1.A Case of Acute Lymphoblastic Leukemia Preceded by Aleukemic Prodrome.
Byoung Su PARK ; Hwang Min KIM ; Baek Keun LIM ; Seok Won PARK ; Young UH ; Mee Yon CHO
Korean Journal of Pediatric Hematology-Oncology 2001;8(1):120-125
Acute lymphoblastic leukemia (ALL), in general, can be diagnosed by detecting blasts in peripheral blood or bone marrow. Some of the cases of ALL do not show typical leukemic features, and only manifest as refractory anemia, thrombocytopenia, myelofibrosis and lymphocytic infiltration into bone marrow. Several months after presentation, they may reveal typical leukemic features and are diagnosed as ALL. This kind of leukemia is called ALL with aleukemic prodrome. Although the incidence of ALL with aleukemic prodrome is 1.5~2.2% of childhood ALL cases, it is rarely reported in Korea. We experienced a 6 month-old female infant who presented with refactory anemia and thrombocytopenia, and two serial of bone marrow examination revealed only myelofibrosis. She subsequently developed ALL 3 months later. We report this case with a brief review of related literatures.
Anemia
;
Anemia, Refractory
;
Bone Marrow
;
Bone Marrow Examination
;
Female
;
Humans
;
Incidence
;
Infant
;
Korea
;
Leukemia
;
Precursor Cell Lymphoblastic Leukemia-Lymphoma*
;
Primary Myelofibrosis
;
Thrombocytopenia
2.A case of bronchiolitis obliterans organizing pneumonia associated with wheezing.
Jae Seok LEE ; Do Jin KIM ; Young Soo AHN ; Sang Moo LEE ; Hyeon Tae KIM ; Soo Taek UH ; Yong Hoon KIM ; Choon Sik PARK
Tuberculosis and Respiratory Diseases 1993;40(6):730-735
No abstract available.
Bronchiolitis Obliterans*
;
Bronchiolitis*
;
Cryptogenic Organizing Pneumonia*
;
Respiratory Sounds*
3.Hemophagocytic Syndrome with Kawasaki Disease and Peripheral Gangrene.
Hwa Jun YUN ; Ko Woon JEON ; Hwang Min KIM ; Seok Won PARK ; Young UH
Journal of the Korean Pediatric Society 2002;45(5):664-668
A twenty six months-old boy developed hemophagocytic syndrome during the course of Kawasaki disease. Despite the appropriate treatment modalities for Kawasaki disease, he developed thrombocytopenia, hepatomegaly, high-grade fever, hypertriglyceridemia, peripheral gangrene, and evidence of hemophagocytosis in bone marrow biopsy. Although the course was stormy, he responded well to a combination therapy of corticosteroid and etoposide.
Biopsy
;
Bone Marrow
;
Etoposide
;
Fever
;
Gangrene*
;
Hepatomegaly
;
Humans
;
Hypertriglyceridemia
;
Lymphohistiocytosis, Hemophagocytic*
;
Male
;
Mucocutaneous Lymph Node Syndrome*
;
Thrombocytopenia
4.Prevalence of the Extended-Spectrum beta-Lactamase and qnr Genes in Clinical Isolates of Escherichia coli.
Yongjung PARK ; Hyun Kyung KANG ; Il Kwon BAE ; Juwon KIM ; Jae Seok KIM ; Young UH ; Seok Hoon JEONG ; Kyungwon LEE
The Korean Journal of Laboratory Medicine 2009;29(3):218-223
BACKGROUND: This study was performed to investigate the prevalence of qnr genes in clinical isolates of Escherichia coli from Korea that produce extended-spectrum beta-lactamases (ESBLs). METHODS: During the period of May to June 2005, we collected clinical isolates of E. coli that were intermediate or resistant to ceftazidime and/or cefotaxime from 11 Korean hospitals. Antimicrobial susceptibility was determined by the disk diffusion and agar dilution methods. ESBL production was confirmed phenotypically by the double-disk synergy test. ESBL and qnr genes were searched for by PCR amplification, and the PCR products were then subjected to direct sequencing. RESULTS: Double-disk synergy tests were positive in 84.3% (118/140) of ceftazidime- and/or cefotaxime-nonsusceptible E. coli isolates. The most prevalent types of ESBL in E. coli isolates were CTX-M-14 (N=41) and CTX-M-15 (N=58). Other ESBLs were also identified, including CTX-M-3 (N=7), CTX-M-9 (N=8), CTX-M-12 (N=1), CTX-M-57 (N=1), SHV-2a (N=2), SHV-12 (N=17) and TEM-52 (N=4). The qnrA1 and qnrB4 genes were identified in 4 and 7 ESBL-producing isolates, respectively. CONCLUSIONS: CTX-M-type enzymes were the most common type of ESBL in E. coli isolates from Korea, and the qnr genes were not uncommon in ESBL-producing E. coli isolates. Dissemination of E. coli containing both ESBL and qnr genes could compromise the future usefulness of the expanded-spectrum antibiotics for the treatment of infections.
Disk Diffusion Antimicrobial Tests
;
Escherichia coli/*enzymology/genetics/isolation & purification
;
Escherichia coli Proteins/classification/*genetics
;
Humans
;
Inhibitory Concentration 50
;
Polymerase Chain Reaction
;
beta-Lactamases/biosynthesis/genetics/*metabolism
5.A Study of EFFECT and MECHANISM of IL-2on SURVIVAL of EOSINOPHILS.
Hyo Seok KIM ; Young Mok LEE ; Young Soo CHOI ; Kyung Ho KIM ; Geon Il IM ; Sung Whan JEONG ; Seung Hyug MOON ; Hyeon Tae KIM ; Soo Taek UH ; Yong Hun KIM ; Choon Sik PARK
Tuberculosis and Respiratory Diseases 1996;43(3):348-358
BACKGROUND: Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. METHODS: After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. alpha and beta IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. RESULTS: 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-2Ralpha on eosinophils, instead of no effect on the expression of IL-2Rbeta. CONCLUSION: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.
Animals
;
Antibodies, Neutralizing
;
Asthma
;
Eosinophilia
;
Eosinophils*
;
Humans
;
Interleukin-2
;
Interleukin-2 Receptor alpha Subunit
;
Interleukin-5
;
Lymphocytes
;
Mucous Membrane
;
Receptors, Interleukin-2
;
Survival Rate
;
Trypan Blue
6.A Case of Churg-Strauss Syndrome with Interstinal Perforation.
Jung Hoon PARK ; Yun Seok JUNG ; Yang Ki KIM ; Young Mok LEE ; Jung Hwa HWANG ; Ki Up KIM ; Dong Won KIM ; Soo Taek UH ; Jea Jun KIM
Tuberculosis and Respiratory Diseases 2009;66(5):374-379
Churg-Strauss syndrome (CSS) or allergic granulomatous angiitis is a rare syndrome that is characterized by hypereosinophilic systemic necrotizing vasculitis affecting small- to medium-sized arteries and veins. In general, it occurs in individuals with pre-existing allergic asthma. When CSS appears in patients, it has the following characteristics: eosinophilia of more than 10% in peripheral blood, paranasal sinusitis, pulmonary infiltrates, histological proof of vasculitis with extravascular eosinophils, and mononeuritis multiplex or polyneuropathy. Therapeutic trials dedicated to Churg-Strauss syndrome have been limited due to the rarity of this disorder and the difficulty in making a histological diagnosis. Proper treatment of patients with CSS is not widely known. In this case study, we report on our experience with an unusual patient case, characterized by purpura and a perforation of the small intestine after inadequate steroid therapy.
Arteries
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Asthma
;
Churg-Strauss Syndrome
;
Eosinophilia
;
Eosinophils
;
Humans
;
Intestinal Perforation
;
Intestine, Small
;
Mononeuropathies
;
Polyneuropathies
;
Purpura
;
Sinusitis
;
Vasculitis
;
Veins
7.Antimicrobial Resistance of Clinically Important Bacteria Isolated from Hospitals Located in Representative Provinces of Korea.
Seong Geun HONG ; Dongeun YONG ; Kyungwon LEE ; Eui Chong KIM ; Wee Kyo LEE ; Seok Hoon JEONG ; Won Keun SONG ; Yeon Jun PARK ; Mi Na KIM ; Young UH ; Jong Hee SHIN ; Jongwook LEE ; Ji Young AHN ; Sun Wha LEE ; Jae Seok KIM ; Hee Bong SHIN
Korean Journal of Clinical Microbiology 2003;6(1):29-36
BACKGROUND: A rapid increase of antimicrobial-resistant bacteria has become a serious problem in many countries. The aim of this study was to determine the prevalence of resistance among frequently isolated gram-positive and -negative bacteria in Korea. METHODS: Data of routine antimicrobial susceptibility test for medically important bacteria, isolated during 3 months of 2002, were collected from 12 university and 1 commercial laboratories in Korea. RESULTS: The proportions of methicillin-resistant Staphylococcus aureus (MRSA) were 60-88%, but vancomycin-resistant S. aureus was not detected. Among the Enterococcus faecium isolates, the resistance rate to vancomycin was 29%. The resistance rates of Escherichia coli and Klebsiella pneumoniae: 11% and 24% to cefotaxime, respectively, and 12% and 21% to cefoxitin, respectively. The resistance rates of Citrobacter freundii, Enterobacter cloacae, and Serratia marcescens: 28%, 34% and 21% to cefotaxime, respectively, <1%, 8% and 14% to cefepime, respectively. The resistance rates of Acinetobacter baumannii and Pseudomonas aeruginosa were: 65% and 37% to piperacillin, 64% and 19% to ceftazidime, 13% and 20% to imipenem, respectively. The resistant rates varied according to the hospital size. The resistance rates were generally higher among the isolates in the hospitals with more than 1,000 beds. The rates of penicillin-nonsusceptible Streptococcus pneumoniae were 58-90%. Among the Haemophilus influenzae isolates, 55-68% were resistant to ampicillin. CONCLUSIONS: Antimicrobial resistant strains were prevalent among the medically important clinical isolates, especially, MRSA, vancomycin-resistant enterococci, extended-spectrum -lactamase- or AmpC -lactamase-producing E. coli and K. pneumoniae, third generation cephalosporin-resistant C. freundii, E. cloacae and S. marcescens, imipenem-resistant A. baumannii and P. aeruginosa, penicillin-nonsusceptible S. pneumoniae and ampicillin-resistant H. influenzae. The antimicrobial resistance has become a serious problem in Korea.
Acinetobacter baumannii
;
Ampicillin
;
Bacteria*
;
Cefotaxime
;
Cefoxitin
;
Ceftazidime
;
Citrobacter freundii
;
Cloaca
;
Enterobacter cloacae
;
Enterococcus faecium
;
Escherichia coli
;
Haemophilus influenzae
;
Health Facility Size
;
Imipenem
;
Influenza, Human
;
Klebsiella pneumoniae
;
Korea*
;
Methicillin-Resistant Staphylococcus aureus
;
Piperacillin
;
Pneumonia
;
Prevalence
;
Pseudomonas aeruginosa
;
Serratia marcescens
;
Streptococcus pneumoniae
;
Vancomycin
8.A novel method of brachytherapy using local delivery of 99mTc-HMPAO for coronary stent restenosis.
Weon KIM ; Myung Ho JEONG ; Sung Hee KIM ; Uh Seok PARK ; Ok Young PARK ; Ju Han KIM ; Hee Seung BOM ; Hwan Jung JEONG ; Young Keun AHN ; Jeong Gwan CHO ; Jong Chun PARK ; Jung Chaee KANG
Korean Journal of Medicine 2003;64(5):523-534
BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) still remains a matter to be solved. We examined the inhibitory effects of local delivery of 99mTc-HMPAO (hexamethylprophylene amine oxime), a radioisotope, on neointimal hyperplasia after coronary stenting through an animal experiment, and observed its safety and efficacy for the patients with coronary stent restenosis. METHODS: Stent overdilation injuries were performed in coronary arteries of 10 pigs. After stent overdilation injury, local radioisotope delivery using a 99mTc-HMPAO were performed in one coronary artery (Group I) and control therapy in another coronary artery in each pig (Group II). Follow-up coronary angiogram (CAG) and histopathologic assessment were performed at 4 weeks after stenting. Eleven patients (10 males, 62.4+/-5.7 years of age) underwent local administration of 30 mCi/ 2 mL of 99mTc-HMPAO shortly after PCI via Dispatch CatheterTM, and whole body bone scan and thallium-SPECT afterwards. Major adverse cardiac events (MACE) were assessed during one-year clinical follow-up. RESULTS: On histopathologic analysis, neointimal area was 1.2+/-0.6 mm2 in Group I and 2.7+/-0.4 mm2 in Group II (p=0.002), and histopathologic area stenosis was 27.1+/-6.3% in Group I, 53.4+/-5.2% in Group II (p=0.001). In clinical study, eleven patients with coronary in-stent restenosis were enrolled. There was no in-hospital MACE. On quantitative coronary angiographic analysis minimal luminal diameter and diameter stenosis increased from 0.4+/-0.3 mm and 84.2+/-9.5% to 2.9+/-0.2 mm and 16.3+/-11.0% after PCI, respectively. Follow-up CAG was performed in 9 cases (81.8%) and restenosis occurred in 2 cases (22.2%). On follow-up CAG minimal luminal diameter was 2.0+/-0.8 mm, diameter stenosis rate 27.7+/-2.9 %, lumen loss 0.7+/-0.7 mm and loss index 0.2+/-0.3. During one-year clinical follow-up there were no cases of death and acute MI, but two cases of target vessel revascularization (18.2%). CONCLUSION: Local delivery of 99mTc-HMPAO, one of the novel radiotherapies, can be used safely and effectively for coronary stent restenosis.
Animal Experimentation
;
Brachytherapy*
;
Constriction, Pathologic
;
Coronary Artery Disease
;
Coronary Vessels
;
Follow-Up Studies
;
Humans
;
Hyperplasia
;
Male
;
Percutaneous Coronary Intervention
;
Phenobarbital
;
Radioisotopes
;
Radiotherapy
;
Stents*
;
Swine
;
Technetium Tc 99m Exametazime*
9.The Effect of Passive Smoking on Asthma Symptoms, Atopy, and Airway Hyperresponsiveness in Schoolchildren.
An Soo JANG ; In Seon CHOI ; Soong LEE ; Hae Sung NAM ; Sun Seok KWEON ; Myung Ho SON ; June Hyuk LEE ; Sung Woo PARK ; Do Jin KIM ; Soo Taek UH ; Yong Hoon KIM ; Choon Sik PARK
Journal of Korean Medical Science 2004;19(2):214-217
Passive smoking is a major cause of respiratory morbidity, and is associated with increased bronchial responsiveness in children. To evaluate the effect of smoking by a parent on asthma symptoms, atopy, and airway hyperresponsiveness (AHR), we conducted a cross-sectional survey of 503 schoolchildren that involved questionnaires, spirometry, allergy testing, and a bronchial challenge test. If the PC20 methacholine was less than 16 mg/mL, the subject was considered to have AHR. The prevalence of a parent who smoked was 68.7%. The prevalence of AHR was 45.0%. The sensitization rate to common inhalant allergens was 32.6%. Nasal symptoms such as rhinorrhea, sneezing, nasal itching, and nasal obstruction were present in 42.7%. Asthma symptoms such as cough and wheezing were present in 55.4%. The asthma symptoms were significantly more prevalent in children who had a parent who smoked than in those whose parents did not. The nasal symptoms, atopy, and AHR did not differ according to whether a parent smoked. In a multiple logistic regression model, the asthma symptoms and atopy were independently associated with AHR, when adjusted for confounding variables. Passive smoking contributed to asthma symptoms in schoolchildren and was not an independent risk factor of airway hyperresponsiveness in an epidemiological survey.
Adult
;
Asthma/*epidemiology/physiopathology
;
Bronchial Hyperreactivity/*epidemiology/physiopathology
;
Child
;
Data Collection
;
Female
;
Human
;
Hypersensitivity/*epidemiology/physiopathology
;
Male
;
Parents
;
Prevalence
;
Risk Factors
;
Support, Non-U.S. Gov't
;
Tobacco Smoke Pollution/*adverse effects/*statistics & numerical data
10.Mechanism of VanB Phenotype in Vancomycin-Resistant Enterococci carrying vanA gene.
Il Joong PARK ; Wee Gyo LEE ; Hyukmin LEE ; Dongeun YONG ; Kyungwon LEE ; Eui Chong KIM ; Seok Hoon JEONG ; Yeon Jun PARK ; Tae Yeal CHOI ; Young UH ; Jong Hee SHIN ; Jongwook LEE ; Ji young AHN ; Sung Hee LEE ; Gun Jo WOO
The Korean Journal of Laboratory Medicine 2006;26(6):412-417
BACKGROUND: Recently, vancomycin-resistant enterococci (VRE) with the vanA genotype that are susceptible to teicoplanin have been described in Japan, Taiwan, and Korea. The investigators suggested three point mutations in the putative sensor domain of vanS or impairment of accessory proteins VanY and VanZ as an explanation for the VanB phenotype-vanA genotype VRE. In this study, we analyzed Tn1546-like elements to determine the molecular mechanisms responsible for the impaired glycopeptide resistance of clinical VRE isolates with VanB phenotype-vanA genotype from Korea. METHODS: From 2001 to 2004, 28 clinical isolates of Enterococcus faecium with VanB phenotypevanA genotype were collected from 8 different university hospitals in diverse geographic areas in Korea. For structural analysis of Tn1546-like elements, PCR amplifications for internal regions of Tn1546 were performed. The purified PCR products were directly sequenced with an ABI Prism 3100 DNA sequencer. RESULTS: The sequence data of the vanS regulatory gene revealed that none of the isolates had any point mutations in this gene. All 28 isolates had a complete or incomplete deletion of vanY gene. Of these, 13 strains represented a complete deletion of vanZ, and 2 strains showed the deletion of nucleotides near the end point of vanX. CONCLUSIONS: The mechanism of VanB phenotype-vanA genotype in VRE isolates from Korea is not point mutations of vanS but the rearrangements of vanX, vanY and vanZ.
DNA
;
Enterococcus faecium
;
Genes, Regulator
;
Genotype
;
Hospitals, University
;
Humans
;
Japan
;
Korea
;
Nucleotides
;
Phenotype*
;
Point Mutation
;
Polymerase Chain Reaction
;
Research Personnel
;
Taiwan
;
Teicoplanin