232 Original Clinical
TSBAb (TSH-Stimulation Blocking Antibody) and TSAb
(Thyroid Stimulating Antibody) in TSBAb-Positive Patients with
Hypothyroidism and Graves Patients with Hyperthyroidism
N. Takasu 1, K. Yamashiro 1, Y. Ochi 2, Y. Sato 2, A. Nagata 3, I. Komiya 1, H. Yoshimura 3
1
Department of Internal Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
2
Research Institute for Production Development, Morimoto, Shimogamo, Sakyou-ku, Kyoto, Japan
3
Ito Hospital, Jinguumae, Shibuya-ku, Tokyo, Japan
nnnn There are two types of TSH receptor antibodies (TRAb); thy-
roid stimulating antibody (TSAb) and TSH-stimulation blocking
antibody (TSBAb). TSAb causes Graves hyperthyroidism. TSBAb
causes hypothyroidism. Both TSAb and TSBAb block TSH-binding
to thyroid cells as TSH receptor antibodies (TRAb). TSBAb-posi-
tive patients with hypothyroidism and Graves patients with hy-
perthyroidism may have both TSBAb and TSAb. We studied
TSBAb and TSAb in 43 TSBAb-positive patients with hypothyroid-
ism and in 55 untreated Graves patients with hyperthyroidism.
TSBAb-activities were expressed as percentage inhibition of bo-
vine (b) TSH-stimulated cAMP production by test IgG. Two
formulas were used to calculate TSBAb-activities; TSBAb-A
(%) = [1 ± (c ± b)/(a ± b)] ” 100 and TSBAb-B (%) = [1 ± (c ± d)/(a ±
b)] ” 100, where a: cAMP generated in the presence of normal
IgG and bTSH, b: cAMP generated in the presence of normal
IgG, c: cAMP generated in the presence of test IgG and bTSH,
and d: cAMP generated in the presence of test IgG. TSAb
(%) = [d/b] ” 100. All of the 43 TSBAb-positive patients with hy-
pothyroidism had strongly positive TSBAb-A and -B. Some of
them had weakly positive TSAb (< 240 %). All 55 untreated
Graves patients had positive TSAb (205 ± 2509 %). Some of them
had both TSAb and TSBAb. TSBAb-positive patients with hypo-
thyroidism had a limited distribution of TSBAb- and TSAb-activ-
ities (TSBAb-A + 75 ± + 103 %, TSBAb-B + 87 ± + 106 %, TSAb 92 ±
240 %), but Graves patients with hyperthyroidsim had a wide
distribution of TSAb- and TSBAb-activities (TSAb 205 ± 2509 %,
TSBAb-A ± 158 ± + 43 %, TSBAb-B ± 14 ± + 164 %). TSBAb-A ignores
TSAb activity in serum, and might give low TSBAb activity. How-
ever, TSBAb-A clearly differentiates TSBAb-positive patients with
hypothyroidism from Graves patients with hyperthyroidism;
thus, we favor TSBAb-A over TSBAb-B. Some of TSBAb-positive
patients with hypothyroidism and Graves patients with hyper-
thyroidism have both TSBAb and TSAb.
n Key words: TSBAb: TSH-Stimulation Blocking Antibody ±
TSAb: Thyroid Stimulating Antibody ± TRAb: TSH-Receptor Anti-
body ± Graves Disease ± TSBAb-Positive Hypothyroidism ±
TRAb Disease
Horm Metab Res 2001; 33: 232 ± 237
 Georg Thieme Verlag Stuttgart ´ New York
ISSN 0018-5043
Introduction
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There are two types of TSH receptor antibody (TRAb); thyroid
stimulating antibody (TSAb) and TSH-stimulation blocking an-
tibody (TSBAb) [1, 2]. TSAb stimulates thyroid glands and
causes Graves hyperthyroidism. TSBAb blocks TSH-stimula-
tion of thyroid glands and causes hypothyroidism. Both TSAb
and TSBAb block TSH-binding to thyroid cells as TSH-receptor
antibody (TRAb), which has been measured as TSH-binding in-
hibitory immunoglobulin (TBII). TRAb has been measured by
different assay methods and given various names. Among
them, TBII [3, 4] and TSAb [5 ± 8] have been measured as TRAb
to diagnose Graves disease and to follow Graves patients. TBII
is measured as a receptor assay. TSAb is measured as a stimu-
lator assay, and TSBAb as a TSH-stimulation blocking assay.
The former TRAb is a stimulating antibody (TSAb) [5 ± 8], and
the latter TRAb is a blocking antibody (TSBAb) [1, 9 ± 12].
It has been generally believed that Graves patients have TSAb
but do not have TSBAb, and that blocking antibody(TSBAb)-po-
sitive patients with hypothyroidism have TSBAb but do not
have TSAb. However, we have seen many Graves patients
who had both TSAb and TSBAb. We have also encountered sev-
eral TSBAb-positive patients with hypothyroidism who had
both TSBAb and TSAb. Graves patients and TSBAb-positive pa-
tients with hypothyroidism were sporadically reported to have
both TSAb and TSBAb [11,13 ± 17]. We studied 43 TSBAb-posi-
tive patients with hypothyroidism and 55 untreated Graves
patients with hyperthyroidism. TSBAb-positive patients with
hypothyroidism and Graves patients with hyperthyroidism
may have both TSBAb and TSAb. The balance of TSBAb and
TSAb determines whether a patient will have hypo- or hyper-
thyroidism. Two formulas (one in the earlier reports [9,10] and
the other in the recent reports [1,12]) have been used to calcu-
late TSBAb-activities. We compared these two.
Received: 3 July 2000 Accepted after revision: 9 November 2000
TSBAb and TSAb in TSBAb-Induced Hypothyroidism and Graves Hyperthyroidism
Subjects and Methods
Subjects
We studied 43 thyroxine-treated TSBAb-positive patients with
hypothyroidism (age 35  16 years old [mean  SD], males : fe-
males [10 : 33]) and 55 untreated Graves patients with hyper-
thyroidism (age 38  18 years, males:females [15:40]). TSBAb-
positive patients with hypothyroidism were diagnosed on the
basis of the patients history, signs of hypothyroidism and the
laboratory findings, including positive TSBAb (> + 40 %) and de-
creased serum thyroxine (T4) and triiodothyronin (T3) with
high serum TSH. They were treated with thyroxine and were
euthyroid. Serum TSH levels were always within normal
ranges in all sera studied. TBII-values were 88  10 % (mean 
SD). TSAb and TSBAb values are shown in the figures and table.
Graves patients with hyperthyroidism were diagnosed on the
basis of the patients history and signs of hyperthyroidism with
diffuse goiter and the laboratory findings, including positive
TRAb (TSAb and/or TBII) and elevated serum thyroxine (T4)
and triiodothyronin (T3) with low serum TSH. TBII-values were
44  18 % (mean  SD). TSAb and TSBAb values are shown in the
figure and table. The 55 Graves patients were not treated with
antithyroid drugs, and were in hyperthyroid states. The study
plan was reviewed and approved by our institutional review
committee. Informed consent was obtained from the patients
and the control subjects.
Porcine thyroid cell cyclic AMP production;
TSAb- and TSBAb activities
TSAb-activities were measured as before [5,18]. Cyclic AMP
production was determined according to the instruction in a
commercial TSAb assay kit (Yamasa, Chosi, Chiba, Japan).
Crude IgG, obtained as PEG (6000) 12.5 % (final concentra-
tion)-precipitated fraction from 0.2 ml aliquot of test serum,
was dissolved in modified Hanks solution without NaCl. Por-
cine thyroid cells were incubated with test-IgG in 0.25 ml
Hanks solution without NaCl, pH 7.5, containing 1.5 % bovine
serum albumin, 20 mM Hepes, and 0.5 mM 3-isobutyl-l-me-
thylxanthine. Cyclic AMP production during 5 h incubation at
37 8C was measured by radioimmunoassay (RIA), using a com-
mercial kit (Yamasa, Chosi, Chiba, Japan). The TSAb activities
were expressed as percentage cAMP production compared
with the mean values for 118 normal subjects (normal values
were less than 180 %); TSAb (%) = [d/b] ” 100, where b: cAMP
generated in the presence of normal IgG, and d: cAMP gener-
ated in the presence of test IgG.
To measure TSBAb activities, crude IgG was incubated with
porcine thyroid cells in the presence of 25 U bTSH (100 mU/
L, final concentration), as before [1, 9,10,12,19]. Cyclic AMP
production during 5 h incubation was measured. TSBAb activ-
ities were expressed as percentage inhibition of bTSH-stim-
ulated cAMP production by test IgG. Formulas A (TSBAb-A)
and B (TSBAb-B) were used to calculate TSBAb-activities;
TSBAb-A (%) = [1 ± (c ± b)/(a ± b)] ” 100 [9,10, 20 ± 24] and
TSBAb-B (%) = [1 ± (c ± d)/(a ± b)] ” 100 [1,12, 25, 26], where a:
cAMP generated in the presence of normal IgG and bTSH, b:
cAMP generated in the presence of normal IgG, c: cAMP gener-
ated in the presence of test IgG and bTSH, and d: cAMP gener-
ated in the presence of test IgG.
Horm Metab Res 2001; 33 233
Test IgG and normal IgG were the 12.5 % PEG-precipitated frac-
tions from test serum and normal human serum, respectively.
The TSBAb-A and B activities were studied in 85 normal sub-
jects (normal values were less than + 40 %). These were more
than + 40 % in all of the 43 TSBAb-positive patients with
hypothyroidism.
TSH-binding inhibitory immunoglobulin (TBII)
TBII was measured by radioreceptor assay with a commercial
kit (R.S.R. Limited, Cardiff, U. K.). Assay results were expressed
as the percentage inhibition of I125-TSH-binding to thyroid
plasma membranes as before [4]. Normal values were calculat-
ed from 125 normal control subjects and were less than 10 %.
Statistical analysis and others
All samples were tested in duplicate or triplicate. Statistical
analysis was performed using Student t-test or c2-test. P val-
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ues less than 0.05 were considered to be statistically signifi-
cant. Serum concentrations of T4, T3, and TSH were determined
by RIA using commercially available kits. The normal ranges
for serum T4 and T3 were 6 ± 12 g/dl (77 ± 155 nmol/liter) and
78 ± 182 ng/dl (1.2 ± 2.8 nmol/liter), respectively. The normal
range for serum TSH was 0.3 ± 4.5 mU/liter.
Results
TSBAb and TSAb in 43 TSBAb-positive patients with hypo-
thyroidism and 55 Graves patients with hyperthyroidism
Table 1 shows 5 TSBAb-positive patients with hypothyroidism
(Patients 1 ± 5) and 5 untreated Graves patients with hyper-
thyroidism (Patients 6 ± 10). We calculated TSBAb-A and
TSBAb-B. In the absence of TSAb (Patients 1 ± 4 [4 TSBAb-posi-
tive patients with hypothyroidism]), TSBAb-A activity was
about equal to TSBAb-B-one. In the presence of TSAb (Patient
5 [a TSBAb-positive patient with hypothyroidism] and Patients
6 ± 10 [5 untreated Graves patients]), TSBAb-B activity was
higher than TSBAb-A. TSBAb-A ignored TSAb-activity in the
sera. In the presence of TSAb, TSBAb-A activities might not re-
flect the true TSBAb activities, since TSAb in the sera could
stimulate cAMP synthesis; this possible TSAb-stimulated
cAMP synthesis was ignored in TSBAb-A. In the presence of
TSAb, the values of TSBAb-B were always higher than those of
TSBAb-A; the latter were lower than the former.
Patients 1 ± 5 had positive TSBAb-A and B, and hypothyroidism.
Patients 1 ± 4 did not have TSAb, but Patient 5 had it. IgG, pre-
pared from Patients 1 ± 4, inhibited TSH-stimulated cAMP re-
sponses; they had positive TSBAb-A and B. Their IgG did not
stimulate cAMP synthesis. They did not have TSAb. IgG, pre-
pared from Patient 5, inhibited TSH-stimulated cAMP re-
sponse; she had positive TSBAb-A and B. Her IgG stimulated
cAMP synthesis. She had positive TSBAb (TSBAb-A: 86 %,
TSBAb-B: 95 %) and positive TSAb (200 %). Patients 1 ± 5 had
strongly positive TSBAb-A and B, and had hypothyroidism.
Untreated Graves patients with hyperthyroidism (Patients 6 ±
10) had positive TSAb. All of them had positive TSAb and nega-
tive TSBAb-A. Patients 6 ± 8 had negative TSBAb-B, but Patients
9 and 10 had positive TSBAb-B. Patients 9 and 10 had positive
TSAb (693 % and 636 %, respectively) and positive TSBAb-B
234 Horm Metab Res 2001; 33 Takasu N et al

Table 1 TSBAb (TSH-stimulation blocking antibody) and TSAb (thy- a

roid stimulating antibody) in 5 TSBAb-positive patients with hypothy-
roidism and 5 untreated Graves patients with hyperthyroidism

Patients TBII (%) TSBAb (%) TSAb (%)

TSBAb-A +/±* TSBAb-B +/±* +/±**

I TSBAb-positive patients with hypothyroidism

1 88 96 + 97 + 109 ±
2 90 96 + 98 + 112 ±
b
3 70 94 + 99 + 124 ±
4 77 92 + 94 + 110 ±
5 75 86 + 95 + 200 +
II Untreated Graves patients with hyperthyroidism
6 76 ± 22 ± 12 ± 450 +
7 68 3 ± 22 ± 352 +
8 45 7 ± 29 ± 426 +

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9 32 30 ± 90 + 693 +
10 42 31 ± 82 + 636 + Fig. 1 TSBAb-A and TSAb in 43 TSBAb-positive patients with hypo-
Five TSBAb-positive patients with hypothyroidism (I) and 5 untreated Graves a TSBAb-A and TSAb activity in 43 TSBAb-positive patients with hy-
patients with hyperthyroidism (II) were studied. TSBAb activity was expressed
as percentage inhibition of bovine (b) TSH-stimulated cAMP production by test
IgG; TSBAb-A (%) = [1 ± (c ± b)/(a ± b)] ” 100 and TSBAb-B (%) = [1 ± (c ± d)/(a ±
b)] ” 100. TSAb (%) = [d/b] ” 100. In these equations, a: cAMP generated in
the presence of normal IgG and bTSH, b: cAMP generated in the presence of
normal IgG, c: cAMP generated in the presence of test IgG and bTSH, and d:
cAMP generated in the presence of test IgG. In the absence of TSAb (Patients
1 ± 4), TSBAb-A was about equal to TSBAb-B. In the presence of TSAb (Patients
5 ± 10), TSBAb-B was higher than TSBAb-A, since the d-values in TSBAb-B were
higher than b-values in TSBAb-A. * TSBAb-A and B were +, when TSAb-A and B
activities were more than 40 %. ** TSAb was +, when the activity was more
than 180 %.
(90 % and 82 %, respectively), although they had negative
TSBAb-A. All of Patients 6 ± 10 had positive TSAb, and had hy-
perthyroidism.
thyroidism (&) and 55 Graves patients with hyperthyroidism (*).
pothyroidism and 55 Graves patients with hyperthyroidism.
b TSBAb-A and TSAb activity of the 43 TSBAb-positive patients with
hypothyroidism and 20 of the 55 Graves patients, whose TSAb activ-
ity was less than 500 %. All of the 43 TSBAb-positive patients with hy-
pothyroidism (&) had strongly positive TSBAb-A [+ 75 ± + 103 %,
mean  SD = + 94  6 %]. Some of them had weakly positive TSAb
(< 240 %). All of the 55 untreated Graves patients with hyperthyroid-
ism (*) had positive TSAb. One of them had positive TSBAb-A
(+ 43 %). TSBAb-positive patients with hypothyroidism had a limited
distribution of TSAb and TSBAb-A activity, but Graves patients with
hyperthyroidism had a wide distribution of TSAb and TSBAb-A activ-
ity. Each point is mean of 2 ± 3 determinations. TSBAb-A (%) = [1±
(c ± b)/(a ± b)] ” 100, where a: cAMP generated in the presence of
normal IgG and bTSH, b: cAMP generated in the presence of normal
IgG, and c: cAMP generated in the presence of test IgG and bTSH.
TSAb (%) = [d/b] ” 100.

We studied 43 thyroxine-treated TSBAb-positive patients with
hypothyroidism and 55 untreated Graves patients with hyper-
thyroidism (Figs. 1 ± 3). Fig. 1 demonstrates the activity of
TSBAb-A and TSAb. All of the 43 TSBAb-positive patients with
hypothyroidism had strongly positive TSBAb-A [+ 75 ± +103 %,
mean  SD = + 94  6 %]. Some of them had weakly positive
TSAb. Their TSAb activity ranged from 92 % to 240 %. The TSAb-
activities were 180 ± 240 % in 10 (22 %) of the 43 TSBAb-positive
patients with hypothyroidism and were less than 180 % in the
other 38 patients; 10 (22 %) of the 43 TSBAb-positive patients
with hypothyroidism had positive TSAb. All 55 untreated
Graves patients had positive TSAb (205 ± 2509 %). One Graves 205 ± 2509 %, TSBAb-B ± 14 ± + 164 %). The TSBAb-B activities
patient had positive TSBAb-A (+ 43 %). Graves patients with hy-
perthyroidism had a wide distribution of TSAb and TSBAb-A ac-
tivities (TSAb 205 ± 2509 %, TSBAb-A ± 158 ± + 43 %). TSBAb-A
activity was more than 40 % in one (2 %) of the 55 untreated
Graves patients and were less than 40 % in the other 54 pa-
tients; only one of 55 untreated Graves patients had positive
TSBAb-A. TSBAb-A activity was less than 50 % in all 55 un-
treated Graves patients. TSBAb-positive patients with hypo-
thyroidism had a limited distribution of TSAb and TSBAb activ-
ity (TSAb 92 ± 240 %, TSBAb-A + 75 ± + 103 %), but Graves pa-
tients with hyperthyroidism had a wide distribution (TSAb
205 ± 2509 %, TSBAb-A ± 158  43 %).
Fig. 2 demonstrates the activities of TSBAb-B and TSAb. All 43
TSBAb-positive patients with hypothyroidism had strongly po-
sitive TSBAb-B [+ 87 ± + 106 %, mean  SD = + 99  3 % ]. Some of
them had weakly positive TSAb. Their TSAb activity ranged
from 92 % to 240 %. The TSAb activity was 180 ± 240 % in 10
(22 %) of the 43 TSBAb-positive patients with hypothyroidism
and were less than 180 % in the other 33 patients; 10 (22 %) of
the 43 TSBAb-positive patients with hypothyroidism had posi-
tive TSAb. All of the 55 untreated Graves patients had positive
TSAb (205 ± 2509 %). Graves patients with hyperthyroidism
had a wide distribution of TSAb and TSBAb activity (TSAb
were + 40 ± + 164 % in 35 (64 %) of the 55 untreated Graves pa-
tients and were less than + 40 % in the other 20 patients; 35
(64 %) untreated Graves patients had both positive TSBAb-B
and TSAb. TSBAb-positive patients with hypothyroidism had a
limited distribution of TSAb and TSBAb-B activitiy (TSAb 92 ±
240 %, TSBAb-B + 87  106 %), but Graves patients with hyper-
thyroidism had a wide distribution of TSAb and TSBAb-B activ-
ity (TSAb 205 ± 2509 %, TSBAb-B ± 14  164 %).
Fig. 3 shows the frequency distribution of TSBAb-A (left),
TSBAb-B (middle), and TSAb (right) in 43 TSBAb-positive pa-
tients with hypothyroidism and 55 Graves patients with hy-
perthyroidism. TSBAb-positive patients with hypothyroidism
 TSBAb and TSAb in TSBAb-Induced Hypothyroidism and Graves Hyperthyroidism
Fig. 2 TSBAb-B and TSAb in 43 TSBAb-positive patients with hypo-
thyroidism (&) and Graves patients with hyperthyroidism (*). a TS-
BAb-B and TSAb activity in 43 TSBAb-positive patients with hypothy-
roidism and 55 Graves patients with hyperthyroidism. b TSBAb-B
and TSAb activity of the 43 TSBAb-positive patients with hypothy-
roidism and 20 of the 55 Graves patients, whose TSAb activity was
less than 500 %. All of the 43 TSBAb-positive patients with hypothy-
roidism (&) had strongly positive TSBAb-B [+ 87 ± + 106 %, mean 
SD = + 99  3 %]. Some of them had weakly positive TSAb (< 240 %).
All of the 55 untreated Graves patients with hyperthyroidism (*)
had positive TSAb. Some of them had both positive TSAb-A and
TSBAb-B. TSBAb-positive patients with hypothyroidism had a limited
distribution of TSAb and TSBAb-B activity, but Graves patients with
hyperthyroidism had a wide distribution of TSAb- and TSBAb-B activ-
ity. Each point is mean of 2 ± 3 determinations. TSBAb-B (%) = [1±
(c ± d)/(a ± b)] ” 100, where a: cAMP generated in the presence of
normal IgG and bTSH, b: cAMP generated in the presence of normal
IgG, c: cAMP generated in the presence of test IgG and bTSH, and d:
cAMP generated in the presence of test IgG. TSAb (%) = [d/b] ” 100.
had limited distributions of TSBAb-A (+ 75  103 %) (left), and B
(+ 87 ± + 106 %) (middle), and TSAb (TSAb 92 ± 240 %) (right).
However, Graves patients with hyperthyroidism had wide dis-
tributions of TSBAb-A (± 158 ± + 43 %) (left), B (± 14 ± + 164 %)
(middle), and TSAb (205 ± 2509 %) (right). All 43 TSBAb-posi-
tive patients with hypothyroidism had strongly positive
TSBAb-A and B. Some of them had weakly positive TSAb
(< 240 %). All of the 55 untreated Graves patients had positive
TSAb (205 ± 2509 %). All TSBAb-positive patients with hypo-
thyroidism had strongly positive TSBAb-A, but only one
Graves patient with hyperthyroidism had positive TSBAb-A
(left). TSBAb-A was 43 % in one of the 55 untreated Graves pa-
tients and less than 40 % in the other 54 patients; one Graves All 43 TSBAb-positive patients with hypothyroidism had
patient had positive TSBAb-A. All of the TSBAb-positive pa-
tients with hypothyroidism had high TSBAb-A activity (> 75 %)
and all of the 55 untreated Graves patients with hyperthyroid-
ism had low TSBAb-A activities (< 50 %) (left). TSBAb-A differ-
entiates TSBAb-positive hypothyroidism from Graves hyper-
thyroidism. However, TSBAb-B values were not different
between TSBAb-positive patients and Graves patients; (64 %)
of the 55 untreated Graves patients had positive TSBA-B.
Horm Metab Res 2001; 33 235
Fig. 3 Frequency-distributions of TSBAb-A (left), TSBAb-B (middle),
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and TSAb (right) in 43 TSBAb-positive patients with hypothyroidism
(upper) and 55 Graves patients with hyperthyroidism (lower). All 43
TSBAb-positive patients with hypothyroidism had strongly positive
TSBAb-A (left) and B (middle). All 55 untreated Graves patients had
positive TSAb (right). TSBAb-positive patients with hypothyroidism
had limited distributions of TSBAb-A (+ 75 ± + 103 %) (left), and B
(+ 87 ± + 106 %) (middle) and TSAb (TSAb 92 ± 240 %) (right). Graves
patients with hyperthyroidism had wide distributions of TSBAb-A
(± 158 ± + 43 %) (left), B (± 14 ± + 164 %) (middle), and TSAb (205 ±
2509 %) (right). All of the 43 TSBAb-positive patients with hypothy-
roidism had strongly positive TSBAb-A and B. Some of them had
weakly positive TSAb (< 240 %). All of the 55 untreated Graves pa-
tients had positive TSAb (right); TSBAb-A was + 43 % in one of the
55 untreated Graves patients and less than + 40 % in the other 54
patients. All of the 43 TSBAb-positive patients with hypothyroidism
had high TSBAb-A (> + 75 %) and all of the 55 untreated Graves pa-
tients with hyperthyroidism had low TSBAb-A activities (< + 50 %)
(left). TSBAb-A differentiates TSBAb-positive hypothyroidism from
Graves hyperthyroidism. However, TSBAb-B does not differentiate
the former from the latter; 35 (64 %) of the 55 untreated Graves pa-
tients had positive TSBAb-B.
Discussion
We studied 43 TSBAb-positive patients with hypothyroidism.
Some of TSBAb-positive patients with hypothyroidism and
Graves patients with hyperthyroidism had both positive
TSBAb and TSAb. We calculated TSBAb as TSBAb-A (formula
A) and B (formula B). TSBAb-A ignored TSAb activity of the
sera, and TSBAb-B calculated it. TSBAb-A differentiates
TSBAb-positive patients with hypothyroidism from Graves pa-
tients with hyperthyroidisms, so we favor TSBAb-A over
TSBAb-B.
strongly positive TSBAb-A and B. Some of them had weakly po-
sitive TSAb. All of the 55 untreated Graves patients had posi-
tive TSAb. Some of them had both TSAb and TSBAb. Graves pa-
tients with hyperthyroidism had a wide distribution of TSAb-
and TSBAb activity, but TSBAb-positive patients with hypo-
thyroidism had a limited distribution of TSAb and TSBAb activ-
ity. Limited numbers of TRAb-positive patients became hypo-
thyroid. The numbers of TRAb-positive patients with TSBAb-
induced hypothyroidism were lower than those with TSAb-in-
duced hyperthyroidism (Graves disease). The TRAb-positive
patients with strongly positive TSBAb and with negative (or
236 Horm Metab Res 2001; 33
weakly positive) TSAb had hypothyroidism. When TSBAb is
strongly positive, the patients condition may develop into hy-
pothyroidism. It should be noted that all of the 43 TSBAb-posi-
tive patients with hypothyroidism had high levels of TBII.
TSBAb-positive hypothyroidism and Graves hyperthyroidism
may be two aspects of one disease (TRAb disease).
To calculate TSBAb-activities, TSBAb-A was used in the earlier
reports [9,10], and TSBAb-B in the recent reports [1,12].
TSBAb-A ignored TSAb activity in serum, and TSBAb-B took ac-
count of it. TSBAb-B might be used in the presence of TSAb. In
the absence of TSAb, TSBAb-A was about equal to TSBAb-B. In
the presence of TSAb, TSBAb-B was lower than TSBAb-A, since
the d-values were higher than b-values. TSBAb-A ignored TSAb
activity in the patients serum. In the presence of TSAb, TSBAb-
A might not reflect the true TSBAb-activities, since TSAb in the
serum could stimulate cAMP synthesis. In the presence of
TSAb, TSBAb-B activity was higher than TSBAb-A. In its pres-
ence, TSBAb-B could be used. However, TSBAb-A differentiates
TSBAb-positive patients with hypothyroidism from Graves pa-
tients with hyperthyroidism. Fig. 3 (left) demonstrates that all
of the TSBAb-positive patients with hypothyroidism had
strongly positive TSBAb-A, and that only one Graves patient
with hyperthyroidism had positive TSBAb-A.
In conclusion, some TSBAb-positive patients with hypothy-
roidism and Graves patients with hyperthyroidism have both
TSBAb and TSAb. TSBAb-positive patients with hypothyroid-
ism had a limited distribution of TSBAb and TSAb activity, but
Graves patients had a wide distribution of TSAb and TSBAb ac-
tivity; the former are less numerous than those of the latter.
TSBAb-A differentiates TSBAb-positive patients with hypothy-
roidism from Graves patients with hyperthyroidism.
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