RESUMO
Intramuscular hemangioma (IMH) represents less than 1% of all hemangiomas. In the head and neck region, it occurs mostly in the masseter, temporalis and sternocleidomastoid muscles. Despite its infiltrative growth pattern and several worrisome histological features, such as increased mitotic activity, plumpness of the nuclei, intraluminal papillary projections or perineural infiltration, the lesion is benign, and complete surgical excision is the preferred treatment for such oral lesions. Herein, we report three rare cases of IMH in the tongue and lip, discuss the clinical and histological aspects, and review the literature regarding this lesion.
Assuntos
Hemangioma , Neoplasias Bucais , Neoplasias Musculares , Idoso , Feminino , Hemangioma/metabolismo , Hemangioma/patologia , Hemangioma/cirurgia , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Bucais/metabolismo , Neoplasias Bucais/patologia , Neoplasias Bucais/cirurgia , Neoplasias Musculares/metabolismo , Neoplasias Musculares/patologia , Neoplasias Musculares/cirurgiaAssuntos
Hemangioma/diagnóstico por imagem , Hemossiderose/diagnóstico por imagem , Neoplasias Cutâneas/diagnóstico por imagem , Adulto , Dermoscopia , Feminino , Hemangioma/metabolismo , Hemangioma/patologia , Hemossiderina/metabolismo , Hemossiderose/metabolismo , Humanos , Microscopia Confocal , Pessoa de Meia-Idade , Neoplasias Cutâneas/metabolismo , Neoplasias Cutâneas/patologiaRESUMO
The aim of this study was to investigate the mechanism of propranolol on the regression of hemangiomas. Propranolol-treated hemangioma tissues were collected and the expression of hypoxia inducible factor-1α (HIF-1α) was examined. We also established HIF-1α overexpression and knockdown hemangioma cells, and determined the effects of HIF-1α on the hemangioma cells proliferation, apoptosis, migration and tube formation. Significantly increased HIF-1α level was found in the hemangioma tissues compared to that in normal vascular tissues, whereas propranolol treatment decreased the HIF-1α level in hemangioma tissues in a time- and dose-dependent manner. Moreover, propranolol treatment significantly decreased cell proliferation, migration and tube formation as well as promoted cell apoptosis in HIF-1α overexpression and knockdown hemangioma cells. Propranolol suppressed the cells proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms. HIF-1α could serve as a novel target in the treatment of hemangiomas.
Assuntos
Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Hemangioma/tratamento farmacológico , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Propranolol/uso terapêutico , Vasodilatadores/uso terapêutico , Apoptose/efeitos dos fármacos , Hemangioma/metabolismo , HumanosRESUMO
The aim of this study was to investigate the mechanism of propranolol on the regression of hemangiomas. Propranolol-treated hemangioma tissues were collected and the expression of hypoxia inducible factor-1α (HIF-1α) was examined. We also established HIF-1α overexpression and knockdown hemangioma cells, and determined the effects of HIF-1α on the hemangioma cells proliferation, apoptosis, migration and tube formation. Significantly increased HIF-1α level was found in the hemangioma tissues compared to that in normal vascular tissues, whereas propranolol treatment decreased the HIF-1α level in hemangioma tissues in a time- and dose-dependent manner. Moreover, propranolol treatment significantly decreased cell proliferation, migration and tube formation as well as promoted cell apoptosis in HIF-1α overexpression and knockdown hemangioma cells. Propranolol suppressed the cells proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms. HIF-1α could serve as a novel target in the treatment of hemangiomas.
Assuntos
Humanos , Propranolol/uso terapêutico , Vasodilatadores/uso terapêutico , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Hemangioma/tratamento farmacológico , Apoptose/efeitos dos fármacos , Hemangioma/metabolismoRESUMO
Glut1 is a marker of infantile hemangioma, and its positivity has resulted in defining this tumor at several sites (eg, skin, breast, salivary glands, liver, and placenta). We herein report on the presence of Glut1 positivity in the endothelial cells of 2 examples of intramuscular hemangioma, a peculiar tumor considered to be most probably congenital. The finding expands the sites where infantile hemangioma may be recognized and suggests that this intramuscular variety should be renamed intramuscular infantile hemangioma. An additional previously unreported finding was the presence of a strong membranous pattern of staining for Glut1 in the intralesional fat cells, a known component of the tumor, which parallels that of another endothelial marker, namely CD34. These findings could prove useful for diagnostic purposes in small biopsies.
Assuntos
Músculos Abdominais/metabolismo , Endotélio Vascular/metabolismo , Transportador de Glucose Tipo 1/metabolismo , Neoplasias de Cabeça e Pescoço/metabolismo , Hemangioma/metabolismo , Neoplasias de Tecidos Moles/metabolismo , Músculos Abdominais/patologia , Biomarcadores Tumorais/metabolismo , Pré-Escolar , Endotélio Vascular/patologia , Feminino , Neoplasias de Cabeça e Pescoço/patologia , Neoplasias de Cabeça e Pescoço/cirurgia , Hemangioma/patologia , Hemangioma/cirurgia , Humanos , Imuno-Histoquímica , Neoplasias de Tecidos Moles/patologia , Neoplasias de Tecidos Moles/cirurgiaRESUMO
AIM: To compare the expression of p57 as indirect marker of genomic imprinting of CDKN1C in a series of infantile hemangiomas (IH) of patients with and without Beckwith-Wiedemann syndrome. MATERIALS AND METHODS: Cases of mammary, salivary gland, liver (one each), and placental (2 cases) capillary hemangiomas all with histological features akin to IH as well as typical examples of cutaneous (8 cases) IH were analyzed by immunohistochemistry with antibody against p57(KIP2). This protein is the product of CDKN1C an imprinted, maternally expressed gene. The liver hemangioma and both chorioangiomas were from patients with Beckwith-Wiedemann syndrome. Positive and negative controls included normal placental tissue and complete hydatidiform mole, respectively. Positive staining was localized to nuclei. RESULTS: Endothelial cells from the skin, breast and salivary gland hemangiomas were p57(KIP2) positive while chorioangiomas and liver IH presenting in patients with Beckwith-Wiedemann syndrome were negative. Controls reacted appropriately. CONCLUSIONS: Endothelial cells of IH not associated with BWS normally express p57(KIP2) while chorioangiomas and IH of the liver associated with BWS do not. These results suggest that the BWS IH may result from dysregulation of the cell cycle.
Assuntos
Hemangioma/metabolismo , Proteínas Nucleares/biossíntese , Síndrome de Beckwith-Wiedemann/genética , Síndrome de Beckwith-Wiedemann/metabolismo , Síndrome de Beckwith-Wiedemann/patologia , Biomarcadores , Neoplasias da Mama/genética , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Ciclo Celular/fisiologia , Criança , Pré-Escolar , Inibidor de Quinase Dependente de Ciclina p57 , Feminino , Hemangioma/genética , Hemangioma/patologia , Humanos , Imuno-Histoquímica , Lactente , Recém-Nascido , Masculino , Proteínas Nucleares/genética , Doenças Placentárias/genética , Doenças Placentárias/metabolismo , Doenças Placentárias/patologia , Gravidez , Neoplasias Cutâneas/genética , Neoplasias Cutâneas/metabolismo , Neoplasias Cutâneas/patologia , Fixação de TecidosAssuntos
Fatores de Crescimento Endotelial/metabolismo , Fator 2 de Crescimento de Fibroblastos/metabolismo , Hemangioma/metabolismo , Neoplasias Hepáticas/metabolismo , Linfocinas/metabolismo , Feminino , Hemangioma/patologia , Humanos , Lactente , Neoplasias Hepáticas/patologia , Isoformas de Proteínas/metabolismo , Fator A de Crescimento do Endotélio Vascular , Fatores de Crescimento do Endotélio VascularRESUMO
A 5-year-old boy was found to have severe rickets in association with hyperpigmented, linear, verrucous, epidermal tumors, typical of the epidermal nevus syndrome. Normocalcemia (9.6 mg/dl), hypophosphatemia (2.0 mg/dl), elevated serum alkaline phosphatase concentration (313 IU), decreased renal tubular reabsorption of phosphorus (35%), radiologic evidence of rickets, and lack of response to usual therapeutic doses of vitamin D suggested hypophosphatemic vitamin D-resistant rickets. Therapy with vitamin D in doses to 750,000 IU and oral phosphate, 2.0 gm/day, failed to induce healing of the rickets. A subtotal parathyroidectomy performed when the patient was 9 years old was also without effect. When he was 12 years old several fibroangiomas on the face and left lower limb were excised. Within three months all biochemical abnormalities resolved and radiologic evidence of healing was observed. A portion of excised tissue was homogenized and injection of the supernate into a 6-week-old puppy induced excessive phosphaturia. The data suggest that the rickets was induced by a phosphaturic substance extractable from the tumors.