알레르기 질환에서 피부단자시험과 RAST 성적에 관한 연구

이은직(Eun Jig Lee),김준명(June Myeong Kim),이수곤(Soo Gon Lee),박해심(Hae Sim Park),오승헌(Seung Heon Oh),홍천수(Chein Soo Hong) 대한내과학회 1987 대한내과학회지 Vol.32 No.4

N/A The prick skin test and RAST were used commonly in demonstrating the presence of skin sensitizing antibody in the diagnosis of allergic diseases. The agreement rate and correlation between skin test and RAST were studied by using Phadebas RAST kits and Bencard allergen extracts of 37 common allergens. The following results were obtained; 1) Total agreement rate of 37 allergens between skin test and RAST was 62.3% in 1840 samples. 2) The positive rate of RAST was 20,3% in the + positive group of skin test in all allergens 34.4% in %, and 83.19o in %. 3) Correlation coefficient between skin test and RAST was 0.79 in D. pteronyssinus, 0.67 in D. farinae, and 0.55 in house dust. 4) RAST positive rate of positive skin test and RAST negatvie rate of negative skin test were 68.7%, 94.4% in D. pteronyssinus, 57.8%, 91.3% in D. farinae 47.5%, 96.1 % in Artemisia, 42.4%, 84.3% in Ambrosia, and 32.8%, 97.9% in house dust. 5) RAST positive rate of D. pteronyssinus, D. Farinae, house dust, cat epithelium, cockroach, Ambrosia, Artemisia, mold were 31.0%, 35.1%, 16.4%, 21.7%, 53.8 %, 10.0%, 13.3%, 47,1% in patients with asthma, 59.6%, 55.8%, 30.0%, 18.2%, 22.2%, 48.0%, 39.4%, 34.1% in allergic rhinitis, 60.2%, 56.9%, 37.4%, 34.1%, 40.0%, 21.2 %, 23.2%, 20.0% in asthma associated with allergic rhinitis, 6) The positive RAST rate of D. pteronyssinus was 88.1% when RAS1 of D. Farinae was positive, and positive RAST rate of D. farinae 88.8% when RAST of D. pteronyssinus positive.

면역세포화학 염색법과 전자 현미경검사를 통한 뇌하수체 선종의 특징

이은직(Eun Jig Lee),이현철(Hyun Chul Lee),양우익(Woo Ik Yang),김경래(Kyung Rai Kim),김현만(Hyun Man Kim),안광진(Kwang Jin Ahn),정윤석(Yoon Sok Chung),임승길(Sung Kil Lim),김태승(Tae Seung Kim),박찬일(Chan Il Park),최인준(In Joon choi 대한내과학회 1992 대한내과학회지 Vol.43 No.2

N/A Background: The development of immunocytochemistry and the application of electron microscopy improved the knowledge of the pathology and classification of the pitutiary adenomas. We investigated the characteristics of the pituitary adenomas examined by the immunocytochemistry and electron microscopy. Methods: 44 patients with the pituitary adenomas were investigated, using immunocytochemical techniques in paraffin-embedded tissue, and electron microscopy in fresh tissue. Results: The mean age was 38±13 years, and the ratio of male to female was 1: 2.4 and 18 were prolactinomas, 8 acromegalies, 3 acromegalies with hyperprolactinemia, 3 Cushing`s diaseases, 3 FSH secreting adenomas, 1 TSH secreting adenomas, and 6 nonfunctioning adenomas among 44 patients. The agreement between serum prolactin and prolactin immunocytochemistry was 77.3% if the serum prolaetin level to predict lactotrope adenoma was above 50ng/ml; however, the agreement was 93,2% if the serum prolatin level above 100ng/ml. The serum levels of prolactin and growth hormone in sparsely granulated lactotrope and somatotrope adenomas were 1149.6, 109.5ng/ml, respectively, which were higher than those (129.6, 35.9ng/ml) of densely granulated ones. Immunocytochemical and electron microscopic analysis revealed that thirteen were lactotrope adenomas (12 sparsely granulated, and 1 densely granulated), 9 somatotrope adenomas (6 sparsely granulated and 3 densely granulated), 6 gonadotrope, 4 corticotrope (3 symtomatic and 1 silent), 1 mixed somatotrope and lactotrope, 1 mammosomatotrope, 1 thyrotrope, and 9 null cell (6 nononcocytic, and 3 oncocytic) adenomas. Conclusion: The immunocytochemistry, permitting the visualization of intracellular hormones in the tissue of the pituitary adenoma, made exact histologic diagnosis. So, we have known whether the cause of hyperprolactinemia was lactotrope adenoma or functional hyperprolactinemia due to PIF inhibiton. And it was also possible to diagnose silent corticotrope adenoma and gonadotrope adenoma which had no apparent clinical manifestation. Electron microscopic examination of the pituitary adenoma diagnosed by immunocytchemistry showed ultrastructrural characteristics of the adenoma cells containing each hormones, Accordingly, we could subclassify the pituitary adenoma. However, the identification of the adenomas with somewhat similar ultrastrutural features such as null cell, gonadotrope, and thyrotrope adenoma, may be facilitated by immunocytochemistry. Accordingly, both immunocytochemistry and electron microscopy are necessary for the identification and characterization of the pituitary adenomas.

뇌하수체 성선자극호르몬 분비세포 선종

이은직(Eun Jig Lee),이현철(Hyun Chul Lee),안광진(Kwang Jin Ahn),임세중(Se Joong Rim),정윤석(Yoon Sok Jung),이관우(Kwan Woo Lee),임승길(Sung Kil Lim),김경래(Kyung Rae Kim),허갑범(Kap Bum Huh),양우익(Woo Ik Yang),박찬일(Chan Il Park),최 대한내과학회 1991 대한내과학회지 Vol.41 No.6

N/A This retrospective study concerns 73 patients with nonfunctioning pituitary adenoma who were operated on during an 9-year period from 1981 to 1989. Among them, 7 men showed positive immunocytochemistry for FSH and negative for other pituitary hormones. Six of them had elevated serum FSH levels, and LH levels were normal. Testosterone levels were low in six patients tested. Their major symptoms were visual impairment, headache, and impotence, which had developed from two months to 2 years before sugery. Primary hypogonadism could be eliminated on clinical grounds (recent onset of hypogonadism, previous fertility, and posttreatment-improvement). Transsphenoidal adenomectomies were performed in all patients, and radiation-therapies were paralleled in 6 of them. Clinical recovery occurred in all patients. One patient who did not received radiation therapy showed regrowth of tumor mass after 18 months. In remaining 6 patients, we haven't found any evidence of tumor recurrence during follow-up period from 10 months to 6.3 years. We conclude that these 7 men had primary gonadotrope adenoma of the pituitary, and present them with a literature review.

뇌하수체 Prolactin 분비 미세 선종의 추적 관찰

이은직(Eun Jig Lee),김경래(Kyung Rae Kim),안광진(Kwang Jin Ahn),정윤석(Yoon Sok Chung),정재희(Jae Hee Jung),김미림(Mi Rim Kim),임승길(Sung Kil Lim),이현철(Hyun Chul Lee),정태섭(Tae Seop Jung),김동익(Dong Ik Kim),이병석(Byung Seok Lee 대한내과학회 1992 대한내과학회지 Vol.43 No.5

N/A N/A

TSH 분비 뇌하수체 선종 환자들의 임상적, 생화학적 특징과 치료

이우경 ( Woo Kyung Lee ),황세나 ( Se Na Hwang ),임정수 ( Jung Soo Lim ),김현민 ( Hyun Min Kim ),이은영 ( Eun Young Lee ),이상국 ( Sang Kook Lee ),김선호 ( Sun Ho Kim ),이은직 ( Eun Jig Lee ) 대한내과학회 2011 대한내과학회지 Vol.80 No.1

Background/Aims: Thyrotropin (TSH)-secreting pituitary adenoma (TSHoma) is rare and represents 1~2% of all pituitary adenomas. TSHoma should be distinguished from the thyroid hormone resistance syndrome. Patients with TSHoma may be misdiagnosed with primary hyperthyroidism and often receive inappropriate thyroid gland treatment. Methods: We assessed the clinical characteristics of patients with TSHoma who presented to Severance Hospital at the Yonsei University College of Medicine, Seoul, Korea between 2005 and 2009. Results: Of 484 patients who underwent pituitary tumor resection, eight (1.65%; five women and three men) were found to have TSHoma. The mean age was 40.6±8.9 years at diagnosis (range, 28~55 years). The median duration from onset of symptoms to diagnosis was 17 months (range, 4~60 months). Four patients had overt symptoms of hyperthyroidism and two had visual field defect. Six patients had elevated free thyroxine (FT4) levels with elevated or inappropriately normal TSH levels, and two patients had symptoms associated with Hashimoto`s thyroiditis. The serum levels of free α-subunit measured in two patients were elevated. Six of the tumors were macroadenomas (>10 mm) and two were microadenomas. Complete tumor removal was achieved in all patients. Five patients had preoperative anterior pituitary dysfunction; three patients recovered from this after surgery. Three patients were lost to follow up and five patients showed no evidence of recurrence or hyperthyroidism in the follow-up period (mean, 30.8 months, range, 3~57). Conclusions: Early diagnosis and complete removal of the tumor mass may improve the neurological and endocrine deficits. (Korean J Med 2011;80:47-55)

갑상선질환에서 혈청 Lipoprotein ( a )

조재식(Jae Sik Cho),이은직(Eun Jig Lee),김경래(Kyung Rae Kim),이경미(Kyeong Mi Lee),남문석(Moon Suk Nam),조재화(Jae Hwa Cho),신은택(Eun Tack Shin),임승길(Sung Kil Lim),이현철(Hyun Chul Lee),허갑법(Kap Bum Huh),김정호(Jeong Ho Kim),송경 대한내과학회 1994 대한내과학회지 Vol.47 No.1

N/A Background: Thyroid hormone closely relates with lipid metabolism and especially Hypothyroidism associates with hypercholesterolemia which accelerates atherosclerosis. The purpose of this study was to determine the relationship between thyroid disease and Lp (a). Methods: We evaluated 14 patients with hypothyroidism, 24 patients with hyperthyroidism and 50 normal subjects. Serum Lp (a) was measured by ELISA (IM- MUNOZYM GMBH, Germany), thyroid hormones were measured by ELISA and other lipid profiles by conventional methods. Results: Serum Lp(a) concentrations (median) of hypothyroidism (29.3 mg/dl) were significantly higher than those of hyperthyroidism (4 mg/dl and controls (10 mg/dl)(p<0.05), Total cholesterol and LDL-cholesterol of hypothyroidism (199.0±75.7 mg/dl, 134.6±57.5 mg/dl) were patients had higher total cholesterol (136.1±31.2 mg/dl) and LDL-cholesterol (66.7±31.4 mg/dl) than controls (p<0.05). Serum Lp (a) concentration had negative correlation with the levels of serum T₃, T₄, FT₄ and positive correlation with TSH (p<0.05). Conclusion: These results suggest that thyroid hormones have an influence on Lp (a) concentration.

인슐린 비의존형 당뇨병 환자의 직계자식에서 당수송체 유전자의 다형성과 인슐린 분비능 및 말초조직의 포도당 이용율 등의 대사적 측면과의 상호연관성에 관한 연구

이현철(Hyun Chul Lee),이영식(Young Sik Lee),박석원(Seog Won Park),정윤석(Yoon Sok Chung),안광진(Kwang Jin Ahn),이은직(Eun Jig Lee),임승길(Sung Kil Lim),김경래(Kyung Rae Kim),허갑범(Kap Bum Huh),김태연(Tae Yeun Kim),임정수(Jung Soo Rh 대한내과학회 1993 대한내과학회지 Vol.45 No.1

N/A Background: First-degree relatives of non-insulin dependent diabetes mellitus are generally accepted to be high risk group for development of non-insulin dependent diabetes mellitus. So we are intended to identify the early metabolic defects in the young first-degree relatives of non-insulin dependent diabetes mellitus. Methods: Ten offsprings of non-insulin dependent diabetes mellitus and ten healthy men were included in this study. They were all third decade male subjects and matched well with age and body mass indices. Both groups were not different in anthropometric measurements (IBW, BMI, WHR), dilay calorie intake and total energy consumptions (total energy expenditure, physical activity). Results: 1) Oral glucose tolerance test showed normal responses of plasma glucose levels and C-peptide levels in both groups. 2) There were statistically significant differences (p<0.05) in plasma glucose, C-peptide and insulin levels at 60 minutes between two groups (Glucose 100±19 vs. 77±19mg/dl; C-peptide 5.47±1.7 vs. 3.32±1.88ng/ml; Insulin 90.3±41.3 vs. 38.6±29.4 μU/ml). 3) The result of euglycemic hyperinsulinemic clamp study showed that offsprings of non-insulin dependent diabetes mellitus had significantly diminished rates of insulin-mediated glucose disposal compared to the control group (5.61±1.01 vs. 8.87±0.92mg/kg B.W/min, p<0.01). 4) Simple linear regression analysis showed a good correlation between peripheral glucose utilization rates and the lean mass composition measured by body composition analyzer (Futrex-5000, Futrex Co., USA). As the lean mass percentage increases, peripheral glucose utilization rate also increases with positive 1inear relationship (r2=0.49, p<0.05). 5) By the method of restriction fragment length polymorphism, we found two polymorphic Kpn I sites of 6.5 kb and 5.8 kd as described previously without any new polymorphism for GLUT4 gene DNA in both groups. We also used other two restriction endonucleases, Bam HI and Eco RI, but did not discover polymorphism at GLUT4 gene locus. Conclusion: This study supports the genetic tendency of non-insulin dependent diabetes mellitus and showed that the early metabolic defect in the young offsprings is expressed as insulin resistance rather than pancreatic beta-cell dysfunction, The insulin resistance is in the negative linear relationship with the lean mass composition and seems to arise from the skeletal muscle tissue. For preventing the development of glucose intolerant status and overt diabetes, the avoidance of obesity and maintenance of muscle mass by means of careful diet control and continuous exercise program may be helpful.

당뇨병성 백서에서 Vanadate 투여후 혈당의 변화와 근육세포내 포도당운반체 활성도 및 유전자의 조절

이현철(Hyun Chul Lee),남문석(Moon Suk Nam),이은직(Eun Jig Lee),임승길(Seung Kil Lim),김경래(Kyung Rae Kim),허갑범(Kap Bum Huh),정윤석(Yoon Sok Chung),이관우(Kwan Woo Lee),조용욱(Yong Wook Cho) 대한내과학회 1995 대한내과학회지 Vol.48 No.3

N/A Objectives: Vanadate is known to mimic several effect of insulin including the stimulation of glucose uptake and oxidation, glycogen synthesis as well as the anti-lipolytic effect. But mechanisms for these effects of vanadate are still not completely understood. The aim of this study was to elucidate the effects of vanadate on intrinsic activity of the glucose transporter and the regulation of the glucose transporter mRNA. Methods: Using age and weight-matched male Sprague-Dawley rats (average weight 250 g), the experimental groups were divided into nondiabetic rats (n= 6), streptozotocin (STZ)-induced diabetic rats (n=6), metavanadate and pervanadate treated diabetic rats (n =12). We measured weight, blood glucose, glucose transporter activity, and glucose transporter 4 (GLUT4) mRNA change. Results: 1) STZ-induced diabetic rats became catabolic and they lost their weight, but after 3 to 4 weeks of treatment with metavanadate or pervanadate, body weights were increased. Blood glucose levels in metavanadate or pervanadate treated rats were significantly lower than STZ-induced diabetic rats after 1 week treatment. 2) There was no significant toxicity in vanadates treated rats, compared with STZ-induced diabetic rats and there was no abnormal change in kidney and liver of rats under light microscope 8 weeks after vanadates treatment. 3) The glucose transporter activity of diabetic rats was significantly decreased, compared with that of normal control rats, and increased after vanadates treatment. 4) The glucose transporter mRNA of diabetic rats was markedly decreased, compared with that of normal control rats, and increased after vanadates treatment. Conclusion: In STZ-induced diabetic rats, vanadates treatment may improve insulin sensitivity through in- creased expression of GLUT4 gene.

비만증에서 Pyridostigmine , Acipimox 투여에 따른 성장호르몬 방출호르몬 자극에 의한 성장호르몬의 분비반응

남수연(Su Youn Nam),이은직(Eun Jig Lee),남문석(Moon Suk Nam),조재화(Jae Hwa Cho),김인재(In Jai Kim),김정환(Jung Hwan Kim),김경래(Kyung Rae Kim),임승길(Sung Kil Lim),이현철(Hyun Chul Lee),허갑범(Kap Bum Huh) 대한내과학회 1996 대한내과학회지 Vol.50 No.3

N/A Objectives: Obesity is associated with an impairment of normal GH secretion and blunted responses to all stimuli. Recent reports suggests that increased somatostatinergic activity is the basis for the GH derangement of obesity. However, the basic mechanism of this alteration is till being debated, The high plasma free fatty acid(FFA) is frequently observed in obesity. FFA participates in the regulation of pituitary GH secretion. To determine whether the derangement of GH secretion in obesity is associated with a high plasma FFa levels. Methods: Several tests with GH-releasing hormone(GHRH) with or without pyridostigmine (PYR) and acipimox(ACX), antilipolytic agents able to decrease FFA, were undertaken in both six obese and seven normal control subjects. Results: 1) In obese subjects, the GH response(mean peak±SEM:8.0±1.1 μg/L) to GHRH-(1-29)(1 μg/kg, iv) was significantly blunted when compared to normal controls(25.7±1.8 μg/L; p<0.05). 2) After PYR(120 mg), the response to GHRH only, but remained significantly reduce compared to controls treated with PYR plus GHRH 943.2±6.0 μg/L; p<0.05). 3) Basal FFA levels were higher than those of normal controls(p<0.05), ACX(500 mg) decreased FFA levels in both obese and normal subjects; the lowest FFA levels at 0.15 min were similar to those of normal cantrols, ACX also potentiated GHRH stimulated GH response in both obese and normal subjects. The GH responses potentiated by ACX in obesity(22.7±5.5 μg/L) were similar with those of PYR plus GHRHub ibese sybhects and GHRH in normal controls, but lower than control treated with ACX plus GHRH in normal controls, but lower than control treated with ACX plus GHBH(50.8±6.7 μg/L; p<0.05). 4) After the conbined pretreatment with ACX and PYR, GH responses in obesity(44.1±6.0 μg/LO were significantly higher than those to GHRH test, PYR plus GHRH, and ACX plus GHRH in normal controls. However their enhanced GH responses reduced compared to the control with ACX plus PYR plus GHRH(64.9±4.5 μg/L p<0.05). Conclusion: Our results are in agreement with hypothalamic hypothesis; an increase in somatostatinergic tone is responsible for the blunted GH response to GHRH in obesity. In addition, the demonstation that the decreased FFa levels induced by ACX potentiate the somatotrope responsiveness, likely acting at pituitary level, suggests that high plasma FFA levels play an important role in GH responsiveness in obesity, although other factors might also be involved in GH derangements.

한국인 인슐린 비의존형 당뇨병 및 이차성 당뇨병 환자에서 글루코키나제 유전자 변이

남재현(Jae Hyun Nam),이현철(Hyun Chul Lee),김연의(Youn Euy Kim),권석호(Suk Ho Kwon),윤용석(Yong Suk Yoon),박석원(Suk Won Park),원영준(Young Jun Won),차봉수(Bong Su Cha),송영득(Young Duk Song),이은직(Eun Jig Lee),임승길(Sung Kil Lim) 대한내과학회 1998 대한내과학회지 Vol.54 No.6

N/A Objectives: Mutations in the glucokinase (GCK) gene are considered a possible cause of maturity-onset diabetes of the young. The purpose of this study was to evaluate the contribution of this gene to the development of non insulin dependent diabetes mellitus (NIDDM), gestational diabetes mellitus (GDM) and post-renal transplantation diabetes mellitus (PTDM). Method: Identification of GCK mutation was attempted on 39 NIDDM patients, 2 GDM patients and 58 selected renal allograft recipients with PTDM and 45 normal controls. The exons in the GCK gene were examined by polymerase chain reaction (PCR), followed by analysis of single-stranded DNA conformational polymorphism (SSCP). The abnormal bands were also confirmed by DNA sequencing analysis. The exons of affected family members were also investigated for mutations of the GCK gene. Results: Two of the 58 PTDM patients (3.4%) were found to have CKK mutations. One had the mutation on exon 5 and the other on intron 7. One control subject had the mutation on intmn 9. The mutation of exon 5 was identified as a substitution of CCT (proline) for CTT (leucine) at codon 164, which has not ever reported before. The family members of the PFDM patient with mutation of exon 5 were analyzed by PCR followed by SSCP, and two of them revealed the same mutation. The abnormal band on the SSCP analysis of exon 7 was identified as the insertion of base C/T at the 39th nucleotide in intron 7. Two family members of this patients also had same band on SSCP. The one mutation of 45 normal controls was CT located at the 8th nucleotide in intron 9, which was a common polymorphism. Conclusion: We found GCK mutations in subjects with PTDM and we speculate that these mutations may be one of the contributing cause of PTDM.