Kim, Yun-Hyun;Shin, Yong-Hwan;Kim, Ji-Young;Seok, Jae-Dong
The Korean Journal of Nuclear Medicine Technology
/
v.13
no.1
/
pp.112-115
/
2009
Purpose: The test had been applied for outpatient by end of 2006, however, it has been included in the medical examination since January 2007, as demand and interests have been gradually increasing in the thyroid gland disease and cancer. thus, we would necessarily evaluate usefulness of the test by comparing the number of patients who are diagnosed as "benignancy" by the medical test with the number of outpatient who attend and are diagnosed as autoimmune thyroid disease among the benign patient, in samsung medical center for a certain period. Materials and Methods: Based on the result for Anti-TPO Antibody test by RIA for the 12,937 patients in samsung medical center from October 2007 to March 2008, for six months, benignancy rate classified by sex and age is measured statistically and number of the patients who are diagnosed as autoimmune thyroid disease are kept tracked on. Results: According to the analysis of the Anti-TPO antibody test 1,135 of 12,937, which is 8.77% are benign and 218 treated patient of them, which is 19.2%, were diagnosed as autoimmune thyroid disease. Conclusions: Based on the statistics, usefulness of the test seem to have co relationship with derivation of autoimmune thyroid disease. this is 19.2% of probability relatively high. this figure, however, does not have strong relationship with specialty of the disease. Thus screening test seems to have somewhat effectiveness, considering other experiments and their margin.
Sweet's syndrome, or acute febrile neutrophilic dermatosis, occurs in association with autoimmune diseases such as Hashimoto's thyroiditis but is rare in Graves' disease, in which all cases are induced by propylthiouracil (PTU). We report a case of Sweet's syndrome in a patient with Graves' disease treated with methimazole (MMI) during three weeks. A 34-year-old man presented with the acute onset of high fever, skin rashes on the whole body, arthralgia, and acroparesthesia. Laboratory results showed leukocytosis and elevated C-reactive protein. MMI first stopped and antibiotics and antihistamine therapy started, but his symptoms dramatically improved after oral prednisolone. Graves' disease has again been treated by MMI because of his aggravated ophthalmopathy. After one year of retreatment with MMI, there has been no recurrence of Sweet's syndrome, supporting that Sweet's syndrome in this case was not related to MMI exposure. To our knowledge, this is the first report of Sweet's syndrome associated with Graves' disease per se but not PTU or MMI use.
The canine thyroglobulin autoantibody assay is to be used for the diagnosis of autoimmune thyroid disease in dogs. Antithyroglobulin antibodies are present in about 50 percent of hypothyroid dogs. In this report, the sera of the five canine patients ($P1{\sim}P5$) referred to the Veterinary Medical Teaching Hospital in Seoul National University were assessed by T4, TSH and thyroglobulin autoantibody (TgAA). P1 was diagnosed as severe hypothyroidism since he showed very high TSH levels with low T4 values. P2 and P3 born with a genetic predisposition were assessed as normal in thyroid function. P4 was normal, but needed follow-up examination for TgAA assay. P5 showed the positive result in TgAA assay, so it was diagnosed as autoimmune thyroiditis. As the cases above show, not only T4 and TSH, but also TgAA assay to be considered for more accurate assessment of the status of the thyroid.
Although normal thyroid epithelial cells do not constitutively express HLA-DR antigen, their expression in wide spread within thyroid glands obtained from the human with autoimmune thyroid disease and with many neoplastic thyroids. We have, therefore, studied immunohistochemically with regard to the expression of HLA-DR antigen of thyroidectomy specimens from 50 patients of various thyroid diseases with use of paraffin-embedded tissue. One or two sections from each case were stained with commercially available mouse monoclonal antibody for class II HLA-DR antigen(HLA-DR/Alpha, DAKO) and examined by semiquantitative counting system for thyrocytes, neoplastic thyrocytes and other cells expressing HLA-DR antigen. All patients with lymphocytic thyroiditis(2/2) and diffuse hyperplasia(Graves' disease)(5/5), most patients with Hashimoto's disease(9/ll) expressed HLA-DR antigens in thyrocyte with abundant HLA-DR expressing lymphocytic infiltrates with lymph follicle formation in its vicinity or adjacent to the lesion. Most patients with papillary carcinoma(9/1l) had HLA-DR antigen detected in malignant thyrocytes ; while follicular carcinoma(0/3) and follicular adenoma(0/5) did not have detactable HLA-DR immunoreactivity. Adenomatous goiter(3/7) had HLA-DR antigen detected focally in lesser than half cases. Conversely, in four papillary carcinomas and three adenomatous goiters, HLA-DR expression of thyrocytes was found in the absence of HLA-DR expressing lymphoid infiltrates. In such cases therefore other factors more than thyroid autoimmunity must be causative for HLA-DR immunoreactivity. The results of this study indicate as follows. 1) The expression of HLA-DR on thyrocytes involved in autoimmune reactions appeared to be secondary to cytokine release from associated lymphocytic infiltrates. 2) Thyrocytes in thyroid lesions with equal degrees of lymphocytic infiltration without HLADR expression exhibited no HLA-DR immunoreactivity. 3) In neoplastic thyrocytes, most papillary carcinoma(9/11) exhibited detactable HLA-DR expression, while follicular carcinoma/adenoma(0/3/0/5) exhibited no detactable HLA-DR immunoreactivity which suggest the existence of divergent mechanisms inducing and modulating HLA-DR expression of different types of neoplastic thyrocytes.
Kim, Mee-Kyung;Shon, Yun-Hee;Nam, Kyung-Soo;Son, Ok-Lye;Kim, Cheorl-Ho;Jeon, Byung-Hun
Journal of Physiology & Pathology in Korean Medicine
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v.19
no.3
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pp.623-627
/
2005
Abnormal thyroid cell proliferation has a very important role in hypothyroidism. Thyroid stimulating hormone (TSH) stimulates proliferation and maintains differentiated function in thyroid follicular cells. A functioning rat thyroid cell line (FRTL) was used to study the effect of Gamgung-tang (GGT, Glycyrrhizae Radix, black beans, Angelicae Radix and Cnidii Rhizoma) on proliferation and cAMP accumulation of thyrocytes. Proliferation of cell was assessed by DNA synthesis and incorporation of $[^3H]thymidine$ into DNA. The concentration of cAMP was measured simultaneously with growth assessment. Extract of GGT ($0.15{\sim}0.9\;mg/ml$ increased DNA synthesis in a dose-dependent manner. GGT at 0.6 (p<0.05) and 0.9 mg/ml (p<0.01) significantly increased $[^3H]thymidine$ incorporation. A comparable effect was observed with TSH. GGT also enhanced cAMP accumulation. These results indicate that GGT increases the proliferation of thyrocytes and may be considered a promising agent for the treatment of autoimmune thyroid disease.
Choi, In Su;Kim, Han Kyul;Han, Dong Kyun;Baek, Hee Jo;Jang, Hae In;Kim, Chan Jong;Kook, Hoon
Clinical and Experimental Pediatrics
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v.58
no.7
/
pp.267-269
/
2015
Antithymocyte globulin (ATG) is used as an immunosuppressive treatment (IST) to deplete clonal suppressor T cells in patients with severe aplastic anemia (SAA). The depletion of suppressor T cells by ATG may affect the activation of B cells, which results in an increased risk for autoimmune conditions. A 12-year-old boy was diagnosed with idiopathic SAA. As he did not have an human leukocyte antigen-matched sibling, he was treated with rabbit ATG (3.5 mg/kg/day for 5 days) and cyclosporine. Five months later, he became transfusion independent. However, 23 months after IST, he complained of mild hand tremors, sweating, weight loss, palpitations, and goiter. Results of thyroid function tests revealed hyperthyroidism (free thyroxine, 3.42 ng/dL; thyroid stimulating hormone [TSH], <0.01 nIU/mL; triiodothyronine, 3.99 ng/mL). Results of tests for autoantibodies were positive for the antimicrosome antibody and TSH-binding inhibitory immunoglobulin, but negative for the antithyroglobulin antibody and antinuclear antibody. He was treated with methimazole, and his symptoms improved. The patient has been disease free for 39 months after IST and 9 months after methimazole treatment. This case report suggests that although rare, rabbit ATG may have implications in the pathogenesis of autoimmune hyperthyroidism. Our findings suggest that thyroid function tests should be incorporated in the routine follow-up of SAA patients treated with ATG.
Transient and permanent hypocalcemia after various types of thyroidectomy are well-known complications, and are more common after bilateral subtotal thyroidectomy for Graves' disease. However, their causative mechanisms are not well explained. Four hundred thirty patients with Graves' disease who underwent bilateral subtotal thyroidectomy from January 1983 through December 1992 were analyzed to determine the incidence and risk factors for the development of postthyroidectomy hypocalcemia. Of the 430 patients underwent bilateral subtotal thyroidectomy, symptomatic transient and permanent hypocalcemia developed in 24.2 % (104/430) and 0.5 % (2/430), respectively. With analysis of potential risk factors, the increase in incidence of the postthyroidectomy hypocalcemia was found to be statistically related to the larger thyroid gland, the larger amount of blood loss during thyroidectomy, the smaller remnant thyroid tissue, the higher levels of serum alkaline phosphatase and TBII titers. Our data suggest that impairment of parathyroid gland blood supply, degree of thyrotoxic osteodystrophy and autoimmune process of each patient are regarded as main mechanisms of postthyroidectomy hypocalcemia in patients with Graves' disease.
To evaluate the values of the thyroid autoantibody measured by radioimmunoassay (RIA) and compare it with hemagglutination method (HA) in the normal and the thyroid disease, data were obtained from total 618 persons; 236 healthy persons, 217 patients with Graves' disease (including 113 patients with undertreated Graves' disease), 100 Hashimoto's disease, 31 thyroid nodule, and 34 simple goiter. RSR kit made in England was used and could be detected to at least 3 U/ml. The positive rates of normal group were antimicrosomal antibody (AMA) 31.8%, antithyroglobulin antibody (ATA) 44.5% by RIA and there was no considerable change in sex and age distribution. In Graves' disease, the positive rates of AMA and ATA were 90.4, 76.9% by RIA, 85, 39% by HA. In Hashimoto's disease, 94,91 % by RIA, and 87,48% by HA, respectively. The autoantibody titer by RIA in thyroid autoimmune disease as well as in normal group was more senisitive than that by HA, especially in ATA. There were linear relationships between the titer of RIA and that of HA in AMA of Graves' disease and AMA and ATA of Hashimoto's disease. There was no relationship among thyroid autoantibody, free $T_4$ index, TBII, and TSH. The titers of AMA and ATA were found to decrease in patients with Graves' disease during the course of antithyroid drug therapy. Of the 236 normal subjects, thirty-seven (15.7%) had concentrations of above 7.5 U/ml in AMA, forty. four (18.6%) above 9 U/ml in ATA. These values were considered as the upper limit for the normal range. In Graves' disease, 82.7, 53.8% were above 7.5, 9 U/ml, respectively; In Hashimoto's disease, 82, 79% were positive. We conclude that RIA was more sensitve than HA in measuring the thyoird autoantibody, but we will study further more for determining the normal range and its interpretation.
Objective: Graves' disease, the most common cause of primary hyperthyroidism, is a thyroid specific autoimmune disorder. When resistance to medication is shown in spite of long term therapy with anti-thyroid drugs, radioactive iodine therapy would be chosen in Western medicine. However, this therapy has often been reported to cause patients have hypothyroidism, thus requiring them to take levothyroxine for the rest of their lives. In this study, we evaluate the clinical efficacy and safety of Ahnjeonbaekho-tang (AJBHT) on patients with Graves' disease. Methods: We prescribed AJBHT for 3 months to two groups: patients who had been taking antithyroid drugs were administered AJBHT after discontinuing the antithyroid drugs ($Com-Tx{\rightarrow}Single-Tx$), and patients who had not been taking antithyroid drugs were started with AJBHT (Single-Tx) immediately. We evaluated the thyroidal function test (TFT) and visual analogue scale (VAS) for clinical symptoms for 3 months. Results: Serum T3 and fT4 were significantly decreased in both groups and remission rate of thyroidal hormones were significantly improved in the Single-Tx group. The clinical symptoms of palpitation, fatigue, and heat intolerance were significantly improved in both groups. In the safety analysis, all patients were in normal range of liver, renal function blood test and common blood count. Conclusion: From these results, we suggested that AJBHT was effective on TFT and clinical symptoms of Graves' disease. The study supports that AJBHT may be a useful agent for patients with Graves' disease who are resistant to antithyroid medication or radioactive iodine therapy, and for patients at first diagnosis.
To evaluate the clinical and pathogenetic roles of TSH receptor antibodies in autoimmune thyroid diseases, TBII were measured by TSH-radioreceptor assay methods in 352 patients with Graves' disease, 108 patients with other thyroid diseases and 69 normal persons. The normal range of TBII activity was less than 15%. The frequencies of detectable TBII in 169 patients with untreated Graves' disease, 31 patients with hyperthyroidism under treatment and 70 patients with euthyrodism under treatment were 92.4%, 87.1% and 54.3% respectively. However 12 (21.8%) out of 55 patients who have been in remission more than one year after discontinuation of antithyroid drugs treatment had detectable TBII activities in their sera. In 196 patients with untreated Graves' disease, the frequency of TBII increased by increasing size of goiter and the frequency of proptosis was significantly high in patients whose TBII activities were more than 60%. TBII activities were roughly correlated with total $T_3,\;T_4$ and free $T_4$ index but low $\gamma^2$ value(less than 0.1). In 67 patients with Graves' disease who were positive TBII before antithyroid drugs treatment, TBII activities began to decrease from the third months and it was converted to negative in 35.8% of patients at 12 months after treatment. There were no significant differences of the declining and disappearing rates of TBII activities between high dose and conventional dose groups. TBII activities were significantly increased initially (2-4 months) and then began to decrease from 5-9 months after $^{131}I$ treatment. There were two groups, one whose TBII activities decreased gradually and the other did not change untill 12 months after subtotal thyroidectomy. Although preoperative clinical and laboratory findings of both groups were not different, TBII activities of non-decreasing group were significantly higher than those of decreasing group$(74.6{\pm}18.6%\;vs\;39.2{\pm}15.2%;\;P<0.01)$. Thirty three(55.9%) out of 59 patients with Graves' disease relapsed within 1 year after discontinuation of antithyroid drugs. The positive rate of TBII at the end of antithyroid drug treatment in relapse group(n=33) was significantly higher than those in remission group (n=26) (63.6% vs 23.1%; P < 0.05). The mean value of TBII activities at the end of antithyroid drug treatment in relapse group was significantly elevated $(29.7{\pm}21.4%\;vs\;14.7{\pm}11.1%,\;P<0.05)$. Positive predictive value of TBII for relapse was 77.8%, which was not different from those of TRH nonresponsiveness(78.6%). The frequencies of detectable TBII in 68 patients with Hashimoto's thyroiditis, 10 patients with painless thyroiditis and 5 patients subacute thyroiditis were 14.7%, 20% and 0%, respectively. However in 25 patients with primary nongoitrous myxedema, 11 patients(44%) showed TBII activities in their sera. 9 out of 11 patients who had TBII activities in their sera showed high TBII activities(more than 70% binding inhibition) and their IgG concentrations showing 50% binding inhibition of $^{125}I-bTSH$ to the TSH receptor were ranges of 0.1-2.6 mg/dl. One patient who had high titer of TBII in her serum delivered a hypothyroid baby due to transplacental transfer of maternal TBII. These findings suggested that 1) TSH receptor antibodies are closely related to a pathogenetic factor of Graves' hyperthyroidism and of some patients with primary non-goitrous myxedema, 2) measurement of TSH receptor antibodies is helpful in evaluating the clinical outcome of patients with Graves' disease during antithyroid drug treatment and in predicting the neonatal transient hypothyroidism of baby delivered from primary myxedema patients. 3) there are 2 or more different types of TSH receptor antibodies in autoimmune thyroid diseases including one which stimulates thyroid by binding to the TSH receptor and another which blocks adenylate cyclase stimulation by TSH.
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