[Show abstract][Hide abstract] ABSTRACT: We examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from aggravation of Hashimoto's thyroiditis, both the numbers and proportions of αβ T cell receptor (TCR) negative T (WT31− CD3+) cells and CD8 (CD4− CD8+) cells decreased and those of CD4+ CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+ CD8−) cells. non-T, non-B (CD5− CD19−) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, αβ+ TCR T (WT31+ CD3+) cells, CD8 cells, and non-T, non-B cells. A serial study of some of the patients showed opposite changes in αβ TCR− T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. αβ TCR− T cells were mostly γδ TCR+ T (IIF2+ CD3+) cells in these patients. These data suggest that αβ TCR T (γδTCR+ T), CD8, and CD4+ CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells arc important in thyroid stimulation in Graves' disease.
[Show abstract][Hide abstract] ABSTRACT: We followed up 5 patients with transient neonatal thyroid dysfunction born to mothers with Graves' disease from 5 to 10 years and assessed their outcome in physical growth and intellectual development as well as thyroid function. The patients consisted of 3 girls, including a pair of siblings, and 2 boys. Four of them had transient neonatal hyperthyroidism and the other boy had transient neonatal hypothyroidism with normal thyrotropin. The mother of the latter patient developed hyperthyroidism during the second trimester of her pregnancy. The mothers of the former patients were found hyperthyroid before bearing the children. We analyzed physical findings, growth and intellectual development as well as thyroid function including anti-thyroid antibodies and anti-TSH receptor antibody. Mild thyromegaly developed in 2 patients with transient neonatal hyperthyroidism. Short stature was seen in a patient with neonatal hyperthyroidism in whom an excess band on the X chromosome was found. One patient had only a borderline IQ but the other three with neonatal hyperthyroidism had above average ability, whereas moderate delay in psychomotor development was seen in the patient with neonatal hypothyroidism. In the sibling patients, anti-thyroid antibodies have been positive since 6 years of age. Further follow-up is required to know the final outcome of these patients.
[Show abstract][Hide abstract] ABSTRACT: A novel high-molecular-weight (MW) form of immunoreactive TSH [35,000 Da on Sephacryl S-200HR gel chromatography (S-200 chromatography)] was documented in a 32-year-old healthy woman who delivered two neonates with transient hyperthyrotropinemia. Her TSH levels ranged from 21.2 to 53.9 mU/L on different days or from 11.0 to 48.1 mU/L by the different immunoradiometric assay methods. The IgG fractions showed specific 125I-labeled hTSH binding and inhibited in vitro cAMP increase induced by hTSH but not that induced by bTSH. On protein G Superose HR affinity chromatography (protein G chromatography) equilibrated with 10 mmol/L sodium/potassium phosphate buffer (PB) followed by elution with 0.1mol/L glycine buffer, 95-99% of her TSH immunoreactivity eluted in the latter (bound) fraction while almost all was in the former (unbound) fraction in the control serum containing authentic hTSH. However, after dialysis of this bound fraction overnight with PB adding 0.5 mol/L NaCl (PB/NaCl), which exhibited greater ionic strength than PB, almost all TSH immunoreactivity changed from the bound fraction into the unbound fraction on the protein G chromatography equilibrated with PB/NaCl. These data indicate that the novel immunoreactive TSH was due to hTSH and hTSH-specific antibody complex, and dissociation of the complex may be incomplete on direct S-200. The immunoreactive TSH showed high MW form (35,000 Da). The dissociation may be almost complete during dialysis with greater ionic strength; the native TSH then appeared to be of formal size.
[Show abstract][Hide abstract] ABSTRACT: We examined 13 patients with euthyroid Graves' disease suspected ophthalmologically, by comparing them with 20 patients with untreated Graves' disease and by following them up for 5 to 10 years. They had Graves' ophthalmopathy (NOSPECS class II-IV) without other ocular diseases, normal levels of serum thyroid hormones, and no previous history of Graves' disease. Proptosis in euthyroid Graves' disease was not significantly different from that in untreated Graves' disease. In 3 patients with euthyroid Graves' disease, TSH was suppressed. There was either no TSH response to TRH or it was low in 7 of 12 patients examined. The result of a T3-suppression test was abnormal in 8 of 11 patients examined. Titers of serum TGHA, MCHA, TSH-binding inhibitory immunoglobulin (TBII), and thyroid stimulating antibody (TSAb) were significantly lower in patients with euthyroid Graves' disease compared than in patients with untreated Graves' disease. TSAb, however, was positive in 12 of 13 (92%) patients. In spite of positive TSAb, 9 of 13 patients with euthyroid Graves' disease had normal radioactive iodine uptake (RAIU). During the observation period, various abnormalities in thyroid function developed: persistent hyperthyroidism in 5 patients (38%), transient thyrotoxicosis in 2 (15%) and transient hypothyroidism in 1 (8%). We conclude that euthyroid Graves' disease is a subtype of Graves' disease that minimally develops thyrotoxicosis in spite of the existence of TSAb due to some mechanism inhibiting thyroid growth or stimulation, and that the measurement of TSAb provides a useful marker for the diagnosis of this disease.
[Show abstract][Hide abstract] ABSTRACT: We reported that gestational thyrotoxicosis is induced by thyroid- stimulating activity (TSA) of circulating hCG. However, the serum immunological hCG concentration did not correlate to TSA. To elucidate this, we examined the relation of carbohydrate moieties of hCG to bioactivity in 79 early pregnant women, divided into 4 groups: no emesis, mild emesis, hyperemesis, and gestational thyrotoxicosis with hyperemesis. Serum free T4 (FT4) and free T3 (FT3) levels were significantly higher and TSH was lower in the hyperemesis (FT4, 23.42 ± 5.02 pmol/L; FT3, 6.26 ± 1.80 pmol/L; TSH, 0.30 ± 0.44 mU/L) and in gestational thyrotoxicosis (FT4, 48.65 ± 14.80 pmol/L; FT3, 14.71 ± 3.47 pmol/L; TSH, <0.04 mU/L) groups than in the no emesis group (FT4, 16.99 ± 2.48 pmol/L; FT3, 5.51 ± 0.75 pmol/L; TSH, 1.37 ± 1.23 mU/L; P < 0.0005). TSA was also significantly higher in the hyperemesis (566 ± 187%) and gestational thyrotoxicosis (832 ± 168%) groups than in the no emesis group (321 ± 135%). We found no significant difference among serum hCG concentrations measured by immunoassay in the four groups. To characterize the carbohydrate chains, serum hCG was fractionated by Concanavalin-A and ricin lectin affinity chromatography. The fraction firmly bound to Concanavalin-A, which contains hCG with high mannose and hybrid- type carbohydrate chains, was significantly higher in the hyperemesis group (91.07 ± 2.06%; n = 15) than in the no emesis group (89.61 ± 2.38%; n = 24; P < 0.04). The fraction firmly bound to ricin column, which contains hCG with asialo-carbohydrate chains, was significantly increased in the gestational thyrotoxicosis group (3.44 ± 1.70%; n = 5) compared with that in the no emesis group (1.77 ± 0.49%; n = 24; P < 0.03). Serum FT4 positively correlated to the hCG fraction firmly bound to ricin column (r = 0.61; P < 0.001). We conclude that thyrotoxicosis with hyperemesis may be caused by circulating asialo-hCG with higher thyrotropic bioactivity.
[Show abstract][Hide abstract] ABSTRACT: We measured serum concentrations of apolipoproteins (apo A-I, A-II, B, C-II, C-III and E) in patients with thyroid disease (hyperthyroidism; n = 44, hypothyroidism; n = 15) and in normal subjects (n = 89). We found that apoA-II, B and C-III concentrations revealed significant difference among three groups of the normal (apoA-II; 31.4 +/- 4.9 mg/dl, apoB; 85.8 +/- 16.3 mg/dl, apoCIII; 7.45 +/- 2.99 mg/dl), hyperthyroidism (apoA-II; 29.8 +/- 5.4, apoB; 63.4 +/- 18.9, apoC-III; 6.28 +/- 2.45) and hypothyroidism (apoA-II; 27.5 +/- 5.3, apoB; 108.0 +/- 30.9, apoC-III; 9.43 +/- 2.74). Thyroid hormones showed clear negative correlation to apoB (r = 0.70, p < 0.001). Furthermore, apoC-III was also found to be negatively correlated with thyroid hormone concentrations (r = 0.47, p < 0.001).
[Show abstract][Hide abstract] ABSTRACT: We evaluated the effect of the beta-adrenergic receptor blocking agent nadolol on serum levels of free thyroid hormones in 20 untreated patients with Graves' disease, aged between 17 and 57 years (mean +/- SD, 32.9 +/- 10.5). All the patients were treated with 30 mg of nadolol alone once-daily for 2 weeks, and clinical and laboratory parameters before and after the treatment were compared. Systolic blood pressure was depressed significantly (P < 0.001) from 132.7 +/- 11.1 mmHg to 122.8 +/- 10.9 mmHg. The resting pulse rate was also reduced significantly (from 110.3 +/- 9.2/min to 86.0 +/- 13.2/min, P < 0.001). Serum free thyroxine levels were reduced significantly from 7.1 +/- 3.1 ng/dl to 5.7 +/- 3.6 ng/dl (P < 0.05) and serum free triiodothyronine levels were reduced from 21.9 +/- 5.6 pg/ml to 17.2 +/- 6.9 pg/ml (P < 0.01). In the present study, the beta-adrenergic receptor blocking agent nadolol was newly found to have a reducing effect on serum free thyroxine, as well as free triiodothyronine concentrations.
[Show abstract][Hide abstract] ABSTRACT: Destruction-induced thyrotoxicosis and Graves' thyrotoxicosis must be differentiated, since they are treated differently. To find a useful marker, we examined serial changes in serum thyroglobulin (Tg) concentrations in 20 patients with postpartum thyroid disease (9, euthyroid Hashimoto's disease; 11, Graves' disease in remission in early pregnancy). Serum Tg was measured by a new multisite immunoradiometric assay that allows little influence of anti-Tg autoantibodies. Eight women developed destruction-induced thyrotoxicosis 1 to 4 months postpartum, 6 had relapse of Graves' thyrotoxicosis 2 to 4 months postpartum, and 6 remained euthyroid. In destruction-induced thyrotoxicosis, serum Tg 2 months before the onset was 13.3 +/- 11.4 micrograms/L, then clearly increased 1 month before (34.5 +/- 31.9 micrograms/L) and was even higher at the onset of thyrotoxicosis (116.5 +/- 137.1 micrograms/L). In contrast, serum Tg increased only at the onset in Graves' thyrotoxicosis (from 25.9 +/- 25.2 micrograms/L 1 month before to 76.1 +/- 75.3 micrograms/L at the onset, p < 0.05). There was no difference in serum Tg level at the onset between the two disorders. However, when data were expressed as the percent increase from the level one month before, and the cut-off value were taken at 150%, all 7 patients above the cut-off developed destruction-induced thyrotoxicosis, and 6 of 7 below had recurrent Graves' thyrotoxicosis. Thus, serial measurement of serum Tg is useful for the differentiation of destruction-induced thyrotoxicosis from Graves' thyrotoxicosis after delivery.
[Show abstract][Hide abstract] ABSTRACT: Autoimmune thyroid diseases often occur after delivery. However, it has been difficult to predict who will develop Graves' thyrotoxicosis after delivery. We tried to establish a systematic method for predicting post-partum onset of Graves' thyrotoxicosis.
We followed up the pregnant women with antithyroid microsomal antibody (MCAb) from early pregnancy to the post-partum period and analysed the relation between the activities of thyroid stimulating antibodies (TSAb) in early pregnancy and post-partum occurrence of Graves' disease.
Seventy-one women with positive MCAb in early pregnancy were studied. They were randomly selected from 262 MCAb-positive subjects found in 3405 consecutive early pregnant women who attended our maternity clinic during the last ten years.
MCAb was measured with a commercially available agglutination kit. For 71 MCAb-positive subjects, TSH-binding inhibitory immunoglobulin (TBII) and TSAb were measured in early pregnancy, and serially until 6 months after delivery for the subjects with either positive TBII or TSAb. Thyroid function and goitre size were recorded at every observation.
Among the 71 subjects, 7 showed positive TSAb in early pregnancy without any thyroid dysfunction; all 7 developed thyroid dysfunction in the post-partum period. Five of them (70% of TSAb-positive subjects) developed Graves' disease, two showing persistence and three transiently. None of 64 TSAb-negative subjects developed Graves' thyrotoxicosis, though 44 developed various types of thyroid dysfunction as a result of post-partum autoimmune thyroiditis.
The individuals at high risk of post-partum onset of Graves' thyrotoxicosis can be found early in their pregnancy by the detection of TSAb. Overall occurrence of post-partum Graves' disease in the general population is estimated above 0.54%, that is, one in 200 post-partum women may develop Graves' thyrotoxicosis, although thyrotoxicosis may be transient in half of the patients.
[Show abstract][Hide abstract] ABSTRACT: To assess the prevalence of postpartum onset of disease among the patients with Graves' disease, we performed a retrospective examination of 289 consecutive female patients with Graves' disease who attended our thyroid clinic. Of these patients, 92 were female of child-bearing age (20-39 y.o.) who have had one or more deliveries, and at least 37 patients revealed clear evidences of postpartum onset of the disease. That is, at least 40% of Graves' patients of 20-39 y.o. developed their disease during the postpartum period.
[Show abstract][Hide abstract] ABSTRACT: Effect of theophylline on the thyroid function was studied in 9 healthy subjects. Theophylline (200mg) was taken two times (AM8:00, PM10:00) and blood was collected two times (AM9:00, PM4:00) a day for five days. Five of these 9 subjects took same dose two times (AM8:00, PM10:00) a day and blood was collected once (AM9:00) a week for four weeks. In short-term medication, serum free thyroxine (FT4) increased significantly (1.19 +/- 0.19 ng/dl, before medication) in 4th day AM (1.29 +/- 0.14 ng/dl, p < 0.05), in 4th day PM (1.30 +/- 0.12 ng/dl, p < 0.05) and in 5th day AM (1.30 +/- 0.16 ng/dl, p < 0.05). Serum free triiodothyronine (FT3) increased significantly (3.9 +/- 0.36 pg/ml, before medication) in 4th day AM (4.3 +/- 0.66 pg/ml, p < 0.05) and in 5th day AM (4.3 +/- 0.61 pg/ml, p < 0.05). Serum thyroid stimulating activity (TSA), which was measured as an increase in cAMP in FRTL-5 cells, increased significantly (116.5 +/- 49.5%, before medication) in 1st day PM (152.3 +/- 60.0%, p < 0.05), in 2nd day PM (192.6 +/- 86.7%, p < 0.05), in 3rd day PM (208.5 +/- 94.1%, p < 0.05) and in 4th day AM (183.5 +/- 80.1%, p < 0.05). In contrast, serum FT4, FT3, TSH, and TSA did not increase significantly in long-term medication.(ABSTRACT TRUNCATED AT 250 WORDS)
Rinsho byori. The Japanese journal of clinical pathology 01/1994; 41(12):1343-8.
[Show abstract][Hide abstract] ABSTRACT: Graves' disease is frequently aggravated during antithyroid drug therapy; however, little is known of its aggravating factors. We studied 83 patients with Graves' disease who were euthyroid for at least 6 months under antithyroid maintenance therapy, and we examined the relationship between thyrotoxicosis relapse, attack of allergic rhinitis, and peripheral eosinophil increase. Forty-one patients showed thyrotoxicosis relapse; of these, 22 (54%) showed peripheral eosinophil increase, and 14 (34%) had attacks of allergic rhinitis. In the remaining 42 patients without thyrotoxicosis relapse, only 4 (10%, P < 0.001) showed an increase in peripheral eosinophils, and only 3 (7%, P < 0.01) had allergic rhinitis. Recurrence of thyrotoxicosis was observed with the increase in serum levels of TSH-receptor antibodies and increase in eosinophils 2 months after the attack of allergic rhinitis. Three patients with seasonal allergic rhinitis showed thyrotoxicosis relapse at the same time of year within 2 consecutive years. Our findings indicate that allergic rhinitis can be an aggravating factor of Graves' disease and suggest that the preceding increase in peripheral eosinophils can be a predictive indicator of recurrence of thyrotoxicosis during antithyroid drug therapy.
[Show abstract][Hide abstract] ABSTRACT: The thyroid gland is physiologically stimulated in normal early pregnancy. However, clinical thyrotoxicosis in normal pregnancy has not been well described. In order to clarify this we examined thyroid function and thyrotoxic symptoms in relation to emesis in normal pregnancy. We also investigated the possible mechanism of gestational thyrotoxicosis.
Thyroid function was evaluated in view of the clinical thyrotoxic symptoms and the severity of gestational emesis in early pregnancy of 51 normal women. Two pregnant women who showed clinical thyrotoxicosis were followed serially during and after pregnancy.
Serum free T4, free T3 and TSH were measured by radioimmunoassay and hCG by fluoroimmunoassay. Thyroid-stimulating activity of pregnancy sera was measured by cAMP increase in cultured FRTL-5 cells.
Fifty-one pregnant women were divided into three groups: those without emesis (n = 24), with emesis (n = 19) and with hyperemesis (n = 8). Serum free T4 and free T3 were higher in the hyperemesis group (P < 0.01) and the emesis group (P < 0.01), and serum TSH was suppressed to less than 0.1 mU/l in both groups, while serum hCG was not significantly different among these three groups. However, serum thyroid-stimulating activity was remarkably high in the hyperemesis group (P < 0.01). Thus the ratio of thyroid-stimulating activity to hCG was higher in the hyperemesis group (P < 0.05) and the emesis group (P < 0.05) compared with that in the group without emesis. These thyroid-stimulating activities were abolished by treatment of the serum with anti-hCG antibody. Two of eight women with hyperemesis, who had the highest free T4 and thyroid-stimulating activity/hCG ratio, showed overt clinical symptoms of thyrotoxicosis; all the symptoms disappeared in association with a fall in thyroid-stimulating activity and free T4.
Clinical thyrotoxicosis is caused by circulating hCG with higher biological activity in pregnant women with hyperemesis. A new clinical entity of 'gestational thyrotoxicosis' is proposed and tentative characteristics are discussed.
[Show abstract][Hide abstract] ABSTRACT: Thyrotoxicosis in Graves' disease is often aggravated in early pregnancy and is closely associated with postpartum recurrence of stimulative thyrotoxicosis. To examine whether thyroid-stimulating TSH receptor antibody (TSAb) or human chorionic gonadotropin (hCG), which also has thyroid-stimulating activity (TSA), was responsible for this early aggravation, the respective TSA due to TSAb or hCG was evaluated by a highly sensitive cAMP accumulation assay using FRTL-5 cells. TSA was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG concentration, and was abolished completely by the pretreatment of serum sample with the solid-phase hCG antibody coupled with Sepharose 4B. The model serum samples of Graves' disease with pregnancy were made by the mixture of normal pregnant and Graves' sera, and their TSA were reduced by the pretreatment with the solid-phase hCG antibody, just corresponding with the reduction in hCG-induced TSA. TSA of early pregnant sera in 20 patients with Graves' disease decreased significantly but were still positive even after the pretreatment with the hCG antibody. Serial changes in TSAb and hCG-induced TSA were measured in 5 of these 20 pregnant patients. hCG-induced TSA increased associated with the increase in free thyroxine, while TSAb did not show striking change in early pregnancy. These data indicate that (1) respective TSA due to TSAb or hCG can be measured distinctively by using the solid-phase hCG antibody and (2) hCG plays a crucial role in the aggravation of Graves' thyrotoxicosis in early pregnancy.
[Show abstract][Hide abstract] ABSTRACT: Thyrotoxicosis in Graves' disease is often aggravated in early pregnancy and this aggravation is associated with postpartum relapse of thyrotoxicosis. To examine whether thyroid-stimulating TSH receptor antibody (TSAb) or human chorionic gonadotropin (hCG), which also has thyroid-stimulating activity (TSA), is responsible for this early aggravation, the respective TSA due to TSAb or hCG were evaluated with a sensitive cAMP accumulation assay using FRTL-5 cells. TSA, which was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG level, but was abolished completely by the pretreatment of serum samples with the solid-phase hCG antibody coupled with Sepharose-4B. Total TSA in the model samples of mixture of Graves' and pregnant sera (Gr + Preg), was reduced by the pretreatment with the solid-phase antibody, just corresponding with the reduction in hCG-induced TSA. Total TSA in early pregnant sera in 15 patients with Graves' disease, decreased significantly but was still positive even by the pretreatment with the hCG antibody. Pregnancy-associated changes in TSA was examined serially in a patient with Graves' disease, and hCG-induced TSA increased predominantly along with the serum thyroid hormone in early aggravation period. These data indicate that (1) the respective TSA due to TSAb or hCG can be differentially measured by using the solid-phase hCG antibody and (2) hCG plays an important role for aggravation of Graves' thyrotoxicosis in early pregnancy.
Rinsho byori. The Japanese journal of clinical pathology 10/1992; 40(9):941-7.
[Show abstract][Hide abstract] ABSTRACT: To identify risk factors for disorders of fetal growth and thyroid function in the presence of maternal Graves disease.
Two hundred thirty pregnancies in gravidas with Graves disease were analyzed. Maternal thyroid status was evaluated by serum free thyroxine (T4) or free T4 index, TSH, and TSH-receptor antibody; personal history of thyrotoxicosis and total dose of antithyroid drugs during pregnancy were also noted. Neonatal thyroid function was assessed at birth and on the fifth day after birth.
Fifteen neonates (6.5%) were small for gestational age (SGA), and this occurrence was significantly associated with thyrotoxicosis lasting for 30 weeks or more of pregnancy, TSH-receptor antibody level of 30% or more at delivery, history of Graves disease of 10 years or longer, and onset of Graves disease before 20 years of age. However, no significant correlation was found between maternal thyroid hormone level and SGA neonates. Thyroid dysfunction developed in 38 infants (16.5%), of whom only four were SGA; development of this dysfunction was significantly related to the mother's total dose of antithyroid drugs, duration of thyrotoxicosis in pregnancy, and/or TSH-receptor antibody level at delivery.
Duration of maternal Graves disease or thyrotoxicosis, either mild chemical or overt, in pregnancy is significantly associated with SGA neonates. Neonatal thyroid dysfunction is associated with the maternal thyroid condition, especially the serum TSH-receptor antibody level.
[Show abstract][Hide abstract] ABSTRACT: Using newly developed ultrasensitive enzyme immunoassay (EIA) for thyroglobulin antibody (TgAb), we have evaluated physiological and pathological implications of the antibody in healthy subjects as well as in autoimmune thyroid diseases.
This EIA was based on the immune complex transfer method, and was 10(4)-fold more sensitive compared with the conventional haemagglutination assay (HA); the detection limit was 0.1 micrograms IgG/I, and the specificity of the assay was confirmed from the unequivocal decrease in the fluorescence intensity by the preincubation of test serum with Tg and/or inactive beta-D-galactosidase which blocks antibodies to the enzyme.
TgAb was detectable in 159 (91%) of 175 healthy subjects aged 3rd to 7th decade (96 men and 79 women), and did not exhibit age or sex-associated change. In nine healthy women, the TgAb level significantly decreased as pregnancy progressed but increased transiently after delivery. TgAb was detectable in 52 (98%) of 53 patients with Graves' disease and all (100%) of 107 patients with chronic thyroiditis. Abnormal high TgAb values (> 40 micrograms/I), determined from the 95th percentile in healthy subjects, were shown in 40 (75%) with the former disease and 94 (88%) with the latter disease. Moreover, in 14 goitrous patients with biopsy-proved chronic thyroiditis with negative HA results, 12 (86%) showed abnormal high TgAb levels. In 69 patients with post-partum thyrotoxicosis in Graves' disease, 15 (79%) of 19 patients with the TgAb level of more than 2 x 10(3) micrograms/I in early pregnancy showed destructive thyrotoxicosis and 46 (92%) of 50 with less than this level showed stimulative thyrotoxicosis. This TgAb test could discriminate the two types of thyrotoxicosis more clearly than could the conventional TGHA test. In chronic thyroiditis, the mean TgAb value in early pregnancy was significantly higher in patients with postpartum hypothyroidism than in those without thyroid dysfunction. Hypothyroidism developed in 80% of the patients with a TgAb value of more than 10(3) micrograms/I.
The ultrasensitive TgAb EIA was useful for detecting the physiological changes in autoantibody formation in healthy subjects and the TgAb value was useful for predicting post-partum thyroid dysfunction in autoimmune thyroid diseases. This EIA is useful for the evaluation of the immune surveillance in patients with autoimmune thyroid diseases as well as in healthy subjects.
[Show abstract][Hide abstract] ABSTRACT: We examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from alpha beta T cell receptor (TCR) negative T (WT31-CD3+) cells and CD8 (CD4-CD8+) cells decreased and those of CD4+CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+CD8-) cells, non-T, non-B (CD5-CD19-) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, alpha beta+ TCR T (WT31+CD3+) cells, CD8 cells, and non-T, non-B cells. A serial study of some of the patients showed opposite changes in alpha beta TCR- T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. alpha beta TCR- T cells were mostly gamma delta TCR+ T (IIF2+ CD3+) cells in these patients. These data suggest that alpha beta TCR-T (gamma delta TCR+ T), CD8, and CD4+ CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells are important in thyroid stimulation in Graves' disease.
[Show abstract][Hide abstract] ABSTRACT: Sequential changes in serum levels of IgG, IgA, and IgM, and C3 and C4 during and after pregnancy were studied in 8 healthy women. Serum IgG decreased gradually during pregnancy, but increased markedly during the six months following delivery. Serum IgA and IgM levels also showed patterns similar to IgG. In contrast, C3 and C4 levels increased significantly and reached maximum levels in the last trimester during pregnancy, but decreased gradually for six months after delivery. Reciprocal changes between immunoglobulins and complements were clarified for the first time, and were suggestive of a compensatory autoregulatory mechanism in the suppression of the humoral immune system during pregnancy.
Journal of clinical & laboratory immunology 02/1992; 38(3):137-41.
[Show abstract][Hide abstract] ABSTRACT: Sequential changes in serum levels of the immunoglobulins IgG, A and M and of the complements C3 and C4 during pregnancy and the postpartum period were studied in 8 healthy women. Serum IgG and A levels decreased gradually during pregnancy, but increased significantly during the first three months following delivery. Serum IgM level also decreased during pregnancy, reaching its minimum during the second trimester, but increased thereafter. In contrast, C3 and C4 levels increased significantly during pregnancy and reached their maximum levels during the last trimester. After delivery, levels of these two components decreased gradually for the next six months. The complement system may operate as a compensatory autoregulatory mechanism in the suppression of the humoral immune system during pregnancy.
Rinsho byori. The Japanese journal of clinical pathology 12/1991; 39(11):1195-8.