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PubMed1998

Use of radioactive iodine for thyroid remnant ablation in well-differentiated thyroid carcinoma to replace thyroid reoperation.

Complete thyroidectomy was recommended for patients with well-differentiated thyroid carcinoma to remove any potential residual contralateral cancer tissue and to facilitate detection of metastatic lesions by radioactive iodide (131I). Unfortunately, 8-32% incidence of severe complications were noted after reoperation. At present, there are still not enough data about the ablative effect of 131I for such conservative surgical treatment of well-differentiated thyroid cancers. The major goal of the present study was to examine the effects of 311I for ablation of thyroid remnants in order to obviate the severe complications associated with reoperation. From January 1977 to December 1995, 210 papillary or follicular thyroid carcinoma patients received subtotal thyroidectomy or lobectomy. After the operation, 46 of the 210 patients received 131I for remnant ablation. At doses of > or = 30 mCi 131I, 38 thyroid remnants were successfully ablated; 25 of 38 (65.8%) patients successfully ablated patients received 30 mCi 131I one-four times. Five patients expired during the follow-up period, including two follicular carcinoma patients who were misinterpreted as having benign lesions in the first operation. Patients in the overall failure versus success group for thyroid remnant ablation revealed increased age, histopathology of follicular carcinoma, higher postoperative 131I uptake in the neck bed, higher postoperative thyroglobulin levels, bigger tumor size, and higher mortality. In conclusion, repeated 30 mCi 131I treatments were adequate for most thyroid remnant ablations following subtotal thyroidectomy or lobectomy in well-differentiated thyroid cancer patients. Misinterpretation of follicular cancer as benign lesions and unresectable tumor comprised the main reasons for mortality.

Adenocarcinoma, Follicular↗
PubMed2003

Thyroid gland clonality revisited: the embryonal patch size of the normal human thyroid gland is very large, suggesting X-chromosome inactivation tumor clonality studies of thyroid tumors have to be interpreted with caution.

It is widely assumed thyroid carcinomas, adenomas, and many hyperplastic nodules are monoclonal. This belief is based on X-chromosome inactivation analyses of thyroid tumors. However, X-chromosome inactivation studies of tumors are informative only when interpreted in the context of the clonal composition of the surrounding normal tissue, and in the case of thyroid tissue, such analyses have never been systematically performed in humans. The aim of this study was to determine the embryonal patch size of the human thyroid gland. We performed human androgen receptor (HUMARA) assay-based X-chromosome inactivation analysis on 20 microdissected normal thyroid specimens from 16 female subjects. Monoclonality was observed in 70% of tested specimens, and polyclonal X-inactivation patterns were present in only 30% of specimens. According to our results the monoclonal patch size of normal human thyroid tissue is between 48 mm(2) and 128 mm(2) (1-4 x 10(5) thyrocytes). Our data indicate that normal thyroid epithelium is organized into large stem cell-derived monoclonal patches. Therefore, monoclonality in neoplastic and hyperplastic lesions may just be a reflection of normal thyroid epithelium clonal composition.

Adult↗
PubMed1987

Comparison of serum thyroid microsomal and thyroid peroxidase autoantibodies in thyroid diseases.

Recent evidence indicates that human thyroid peroxidase (TPO) has most of the characteristics of the thyroid microsomal antigen. The question of whether TPO accounts for part or all of the antigenic activity recognized by circulating anti-microsomal antigen autoantibody (anti-M Ab) remains to be determined. The availability of an anti-TPO monoclonal antibody and of a highly purified TPO preparation allowed the development of specific and sensitive radioassays for anti-TPO autoantibody (anti-TPO Ab). In this study we compared anti-M Ab and anti-TPO Ab levels in serum from 128 subjects, including patients with Hashimoto's thyroiditis (n = 31), idiopathic myxedema (n = 11), hyperthyroid Graves' disease (n = 45), miscellaneous nonautoimmune thyroid disorders (n = 9), and normal subjects (n = 32). Anti-M Ab and anti-TPO Ab were measured by radioimmunological methods employing two different assay designs: 1) competitive radioassay (CR), based on the inhibition of radioiodinated antibody binding to human thyroid microsomes coated on microtiter wells, using a) [125I]immunoglobulin G (IgG) containing a high anti-M Ab titer (for anti-M Ab determinations), or b) [125I]anti-TPO monoclonal antibody (for anti-TPO Ab); and 2) sandwich immunoradiometric assay (IRMA) using microtiter wells coated with thyroid microsomes (for anti-M Ab determinations) or immunoaffinity-purified TPO (for anti-TPO Ab determinations) and [125I]anti-human IgG antibody. Anti-M Ab also was measured by passive hemagglutination. Anti-M Ab titers by PH closely correlated with anti-TPO Ab levels whether assayed by IRMA (r = 0.905; P less than 0.00001) or CR (r = 0.922; P less than 0.00001). Even closer correlations were found when anti-M Ab and anti-TPO Ab both were measured by the same type of radioassay procedure (IRMA, r = 0.945 and P less than 0.00001; CR, r = 0.957 and P less than 0.00001). No differences in the correlation between anti-M Ab and anti-TPO Ab results were found when the data in patients with different autoimmune thyroid disorders were analyzed separately. Further and more direct evidence for the identity of anti-M Ab and anti-TPO Ab was provided by the ability of purified TPO to completely inhibit the binding to thyroid microsomes of radioiodinated IgG preparations containing high anti-M Ab titers. In conclusion, our results provide strong support for the concept that TPO accounts for virtually all of the antigenic determinants reacting with the autoantibodies commonly termed anti-M antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigens↗
PubMed2000

Expression and regulation of regulated on activation, normal T cells expressed and secreted in thyroid tissue of patients with Graves' disease and thyroid autonomy and in thyroid-derived cell populations.

Thyroid glands affected by Graves' disease (GD) show striking lymphocytic infiltration, mainly by CD45RO(+) T cells. The mechanisms by which the various lymphocytic subsets are recruited and maintained in the thyroid are unknown. RANTES (regulated on activation, normal T cells expressed and secreted) in interaction with its receptors (CCR1, CCR3, CCR4 and CCR5) may be one of the favorite chemokines involved in the cell trafficking and maintenance. RANTES messenger RNA (mRNA) was quantified in the thyroid tissue of 16 patients with GD and 7 patients with thyroid autonomy (TA), using competitive RT-PCR. We found a clear correlation between the RANTES mRNA level and 1) the degree of T-cell infiltration (r = 0.68), and 2) the level of serum antibodies to thyroid peroxidase (r = 0.76) in GD but not in TA patients. There was no difference between the autonomous nodules and the quiescent surrounding tissue in TA patients. To define the cellular source of RANTES mRNA and protein, we examined various thyroid-derived cells. Lymphocytes showed a markedly higher basal RANTES mRNA and protein level (mean +/- SEM; pg/mL, n = 3; 140 +/- 30) than thyrocytes (12 +/- 5) and fibroblasts (9 +/- 2). Lymphocyte stimulation with PMA enhanced RANTES secretion significantly (4490 +/- 200). Fibroblasts responded to stimulation with interleukin 1 (530 +/- 220) and tumor necrosis factor alpha (2780 +/- 1790), whereas thyrocytes did not. However, some thyroid carcinoma cell lines showed very high basal and stimulated RANTES expression. Lymphocytes expressed the mRNA of all chemokine receptors that bind RANTES. The number of CCR3(+) and CCR5(+) T cells was significantly higher in thyroid-derived leukocytes than in those in the peripheral blood stream. We conclude that RANTES expression, mainly by lymphocytes, is perhaps involved in the maintenance of lymphocytic infiltration and, therefore, in the autoimmune responses in GD.

Cells, Cultured↗
PubMed1985

Thyroid function after resection for non-toxic goitre with special reference to thyroid lymphocytic aggregation and circulating thyroid autoantibodies.

A series of 91 patients operated on for non-toxic goitre was followed systematically during 24 months post-operatively with regard to thyroid function. A thyroid remnant of at least 5 to 8 g was left in the majority of cases, and thyroid replacement was not given. Histopathological grading was performed on goitrous specimens with reference to lymphocytic infiltration. Thyroglobulin antibodies and thyroid microsomal antibodies were determined pre-operatively. Goitre resection provoked a high, but transient increase in serum thyroid stimulating hormone (TSH) levels with peak values 3 to 6 months after operation. Twenty-four months after surgery serum TSH values had normalized, but were still slightly elevated in patients with bilateral surgery and high lymphocytic infiltration, 9% of the patients. The concentration of serum free thyroxine index (FT4I) and serum total triiodothyronine (TT3) decreased after operation, but within reference range. Twenty-four months after surgery, serum FT4I was back to baseline values, while serum TT3 was still lowered compared to the pre-operative level. None of the patients developed overt hypothyroidism. Occurrence of circulating thyroid autoantibodies was not related to post-operative changes in thyroid parameters. We conclude that thyroid replacement therapy seems not to be indicated routinely following resection for non-toxic goitre, but precaution should be taken in case of bilateral resection and high lymphocytic infiltration of goitrous specimens.

Adolescent↗
PubMedDate not supplied

[Relationship between thyroid echogram and thyroid function in Hashimoto's thyroiditis].

Seventeen cases of untreated Hashimoto's thyroiditis were selected from the files of the Taipei Municipal Jen-Ai Hospital during the period from Jan. 1985 to Jan. 1986. All the cases were confirmed by a physical examination, determination of thyroid antibodies and fine needle aspiration cytology. Thyroid function was also determined. According to the echogenicity of the thyroid, they were divided into 2 groups, group A (8 cases) and group B (9 cases). In group A, homogeneous hypoechogenicity of the thyroid was noted and was lower than that of the adjacent muscles. In group B, heterogeneous echogenicity of the thyroid with equal or higher echogenicity than that of the adjacent muscles was noted. Group A showed a significantly lower serum T4, T3 and a higher serum TSH in comparison with group B. Five cases in group A presented hypothyroidism clinically while only 1 in group B presented. In conclusion, in the cases of Hashimoto's thyroiditis, the homogeneous hypoechogenicity of the thyroid echogram suggested the possibility of hypothyroidism. Statistically, the sensitivity was 83.3%, specificity 72.8%, positive prediction value 62.5% and the negative prediction value was 88.9%.

Adolescent↗
PubMed1983

Free thyroid hormone index, thyroid hormone/thyroxin-binding globulin ratio, triiodothyronine uptake, and thyroxin-binding globulin compared for diagnostic value regarding thyroid function.

The thyroid hormone/thyroxin-binding globulin (TBG) ratio and the free thyroid hormone index (FTI) were compared in 372 subjects classified according to age, sex, and biochemical and clinical findings. Age-related variations in thyroid function tests were investigated, as was the relationship between triiodothyronine uptake and TBG. Men, but not women, showed significant age-dependent changes in concentrations of thyroid hormones. FTI was as good as the thyroid hormone/TBG ratio in hyperthyroidism and was a better index of thyroid status in pregnancy, TBG deficiency, and hypothyroidism. In addition, the triiodothyronine uptake correlated extremely well with TBG (r = -0.95, p less than 0.001) and was very efficient in detecting decreased and significantly increased concentrations of TBG. I conclude that FTI is a better discriminator of functional status of the thyroid over a wider range of TBG values than is the thyroid hormone/TBG ratio. Further, the triiodothyronine uptake test produced diagnostic information equivalent to that of TBG estimation and thus should not be replaced in routine use.

Adolescent↗
PubMed2003

Effects of a dietary thermally oxidized fat on thyroid morphology and mRNA concentrations of thyroidal iodide transporter and thyroid peroxidase in rats.

BACKGROUND/AIM: Recent studies demonstrated that feeding oxidized fats increases the concentrations of total and free thyroxine in blood of rats and pigs. This finding suggested that oxidized fats affect the function of the thyroid gland. This study investigates the effects of a thermally oxidized dietary fat on the morphology of the thyroid gland and on the expression of proteins (Na(+)/I(-) symporter, thyroid peroxidase) involved in the synthesis of thyroid hormones in rats at different dietary iodine concentrations. METHODS: An experiment was conducted with 48 growing male Sprague-Dawley rats which were allotted to four groups of 12 animals each. According to a bifactorial experimental design, the rats received semisynthetic diets with 10% of either a fresh or an oxidized fat, with low (50 microg/kg) or adequate (400 microg/kg) iodine concentrations, over a period of 38 days. The oxidized fat was prepared by heating sunflower oil at a temperature of 55 degrees C for a period of 5 weeks. The oxidized fat had much higher concentrations of lipid peroxidation products than the fresh fat as assessed by determining the peroxide concentrations (877 vs. 33 mEq O(2)/kg) and those of thiobarbituric acid reactive substances (25 vs. 0.7 micromol/kg). RESULTS: Rats fed the diets containing oxidized fat had higher concentrations of total and free thyroxine in plasma, a greater height of thyroid epithelial cells, a smaller diameter of thyroid follicle lumen, a lower Na(+)/I(-) symporter mRNA concentration, and a higher thyroid peroxidase mRNA concentration than rats fed the fresh fat (p < 0.05 for all effects). The concentrations of triiodothyronine and thyrotropin were not different between rats fed the fresh fat and those fed the oxidized fat. The dietary iodine supply also had significant effects on some of the parameters analyzed. There were no interactions between type of fat and dietary iodine concentrations. CONCLUSION: The rat model used here shows that dietary oxidized fats affect the morphology and the function of the thyroid gland, irrespective of the dietary iodine supply.

Animals↗
PubMed1991

Asialoagalacto-human chorionic gonadotropin, a carbohydrate-modified variant of human chorionic gonadotropin, antagonizes the stimulatory actions of bovine thyroid-stimulating hormone on thyroid function and HLA-DR expression in human thyroid in vitro and in vivo.

The concept of using thyroid-stimulating hormone (TSH) receptor antagonists in the management of Graves' disease is intriguing. Therefore, we investigated a TSH receptor antagonist derived from human chorionic gonadotropin (hCG) with respect to TSH receptor binding, adenylate cyclase activity, thyroid hormone release, and HLA class II antigen expression in vitro and in an in vivo model. A variant of hCG, asialoagalacto-hCG, like asialo-hCG and unlike hCG itself, inhibited both 125I-bTSH binding and cAMP response to bTSH in human thyroid membranes. However, like intact or deglycosylated hCG and unlike asialo-hCG, asialoagalacto-hCG displayed a limited affinity for hepatic asialoglycoprotein receptors, a likely marker for its in vivo turnover rate. It proved capable of inhibiting bTSH-stimulated thyroid hormone release in human thyroid slices as well as in the nude mouse bearing human thyroid transplants. It also prevented bTSH induced hypertrophy of transplanted thyrocytes. Further, HLA-DR expression induced by bTSH in the presence of gamma-interferon on human thyrocytes was inhibited. In conclusion, we present evidence that asialogalacto-hCG antagonizes bTSH actions on thyroid function and HLA-DR expression in human thyroid in vitro and, more importantly, in an in vivo model. Hence, the hCG variant described here or similar agents should warrant further exploration in the study and treatment of Graves' disease.

Adenylyl Cyclases↗
PubMed1995

Stimulation by thyroid-stimulating hormone and Grave's immunoglobulin G of vascular endothelial growth factor mRNA expression in human thyroid follicles in vitro and flt mRNA expression in the rat thyroid in vivo.

To elucidate the pathogenesis of thyroid gland hypervascularity in patients with Graves' disease, we studied the expression of mRNAs for vascular endothelial growth factor (VEGF) and its receptor, Flt family, using human thyroid follicles in vitro and thiouracil-fed rats in vivo. Human thyroid follicles, cultured in the absence of endothelial cells, secreted de novo-synthesized thyroid hormone in response to thyroid-stimulating hormone (TSH) and Graves' IgG. The thyroid follicles produced VEGF mRNA but not flt-1 mRNA. The expression of VEGF mRNA was enhanced by insulin, tumor-promoting phorbol ester, calcium ionophore, dibutyryl cAMP, TSH, and Graves' IgG. When rats were fed thiouracil for 4 wk, their serum levels of TSH were increased at day 3. VEGF mRNA was also increased on day 3, accompanied by an increase in flt family (flt-1 and KDR/ flk-1) mRNA expression. These in vitro and in vivo findings suggest that VEGF is produced by thyroid follicles in response to stimulators of TSH receptors, via the protein kinase A and C pathways. VEGF, a secretable angiogenesis factor, subsequently stimulates Flt receptors on endothelial cells in a paracrine manner, leading to their proliferation and producing hypervascularity of the thyroid gland, as seen in patients with Graves' disease.

Animals↗
PubMed2000

Developmental regulation of thyrotropin receptor gene expression in the fetal and neonatal rat thyroid: relation to thyroid morphology and to thyroid-specific gene expression.

The TSH receptor plays a pivotal role in thyroid gland function, growth, and differentiation, but little is known about its role or regulation in the fetus and neonate. To explore these questions, we systematically evaluated TSH receptor gene expression at the level of messenger RNA (mRNA) in thyroid glands obtained from rat fetuses and neonates, from 14 days gestation to day 5 of postnatal life. Results were compared with histological evidence of differentiation and to thyroid-specific gene expression. Northern blot and RT-PCR analysis revealed that TSH mRNA was first detected at low levels on fetal day 15, but it increased 3- to 15-fold on fetal days 17-18. Up-regulation of TSH receptor mRNA on fetal day 17-18 was accompanied by the first appearance of colloid formation and of follicular development on morphological examination. It was also paralleled by increased expression of the thyroid-specific genes thyroglobulin (Tg) and thyroid peroxidase. Unexpectedly, TSH mRNA abundance was 2- to 3-fold higher in pregnant dams than in nonpregnant adult females or adult males. In view of the 8-day lapse between the first appearance of the thyroid diverticulum and up-regulation of TSH receptor gene expression, we conclude that pituitary TSH, acting through its receptor, plays an important role in terminal thyroid maturation, but it is not involved earlier in gestation. Similarly, these data support previous evidence that the weak thyrotropic activity of human CG could not be of significance in early fetal thyroid gland development. The increased TSH receptor mRNA on fetal day 17-18 may be attributable to up-regulation by TSH, which is first secreted into the fetal circulation at this time. The significance of the increased TSH receptor expression during pregnancy remains to be explored.

Animals↗
PubMed1975

[Clinical studeis on the regulatory system of thyroid hormone secretion and serum triiodothyronine. Part III. Studies on thyroid hormone change and its relationship when TSH in cases with subclinical hypothyroidism (Hashimoto's thyroiditis and 131I treated Graves' disease)].

Changes in thyroid hormone levels and their relationship with TSH in cases with Hashimoto's thyroiditis and 131I treated Graves' disease in subclinical hypothyroid state were investigated: 1) In 34 cases with Hashimoto's thyroiditis, TSH levels was 14.7 +/- 26.8 muU/ml (mean +/- s.d.), T3 144.5 +/- 33.6 Rg/100 ml; T4 6.7 +/- 2.4 MUG/100 ML; T3RU 25.4 +/- 3.2%; F.T.I. 2.0g +/- O.89; T3/T4 2.46+/- 1.04%. It was noted that TSH levels revealed significant positive correlation with T3/T4 (r=0.77); significant inverse correlation with F.T.I. (r= - 0.51); and non-significant inverse correlation with T3 levels (r= - 0.06). These results indicate that T3 might play a more important role than T4 in maintaining normal thyroid function (so-called T3 euthyroidism). This is probably based on metabolic disturbance of iodine which is common in Hashimoto's thyroid. In several cases with rather high normal basal T3 levels, no significant elevation in T3 was observed in spite of elevated TSH level following TRH administration. This might indicate that the thyroid is fully functioning and that no more reserve is left for the thyroid to respond further to elevated TSH. 2) In 30 cases with 131I treated Graves' disease, TSH concentration was 22.3 +/- 29.8 muU/ml (mean +/- s.d.); T3 100.7 +/- 35.4 ng/100 ml: T4 6.2 +/- 2.9 MUG/100 ML; T3RU 25.6 +/- 2.3%; F.T.I. 1.87 +/- 0.85; T3/T4 1.80 +/- 0.64. Significant inverse correlation was noted between TSH levels and F.T.I. as well as T3 levels. Although TSH levels showed significant positive correlation with T3/T4 (r=0.44), its degree of correlation was not as good as that with F.T.I. (r= - 0.71) and T3 (r= - 0.53). These results indicate that there is no preference in T3 production. From the responsiveness of thyroid and pituitary following TRH administration, assumption can be drawn that 131I treated Graves' patients, who became euthyroid, may in fact be on the way to hypothyroidism.

Follow-Up Studies↗
PubMed1998

Hyperfunctioning thyroid adenoma concomitant with papillary thyroid carcinoma, follicular thyroid adenoma and primary hyperparathyroidism.

A case of 67-year-old woman with hyperthyroidism due to functioning thyroid adenoma is reported. The patient had concomitant follicular thyroid adenoma and primary hyperparathyroidism in addition to functioning adenoma. Histological examination of the excised thyroid tissue revealed occult papillary carcinoma within a functioning adenoma. Genetic analysis of such tumors indicated that functioning adenoma and papillary carcinoma may be etiologically independent. There have been a number of case reports on the coexistence of functioning thyroid adenoma and thyroid cancer or hyperparathyroidism, but none of the studies had examined the etiologic relationship of these lesions on a genetic basis. Furthermore, to our knowledge, this is the first report of the concurrence of four tumors in the neck, functioning thyroid adenoma, papillary thyroid carcinoma, follicular thyroid adenoma and parathyroid adenoma.

Adenoma↗
PubMed1991

Thyroid microsomal antigen in Graves' thyroid is not different from that in normal thyroid.

Differences from normal in microsomal antigen (M-Ag) may be involved in the development of autoimmune thyroid disease. We compared the M-Ag in Graves' thyroid immunologically and biochemically to that in normal thyroid. The concentration of M-Ag, measured with an enzyme-linked immunosorbent assay, was significantly greater in the Graves' microsomes than in normal microsomes. Binding of a patient's microsomal antibody to Graves' microsomes was completely inhibited when the serum was first incubated with normal thyroid microsomes. Sodium dodecylsulfate-polyacrylamide gel electrophoresis and Western blotting were done with a monoclonal antibody to denatured M-Ag. In both Graves' and normal thyroids, M-Ag existed as 107-, 101-, and 95-kDa peptides. After incubation with V8 protease, the residual antigenic peptide had a molecular weight of less than 60,000 and after incubation with trypsin, 95- and 87-kDa peptides and several smaller antigenic peptides were found. There were no significant differences in the pattern of normal and Graves' microsomes after digestion. Two-dimensional gel electrophoresis of Graves' microsomes showed that the isoelectric point for the 107-kDa peptide was at pH 7.2; that for the 101-kDa peptide was at pH 6.2, and that for the 95-kDa peptide was at 6.5. These values were not different from those observed for normal microsomes. These results indicate that M-Ag in Graves' thyroid does not differ from that in normal thyroid, and that microsomal antibodies in autoimmune thyroid disease probably do no arise from differences in the antigen.

Autoantigens↗
PubMed2006

The evaluation of thyroid functions, thyroid antibodies, and thyroid volumes in children with epilepsy during short-term administration of oxcarbazepine and valproate.

PURPOSE: The aim of this study was to evaluate the effects of short-term oxcarbazepine (OXC) and valproate (VPA) monotherapy on thyroid functions in children. METHODS: Fifty-five newly diagnosed epileptic children with normal thyroid functions (confirmed with the thyrotropin releasing hormone stimulation test) participated in this study. VPA treatment was started in 30 patients and OXC in 25 patients. Serum thyroxine (T(4)), free thyroxine (fT(4)), triiodothyronine (T(3)), free triiodothyronine (fT(3)), reverse T3 (rT(3)), thyroid peroxidase antibodies (TPO-ab), and urine iodine levels were evaluated at baseline and at the third and sixth months of therapy. RESULTS: In the OXC group, serum T(4), fT(4), T(3), fT(3), and rT(3) levels were found to be decreased at the third and sixth months, the differences were significant compared to the baseline values except for fT(3) levels at the third month and fT(4) and rT(3) levels at the sixth month (p < 0.05). At the sixth month, serum T(4) level dropped below the normal reference value in 8 (32%), fT(4) in 5 (20%), T(3) in 4 (16%), and fT(3) in 3 (12%) patients. In the VPA group, mean T(4), fT(4), T(3), fT(3), and rT(3) levels at 3 and 6 months remained similar compared to the baseline values (p > 0.05). Mean serum thyroid stimulating hormone levels increased significantly at the sixth month compared to the baseline values in the VPA group (p < 0.05) while it remained unchanged in the OXC group (p > 0.05). There was no effect of either drug on urinary iodine excretion and serum TPO-ab levels remained in normal ranges throughout the study. CONCLUSIONS: In this prospective study, it is documented that children under short-term OXC or VPA therapy showed altered thyroid functions similar to the changes observed after long-term treatment. Although, the clinical significance of these results need to be evaluated with future studies, this observation of altered thyroid functions points out that thyroid functions may need to be monitored closely in children receiving antiepileptic treatment, even in the short-time interval.

Antibodies↗
PubMed1988

[Clinical studies on abnormal thyroid stimulators in patients with Graves' disease. I. A sensitive assay for thyroid-stimulating antibodies using cultured porcine thyroid cells and polyethylene glycol precipitation of serum].

The activities of thyroid-stimulating antibody (TSAb) in serum from patients with Graves' disease were measured by a sensitive assay, using cultured porcine thyroid cells and the precipitation from serum with polyethylene glycol (PEG), and the activities were compared with those of thyrotropin binding inhibitor immunoglobulin (TBII), measured by the commercial assay kit. Porcine thyroid cells after digestion were cultured for 15-18 hours with TSH of 1-10,000 microU/ml or the precipitations of sera from normal subjects and patients with Graves' disease or Hashimoto's thyroiditis, and then the cAMP levels in the culture medium were determined by the commercial RIA assay kit (Yamasa). The precipitation was obtained by adding 0.5 ml of 30% PEG solution to 0.5 ml serum, and was resuspended with 0.6 ml of Hanks' medium without NaCl, containing 1.5% bovine serum albumin, 20mM Hepes and 0.5 mM 3-isobutyl-1-methylxanthine. The precipitation contained about 85% of immunoglobulin and 63% of albumin of the original amount of the serum, as well as substantial TSH, when the original serum contained TSH more than 40 microU/ml. When the PEG precipitations from 10 normal subjects were incubated with the thyroid cells of 4 X 10(5) cells, the cAMP releases into the medium ranged from 83 to 124%, when the mean value was calculated as 100%. Therefore, the cAMP release of more than 130% of the amount released into the culture medium incubated with normal IgG was judged as positive TSAb activity. The minimum detectable quantities were regarded as about 5 microU/ml TSH equivalent. TSAb and TBII activities were detected in 48 (92%) and 50 (96%) of 52 patients with untreated hyperthyroid Graves' disease, respectively, and either TSAb or TBII activities were detected in 16 (80%) of 20 patients with Graves' disease maintained in a clinically euthyroid state by treatment with antithyroid drugs. TBII was positive in 10(50%) of these patients. Some patients showed distinct discrepancies in these two activities, although there was a significant positive correlation between TSAb and TBII activities (r = 0.53, p less than 0.01) in patients with untreated Graves' disease. In these patients, TSAb activities showed a significant positive correlation with values for 99mTc thyroid uptake, determined 30 min after the injection. However, they did not show any significant correlation with serum T4 or T3 concentrations. Similarly, TBII showed significant correlations with goiter size and 99mTc thyroid uptake. To conclude, the present assay for TSAb is sensitive and reproducible.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗