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Erythema Nodosum Masking Kawasaki Disease with an Initial Manifestation of Skin Lesions
Seigo Okada,Yuichi Ishikawa,Maiko Shimomura,Shinpei Sunagawa,Reiji Hirano,Shinnosuke Fukunaga,Akiko Miyake,Yusuke Okada,Takashi Maki 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.3
We report the first case demonstrating an association between Kawasaki disease (KD) and erythema nodosum (EN). A 3-year-oldgirl presented with EN as an initial manifestation of KD. At the initial visit, she showed high fever of 40°C, injection of the oropharynx,cervical lymphadenopathy, and red-purple cutaneous nodules, particularly on the lower limbs. She complained of severepain in the neck and cutaneous lesions. Initially, the development of EN was attributed to Salmonella spp infection, which wasdetected in stool culture. However, the patient did not respond to high-dose ampicillin/sulbactam to which the Salmonella spp issensitive. Echocardiography performed as screening for fever of unknown origin revealed medium-sized aneurysms of the leftanterior descending artery. EN masked the diagnosis of KD, and the patient developed a coronary artery lesion. KD should beconsidered in the differential diagnosis of refractory EN in pediatric patients.
Yuji Kasukawa,Naohisa Miyakoshi,Michio Hongo,Yoshinori Ishikawa,Daisuke Kudo,Ryota Kimura,Yuichi Ono,Jumpei Iida,Chiaki Sato,Yoichi Shimada 대한척추외과학회 2019 Asian Spine Journal Vol.13 No.5
Study Design: Retrospective and comparative study. Purpose: We assessed surgical treatment outcomes in patients with thoracic myelopathy due to ossification of the ligamentum flavum (OLF), and OLF combined with ossification of the posterior longitudinal ligament (OPLL) or vertebral fracture (VF) at the same level. Overview of Literature: OLF and OPLL cause severe thoracic myelopathy. Osteoporotic VF commonly occurs at the thoracolumbar junction. There have been no investigations of thoracic myelopathy due to OLF and VF. Methods: Forty patients were divided among three groups: the OLF group (n=23): myelopathy due to OLF, the OLF+OPLL group (n=12): myelopathy due to OLF and OPLL, and the OLF+VF group (n=5): myelopathy due to OLF and VF. We recorded OLF, OPLL, and VF sites and operative procedures. Each patient’s neurological status, according to the Japanese Orthopaedic Association (JOA) score, and walking ability were evaluated pre- and postoperatively. Results: Patients in the OLF+OPLL group were significantly younger than those in the other two groups. The preoperative JOA score was significantly lower in the OLF+VF than OLF group. The final JOA score was significantly lower in the OLF+VF than OLF and OLF+OPLL groups. The JOA score recovery rate was significantly lower in the OLF+VF than OLF group. Final walking ability was significantly worse in the OLF+OPLL and OLF+VF groups than in the OLF group and significantly worse in the OLF+VF than OLF+OPLL group. Conclusions: Thoracic myelopathy due to OLF+VF occurs primarily in older females, who also exhibit worse preoperative and postoperative neurological status, and worse walking ability, than patients with thoracic myelopathy due to OLF or OLF+OPLL.
Lee, Sang-Hoon,Suh, Sung-Wook,Yoo, Kwang-Hyun,Kim, Han-Soo,Ishikawa, Yuichi,Goto, Makoto 대한근골격종양학회 2002 대한골관절종양학회지 Vol.8 No.3
워너 증후군은 상염색체 열성 유전을 하는 희귀한 성인 조로 질환이다. 이 질환은 조기 노화를 보일 뿐만 아니라, 악성 종양의 발생 빈도도 증가하게 되는데, 골연부 조직의 종양이 많이 발생하게 된다. 그러나 악성 종양의 발생 원인은 단순한 조기 노화 현상으로만 보기보다는 하나의 종양 증후군으로 보는 경향이 있으며, 그 이유는 워너 증후군 환자에서 발생하는 종양의 위치, 병리적 소견, 나이 등에서 정상인과는 많은 차이를 보였기 때문이다. 최근의 분자 유전학적 연구들에 의해서 워너 증후군은 DNA의 복제, 복구, 재생에 관여하는 Werner helicase의 유전자 변이와 관련이 있음이 밝혀졌다. 워너 증후군의 유전자 이상은 이러한 DNA 복구과정에 문제를 일으키고, 유전자의 불안정성을 증가시켜 종양의 발생 가능성을 높이게 된다. 육종의 발생과 워너 증후군의 연관성에 관한 향후의 연구들은 정상적인 노화의 과정과 육종의 발생 기전에 관한 많은 정보를 제공할 수 있을 것으로 사료된다. Werner's syndrome is a rare autosomal recessive disorder manifesting as premature aging. It is also known to be characterized by a high frequency of malignant tumors, especially sarcomas. However, Werner's syndrome may be not only a premature aging disease but also a cancer syndrome, because the malignant tumors in these patients are different from those of normal population with respect to involved site, histological type, and age of onset. Recent studies found Werner's syndrome was caused by a mutation of Werner helicase suggesting that WRN helicase may participate in metabolism and repair of DNA. And a dysfunction of WRN helicase may induce the genomic instability causing somatic mutations. Further studies of Werner's syndrome associated with sarcoma might give much informations about the normal aging process and the pathogenesis of sarcomas.