• Journal of Acupuncture Research
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• 제24권4호
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• pp.209-223
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• 2007

Objectives : Facial Nerve Paralysis is one kind of common diseases and it can be treated by natural therapy and the efficiency of treatment is relatively high. In clinical trial, it is not difficult to find patients who were not completely recovered from Facial Nerve Paralysis, so the symptoms are fixed permanently. This leads many doctors and patients to have interests in the progress and prognosis of the disease, so this study was to analyze clinical prognosis factors and verify the effects of Electrodiagnostic Test. Methods : The 378 subjects were chosen from 987 patients who were suffering from Peripheral Facial Palsy, diagnosed with Bell's palsy and Ramsay Hunt Syndrome and had admission treatment. They got Oriental-Western Medicine Treatment within two weeks after outbreaks of the disease and treated at least over 3 weeks using Oriental-Western Medicine Treatment. Results : 1. There was a significant difference in the results of treatment according to gender, age, types of Facial Palsy, existence of Post Auricular Pain, existence of Labyrinth Symptom, HBGS, and existence of onsets of recovery as clinical prognosis factors of Peripheral Facial Palsy, However, a statistically significant difference was not shown in the results of treatment according to the position of Facial Palsy(left or right), existence of a relapse, and diabetes, hypertension. 2. As a result of overall treatment, 77.2% of patients were recovered almost entirely and 22.8% were not, and the quelae of incomplete recovery were Synkinesis, facial contracture, facial spasm, crocodile tears and scheroma in order of frequency. 3. The results of electrodiagnostic test represented useful correlation to predict the final effects of treatment. Conclusion : Based on the above results, the prognosis factors, the degree of recovery, and the sequelae of incomplete recovery were analysed and the effects of electrodiagnostic test was verified.

• 한국임상약학회지
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• 제22권4호
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• pp.356-366
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• 2012

Background: Chemotherapy-induced peripheral neuropathy (CIPN) involving sensory and motor nerve damage or dysfunction is a common and serious clinical problem that affects many patients receiving cancer treatment. This condition may pose challenges for the clinician to diagnose and manage, particularly in patients with coexisting conditions or disorders that involve the peripheral nervous system. Many chemotherapeutic agents used today are associated with the development of serious and dose-limiting CIPN that can adversely affect the administration of planned therapy and can impair quality of life by interference with the patients' activities of daily living. The most important clinical objective in the evaluation of patients with CIPN is to determine their level of functional impairment involving activities of daily living. These findings are used to make medical decisions to continue, modify, delay, or stop treatment. The most commonly reported drugs to cause CIPN include taxanes, platinum agents, vinca alkaloids, thalidomide, and bortezomib. We aimed to determine PN incidence during cisplatin, carboplatin and oxaliplatin administration. Methods: We collected data from 125 patients who received at least one cycle of cisplatin, carboplatin or oxaliplatin. They completed a self-reported questionnaire and items related to their disease and peripheral neuropathy. The investigators filled in part of items about disease and treatment. Patient Neurotoxicity Qeustionnaire developed by Bionumerik company were applied for PN assessment. Results: The incidences of sensory neurotoxicities of cisplatin, carboplatin and oxaliplatin were respectively 23%, 56% and 50%. The incidences of motor neurotoxicities of cisplatin, carboplatin and oxaliplatin were respectively 18%, 42% and 19%. The incidences of severe neurotoxicities of cisplatin, carboplatin and oxaliplatin were respectively 13%, 28% and 14%. The incidences of PN were associated with cumulative dose but not age, gender and concurrent illness. 19.2% of the patients (24/125) were prescribed with gabapentin, nortriptyline or gabapentin plus nortriptyline to reduce these peripheral symptoms and 75% of the patients answered the drug were effective. Conclusion: Incidence of PN after cisplatin or oxaliplatin administration is cumulative dose-related. Physician-based assessments under-reported the incidence and severity of CIPN. To overcome this limitation, diagnostic tools specifically designed to assess peripheral neuropathy severity associated with chemotherapy must be developed.

• Journal of Oral Medicine and Pain
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• 제38권3호
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• pp.247-253
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• 2013

신성골이영양증 (Renal osteodystrophy)은 만성 신질환 환자에서 관찰되는 골격성 변화를 특징으로 하는 질환으로 칼슘과 인 대사의 변화, 그리고 이차성 부갑상선 기능항진증의 결과로 나타난다. 방사선학적으로 지골의 말단, 장골과 악골 부위의 골막하 부위의 침식을 흔하게 관찰할 수 있다. 악안면 영역에서 골변화는 골밀도의 감소, 방사선 투과성 병소 (갈색 종양 : brown tumor), 피질골의 비박화와 치조백선의 소실을 보인다. 그러나 이러한 골변화가 악관절에 발생하는 것은 흔치 않은 일이다. 본 증례는 양측 하악 과두의 골변화를 보인 신성골이영양증 환자를 보고하고자 한다. 지난 10년 간 혈액 투석 치료와 3개월 전 신장암 수술 병력이 있는 41세 남자 환자가 좌측 턱의 통증을 주소로 2011년 2월 단국대학교 치과대학부속 치과병원 구강내과에 내원하였다. 양측 악관절의 골관절염과 유사한 방사선학적 소견을 보였고, 전치부 개방교합이 관찰되었다. CBCT를 이용한 방사선학적 특징과 생화학적 지표를 통해 신성골이영양증으로 인한 양측 턱관절의 골관절염으로 진단 되어 환자는 내과에서 신성골이영양증의 치료 방법의 하나인 칼슘 및 비타민 D 복용고 부갑상선 절제술을 시행 받았고, 그 동안 턱관절의 통증 조절을 위해 본원에서는 행동 요법과 약물 치료, 물리치료만 시행하였다. 약 1년 3개월 후 재검사에서 하악골의 골밀도와 피질골 두께가 증가하였고, 하악 과두 외형이 비교적 명확하게 바뀌었다. 골변화는 만성 신장 질환의 초기 단계부터 시작되므로 치과의사는 이러한 질환의 징후 및 가능성을 신속히 감별할 수 있어야 한다. 또한 골관절염과 신성골이영양증의 치료 프로토콜이 다르기 때문에 두 질환을 감별하는 것이 중요하다.

• 대한소아치과학회지
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• 제38권3호
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• pp.284-289
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• 2011

Lesch-Nyhan syndrome은 purine 대사장애로 인해 나타나는 질환이다. 유아기부터 전신근육의 강직, 발육 저하가 나타나고 손발의 불수의적 운동이나 불규칙적인 운동이 보이며 정신지체, 강박적 자해행위가 나타난다. 자해행위는 대개 1세 전후에 나타나지만 간혹 10대 후반에 나타나기도 한다. 입술, 특히 아랫입술과 혀, 협점막, 손, 손가락 등을 깨물고 입술, 혀, 협점막 등이 손상되거나 심할 경우 절단되기도 한다. 나이가 들면서 자해 행위가 점점 심해지고 상처 부위를 통한 2차 감염 가능성이 있다. 자해행위로 인한 주기적인 연조직 손상은 심할 경우 구강암으로 이행되기도 한다. 이와 같은 자해행위를 억제하기 위해 약물치료, 장치치료, 발치, 외과적 수술 등 여러 가지 방법이 시도되고 있다. 본 증례는 자해행위로 인한 입술손상을 주소로 내원한 Lesch-Nyhan syndrome 환자들을 대상으로 발치 대신 보존적 치료를 위해 가철성, 고정성 장치를 사용한 결과 입술외상의 빈도를 줄이고 심미적으로 양호한 결과를 얻을 수 있었기에 보고하는 바이다.

• BMB Reports
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• 제40권6호
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• pp.1069-1076
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• 2007

Cancer cells, characterized by local invasion and distant metastasis, are very much dependant on the extracellular matrix. The expression of matrix metalloproteinases (MMPs) has been implicated in the invasion and metastasis of cancer cells. In this study, we reported the effects of disulfiram, a clinically used anti-alcoholism drug, on tumor invasion suppression, as well as its effects on the activity of MMP-2 and MMP-9 in human osteosarcoma cells (U2OS). Disulfiram has been used for alcohol aversion therapy. However, recent reports have shown that disulfiram may have potential in the treatment of human cancers. Herewith, we showed that the anti-tumor effects of disulfiram, in an invasion assay using U2OS cells and that disulfiram has a type IV collagenase inhibitory activity that inhibits expression of genes and proteins responsible for both cell and non-cell mediated invasion on pathways. In conclusion, disulfiram inhibited expression of MMP-2 and MMP-9 and it regulated the invasion of human osteosarcoma cells. These observations raise the possibility of disulfiram being used clinical for the inhibition of cancer invasion.

• BMB Reports
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• 제53권11호
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• pp.582-587
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• 2020

It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H₂O₂ exposed HT-22 cells. In the cerebral ischemia/reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury.

• 한국콘텐츠학회논문지
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• 제12권12호
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• pp.335-344
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• 2012

우리나라는 급격한 경제성장과 의료기술의 발달로 고령화 사회가 되면서 골다공증 발병이 증가하고 있다. 또한 서구화된 식생활로 암질환이 증가하였고 항암치료과 방사선 치료 등으로 인해 골다공증이 발생하게 된다. 골다공증은 골밀도의 감소로 인한 것으로 대퇴근위부의 형태학적 구조 변화와도 밀접한 관계를 가지고 있으며, 대퇴 근위부의 형태학적 구조 변화는 고관절 골절의 위험을 나타내는 요인이다. 본 연구는 T-score변화에 따라 정상, 골감소증, 골다공증으로 분류하여 각 군별로 대퇴 근위부의 형태학적 변화를 관찰하고 상관관계를 분석하였다. 조사대상은 부산지역의 D종합병원의 남녀 350명을 대상으로 연령, 성별, T-score변화로 질환을 구분하여 분석하였다. 결과는 연령, 성별에 따라 골다공증의 발병빈도는 유의한 차이를 보였고, T-score변화에 따른 질환 분류와 대퇴근위부 형태학적 특성의 7가지 파라미터로서 Cortical ratio calcar, Cortical ratio shaft, Hip/shaft Angle, Strength index, Section modulus, CSMI, CSA는 유의한 차이를 보였으며 골다공증과 높은 상관관계가 있었다. 그러므로 연구 결과는 T-score변화에 따른 대퇴근위부의 형태학적 변화를 상관관계 분석함으로써 골다공증을 진단하는데 대퇴 근위부의 형태학적 변화가 지표로서 활용가능하리라 사료되며, 향후에 대퇴근위부의 형태학적 파라미터가 골다공증 진단의 정확성을 높이고 예측인자로서 임상활용이 가능하리라 판단된다.

• Clinical and Experimental Pediatrics
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• 제46권11호
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• pp.1112-1117
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• 2003

목 적 : 소아의 악성 종양에 대한 새로운 치료법의 개발로 환아의 생존 기간이 증가하는 추세에 있으나 이로 인한 신경계 합병증의 발생도 증가하고 있다. 저자들은 항암 치료를 시행한 소아 종양 환아에서 나타난 중추 신경계 합병증에 대한 임상 양상을 알아보고자 하였다. 방 법 : 1995년 1월부터 2002년 11월까지 동산병원 소아과에서 항암치료를 시행한 환아 중 신경계 합병증이 동반되었던 15례의 환아를 대상으로 그 임상상을 후향적으로 검토하였다. 결 과 : 전체 15례 중에서 방사선학적 검사로 원인 질환을 밝힌 경우는 모두 13례로 백질뇌병증이 7례, 무기질화 미세혈관병증이 4례, 뇌경색이 3례, 뇌출혈이 1례, 저산소성 허혈성 뇌증이 1례, 2가지 이상의 합병증을 함께 나타낸 경우는 2례였으며, 혈액학적 방사선학적 검사상에서 이상 소견이 없이 MTX의 부작용으로 생각되는 경련성 질환이 2례였다. 뇌출혈과 뇌경색이 나타낸 경우는 예후가 나빴으며 전해질 불균형으로 인한 저산소성 허혈성 뇌증에서는 원인 교정 후 후유증 없이 회복되었다. 결 론 : 소아 종양 환아에서 치료 중 발생한 신경계 합병증은 질환의 예후에 큰 영향을 미치고 신경인지 발달에 장애를 남기므로 이들 합병증에 대한 예방, 진단 및 즉각적인 치료와 추적관찰이 필요할 것이다.

• Clinical and Experimental Pediatrics
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• 제60권3호
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• pp.86-93
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• 2017

Purpose: To evaluate the clinical spectrum of posttransplantation lymphoproliferative disorder (PTLD) after solid organ transplantation (SOT) in children. Methods: We retrospectively reviewed the medical records of 18 patients with PTLD who underwent liver (LT) or kidney transplantation (KT) between January 1995 and December 2014 in Seoul National University Children's Hospital. Results: Eighteen patients (3.9% of pediatric SOTs; LT:KT, 11:7; male to female, 9:9) were diagnosed as having PTLD over the last 2 decades (4.8% for LT and 2.9% for KT). PTLD usually presented with fever or gastrointestinal symptoms in a median period of 7 months after SOT. Eight cases had malignant lesions, and all the patients except one had evidence of Epstein-Barr virus (EBV) involvement, assessed by using in situ hybridization of tumor tissue or EBV viral load quantitation of blood. Remission was achieved in all patients with reduction of immunosuppression and/or rituximab therapy or chemotherapy, although 1 patient had allograft kidney loss and another died from complications of chemotherapy. The first case of PTLD was encountered after the introduction of tacrolimus for pediatric SOT in 2003. The recent increase in PTLD incidence in KT coincided with modification of clinical practice since 2012 to increase the tacrolimus trough level. Conclusion: While the outcome was favorable in that all patients achieved complete remission, some patients still had allograft loss or mortality. To prevent PTLD and improve its outcome, monitoring for EBV infection is essential, which would lead to appropriate modification of immunosuppression and enhanced surveillance for PTLD.

• BMB Reports
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• 제49권7호
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• pp.382-387
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• 2016

Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stress-induced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases.