MIRIAN NACAGAMI SOTTO

(Fonte: Lattes)
Índice h a partir de 2011
17
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/53 - Laboratório de Micologia, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 3 de 3
  • article 5 Citação(ões) na Scopus
    Amantadine-Induced Livedo Racemosa
    (2016) CRIADO, Paulo Ricardo; ALAVI, Afsaneh; VALENTE, Neusa Yuriko Sakai; SOTTO, Mirian Nacagami
    Although livedo reticularis is a known adverse effect of amantadine, only limited studies have addressed this association. Livedo racemosa in contrast to livedo reticularis is characterized by a striking violaceous netlike pattern of the skin similar to livedo reticularis with a different histopathology and morphology (irregular, broken circular segments). In this case report, we present 2 cases of livedo racemosa and edema of lower extremities following amantadine treatment. The cutaneous biopsies in both cases showed intraluminal thrombi in subcutaneous blood vessels without evidence of vasculitis, which is consistent with livedo racemosa.
  • article 6 Citação(ões) na Scopus
    Unilateral Livedoid Vasculopathy Associated With Involutional Phase of Cutaneous Infantile Hemangioma: The Connection to Coagulation Disorders
    (2013) CRIADO, Paulo Ricardo; ALAVI, Afsaneh; HALPERN, Ilana; SOTTO, Mirian Nacagami; KIRSNER, Robert S.
    Livedoid vasculopathy is a bilateral painful and recurrent cutaneous ulcerative disorder of the legs that leads to atrophie blanche, atrophic white-porcelain scars, and is associated with disorders of fibrinolysis and/or coagulation. We present a young boy with an association between livedoid vasculopathy in the area of a previous involuted cutaneous hemangioma. We found 4 uncommon abnormalities associated with thrombo-occlusive events: heterozygous 20210 AG genotype of prothrombin, reduced activity of anticoagulation proteins C and S, and elevated lipoprotein (a).
  • article 11 Citação(ões) na Scopus
    Increased serum levels of vascular endothelial growth factor in pemphigus foliaceus patients with erythroderma
    (2017) MIYAMOTO, D.; SOTTO, M. N.; OTANI, C. S. V.; FUKUMORI, L. M. I.; PEREIRA, N. V.; SANTI, C. G.; MARUTA, C. W.; BURNIER, M. N. N.; REBEIS, M. M.; AOKI, V.
    Background Erythroderma is a clinical skin syndrome shared by patients with cutaneous disorders of distinct aetiologies as a result of the combined actions of chemokines, adhesion molecules, and cytokines, such as vascular endothelial growth factor (VEGF). Objective To evaluate the profile of serum levels of VEGF and soluble vascular endothelial growth factor receptor 1 (sVEGFR-1) in pemphigus foliaceus (PF) patients with erythroderma. Methods We conducted a retrospective study, which included (i) a chart review of all PF patients from the Autoimmune Blistering Clinic, University of Sao Paulo, Brazil, from January 1991 to December 2014, together with an evaluation of demographic variables, hospitalization duration and complications and (ii) analysis of the circulating VEGF and sVEGFR-1 levels in PF patients with erythroderma by ELISA. The controls included patients with pemphigus vulgaris or psoriasis. Results We observed higher serum VEGF levels in PF patients during erythroderma than during the non-erythrodermic phase. PF patients showed increased serum levels of sVEGFR-1 during the erythrodermic phase in comparison to controls. Interestingly, the sVEGFR-1 and antidesmoglein-1 levels were positively correlated during the non-erythrodermic period. Conclusion Erythroderma, which represents one clinical form of PF, implies more severe outcomes. The circulating levels of VEGF, a potent endothelial activator, are increased in PF patients with erythroderma; this result suggests the contribution of the blood vessel endothelium to the pathogenesis of this clinical syndrome. Interestingly, our findings showed a positive correlation between the sVEGFR-1 and antidesmoglein-1 antibody levels, indicating a suppressive response to VEGF augmentation during the erythrodermic phase of PF.