RESUMO
BACKGROUND AND OBJECTIVES: Patent foramen ovale (PFO) has been implicated in the pathogenesis of cryptogenic stroke or transient ischemic attack (TIA) due to paradoxical embolism, and in the pathogenesis of migraine. This paper reports the intermediate and long-term results of transcatheter closure of PFO associated with cerebrovascular accidents (CVAs), TIAs and migraine, using the Amplatzer PFO occluder. This paper also reports a case of pulmonary embolism which developed in one patient after PFO closure. SUBJECTS AND METHODS: From January 2003 to May 2010, 16 patients with PFO (seven males and nine females) with a history of at least one episode of cryptogenic stroke/TIA, CVA, or migraine and who underwent percutaneous transcatheter closure of PFO using the Amplatzer occluder. All the procedures were performed under general anesthesia and were assisted by transesophageal echocardiography. RESULTS: The device was implanted without any significant complications in all the patients, and the PFOs were effectively closed. At an average follow-up period of 54 months, the 15 patients with TIA/CVA had no recurrence of any thromboembolic event. The symptoms in one patient with migraine subsided after occlusion of the PFO. In this study, pulmonary embolism occurred five months after PFO closure in one patient, but the cause of pulmonary embolism was not identified. However, it is believed that the pulmonary embolism occurred without stroke recurrence because occlusion of the PFO was performed when the patient had a stroke event. CONCLUSION: It can be concluded that according to the intermediate and long-term follow-up results, transcatheter PFO closure is an effective and safe therapeutic modality in the prevention of thromboembolic events, especially in the patients with cryptogenic stroke/TIA, and PFO closure is helpful in the treatment of migraine. However, this study involved a small number of patients and also the follow-up period was not long enough. Hence, randomized, controlled trials are necessary to determine if this approach is preferable to medical therapy for the prevention of recurrent stroke or as primary treatment for patients with migraine headache.
RESUMO
Kikuchi-Fujimoto disease is a rare and benign disease, characterized by regional cervical lymphadenopathy with fever of unknown origin, affecting mainly young women. This self-limiting disease of unknown etiology has rarely been reported in children, so it has been frequently confused with malignancies. We describe a case of a child who was initially mistaken for malignant lymphoma because of multiple lymph nodes with 18-fluorodeoxyglucose uptake on positron emission tomography and was finally diagnosed with Kikuchi-Fujimoto disease by excisional biopsy of the affected lymph node.
Assuntos
Linfadenite Histiocítica Necrosante/diagnóstico por imagem , Linfoma/diagnóstico , Tomografia por Emissão de Pósitrons , Biópsia , Criança , Diagnóstico Diferencial , Fadiga/etiologia , Feminino , Febre/etiologia , Radioisótopos de Flúor , Fluordesoxiglucose F18 , Linfadenite Histiocítica Necrosante/diagnóstico , Linfadenite Histiocítica Necrosante/patologia , Humanos , Hiperplasia , Linfonodos/diagnóstico por imagem , Linfonodos/patologia , Necrose , Compostos Radiofarmacêuticos , Indução de Remissão , Redução de PesoRESUMO
Complement C7 deficiency is associated with increased susceptibility to meningococcal infection. The genetic alterations of C7 deficiency are known to be sporadic and heterogeneous worldwide. We investigated molecular basis of C7 deficiency in two unrelated Korean families, in which the index cases suffered from meningococcal meningitis. Exon-specific PCR and direct sequencing of the C7 gene revealed two different mutations: c.1424G > A and c.281-1G > T. In family 1, index case and her brother revealed a homozygous mis-sense mutation (c.1424G > A), a novel mutation, which results in the change of cysteine to tyrosine (C475Y) in exon 10. Index case in family 2 was found to be a homozygote carrying point mutation at the 3' splice acceptor site of intron 3 (c.281-1G > T), which was previously reported in a Korean C7-deficient subject.