Endocrinology and Metabolism

Original Articles

The Changes of Serum Soluble Intercellular Adhesion Molecule-1(ICAM-1) According to the Clinical Course of Graves' Disease Treated with Antithyroid Drug.: Jin Hong Lee, Jae Kyu Shin, So Young Bak, Bong Soo An, Bon Jeong Ku, Mee Ae Ahn, Jun Sik Jeon, Young Kun Kim, Heung Kyu Ro; J Korean Endocr Soc. 1996;11(3):293-301. Published online November 7, 2019

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Abstract PDF: Background
TSH binding inhibiting imunoglobulins(TBII) are autoimmune antibody causing autoimmune thyroid diseases such as Graves disease or Hashimoto's thyroiditis, while intercellular adhesion molecule-1(ICAM-1) is known as a substance expressed at the site of autoimmune reaction in relation with lymphocyte infiltration. The serum TBII activity is used as an index of the disease course and prognosis of Graves disease treated with antithyroid drugs, propylthiouracil or methimazole. The aim of this study is to understand the change of serum ICAM-1 level according to the change of the degree of autoimmunity and clinical course of Graves disease. Methods: In order to study the change of soluble ICAM-1 and relationship to the immune mechanism of Graves' disease, we measured serum levels of TBII and ICAM-1 in patients(n 35) with Graves disease before and after treatment with antithyroid drugs and in relapsed patients using a highly sensitive ELISA method. Results: The serum levels of TBII and ICAM-1 were markedly elevated in patients with Graves disease before treatment than normal controls and there were good correlation between TBII and ICAM-1 level. In patients with normalized TBII levels after 22 months antithyroid drug treatment, the ICAM-1 levels became normal but in the patients with high serum TBII level showed high serum level of ICAM-1 even with clinical remission with same treatment. The serum levels of TBII and ICAM-1 in relapsed patients were elevated as those of patients before treatment. Conclusion: With the above results, we can conclude that not only the TBII level but seru ICAM-1 level also reflect the degree of autoimmune activity of Graves disease and may be used as an index of the disease course and prognosis of Graves disease treated with antithyroid drugs.

Clinical Characteristics of Graves' Disease Patients with Undetectable Thyrotropin Binding Inhibitor Immunoglubulin (TB2).: Bo Youn Cho, Won Bae Kim, Hong Gyu Lee, Chang Soon Koh, Seong Yeon Kim, Seok In Lee, Jae Seok Chun, Kyung Soo Park; J Korean Endocr Soc. 1996;11(1):68-74. Published online November 7, 2019

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Abstract PDF: Background
Graves disease is an autoimmune disease caused by TSH receptor antibodies. Thyrotropin binding inhibitor immunoglobulins(TBII) are detected in most Graves patients, but some patients have no TBII activities in their sera. It is unknown whether the clinical features of TBII-positive patients are different from those of TBII-negative patients. Methods: To evaluate the prevalence of TBII-negative Graves' patients and its clinical differences from TBII-positive patients, we examined TBII by radioreceptor assay in 686 consecutive untreated Graves patients. We found 84 TBII-negative patients(15 men and 69 women, mean age ±EM: 40.9±.4 years) and compared their clinical characteristics with 87 TBII-positive patients (22 men and 65 women, mean age±EM: 39.9±.5 years) who were selected randomly from the same patients group. Results: In this study, TBII was undetectable in 12.2% of patients with Graves' disease(84 of 686). TBII-negative group had a less weight loss than TBII-positive group. However, there was no significant differences in age, sex ratio, prevalence of ophthalmopathy, duration of illness and positive rate of family history for thyroid diseases between TBII-negative and -positive groups. Serum total T or T levels were not different from each other, but T3-uptake was significantly higher in TBII-positive group than that in TBII-negative group, suggesting that the free hormone levels in TBII-negative group might be lower. The thyroid uptake of 99mTcO4 was significantly higher in TBII positive group than that in TBII-negative group. Thyroid autoantibodies, including antimicrosomal and antithyroglobulin antibodies were detected in almost all patients but there were no differences in titers and positive rate between TBII-negative and -positive groups. Conclusion: Although TBII-negative Graves patients showed less weight loss and low 99mTc04 thyroidal uptake compare to TBII-positive patients, the clinical and immunological characteristics of TBII-negative patients are not different from TBII-positive one.

The Change of Pulmonary Artery Pressure in Graves'Disease Before and After Treatment.: Taek Man Nam, Han Soo Cho, Jin Seo Lee, Young Rim Song, Doo Man Kim, Young Cheoul Doo, Cheol Young Park, In Kyung Jeong, Eun Gyung Hong, Seong Jin Lee, Gi Weon Oh, Hyeon Kyu Kim, Jae Myung Yu, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park; J Korean Endocr Soc. 2003;18(5):465-472. Published online October 1, 2003

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Abstract PDF: BACKGROUND
Exertional symptoms, dyspnea and impaired effort tolerance are common in patients with Graves' disease. Proposed explanations include: high-output left heart failure, ineffective oxygen utilization and respiratory muscle weakness. In addition, pulmonary hypertension has also been reported in patients with Graves' disease. A high prevalence of hypothyroidism and positive thyroid autoantibody were also observed in patients with pulmonary arterial hypertension. Therefore, the pulmonary artery pressure in patients with Graves' disease was evaluated. METHODS: Two-dimensional and Doppler echocardiographic examinations (Hewlett Packard Sonos 2500) were performed to determine the pulmonary artery (PA) pressure in 26 Graves' disease patients, both before and after treatment (23 patients with propylthiouracil and 3 with RAI), and in 10 euthyroid controls. The changes in the PA pressure after treatment were evaluated in 13 patients with Graves' disease, who became euthyroid after treatment. RESULTS: The pulmonary artery pressure was increased in the untreated Graves' disease patients compared to the normal controls (23.5+/-2.32 vs. 29.6+/-10.3 mmHg). 38.5% of the Graves' disease patients (10/26) showed pulmonary arterial hypertension (PA>30 mmHg) and the serum TBII levelwas higher in the Graves' disease patients with pulmonary arterial hypertension than in those with normal PA pressure (P<0.05). In the Graves' patients who became euthyroid after treatment, the PA pressure was significantly decreased. CONCLUSION: 38.5% of the untreated Graves' disease patients showed pulmonary arterial hypertension, and the pulmonary artery pressure was significantly decreased in those who became euthyroid after treatment. The pathogenesis and clinical importance of pulmonary arterial hypertension in Graves' disease requires further studies.

Differential Diagnostic Value of TSH Receptor Antibody Measurements in Thyrotoxic Postpartum Patients with History of Graves' Disease.: Seong Jin Lee, Yun Ey Chung, Ha Young Kim, Jung Hee Han, Jong Chul Won, Ahm Kim, Jin Sook Ryu, Dae Hyuk Moon, Il Min Ahn; J Korean Endocr Soc. 2001;16(1):75-84. Published online February 1, 2001

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Abstract PDF: BACKGROUND
It is known that pregnancy markedly influences the clinical course of autoimmune thyroid diseases. In the postpartum period, various kinds of autoimmune thyroid dysfunctions can be observed. Thyroid dysfunction is found in 5.5-7.1% of postpartum women in the general population. Among those who show thyroid dysfunction after delivery, some will develop Graves' disease and others will develop postpartum thyroiditis. It is also known that patients with Graves' disease may manifest thyrotoxicosis in the postpartum period because of postpartum thyroiditis or relapse of the Graves' disease itself. We evaluated the clinical features of postpartum thyrotoxicosis in Graves' disease patients to find diagnostic indices that could be used in differentiating between postpartum thyroiditis and relapse of Graves' disease. METHOD: We reviewed the cases with postpartum thyrotoxicosis in patients that had a history of Graves' disease between 1995 and 2000. The diagnosis of postpartum thyroiditis had been made by means of a 99mTc thyroid scan or by the observation of a typical triphasic thyroid function change, in cases where a 99mTc thyroid scan was not possible because of breast feeding. We measured the serum TSH, free T4, free T3, TSH binding inhibiting immunoglobulin (TBII), anti-thyroid peroxidase (TPO) antibody, and anti- thyroglobulin (Tg) antibody serially from the time of the diagnosis of Graves' disease to the time of postpartum thyroid dysfunction. RESULTS: Eleven patients, 5 patients in the postpartum thyroiditis (PPT group) and 6 patients with relapse of the Graves' disease (GD group), were identified. The mean values of TBII of two groups at the time of diagnosis of Graves' disease were 40.9+/-4.8 IU/mL (PPT group), 58.9+/-23.5 IU/mL (GD group) respectively, which were insignificant. The mean values of TBII of the two groups at early pregnancy were 3.2+/-1.9 IU/mL (PPT group), 41.6+/-22.6 IU/mL (GD group) and this difference was statistically significant (p=0.009). The mean values of TBII of the two groups at the time of postpartum thyrotoxicosis were 1.9+/-1.6 IU/mL (PPT group), 51.5+/-23.2 IU/mL (GD group) which were also statistically significant (p=0.003). The mean values of anti-TPO antibody, anti-Tg antibody, disease duration, and treatment duration between the two groups were not significantly different. The onsets of thyroid dysfunction after delivery in the two groups were 2.6+/-2.0 (PPT group), 4.0+/-3.9 (GD group) months which were statistically insignificant. CONCLUSION: These data suggest that the measurement of TBII at the time of the postpartum thyrotoxic period, could help to differentiate postpartum thyroiditis from a relapse of Graves' disease in those patients that have a history of Graves' disease especially when thyroid scan is not possible because of breast feeding.

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