Graves’ Disease Associated with Elevated Serum Thyroxine-Binding Globulin Concentrations*

1980 ◽  
Vol 51 (2) ◽  
pp. 325-329 ◽  
Author(s):  
YUKIKO YABU ◽  
NOBUYUKI AMINO ◽  
KIYOMI NAKATANI ◽  
KIYOSHI ICHIHARA ◽  
MIZUO AZUKIZAWA ◽  
...  
1984 ◽  
Vol 6 (6) ◽  
pp. 189-190

I have read with great interest "Goiter in Children" by Foley (PIR 1984;5:259). The author stated: "In patients with thyromegaly and mild symptoms of hyperthyroidism, a TRH test will help to discriminate hyperthyroxemia secondary to increased or abnormal serum thyroxine binding proteins from early Graves disease, factitious hyperthyroidism, toxic thyroiditis, and TSH-mediated hyperthyroidism." I would suggest the use of a triiodothyronine (T3) resin uptake as a base-line test. An elevated serum thyroxine (T4) value in conjunction with a diminished T3 resin uptake suggests thyroxine-binding globulin (TBG) excess, which can be confirmed by specific quantitation of TBG. Patients with familial dysalbuminemic hyperthyroxinemia (FDH) have elevated levels of serum T4 and free thyroxine index (FT4l) values but normal T3 resin uptake and TBG levels.


1984 ◽  
Vol 107 (3) ◽  
pp. 352-356 ◽  
Author(s):  
G. A. Sigurdsson ◽  
G. Arnason ◽  
Th. V. Gudmundsson ◽  
M. Kjeld ◽  
L. Franzson ◽  
...  

Abstract. A kindred of four generations with inherited elevation of serum thyroxine binding globulin (TBG) is reported. To our knowledge this is the twelfth kindred reported with this disorder. Of the 35 family members studied, 10 females and 5 males had elevated serum TBG. The patients were clinically euthyroid. The pedigree data was consistent with an X-chromosome linked mode of inheritance.


1982 ◽  
Vol 99 (3) ◽  
pp. 393-396 ◽  
Author(s):  
J. Penhaligon ◽  
M. L. Wellby

Abstract. A kindred with a high prevalence of hereditary serum thyroxine-binding globulin (TBG) is described. Seventeen of the 29 members of the kindred have the increased TBG trait as demonstrated by a combination of increased serum total thyroxine (T4) and total triiodothyronine (T3) and decreased T3 resin uptake. In 12 of the 17, the anomaly was confirmed by measuring serum TBG activity as maximum binding capacity of T4. The pattern of increased TBG is consistent with X-linked inheritance. One of the affected members had proven thyrotoxicosis and two others were subjected to sub-total thyroidectomy.


1973 ◽  
Vol 72 (2) ◽  
pp. 265-271 ◽  
Author(s):  
J. H. Dussault ◽  
D. A. Fisher ◽  
J. T. Nicoloff ◽  
V. V. Row ◽  
R. Volpe

ABSTRACT In order to determine the effect of alterations in binding capacity of thyroxine binding globulin (TBG) on triiodothyronine (T3) metabolism, studies were conducted in 10 patients with idiopathically low (7 subjects) or elevated (3 subjects) TBG levels and 10 subjects given norethandrolone (7 male subjects) or oestrogen (3 female subjects). Measurements of serum thyroxine (T4) concentration, maximal T4 binding capacity, serum T3 concentration and per cent dialyzable T3 were conducted. Serum T3 was measured both by chemical and radioimmunoassay methods. In patients with idiopathically low TBG, the mean serum T4 concentration was low (2.4 μg/100 ml), the mean serum T3 level low (55 ng/100 ml), the mean per cent dialyzable T3 increased (0.52%), and the calculated free T3 concentration normal (186 pg/100 ml). In patients with idiopathically high TBG levels the mean T4 concentration was high (10.3 μg/100 ml), the mean T3 level slightly elevated (127 ng/100 ml), the% dialyzable T3 low (0.10%) and the calculated free T3 concentration low normal (123 pg/100 ml). The correlation coefficient between the per cent dialyzable T3 and maximal TBG binding capacity in the 20 subjects was 0.68, a value significant at the P < 0.01 level. Thus, alterations in binding capacity of TBG seem to influence T3 and T4 metabolism similarly; the inverse relationship between the % of dialyzable hormone and total hormone concentration tends to keep the absolue levels of free hormones stable.


1983 ◽  
Vol 57 (3) ◽  
pp. 665-667 ◽  
Author(s):  
DAVID SARNE ◽  
KIMBERLY BAROKAS ◽  
NEAL H. SCHERBERG ◽  
REFETOFF REFETOFF

1986 ◽  
pp. 481-484
Author(s):  
Masataka Nanno ◽  
Rieko Ohtsuka ◽  
Noriyuki Kikuchi ◽  
Yutaka Oki ◽  
Shozo Ohgo ◽  
...  

1985 ◽  
Vol 69 (2) ◽  
pp. 113-121 ◽  
Author(s):  
C. A. Ollis ◽  
S. Tomlinson ◽  
D. S. Munro

Graves’ disease is the commonest form of hyperthyroidism in which excessive production of thyroid hormones by the hyperplastic overactive thyroid gland produces elevated serum levels of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). Many of the manifestations of Graves’ disease, increased basal metabolic rate, increased heart rate, heat intolerance, sweating and nervousness, can be attributed to the peripheral actions of the excess thyroid hormones. The pathogenesis of many of the other dramatic features of Graves’ disease, such as the eye involvement or localized skin changes, is not fully understood, but circulating immunoglobulins with thyroid stimulating activity are almost certainly linked to excess thyroid hormone production and thereby cause the hyperthyroidism.


2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Jianhui Li ◽  
Xiaohua Sun ◽  
Danzhen Yao ◽  
Jinying Xia

Background. Antithyroid drug (ATD) treatment occupies the cornerstone therapeutic modality of Graves’ disease (GD) with a high relapse rate after discontinuation. This study aimed to assess potential risk factors for GD relapse especially serum interleukin-17 (IL-17) expression. Methods. Consecutive newly diagnosed GD patients who were scheduled to undergo ATD therapy from May 2011 to May 2014 were prospectively enrolled. Risk factors for GD relapse were analyzed by univariate and multivariate Cox proportional hazard analyses. The association between serum IL-17 expression at cessation and GD relapse was analyzed with relapse-free survival (RFS) by the Kaplan–Meier survival analysis and log-rank test. Results. Of the 117 patients, 72 (61.5%) maintained a remission for 12 months after ATD withdrawal and 45 (38.5%) demonstrated GD relapse. The final multivariate Cox analysis indicated elevated IL-17 expression at cessation to be an independent risk factor for GD relapse within 12 months after ATD withdrawal (HR: 3.04, 95% CI: 1.14–7.67, p=0.021). Patients with higher expressions of IL-17 (≥median value) at cessation demonstrated a significantly higher RFS than those with lower levels by the Kaplan–Meier analysis and log-rank test (p=0.028). Conclusions. This present study indicated elevated serum IL-17 expression at cessation to be a predictor for GD relapse within 12 months.


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