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일차성 점액수종환자에서 차단형 TSH 수용체항체의 유무에 따른 임상상의 차이
이가희(Ka Hee Yi),안종호(Chong Ho Ahn),김원배(Won Bae Kim),정재훈(Jae Hoon Chung),조보연(Bo Youn Cho),이홍규(Hong Kyu Lee),고창순(Chang Soon Koh),송영기(Young Kee Shong) 대한내과학회 1994 대한내과학회지 Vol.47 No.5
N/A Objectives: To elucidate primary myxedema characterized by progressive atrophy of the thyroid gland and primary hypothyroidism is caused by the blocking type TSH receptor antibody and as a end result of Hashimoto's thyroiditis as well. Methods: We measured thyrotropin-binding inhibitory immunoglobulin (TBII) using radioreceptor assay and thyroid-stimuiation blocking antibody (TSBAb) by bioassay using rat thyroid cell line, FRTL-5, in the sera from 84 patients with primary myxedema and from 61 patients with Hashimoto's thyroiditis and compared their clinical characteristics. Results: Among the patients with primary myxedema THII was detected in 39 patients (46%) and TSBAb in 47 patients (64%). In patients with Hashimoto's thyroiditis, TBII was detected only in 3 patients (5%) and TSBAb in 3 patients (8.8%). The prevalences of both TBII and TSBAb were significantly higher in primary myxedema than those in Hashimoto's thyroiditis. TSBAb activity was significantly higher in TRII positive primary myxedema patients when compared with TBII negative and was positively correlated with TBII activity. The activities of both TBII and TSBAb measured in patients with Hashimoto's thyroiditis were much lower than those in primary myxedema. The mean age at the onset of primary myxedema was significantly lower in the patients with TBII. When compared with the patients with Hashimoto's thyroiditis, mean age at the onset of disease was significantly older in the TBII negative primary myxedema patients. But the age of disease onset in TBII positive myxedema was not different from that of Hashimoto's patients. As the patients were younger at the onset of disease, the prevalence of TBII was higher: for the patients under the age of 29, TBII was detected in 76%, for between 30 and 39, 55%, for 40~49, 45%, for 50~59, 16 % and for over 60, 38 %, respectively (ψ²=24.77, df=l, p<0.05). Among the patients with primary myxedema, 24h 1311-thyroid uptake values were significantly lower in patients with TBII compared to those without TBII (1.5±1.1% vs. 4.1±3.9% p<0.05). Conclusion: These results suggest that primary myxedema may be a heterogenous disease: for the development of hypothyroidism, blocking type TSH receptor antibodies play a major role in one group, especially young patients and cell-mediated destructive mechanisms may be important in another group.
이가희(Ka Hee Yi),조보연(Bo Youn Cho),이홍규(Hong Kyu Lee),고창순(Chang Soon Koh),민헌기(Hun Ki Min) 대한내과학회 1991 대한내과학회지 Vol.40 No.3
N/A Both spontaneous and exogenous hyperthyroidism result in osteoporosis by increased bone-remodeling. We studied the effect of long-term suppressive thyroxine therapy on axial bone density in 59 female patients (28 premenopausal, 31 postmenopausal). Bone densities of the lumber spine, femoral neck, femoral trochanter and Wards triangle were measured by dual photon absoptiometry and compared with those of age, sex, menopause-matched normal controls. The levels of serum osteocalcin, alkaline phosphatase, calcium, phosphorus were measured in patients and their correlations with bone densities were analyzed. The degree of change in bone density was quantified with Z transformation. Bone densities of lumbar spine and femur were decreased significantly in postmenoausal patients when compared with controls (lumbar spine: 0.8696±0.116 vs. 0.9264±0.043(g/cm²), femoral neck: 0.7246±0.096vs. 0.8020±0.037(g/cm²), femoral trochanter: 0.6021±0.088 vs 0.6489±0.032(g/cm²), Ward's triangle: 0.6216±0.128 vs. 0.6900±0.048(g/cm²), p<0.05) but in premenopausal women, there were no differences in bone densities between patients and controls. Bone densities were negatively correlated with serum ostocalcin (lumbar spine r=-0.572, femoral neck r=-0.561, femoral trochanter r=0.646, Ward's triangle r =-0.581, p<0.001), and alkaline phosphatase (lumbar spine r= -0.615, femoral neck r =-0.610 femoral trochanter r=-0.452, Ward's triangle r=-0.573, p<0.01) and Z value were negatively correlated with osteocalcin (lumber spine r=-0.427 femoral neck r=-0.473 femoral trochanter r=-0,567 Ward's triangle r=-0.464, p<0.01), and patients age (lumbar spine r=-0.464 femeral neck r=-0. 350, femoral trochanter r=-0.425, Ward. triangle r=-0.310, p<0.05). These results suggest that sucblinical hyperthyroidism induced by suppressive thyroxine therapy can cause osteoporosis by high bone turnover which is severer in older postmenoausal women. Therefore regular evaluation of bone mineral density and warning for osteoporosis will be necessary.
갑상선질환 및 비갑상선질환에서 TSH 측정의 진단적 의의
이가희(Ka Hee Yi),조보연(Bo Youn Cho),이홍규(Hong Kyu Lee),고창순(Chang Soon Koh),민헌기(Hun Ki Min) 대한내과학회 1991 대한내과학회지 Vol.40 No.3
N/A The diagnostic value of basal serum TSH measured by ultrasensitive IRMA was evaluated. For hyperthyroidism, we measured serum TSH by IRMA in 499 patients with thyroid diseases and analysed the causes of undetectable TSH levels in 821 serum samples referred for thyroid function test during one month (May, 1988). For euthyroid sick syndrome in nonthyroidal ill- nesses, we measured serum TSH using IRMA in 411 patients hospitalized due to nonthyroida1 illnesses and in 105 randomly selected patients, T3, T3RU, T4, FT4I, FT4 and rT3 were also measured by RIA. The mean of serum TSH level in 178 normal controls was 1.39±0.76 μU/ml(log mean=1.18)and the 99% confidence range(mean±3SD) was 0.19~7.4 μU/ml. the serum TSH levels of 141 patients with Graves disease were below 0.19 μU/ml and those of 136 patients (96.4%) were undetectable. In patients with thyroid diseases other than Graves disease, the serum TSH levels were decreased below 0.19 uU/ml in 6. The diagnostic sensitivity of TSH by IRMA for hyperthyroidism was 100% (141/141), and specificity was 97.8%(271/277). 176 samples (21.4%) out of 821 sera referred for thyroid function test for one month showed undetectable TSH levels. The undetectable TSH lebels were caused by Graves' hyperthyroidism in 127(72%), Graves' disease under treatment (euthyroidism) in 38(22%), thyoxine treatment in 7(3.4%), subacute thyroiditis in 2(1%), and thyroid nodule in 2(1%). Among 411 patients hospitalized due to nonthyroidal illnesses (NTI), 16 patients (3.9%) showed undetectable or low (<0.19μU/ml) TSH levels and 4 patients (0.9%) showed raised (>7.4 μU/ml) TSH levels. 6(3%) of 20 patients with abnormal TSH levels had received steroid therapy which suppress TSH secretion and 1(5%) had received metoclopropamide which antagonize dopaminergic inhibition of TSH secretion. Only 13(3.2%) out of 411 patients showed abnormal TSH levels due to NTI. Results of thyroid function test in randomly selected 105 patients with NTI showed low total T3 levels in 79(75.2%), low total T4 in 31(29.5%), low FT4I in in 11(10.5%), raised FT4 in 17(16.2%), decreased FT4 in 5(4.8%), raised rT3 in 38(36.2%), decreased rT3 in 13(12.4%). In contrast, TSH levels were abnormal only in 6(5.7%), increased in 2(1.9%) and decreased in 4(3.8%) patients with NTI. Therefore basal seum TSH measured by IRMA can represent status of pituitary-thyroid axis both in patients with thyroid diseases, especially hyperthyroidism and nonthyroidal illnesses.
Park, Min,Yi, Ja-Woon,Kim, Eun-Mi,Yoon, Il-Joo,Lee, Eun-Hee,Lee, Hwa-Youn,Ji, Kon-Young,Lee, Kwang-Ho,Jang, Ji-Hun,Oh, Seung-Su,Yun, Chul-Ho,Kim, Seung-Hyung,Lee, Ki-Mo,Song, Mun-Gyu,Kim, Dong-Hoon,Ka American Diabetes Association 2015 Diabetes Vol.64 No.1
<P>Triggering receptor expressed on myeloid cells 2 (TREM2) is known to be involved in the anti-inflammatory response and osteoclast development. However, the role of TREM2 in adipogenesis or obesity has not yet been defined. The effect of TREM2 on adipogenesis and obesity was investigated in TREM2 transgenic (TG) mice on a high-fat diet (HFD). To block TREM2 signaling, a neutralizing fusion protein specific for TREM2 (TREM2-Ig) was used. TG mice were much more obese than wild-type mice after feeding with an HFD, independent of the quantity of food intake. These HFD-fed TG mice manifested adipocyte hypertrophy, glucose and insulin resistance, and hepatic steatosis. The expression of adipogenic regulator genes, such as peroxisome proliferator–activated receptor γ and CCAAT/enhancer-binding protein α, was markedly increased in HFD-fed TG mice. Additionally, HFD-fed TG mice exhibited decreased Wnt10b expression and increased GSK-3β (glycogen synthase kinase-3β)–mediated β-catenin phosphorylation. In contrast, the blockade of TREM2 signaling using TREM2-Ig resulted in the inhibition of adipocyte differentiation in vitro and a reduction in body weight in vivo by downregulating the expression of adipogenic regulators. Our data demonstrate that TREM2 promotes adipogenesis and diet-induced obesity by upregulating adipogenic regulators in conjunction with inhibiting the Wnt10b/β-catenin signaling pathway.</P>