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At least 19 recordsLinked to original sources
PubMed1977

Hypothyroid Graves' disease.

Graves' disease has recently been shown to exist in a euthyroid form in untreated patients. Sporadic reports of a hypothyroid form are beginning to emerge, thus illustrating the multifaceted nature of this disorder, with thyrotoxicosis at one end of the spectrum and hypothyroidism at the other. Three patients with nonthyrotoxic Graves' disease and concomitant hypothyroidism were seen at Emory University Hospital in one year, and deatailed studies were made to help elucidate the nature of this unusual combination. Results of these studies are reported and briefly discussed. It is suggested that, until more is known about this intriguing aspect of the Graves' disease spectrum, the label "hypothyroid Graves' disease" is justifiable.

Adult↗
PubMed1978

The operation of immunological networks in Graves' disease.

Association between Graves' disease and HLA--B8 has been previously documented, as have been associations between 1 gG heavy chain allotype markers (Gm). We found a significant increase in the phenotype fnb/fb (ie. positivity for fb) in patients with Graves' disease compared to controls, raising the possibility of allotypic restriction of thyroid stimulating antibodies thought to be causally related to the disease. The influence of fb on the susceptibility to Graves' disease was found to be independent of HLA--B8 status suggesting that the immunological network operated by the Histocompatibility-linked genes is independent of that centered around IgG allotypes. It is postulated that, whereas the former genes determine the level of helper T lymphocyte function in the production of thyroid stimulating antibodies in Graves' disease, a person who also happens to carry the Gm marker fb would be assured of the production of IgG antibodies with thyroid stimulatory activity.

Adult↗
PubMed1979

A study of human leukocyte D locus related antigens in Graves' disease.

An association between Graves' disease and the human leukocyte antigen (HLA) system has previously been reported. The disease was more strongly associated with the HLA D locus antigen Dw3 than with HLA B8. Products of the HLA D locus are determined by the interaction of test cells with standard typing lymphocytes, a technically difficult procedure. Recently, it has been possible to type serologically for D locus related (DRw) specificities on peripheral bone marrow-derived (B) lymphocytes. Blood B lymphocytes from 50 unrelated controls and 41 patients with Graves' disease were typed for seven HLA DRw specificities. 28 patients with Graves' disease (68%) were positive for DRw3, in contrast to 14 controls (28%); whereas only 21 patients (50%) were HLA B8 positive, compared with 13 (26%) controls. Thus, positivity for DRw3 afforded a relative risk for Graves' disease of 5.5, whereas that for HLA B8 amounted to 3.0. Additionally, a family with multiple cases of Graves' disease in which the disease was previously shown to be inherited with the haplotype, was linked to DRw2, which suggests that the susceptibility to the disease was inherited in association with that antigen. Two HLA B/glyoxalase recombination events were observed in this family; in both instances HLA DRw followed HLA B. This study thus demonstrates that the disease susceptibility gene for Graves' disease is in strong linkage disequilibrium with DRw3; however, it may be associated with other DRw specificities and inherited within family units in association with them.

Alleles↗
PubMed1979

Reemergence of thyroidectomy as treatment for Graves' disease.

Hyperthyroidism of Graves' disease may be treated very effectively by antithyroid pills, such as PTU and Tapazole, by radioactive iodine therapy, and by subtotal thyroidectomy. Each form of therapy has advantages and disadvantages, and thus treatment should be individualized. While therapy with radioactive iodine would appear to be ideal since it does not require an operation and is less expensive than surgical management, it suffers from a high rate of progressive hypothyroidism and from the fact that the time until a euthyroid state is obtained is often prolonged. In addition, the long-term carcinogenic risk of the therapy for thyroid neoplasia has never been completely defined since the data most often quoted have a mean follow-up time of only eight years. Furthermore, new "low-dose" radioiodine regimens may be more dangerous in this regard. Subtotal thyroidectomy, while not totally without complications, remains a rapid, safe, and effective treatment for Graves' disease. The careful use of propranolol has facilitated the preparation of some patients and has lessened the risk of operation. Thyroidectomy should remain the treatment of choice for young adults with this disease.

Graves Disease↗
PubMed1978

UCLA conference. Autoimmune thyroid diseases--Graves' and Hashimoto's.

Thyroid-related autoimmune diseases (Graves' thyroid disease, Graves' ophthalmopathy, and Hashimoto's thyroiditis) may occur alone or in any association. The diagnosis of Hashimoto's thyroiditis requires multiple criteria; pathologic changes in the thyroid are not due to antibodies but may result from cytotoxic lymphocytes or a deficiency of suppressive T cells. In Graves' and Hashimoto's diseases the increased prevalence of HLA-B8 may not be significant, but that of HLA-AW30 in Hashimoto's disease is. In 48 first-degree relatives of patients with Graves' disease, thyroid abnormalities were frequent but not correlated with HLA type. Elevated serum thyroglobulin levels in all patients with hyperthyroidism fell to normal after surgical resection or radioiodine therapy. Patients whose illness recurred after antithyroid drug treatment was stopped had higher pretreatment thyroglobulin levels and no fall during treatment; those whose illness remitted had lower initial levels and a significant fall during treatment. Sodium ipodate lowered serum triiodothyronine and thyroxine levels in hyperthyroid patients and may be useful in the treatment of hyperthyroidism.

Animals↗
PubMed1977

Transient recurrence of hyperthyroidism after delivery in Graves' disease.

Four patients with Graves' disease whose hyperthyroidism was in remission following antithyroid therapy were studied without any treatment during and after pregnancy. In the 8-9th month of pregnancy, they were in a euthyroid state with serum levels of thyroxine (T4) of 18.9, 11.9, 11.2 and 14.5 mug/100 ml, triiodothyronine (T3) of 273, 190, 162 and 244 ng/100 ml and T3 resin sponge uptake (RT3U) of 22, 14, 19 and 16% respectively (normal pregnant range: T4, 7.0-15.0, T3 140-250, RT3U 15-25). At 1-3 months after delivery, hyperthyroidism recurred, as manifested by T4 levels of 17.2, 14.5, 16.7 and 21.7 mug/100 ml, T3 levels of 320, 225, 390 and 464 ng/100 ml and RT3U levels of 34, 34, 43, and 41% respectively (normal non-pregnant range: T4 5.0-12.0, T3 90-190, RT3U 24-37). The recurrence of hyperthyroidism was also demonstrated by serial measurements of serum free T4 and free T3. The thyroid function of all four patients returned spontaneously to the normal range at 4-6 months after delivery. One patient developed hypothyroidism for a short period before regaining the euthyroid state. The titers of serum anti-thyroid microsomal antibodies and levels of serum immunoglobulins decreased during pregnancy and increased transitorily at the time of hyperthyroidism after delivery. Similarly, increases in the levels of thyroid hormones, anti-thyroid antibodies and immunoglobulins were observed transitorily following spontaneous abortion after 4 months' pregnancy in one case. We suggest that the transient recurrence of hyperthyroidism in Graves' disease may be induced by immunological changes after delivery.

Adult↗
PubMed1978

Responses to TRH and T3 suppression tests in euthyroid subjects with a family history of Graves' disease.

The relationship of Graves' disease and heredity was studied in 97 clinically and biochemically euthyroid relatives (resin T3 uptake and serum T3, T4, and TSH within normal ranges) who had more than two thyrotoxic relatives within the second degree relationship. TRH tests were preformed in all 97 cases. In 56 of the 97, T3 suppression tests were performed shortly after the TRH test. Results revealed that 29 of the 97 (29.9%) showed an abnormal response to TRH. fourteen of these (14.4%) revealed no response or a hyporesponse, and 15 (15.5%) revealed a hyperresponse to TRH. Four of 56 (7.1%) were T3 nonsuppressible. Seven individuals who showed no response or a hyporesponse to TRH consisted of 2 nonsuppressible and 5 suppressible subjects. In 14 non- or hyporesponsive cases, serum T3 (1.51 +/- 0.05 ng/ml; mean +/- SE) and T4 (9.91 +/- 0.31 micrograms/dl) were significantly higher compared with those of normal responders (1.30 +/- 0.04 ng/ml, 8.57 +/- 0.21 micrograms/dl; P less than 0.001) or hyperresponders (1.16 +/- 0.06 ng/ml, 7.77 +/- 0.63 micrograms/dl; P less than 0.01). There was no correlation between TRH responsiveness and T3 suppressibility. A relatively high occurrence of thyroglobulin and microsomal antibodies was observed, further suggesting a hereditary predisposition. The findings indicate that even in euthyroid relatives with a family history of Graves' disease who have no clinical or biochemical abnormalities of thyroid dysfunction, many have abnormalities in TRH responsiveness, T3 suppressibility, and thyroidal antibodies.

Adolescent↗
PubMed1979

Delayed hypocalcemia after thyroidectomy for Graves' disease is prevented by parathyroid autotransplantation.

Late hypocalcemia appears associated with thyroidectomy for Graves' disease more frequently than with thyroidectomy for other conditions. Of 62 total thyroidectomies done by a single surgeon, 28 were done for carcinoma, 18 for benign disease (primarily nontoxic nodules with a history of radiation therapy to the head and neck (RT)) and 16 for Graves' disease. Mean calcium concentrations measured two months or more after surgery were 9.38 +/- 0.07 (SEM)mg/% for patients with cancer, 8.79 +/- 0.31 mg/dl for patients with Graves' disease and 9.38 +/- 0.08 mg/dl for patients with other benign diseases. No patient without Graves' disease developed late hypocalcemia. In contrast, six of 16 patients with Graves' developed significant late hypocalcemia requiring calcium therapy. The incidence of hypocalcemia after total thyroidectomy for Graves' disease was significantly greater than that seen in other conditions (p < 0.01). Since no parathyroids were removed in the patients with Graves' disease, and since branches of the inferior thyroid artery were invariably ligated distal to the parathyroids, we hypothesized that the late hypocalcemia might be associated with a peculiarity in scar formation in the presence of this autoimmune disease. Accordingly, parathyroid autotransplantation was performed synchronously as a prophylactic measure in nine subsequent patients undergoing total thyroidectomy for Graves' disease; no instance of late hypocalcemia has occurred in this group. The decreased incidence of late hypocalcemia is highly significant (p < 0.01). Although the precise etiology of late hypocalcemia after thyroidectomy for Graves' disease remains undetermined, this experience indicates that synchronous parathyroid autotransplantation is beneficial in preventing this complication.

Calcium↗
PubMed1978

The HLA B w4/w6 diallelic system in Graves' disease.

We studied the diallelic system HLA--Bw4/w6 in patients with Graves' disease and control subjects. Twenty-one out of the 22 patients with Graves' disease were found to be HLA--Bw6 positive and 16 of these were homozygous, contrasted with 28 and 9 out of 34 controls, respectively. HLA--Bw6 positivity results in a relative risk for Graves' disease of 3.27; homozygosity for that allele further increases the risk to 7.4. It is possible that the increased risk attached to HLA--Bw6 is secondary to the increase in HLA--B8 previously described in Graves' disease.

Alleles↗
PubMed1977

Short and long term effects of radioiodine and antithyroid drugs on T4 binding proteins, free T4 and T3, during Graves' disease therapy.

Ninety five patients with Graves' disease were studied before and at three months intervals after antithyroid drugs (ATD) (31 cases) or radioiodine (64 cases) therapy until recovery. Before treatment, the T4 maxima binding capacity of TBPA was significantly decreased 253.5 +/- 11.4 mug/100 ml)(mean + se) (control values: 287 +/- 10.4 mug/100 ml) (alpha = 0.04), especially in 53.7% of patients (m = 177 +/- 8 mug/100 ml). The mean of TBG (m = 20.7 +/- 0.9 mug/100 ml) was not different from euthyroid subjects (m = 19.7 +/- 1.7 mug/100 ml) except in 51.2% of patients who had a low TBG (m = 14.3 +/- 1.1 mug/100 ml). An inverse linear correlation was found between TBG-DFT4 (alpha = 0.05) and DF T 3 (alpha = 0.002), TBPA-log DF T4 (alpha = 0.05) but not between TBG and TBPA. The physiological relationship between DFT3, DFT4, TT3, TBG and TBPA was studied in vitro; after adding increased quantities of T4 to a pool of sera collected from eu, hypo or hyperthyroid patients, DFT4, DFT3, FT3 index increased in linear positive relationship with TT4 concentrations, the kinetic of this phenomena was inversely correlated with T4 maximal binding capacity of TBG or TBPA for T4. Addition of T3 to the same sera did not show any effect on the previous parameters. DFT3 depended on the level of T4 in serum more than T3 concentration and was in inverse relationship with the maximal binding capacity of TBG. This data might explain the paradoxal normal or slightly increased values of DFT3 found in T3 thyrotoxicosis. In patients treated with ATD or radioiodine, TBPA but not TBG increased significantly on year after. However, in subjects with an initial very low TGB or TBPA, this phenomenon occurred on the third month after radioiodine or ATD. During the same period, DF T4 and DF T3 were inversely correlated to TBG and TBPA. In conclusion, important changes in T4 binding proteins and free fractions of thyroid hormones were observed in Graves' disease but were corrected by antithyroid therapy. All these data were in good agreement with the normalisation of thyroid function.

Adolescent↗
PubMed1976

Thyroid antigen stimulates lymphocytes from patients with Graves' disease to produce thyroid-stimulating immunoglobulin (TSI).

Circulating lymphocytes from patients with Graves' disease and from control subjects were cultured in vitro alone, with normal human thyroid tissue homogenates, and with other nonthyroid human tissue homogenates. The supernatants of these cultures were assayed for human thyroid-stimulating activity by incubation with human thyroid slices in which increases in cAMP levels were then measured. Human thyroid stimulator activity was demonstrated in 16 out of 20 experiments in which lymphocytes from patients with active untreated Graves' disease (with hyperthyroidism) were cultured with normal thyroid homogenate, in 4 out of 17 experiments when control lymphocytes were similarly cultured, and in one out of 12 experiments in which the lymphocytes from the patients with Graves' disease were cultured with liver or gastric mucosa homogenate. Thyroid-stimulating activity was abolished by precipitation of the globulin from the supernatant by goat anti-human globulin serum. These results demonstrate that normal human thyroid tissue homogenates can specifically stimulate most lymphocytes from patients with Graves' disease and lymphocytes from a few normal subjects to produce human thyroid-stimulating immunoglobulins in vitro. This suggests that the human thyroid-stimulating immunoglobulins are auto-antibodies to normal thyroid constituents, but the possiblity that an antigenic change in the thyroid initiates the disease cannot be entirely excluded. The findings suggest that the prime change in Graves' disease is immunologic, perhaps a failure of immunological suppression.

Antigens↗
PubMed1978

Differentiation of thyrotoxicosis induced by thyroid destruction from Graves' disease.

Thyroid function was tested in untreated patients with Graves' disease or thyrotoxic subacute thyroiditis, and in patients with autoimmune thyroiditis who showed postpartum or spontaneous transient thyrotoxicosis. The serum triiodothyronine/thyroxine ratio (T3/T4) was greater than 20 ng/microgram in Graves' disease but less than 20 in all patients with subacute thyroiditis and 9 of 11 patients with autoimmune thyroiditis. Thus, like radioactive iodine uptake, the serum T3/T4 ratio is useful for differentiating destruction-induced thyrotoxicosis from the stimulation-induced hyperthyroidism of Graves' disease.

Adult↗
PubMed1978

Diabetes and Graves disease complicating pregnancy.

We report here six pregnancies in 5 women with juvenile diabetes and Graves disease. The diabetes was managed in a standard fashion. The Graves disease was managed with propylthiouracil when required. The course of neither the diabetes nor Graves disease was different than expected. When established guidelines for therapy are followed the two have no interaction with one another. One infant was mildly hypothyroid. None developed neonatal Graves disease. Four of the infants had hyperbilirubinemia.

Adult↗
PubMed1979

[Studies on the radioreceptor assay of TSH: the properties of TSH-binding inhibitor immunoglobulins (TBII) in patients with Graves' disease (author's transl)].

In the radioreceptor assay system for TSH, serum immunoglobulin G (IgG) from some patients with Graves' disease has been shown to inhibit the binding of labelled TSH to its receptor sites. In order to clarify the properties of these TSH-binding inhibitor immunoglobulins (TBII) in patients with Graves' disease, TBII were measured in sera from 31 untreated and 51 131I-treated patients, and their relation to clinical and laboratory findings was studied. TBII were detected in 18 (60%) out of 31 patients with untreated Graves' disease. TBII levels in these patients correlated well with thyroidal 99mTc uptake at 30 min and also with the grade of epithelial hyperplasia of thyroid follicles. There was no significant correlation between TBII and serum T3, serum T4, free T4 index, antibody titers against thyroglobulin and microsomes, or association of exophthalmos. There were many patients with Graves' disease whose sera contained high TBII levels but no detectable bioassayable thyroid-stimulating activity (LATS), and in these patients a close correlation was observed between serum levels of TBII and bioassayable LATS-protector activity. In patients with Graves' disease who had been treated by 131I from 5 to 17 years before, the incidence of TBII was very low at 20% (10/51). All except two cases having TBII were found to be still thyrotoxic. Thus, TBII were detected in 8 out of 10 thyrotoxic patients and in only 2 out of 18 euthyroid and none of 23 hypothyroid patients. These findings suggest that TBII in patients with Graves' disease were in close association with human thyroid stimulating activity, and that TBII might be useful as an indicator for checking the effectiveness of the treatment.

Autoantibodies↗
PubMed1977

Triiodothyronine, thyroxine, and iodine in purified thyroglobulin from patients with Graves' disease.

Previous studies have suggested that there is an overproduction of triiodothyronine (T(3)) relative to thyroxine (T(4)) in patients with thyrotoxicosis associated with Graves' disease. To evaluate whether or not an increased ratio of T(3) to T(4) in thyroidal secretion could be contributing to this relative T(3) hyperproduction, T(3), T(4), and iodine were measured in thyroglobulin (Tg) from controls and patients with Graves' disease who had been treated either with propranolol only or with antithyroid drugs plus iodide before surgery. To avoid possible artifacts associated with pulse labeling and chromatography, T(3) and T(4) were determined by radioimmunoassay of Pronase hydrolysates of purified Tg. Results of analyses of Tg from six control patients and seven with Graves' disease, not receiving thiourea drugs or iodide, showed that the iodine content of Graves' disease Tg was not different from normal. Both contained 3.4 residues of T(4)/molecule Tg, but there was 0.39+/-0.08 (mean+/-SD) residue of T(3)/molecule Tg in Graves' Tg as opposed to 0.23+/-0.07 residue T(3) molecule Tg in controls matched for iodine content (P < 0.01). This difference resulted in a significantly lower T(4)/T(3) molar ratio (9+/-2) in Graves' Tg as opposed to control (15+/-2, P < 0.001). In Tg from patients with treated Graves' disease, iodine, T(3), and T(4) were reduced, but the reduction in the latter was more substantial, resulting in a T(4)/T(3) molar ratio of 3.4+/-1. Fractionation of Tg from all groups by RbCl density gradient ultracentrifugation indicated that at physiological levels of Tg iodination, the molar ratio of T(3)/Tg was consistently higher in Graves' disease. The specific mechanism for this difference is not known, but it is not due to iodine deficiency. If T(3) and T(4) are secreted in this altered ratio in patients with Graves' disease, the magnitude of the difference could explain the relative T(3) hyperproduction which is characteristic of this state.

Drug Therapy, Combination↗
PubMed1977

HLA-BW35 and B5 in Japanese patients with Graves' disease.

Thirty-three Japanese patients with Graves' disease and 106 healthy controls living in the Kagoshima area, the southernmost part of the Japanese mainland, were HLA typed by the NIH method. None of them were related to each other. The only antigen showing an increased frequency in Japanese patients with Graves' disease was HLA-BW35 (corrected P less than 0.02). A decreased frequency of B5 in the patients was also statistically significant (corrected p less than 0.02).

Asian People↗