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PubMed2006

Pulmonary hypertension is frequent in hyperthyroidism and normalizes after therapy.

BACKGROUND: In recent years, many authors have described several cases revealing an association between hyperthyroidism and pulmonary hypertension. This observational study was designed to evaluate the prevalence of pulmonary hypertension in hyperthyroidism and to determine the role of methimazole in regulating pulmonary vascular resistance in these patients. METHODS: We studied 114 patients, 78 women and 36 men, whose mean age was 51+/-13years. Forty-seven had Graves' disease and 67 had a nodular goiter. All subjects were ambulatory and were recruited in a consecutive order. The control group (group 2) included 20 healthy subjects matched for age and sex. Transthoracic Doppler echocardiography was performed and systolic pulmonary artery pressure (PAPs) was determined by the tricuspid regurgitation method using the Bernoulli's equation. We performed a 120-day follow-up in the patients with pulmonary hypertension and we divided them into two subgroups: group 1A (n=33), patients treated with methimazole, and group 1B (n=17), subjects treated with partial thyroidectomy. RESULTS: We found a mild pulmonary hypertension in 50 patients in group 1 (43%) and in none of those in the control group. The mean+/-SD PAPs was 27.77+/-6.56 in group 1 and 21.32+/-2.55 in group 2. A negative correlation was found between the T.S.H. value and the level of PAPs (r=-0.85; p<0.001). During the follow-up, group 1A went from a PAPs value of 34.3+/-3.2 to 29.2+/-3.3 after 15days of therapy and group 1B from 34.3+/-3.0 to 34.1+/-2.9 (p<0.001). CONCLUSIONS: The results of the present study demonstrate a frequent association between hyperthyroidism and mild and transient pulmonary hypertension. Subjects treated with methimazole have a more rapid drop in PAPs.

Journal Article↗
PubMed2004

TSH-receptor autoantibodies - differentiation of hyperthyroidism between Graves' disease and toxic multinodular goitre.

Previous studies indicate pre-existing subclinical Graves' disease in many patients with the scintigraphic diagnosis of toxic multinodular goitre type A, equivalent to the in Germany so-called disseminated thyroid autonomy. Furthermore, after radioiodine treatment an increase or the induction of TSH-receptor antibodies (TRAb) in patients with Graves' disease or toxic multinodular goitre has been repeatedly reported. The distinction between both hyperthyroid conditions, Graves' disease and toxic multinodular goitre type A, depends on the diagnostic power of the TSH-receptor antibody determination. Bioassays using CHO cell lines expressing the hTSH-receptor or a new TBII assay based on competitive binding to recombinant human TSH-receptor showed a higher sensitivity for the detection of TSH-receptor antibodies in patients with Graves' disease than previous assays using solubilized porcine epithelial cell membranes. In up to 50 % of patients with toxic multinodular goitre A without antithyroid drug pretreatment TSH-receptor antibodies were detectable with a high correlation between thyroid-stimulating antibodies in the bioassay and the h-TBII assay. Moreover, in a recent study the development of TSH-receptor antibodies after radioiodine treatment was detectable in 36 % of patients with toxic multinodular goitre type A, whereas TSH-receptor antibodies were not detectable in patients with toxic multinodular goitre type B or in patients with toxic adenoma. In conclusion, thyroid-stimulating antibodies in a bioassay or TSH-receptor antibodies detected with the h-TBII assay have the highest diagnostic power to differentiate Graves' disease from toxic multinodular goitre. Because of its less cumbersome assay technique the h-TBII should be performed in all patients with hyperthyroidism to differentiate Graves' disease from non-autoimmune hyperthyroidism such as toxic multinodular goitre to select the appropriate therapy for these patients.

Autoantibodies↗
PubMed1998

Power spectral analysis of variations in heart rate in patients with hyperthyroidism or hypothyroidism.

Power spectral analysis (PSA) of the variation in heart rate is useful in determining the relative activity of the sympathetic and parasympathetic nerves. In this study, PSA was used to investigate the relationship between abnormalities in autonomic nerve function and the presence of thyroid disorders in patients with autoimmune thyroid diseases. The low frequency (LF) or high frequency (HF) components of R-R variations were determined by PSA. The coefficient of variation of the R-R time intervals (CV(R-R)) was positively correlated with HF in healthy subjects. In untreated hyperthyroid patients with Graves' disease, the CV(R-R) and HF values were significantly lower than in healthy controls. Moreover, the LF/HF ratio in patients with untreated Graves' disease was significantly higher, and the LF/HF ratio in hypothyroid patients with Hashimoto's thyroiditis was significantly lower than in healthy controls. A negative correlation was observed between serum levels of free thyroid hormones (FT4 and FT3) and HF in Graves' disease patients. In some hyperthyroid patients, antithyroid drug therapy or beta-blocker administration gradually restored reduced HF values. Present results suggest that relative vagal nerve activity is reduced in hyperthyroid patients and that this reduction is reversible according to the decrease in serum levels of thyroid hormones.

Adrenergic beta-Antagonists↗
PubMed1992

Occurrence of ophthalmopathy after treatment for Graves' hyperthyroidism. The Thyroid Study Group.

BACKGROUND: Ophthalmopathy caused by Graves' disease may first appear or worsen during or after treatment for hyperthyroidism. It is not known, however, whether choosing to treat hyperthyroidism with antithyroid drugs, iodine-131, or surgery affects the development or aggravation of Graves' ophthalmopathy. METHODS: We studied 168 patients with hyperthyroidism caused by Graves' disease, stratified into two age groups--20 to 34 years (54 patients, group 1) and 35 to 55 years (114 patients, group 2). The patients in group 1 were randomly assigned to treatment with methimazole for 18 months or subtotal thyroidectomy, and those in group 2 to either of these two treatments or to iodine-131 therapy. All the patients received thyroxine to avert hypothyroidism, except those treated with iodine-131, who received thyroxine only if hypothyroidism developed. The duration of follow-up was at least 24 months. RESULTS: Twenty-two patients (13 percent) had infiltrative Graves' ophthalmopathy at randomization. During follow-up, ophthalmopathy developed for the first time in 22 patients (13 percent) and worsened in 8 patients (5 percent). The frequency of the development or worsening of ophthalmopathy was similar among the patients in group 1 (medical therapy, 4 of 27 patients [15 percent]; and surgery, 3 of 27 patients [11 percent]). In group 2, ophthalmopathy developed or worsened in 4 of the 38 patients (10 percent) treated medically, 6 of the 37 patients (16 percent) treated surgically, and 13 of the 39 patients (33 percent) given iodine-131 (P = 0.02 for the comparison between the iodine-131 subgroup and the others combined). The risk of the development or worsening of ophthalmopathy increased as pretreatment serum triiodothyronine concentrations increased. CONCLUSIONS: As compared with other forms of antithyroid therapy, iodine-131 is more likely to be followed by the development or exacerbation of Graves' ophthalmopathy.

Adult↗
PubMed1988

Feline hyperthyroidism--a review.

Feline hyperthyroidism is the name given to the multisystemic manifestation of excessive concentrations of circulating thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3). The most common cause is a functional thyroid adenoma involving one or both thyroid lobes. Both multinodular adenomatous hyperplasia and multinodular adenomatous goitre are acceptable descriptions for the histopathological findings. Thyroid adenocarcinoma rarely causes hyperthyroidism in the cat, and when present, seldom metastasizes. This is in contrast to the situation in the dog, where thyroid adenocarcinoma is aggressively malignant Grave's disease, an immune-mediated disease, and the most common cause of hyperthyroidism in man, was until recently thought not to occur in the cat. However, a recent study of 29 cats..

Journal Article↗
PubMed1995

The prevalence of feline immunodeficiency virus infection in hyperthyroid cats.

One hundred and thirty-four male and female hyperthyroid cats (mean age 11.9 years) were tested for the presence of feline immunodeficiency virus antibodies. Thirty-two (23.9%) were positive. The prevalence of feline immunodeficiency virus antibodies was greater in male cats (30.5%) than in female cats (17.2%). The prevalence of feline immunodeficiency virus infection in hyperthyroid cats is similar to the prevalence of feline immunodeficiency virus in the sick cat population and less than that of sick aged cats at the Massey University Clinic and Hospital. The findings of this survey do not support involvement of feline immunodeficiency virus in the pathogenesis of hyperthyroidism in the cat.

Journal Article↗
PubMed1996

Serum antibodies reactive with eye muscle antigens and the TSH receptor in a euthyroid subject who developed ophthalmopathy and Graves' hyperthyroidism.

Serum antibodies reactive with eye muscle autoantigens, in particular a 64-kDa protein that is also expressed in the thyroid, and the TSH receptor, are associated with the ophthalmopathy that occurs in about 50% of patients with Graves' hyperthyroidism. We have had the opportunity to study a euthyroid, apparently normal, 35-year-old woman with a family history of thyroid autoimmunity and "colitis" but no clinical or biochemical evidence for thyroid disease or ophthalmopathy, who developed Graves' hyperthyroidism and ophthalmopathy together 18 months later. Serum taken when the patient was first seen was positive for antibodies reactive with (i) 9 different eye muscle proteins ranging in size from 15 to 130 kDa, notably those of 64, 55, and 50 kDa, by immunoblotting with eye muscle membranes, (ii) eye muscle and Müller's muscle cell membrane antigens in antibody-dependent cell-mediated cytotoxicity (ADCC), (iii) an eye muscle cytoplasmic antigen in indirect immunofluorescence, and (iv) the TSH receptor as measured in a radioreceptor binding inhibition assay. When she developed Graves' disease, serum concentration of antibodies to the 55-kDa protein had decreased from +2 to +/-, those reactive with other eye muscle antigens had not changed significantly, and TSH receptor antibodies had increased 3-fold. This case report suggests that antibodies reactive with eye muscle antigens and the TSH receptor are markers of the ophthalmopathy and able to predict its development in predisposed subjects. The significance of these findings needs to be confirmed in a prospective study of first-degree relatives of patients with thyroid-associated ophthalmopathy and patients with Graves' hyperthyroidism without eye signs.

Adult↗
PubMed1998

An elevation of stem cell factor in patients with hyperthyroid Graves' disease.

Graves' disease is an autoimmune disorder characterized by the presence of antibodies against thyrotropin receptor (TRAb). Stem cell factor (SCF), derived from bone marrow, is known to promote lymphohematopoiesis. To investigate the relation between the alteration in plasma levels of SCF, thyroid hormone status, and TRAb measured by thyrotropin binding inhibition (TBI), 13 untreated, 21 treated, and 4 relapsed hyperthyroid Graves' disease patients, 21 patients with Hashimoto's thyroiditis, 6 patients with subacute thyroiditis, and 11 control subjects were examined. In untreated hyperthyroid Graves' disease patients, serum levels of thyroxine (T4) and triiodothyronine decreased rapidly by methimazole treatment, and TBI decreased progressively, but variably. Simultaneously, the elevated plasma levels of SCF decreased gradually and progressively. The plasma levels of SCF correlated curvilinearly with the serum levels of T4. In 4 patients with relapsed hyperthyroid Graves' disease, TBI was marginally positive in 3 patients and negative in 1, but plasma levels of SCF were elevated significantly in all 4 patients. In patients with subacute thyroiditis and Hashimoto's thyroiditis with or without T4 replacement, plasma levels of SCF did not differ from that of controls. These findings indicate that the elevation of plasma levels of SCF relates to the longstanding thyrotoxic state and that short-term thyrotoxicosis does not significantly affect plasma levels of SCF. It remains to be determined whether the elevation in plasma levels of SCF is induced by excess thyroid hormone, reflecting the hypermetabolic state, or whether the elevation of plasma levels of SCF contributes to stimulation of lymphocytes producing TRAb.

Acute Disease↗
PubMed2000

The prevalence and clinical significance of blocking thyrotropin receptor antibodies in untreated hyperthyroid Graves' disease.

The goal of this study was to evaluate the clinical significance of the blocking thyrotropin receptor antibodies (TSHRAb) in Graves' disease. The amount of blocking and stimulating TSHRAb were measured in 200 patients with untreated hyperthyroid Graves' disease using several cell lines carrying different TSHR chimera. Stimulating TSHRAb were measured in Chinese hamster ovary (CHO) cells with wild-type human TSHR (CHO-hTSHR) or a TSHR chimera with residues 90-165 (Mc2) or 8-165 (Mc1+2) substituted by equivalent residues of rat luteinizing hormone/chorionic gonadotrophin (LH/CG) receptor or in FRTL-5 cells. Blocking TSHRAb were measured in Mc2 cells. The activities of different TSHRAb were assessed and clinical features were compared to patients who were positive or negative for blocking TSHRAb antibodies. Blocking TSHRAbs were detected in 18.5% of patients (37/200) with hyperthyroid Graves' disease. Patients with blocking antibodies had significantly lower mean stimulating TSHRAb activities than those without blocking antibodies in wild-type CHO-hTSHR cells (301 +/- 179 vs. 446% +/- 537%, p = 0.005). Mean stimulating TSHRAb activities measured by FRTL-5, Mc1+2, or Mc2 cells and mean thyrotropin receptor inhibitor immunoglobulin (TBII) activities were not different between the two groups. The patients with blocking antibodies were not different from those without blocking antibodies in age, gender ratio, initial serum free thyroxine (T4) levels, or goiter size. However, the prevalence of exophthalmos was higher (35.1% vs. 17.5%, p = 0.024) in the patients with blocking antibodies than those without. In summary, the presence of blocking TSHRAb is not rare in patients with hyperthyroid Graves' disease when measured with chimeric receptor expressing cells. Blocking TSHRAb in Graves' sera do not strongly antagonize the action of stimulating TSHRAb in vivo, but could be a major factor responsible for underestimation of stimulating TSHRAb activities measured by CHO-hTSHR. The association of blocking TSHRAb with ophthalmopathy suggests that the TSHRAb repertoire of Graves' patients is different in those who do and who do not have ophthalmopathy.

Adult↗
PubMed2000

Development of overt autoimmune hyperthyroidism in a patient therapeutically immunosuppressed after liver transplantation.

Immunosuppression is a therapeutic maneuver directed at preventing transplant rejection. When applied to autoimmunity, immunosuppression is intended to target similar immune processes. We report an unusual case of a 35-year-old woman who developed autoimmune hyperthyroidism of Graves' disease while on immunosuppressive therapy for liver transplantation. Signs and symptoms of hyperthyroidism were already present when, misled by the concomitant toxic hepatic syndrome, liver rejection was first suspected. Despite a therapeutic level of cyclosporine, elevated serum alanine and aspartate aminotransferase levels were noted. Consequently, a liver biopsy was performed to exclude an acute rejection. The findings were consistent with acute hepatitis without evidence of rejection. Then, the diagnosis of Graves' hyperthyroidism was considered and finally confirmed by finding a suppressed thyroid-stimulating hormone, elevated thyroid hormone levels, and a high and homogeneous thyroid uptake from radioactive iodine scan. Thyroid peroxidase antibody and thyroid-stimulating immunoglobulin were markedly elevated. The patient was treated with radioactive iodine, which resulted in improvement of symptoms and resolution of abnormal liver function tests. Although the mechanisms involved in transplant rejection and human autoimmunity are thought to be similar, the development of Graves' disease in this patient despite therapeutic immunosuppression suggests that the immunological processes may be different.

Adult↗
PubMed2000

Remission of Graves' hyperthyroidism predicted by smooth decreases of thyroid-stimulating antibody and thyrotropin-binding inhibitor immunoglobulin during antithyroid drug treatment.

It is important to know whether a patient with Graves' disease will get into remission or not during antithyroid drug (ATD) treatment. Thyrotropin (TSH) receptor antibodies (TRAb) cause Graves' disease. Thyroid-stimulating antibody (TSAb) and TSH-binding inhibitor immunoglobulin (TBII) have been measured as TRAb to diagnose Graves' disease and to follow Graves' patients. Smooth decreases of TSAb and TBII during ATD treatment predict the remission of Graves' hyperthyroidism. We followed serial changes of TSAb and TBII in 58 Graves' patients before, during, and after ATD treatment; TSAb was measured as a stimulator assay, using porcine thyroid cells, and TBII as a receptor assay. Patterns of TSAb and TBII changes during ATD treatment differ from one patient to another. TSAb and TBII activities decreased and disappeared in 52 (group A) but continued to be high in the other 6 (group B); 39 of the 52 group A patients achieved remission, but all of the 6 group B patients with persistently positive TSAb and TBII continued to have hyperthyroidism. No differences in the initial TSAb and TBII activities were noted between the 52 group A patients and the 6 group B patients. Of the 52 group A patients in whom TSAb and TBII had disappeared, 44 had smooth decreases of TSAb and TBII (group A1), and 8 had complex changes of TSAb and/or TBII (group A2); 36 of the 44 group A1 patients (82%) but only 3 of the 8 group A2 patients (37%) continued to be in remission more than 1 year after ATD discontinuation. The number of remission in group A1 was significantly larger than that in group A2. No differences in the initial TSAb and TBII activities were noted between group A1 and group A2. More than 80% of group A1 patients, who had smooth decreases of TSAb and TBII, continued to be in remission longer than 1 year. We demonstrated that smooth decreases of TSAb and TBII during ATD treatment predicted the remission of Graves' hyperthyroidism. The Graves' patients can be classified into A1, A2, and B groups according to the patterns of TSAb and TBII changes during ATD treatment. Group A1 patients, who had smooth decreases of TSAb and TBII, had higher rate of remission than the others. Smooth decreases of TSAb and TBII during the early phase of ATD treatment are a reliable predictor of the remission.

Adult↗
PubMed2006

Rhabdomyolysis associated with hyperthyroidism.

BACKGROUND: Nontraumatic rhabdomyolysis has been associated with alcohol and drug abuse, seizures, strenuous exercise, muscle hypoperfusion, hyperthermia, electrolyte disturbances, diabetic coma, and hypothyroidism. Hyperthyroidism can be associated with several neuromuscular manifestations, such as thyrotoxic myopathy and thyrotoxic periodic paralysis, both associated with weakness and normal creatine phosphokinase levels. There have been only three reported cases of rhabdomyolysis as a result of thyrotoxicosis. We are reporting the fourth case of such association. CASE REPORT: The patient is a 26-year-old black woman with history of hypertension. She presented to the clinic with blurred vision, headaches, palpitations, weight loss, weakness, and persistent high blood pressure. She was found to have exophthalmus, lid lag, and a symmetric, smooth, and diffuse goiter. Ptosis and diplopia were absent; neurologic examination findings was normal. The patient had positive TPO antibodies, elevated free T4 level, and low thyroid-stimulating hormone (TSH) level. Graves disease was diagnosed and propylthiouracil was prescribed. The patient then returned to the clinic 2 weeks later with weakness and myalgias. Her physical examination findings were unchanged except for mild muscle weakness. Laboratory evaluation showed normal electrolytes, normal renal function, and negative urine drug screening. Creatine phosphokinase was 1276 U/L. Her free T4 and T3 levels were elevated and TSH level was low. The patient was treated with aggressive oral fluid resuscitation. Propylthiouracil was continued and free T4 and T3 normalized along with creatine phosphokinase with resolution of symptoms. CONCLUSIONS: Hyperthyroidism may, theoretically, cause rhabdomyolysis by means of increasing energy consumption associated with depletion of muscle energy stores and substrates. Our patient constitutes the fourth reported case of rhabdomyolysis associated with hyperthyroidism.

Adult↗
PubMed2004

Induction of hyperthyroidism in mice by intradermal immunization with DNA encoding the thyrotropin receptor.

Intramuscular injection with plasmid DNA encoding the human thyrotropin receptor (TSHR) has been known to elicit symptoms of Graves' disease (GD) in outbred but not inbred mice. In this study, we have examined, firstly, whether intradermal (i.d.) injection of TSHR DNA can induce hyperthyroidism in BALB/c mice and, secondly, whether coinjection of TSHR- and cytokine-producing plasmids can influence the outcome of disease. Animals were i.d. challenged at 0, 3 and 6 weeks with TSHR DNA and the immune response was assessed at the end of the 8th or 10th week. In two experiments, a total of 10 (67%) of 15 mice developed TSHR-specific antibodies as assessed by flow cytometry. Of these, 4 (27%) mice had elevated thyroxine (TT4) levels and goitrous thyroids with activated follicular epithelial cells but no evidence of lymphocytic infiltration. At 10 weeks, thyroid-stimulating antibodies (TSAb) were detected in two out of the four hyperthyroid animals. Interestingly, in mice that received a coinjection of TSHR- and IL-2- or IL-4-producing plasmids, there was no production of TSAbs and no evidence of hyperthyroidism. On the other hand, coinjection of DNA plasmids encoding TSHR and IL-12 did not significantly enhance GD development since two out of seven animals became thyrotoxic, but had no goitre. These results demonstrate that i.d. delivery of human TSHR DNA can break tolerance and elicit GD in inbred mice. The data do not support the notion that TSAb production is Th2-dependent in murine GD but they also suggest that codelivery of TSHR and Th1-promoting IL-12 genes may not be sufficient to enhance disease incidence and/or severity in this model.

Animals↗
PubMed2005

Adenovirus-mediated gene delivery of interleukin-10, but not transforming growth factor beta, ameliorates the induction of Graves' hyperthyroidism in BALB/c mice.

Interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta) are well known anti-inflammatory cytokines. We have studied the effect of adenovirus-mediated IL-10 and TGF-beta gene delivery on the induction of Graves' hyperthyroidism in our mouse model that involves repeated injections of adenovirus expressing the thyrotropin receptor A subunit (AdTSHR). We first constructed adenoviruses encoding the two cytokines (AdIL10 and AdTGF(beta)) and confirmed expression by in vitro infection of COS cells. Susceptible BALB/c mice were injected twice with AdTSHR alone or together with AdIL10 or AdTGF(beta), and bled two weeks after the second immunization. Significantly elevated serum thyroxine levels were seen in 26% of mice immunized with AdTSHR and AdIL10 versus 61% with AdTSHR alone. Levels of thyroid stimulating antibody, but not nonstimulating antibody, were also decreased, and TSHR-specific splenocyte secretion of interferon-gamma in recall assays was impaired in mice treated with AdIL10. In contrast, AdTGF(beta) had little effect on hyperthyroidism. Overall, our findings demonstrate that gene delivery of IL-10, but not TGF-beta, suppresses the induction of Graves' hyperthyroidism in a mouse model. However, the effect of IL-10 is less powerful than we observed previously with T helper type 2-inducers including adenovirus expressing IL-4, Shistosoma mansoni infection or alpha-galactosylceramide.

Adenoviridae↗
PubMed1983

Single daily dose short term carbimazole therapy for hyperthyroid Graves' disease.

Twenty-one patients with hyperthyroid Graves' disease were treated with carbimazole 30 mg daily, given as a single dose. Propranolol was also given for the first 3 weeks. All became clinically euthyroid with normal serum thyroxine (T4) levels, usually within 1-3 months. Patients with large goitres and raised serum alkaline phosphatase concentrations took longer to respond. In 19 patients a positive thyroid stimulating hormone (TSH) response to intravenous thyrotrophin releasing hormone (TRH) developed. Carbimazole was stopped soon after (median time of treatment 18 weeks, range 9-41 weeks) and 18 patients have been followed. Seven of these (39%) have remained in remission from hyperthyroidism for more than one year (median 77 weeks). Carbimazole 30 mg once daily is a convenient and effective treatment for hyperthyroid Graves' disease. Many patients will achieve prolonged remissions if treatment is stopped when serum T3 and T4 levels are in the low-normal range, usually 2-4 months after clinical euthyroidism has been reached.

Adult↗
PubMed1990

Serum soluble interleukin 2 receptor in hyperthyroid Graves' disease and effect of carbimazole therapy.

To study the activation of T lymphocytes in hyperthyroid Graves' disease, the serum concentrations of soluble interleukin 2 receptors (sIL2R) were determined during active thyrotoxicosis and following the return to a euthyroid state with carbimazole therapy. Serum sIL2R was measured by an enzyme linked immunoassay. The mean +/- SD serum sIL2R concentration during untreated hyperthyroidism was elevated as compared with controls (919.1 +/- 523.4 vs 374.2 +/- 189.4 U/ml, P less than 0.005). However, after carbimazole therapy the serum sIL2R in euthyroid patients fell to 377.9 +/- 90.3 U/ml, which did not differ from healthy controls. Serum sIL2R correlated significantly with the serum free T3 only during hyperthyroidism (r = 0.678, P less than 0.01). Our study suggests that in vivo measurement of serum sIL2R released from activated T lymphocytes is a useful immunological indicator of disease activity.

Adult↗
PubMed1990

Correlation of orbital computed tomography and antibodies in patients with hyperthyroid Graves' disease.

The purpose of this study was to elucidate the incidence of orbital changes in computed tomography, and the relationships of orbital changes with eye-muscle antibody (EMAb), thyrotrophin-binding inhibitor immunoglobulin (TBII), antithyroglobulin antibody (TgAb) and anti-thyroid microsomal antibody (MsAb), in 55 consecutive patients with hyperthyroid Graves' disease. EMAb was demonstrated by an immunoperoxidase technique. The results showed that the prevalence of orbital fat increase, extraocular muscle enlargement, lacrimal gland enlargement and optic nerve swelling were 54.5, 41.8, 21.8 and 16.5% respectively. There were 32.7% of patients without any orbital changes. The patients with extraocular muscle enlargement, lacrimal gland enlargement and optic nerve swelling had higher titres of EMAb than the patients without these orbital changes. The patients with lacrimal gland enlargement had a lower TBII index than those without. There was no difference in TgAb or MsAb between the patients with extraocular muscle enlargement, lacrimal gland enlargement, optic nerve swelling or orbital fat increase and those patients without these orbital changes. The patients with extraocular muscle enlargement, optic nerve swelling and orbital fat increase had a higher degree of exophthalmos than the patients without these orbital changes. EMAb was negatively correlated with TBII. However, there was no correlation between EMAb and TgAb or MsAb. The degree of exophthalmos was positively correlated with EMAb and negatively correlated with age. There was no correlation between exophthalmos and TBII, TgAb or MsAb. In conclusion, although the pathogenesis of orbital changes and hyperthyroidism is different, a close link between these two entities is suggested by the high incidence of orbital changes in hyperthyroid Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Correlation of HLA types and clinical findings in Japanese patients with hyperthyroid Graves' disease: evidence indicating the existence of four subpopulations.

OBJECTIVES: To re-evaluate the associations of HLA types with Japanese patients having hyperthyroid Graves' disease, HLA types and clinical findings were correlated. DESIGN: Four independent clinical findings (ophthalmopathy, family history, age at onset and size of goitre) and two autoantibody titres, thyrotrophin binding inhibitor immunoglobulin (TBII) and anti-thyroid microsmall antibody (anti-M), were analysed. PATIENTS: Eighty-eight Japanese patients with hyperthyroid Graves' disease and 186 control subjects were assessed. MEASUREMENT: Serological HLA typing was performed on 73 antigens in HLA-A, -B, -C, -DR and -DQ loci. HLA-D and -DP (29 antigens) were determined by the restricted fragment length polymorphism (RFLP) methods. TBII and anti-M were measured by commercially available kits. RESULTS: Patients with potent antibody titres had HLA antigens commonly seen among all the patients with Graves' disease. Interestingly, however, HLA-B35 and -Cw11 were found to relate with negative and/or weak TBII, and HLA-B7 and absence of HLA-Aw19 with negative anti-M. Significant associations were observed between HLA-DRw8 and large goitre and absence of ophthalmopathy, and between HLA-DQw4 and a negative family history of diffuse goitre (corrected P less than 0.05). Several other antigens were also found to be significant. Among these antigens, four pairs of MHC classes I and II were found to relate to the clinical findings independently. HLA-DQw4 and negative -A31 pair was closely related to ophthalmopathy, negative family history and late onset of disease. The HLA-B5 and -Dw12 pair was associated with ophthalmopathy, positive family history and early onset of disease. The HLA-A11 and negative -DPw2 pair was associated with ophthalmopathy, negative family history and early onset of disease. The HLA-Bw46 and -DRw8 pair did not increase in frequency above that seen with HLA-DRw8 alone. These four antigen groups (HLA-DRw8, HLA-DQw4 and negative-A31, HLA-B5 and -Dw12, and HLA-A11 and negative -DPw2) were observed in the majority (68%) of patients with Graves' disease and at a significantly higher incidence than in the control group (P less than 0.05). CONCLUSION: There are four subpopulations of Japanese patients with hyperthyroid Graves' disease. This is one of the reasons why the association of HLA types in Japanese patients is rather weak when they are studied as one group.

Adolescent↗