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박무석 대한의사협회 2009 대한의사협회지 Vol.52 No.1
Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is an immunologically mediated granulomatous, inflammatory disease of the lungs caused by repeated inhalation of various antigens. HP may occur in acute, subacute, or chronic forms. Chronic HP may be progressive, irreversible, and evolve to fibrotic interstitial lung disease. The diagnosis of HP can be made from a combination of clinical, laboratory, radiologic, and pathologic findings. A careful environmental and occupational history and establishment of exposure to a known inciting antigen are key factors in making the diagnosis of HP. Serum precipitating antibodies, bronchoalveolar lavage, and lung biopsy may be helpful in making the diagnosis. The pathology of HP is characterized by interstitial lymphocytic infiltration, poorlyformed noncaseating granulomas, cellular bronchiolitis, and fibrosis. In the pathogenesis of HP, recent studies showed that both type III and type IV hypersensitivity reactions are involved and are mediated by immune complexes and Th1 T cells, respectively. IFN-γ is essential for the development of HP, and IL-10 appears to modulate the severity of the disease. TNF-αand TGF- βhave been implicated in development of the pulmonary fibrosis that is seen in chronic HP. Avoidance of organic antigen exposure is the most important factor for the management of HP. There is often an apparent beneficial response to corticosteroids in the cases of severe acute and subacute HP, and for chronic HP that is severe or progressive.
Neurogenic Pulmonary Edema Following Acute Cerebral Infarction
박무석,김정민,윤영철,권오상,배재한 대한신경집중치료학회 2016 대한신경집중치료학회지 Vol.9 No.2
Background: Neurogenic pulmonary edema is non-cardiogenic pulmonary edema due to sudden excessive activation of sympathetic system after central nervous system injury. We report an acute cerebral infarction patient who developed neurogenic pulmonary edema requiring intubation and mechanical ventilation care. Case Report: A 77-year-old Korean woman visited emergency room complaining of sudden onset right side weakness which started one hour ago. She had a history of atrial fibrillation with normal ejection fraction. Neurological examination revealed motor aphasia and right side weakness. Brain computerized tomography angiography showed left middle cerebral artery occlusion without frank ischemic change. Intravenous thrombolytic therapy was considered, but suspended because she suddenly complained of respiration difficulty. Conclusions: This case suggests that large hemispheric infarction can result in acute onset pulmonary edema which is severe enough to require intubation and to delay thrombolytic treatment.
결핵 환자에서 Rifampin에 의한 Henoch-Shönlein Purpura 1예
박무석,김혜련,박병훈,손지영,정지예,안정련,정윤숙,임주은,정주원,문지애,변민광,김영삼,김세규,장준,이광길 대한결핵및호흡기학회 2008 Tuberculosis and Respiratory Diseases Vol.65 No.2
Henoch-Shönlein 자반증은 신장, 피부, 관절, 소화기계 등의 전신을 침범하는 혈관염으로 임상적인 증상을 종합하여 진단하는 질환이며 피부나 신장에서의 조직학적 생검이 진단을 뒷받침해 주는 근거가 될 수 있다. 항결핵제 사용 중에 rifampin으로 인하여 신기능 저하, 관절 통증, 양하지 자반, 복통 등의 임상 양상이 발생하였으며 하지 피부 병변의 조직 검사로 백혈구파쇄성혈관염(leukocytoclastic vasculitis) 소견을 보여 임상적으로 Henoch- Shönlein 자반증으로 진단하였으며 rifampin 복용 중지 후 피부 자반 소실되고, 신장 기능이 회복된 예를 문헌 고찰과 함께 보고하는 바이다. Rifampin is one of the first line drugs for treating tuberculosis, but it might be associated with serious adverse effects, including renal failure. We report here on a case of a 57-year-old patient who developed Henoch-Shönlein purpura during antituberculosis therapy that included rifampin. The patient converted to negative on the AFB smear for tuberculosis two weeks after the initial administration of antituberculosis medication. After treatment for 60 days, this patient was diagnosed with Henoch-Shönlein purpura by the purpura lesion on the lower legs, the leukocytoclastic vasculitis, the renal impairment and the pathological examination. After stopping rifampin, the skin lesions disappeared in about 10 days and his renal function gradually improved. This case study showed that Henoch-Schönlein purpura can be caused by rifampin during antituberculosis therapy and we recommend that the use of rifampin should be restrained when clinical symptoms of Henoch-Shönlein purpura are observed.
The Prevalence of Human Papillomavirus Infection in Korean Non-Small Cell Lung Cancer Patients
박무석,장윤수,신주혜,김대준,정경영,신도환,문진욱,강신명,한창훈,김영삼,장준,김성규,김세규 연세대학교의과대학 2007 Yonsei medical journal Vol.48 No.1
Human papillomavirus (HPV) infection is a co-carcinogen of lung cancer and contributes to its pathogenesis. To evaluate the prevalence of HPV infection, polymerase chain reaction (PCR) was employed to detect HPV 16, 18, and 33 DNA in tumor tissues of 112 patients with non-small cell lung cancer (NSCLC) who underwent curative surgery from Jan. 1995 to Dec. 1998 at Severance Hospital, Seoul, Korea. The patients consisted of 90 men and 22 women. Nineteen patients were under 50 years old (17%), and 92 patients (82%) were smokers. Fifty-three patients had adenocarcinomas, while 59 patients had non-adenocarcinomas. Early stage (I and II) cancer was found in 64 patients (57.1%) and advanced stage (III and IV) found in 48 (42.9%). The prevalence of HPV 16, 18, and 33 were 12 (10.7%), 11 (9.8%), and 37 (33.0%), respectively. Smoking status, sex, and histologic type were not statistically different in the presence of HPV DNA. The presence of HPV 16 was more common in younger patients and HPV 18 was more common in advanced stage patients. This study showed that the prevalence rate of HPV 16 and 18 infections in NSCLC tissue was low, suggesting HPV 16 and 18 infections played a limited role in lung carcinogenesis of Koreans. However, the higher prevalence of HPV 33 infections in Korean lung cancer patients compared to other Asian and Western countries may be important and warrants further investigation.
박무석 대한결핵및호흡기학회 2013 Tuberculosis and Respiratory Diseases Vol.74 No.4
Diffuse alveolar hemorrhage (DAH) is a life-threatening and medical emergency that can be caused by numerous disorders and presents with hemoptysis, anemia, and diffuse alveolar infiltrates. Early bronchoscopy with bronchoalveolar lavage is usually required to confirm the diagnosis and rule out infection. Most cases of DAH are caused by capillaritis associated with systemic autoimmune diseases such as anti-neutrophil cytoplasmic antibody-associated vasculitis, anti-glomerular basement membrane disease, and systemic lupus erythematosus, but DAH may also result from coagulation disorders, drugs, inhaled toxins, or transplantation. The diagnosis of DAH relies on clinical suspicion combined with laboratory, radiologic, and pathologic findings. Early recognition is crucial, because prompt diagnosis and treatment is necessary for survival. Corticosteroids and immunosuppressive agents remain the gold standard. In patients with DAH, biopsy of involved sites can help to identify the cause and to direct therapy. This article aims to provide a general review of the causes and clinical presentation of DAH and to recommend a diagnostic approach and a management plan for the most common causes.