able to reduce enamel surface softening after the erosive challenge