Search Results

You are looking at 1 - 10 of 3,734 items for

  • Abstract: goiter x
  • Abstract: Graves x
  • Abstract: hyperthyroidism x
  • Abstract: hypothyroidism x
  • Abstract: levothyroxine x
  • Abstract: T3 x
  • Abstract: T4 x
  • Abstract: thyroglobulin x
  • Abstract: thyroid x
  • Abstract: thyroiditis x
  • Abstract: thyrotoxicosis x
  • Refine by Access: All content x
Clear All Modify Search
Restricted access

W. A. Scherbaum

Abstract. Among the various autoantibody tests applied in research and clinical practice, the determination of thyroid microsomal (TMAb) and thyroglobulin antibodies (TgAb) still retains its strong value in the screening for thyroid autoimmunity. The presence in the serum of TMAb is almost invariably associated with thyroid autoimmune disease or focal thyroiditis. The appearance of TMAb together with elevated serum-TSH in subclinical autoimmune thyroiditis strongly suggests progression to overt hypothyroidism. Pregnant women with positive TMAb and/or TgAb run an increased risk for post-partum painless thyroiditis with transient thyrotoxicosis and subsequent hypothyroidism. After delivery also a relapse of previously unrecognized Graves' thyrotoxicosis may occur. Thyroid antibody determination is not a valuable tool to discriminate autoimmune thyroiditis from thyroid malignancies. TMAb and TgAb determination helps to recognize individuals with thyroid autoimmunity among patients with non-thyroid autoimmune diseases such as Addison's disease and Type I diabetes mellitus.

Free access

HB Shahbazian, F Sarvghadi, and F Azizi

OBJECTIVE: To determine the prevalence of postpartum thyroiditis (PPT), one of the autoimmune disorders of the thyroid which usually occurs in women in the first year after parturition. PPT presents with periods of transient thyrotoxicosis and hypothyroidism, in many cases resulting in permanent hypothyroidism. DESIGN: The study involved 1040 mothers who had contacted five health centers in Tehran for vaccination of their children. METHODS: Signs and symptoms of hypothyroidism and thyrotoxicosis, and the presence of goiter (using the World Health Organization classification), were sought. Serum T3, T4, TSH, anti-TPO and anti-Tg antibodies were measured at 3, 4.5, 6 and 9 months after parturition. In those with hypothyroidism or thyrotoxicosis and a matched group of normal women, thyroid sonography was performed. RESULTS: The prevalence of thyroiditis was 11.4%. Hypothyroidism and thyrotoxicosis occurred in 68 and 42 mothers respectively. Nine had thyrotoxicosis followed by hypothyroidism. There was one case of Graves' disease. Out of 68 hypothyroid patients, 33 women underwent treatment with levothyroxine (because of the severity of symptoms) for 12 months. Six women showed increased TSH at 6 weeks after discontinuation of thyroxine. Stage II goiter (World Health Organization classification) were observed in 21.8% of patients and in 6.7% of pospartum euthyroid women (P<0.001). Positive anti-TPO was found in 61.5% of patients and in 19% of the control group; positive anti-Tg was found in 58% of patients and in 6% of the control group (P<0.001). Sonographic changes were observed in 96% of the patients and in 7% of the control group (P<0.001). There was no significant correlation between the occurrence of thyroiditis and parity, the age of the mother, a previous history of thyroid disease in the patient or family, breast-feeding, or the gender of the child. CONCLUSION: The results of this study show a high prevalence of PPT in Tehranian women. This may be due to the length and frequency of follow-up and/or the transition from low to adequate iodine intake. The major difference with respect to other studies is the low frequency of the biphasic form of PPT.

Restricted access

C. Ferrari, M. Boghen, A. Paracchi, P. Rampini, F. Raiteri, R. Benco, M. Romussi, F. Codecasa, M. Mucci, and M. Bianco

Abstract. Circulating thyroglobulin antibodies (TgAb) and microsomal antibodies (MsAb) and thyroid function (total and free T4 and T3, TSH basal and after TRH) have been evaluated in 92 hyperprolactinaemic patients (82 females and 10 males; 9 with macroprolactinoma, 22 with microprolactinoma, 4 with acromegaly, 5 with organic lesions of the hypothalamus, 2 with empty sella, 2 with idiopathic hypopituitarism, 2 with primary hypothyroidism, and 46 with idiopathic hyperprolactinaemia). Thyroid function was normal in all cases except 3 with hypothalamic disease and central hypothyroidism, the 2 patients with primary hypothyroidism and 2 with thyrotoxicosis (one due to Graves' disease and one to autonomous thyroid adenoma). High titres of TgAb (≥1/1250) and/or MsAb (≥ 1/1600) were found in the subject with Graves' disease, in one acromegalic, in the 2 primary hypothyroids, and in 12 women with either adenomatous or idiopathic hyperprolactinaemia; low titres of one or both antibodies were found in 9 other euthyroid women and in the one with toxic adenoma. In a control population of 185 subjects studied with the same methods, the prevalence of TgAb and/or MsAb positive (low titres) was 3.3% in females and 2.5% in males. Diffuse thyroid hyperplasia was clinically detectable in 12 euthyroid women and in the one with Graves' disease; 3 others had been previously operated for nodular goitre with histological evidence of Hashimoto's thyroiditis (2 cases) or for a cold nodule; a single thyroid nodule was present in the woman with toxic adenoma and in one euthyroid woman. Most of these subjects also had circulating TgAb and/or MsAb, and a few had increased TSH secretion. No significant differences were found in mean thyroid hormone and TSH levels between euthyroid hyperprolactinaemic subjects and healthy controls, but TRH-stimulated TSH levels were significantly higher in thyroid antibodies positive than negative subjects. These data, in agreement with a few previous reports, suggest that autoimmune thyroid disorders (especially asymptomatic autoimmune thyroiditis) occur in hyperprolactinaemic women with a prevalence far exceeding that observed in many surveys in the general population.

Restricted access

N. J. B. Christiansen, K. Siersbæk-Nielsen, J. E.M. Hansen, and L. Korsgaard Christensen


Serum thyroxine (T4) and other thyroid function tests were studied in 14 patients with subacute thyroiditis and compared with the same parameters in 32 patients with untreated thyrotoxicosis. The mean values of serum T4 and protein-bound iodine (PBI) were found to be elevated to the same extent in the two groups and the calculated T4 iodine did not differ significantly from the PBI in any of the groups. The resin-T3-test and the basal metabolic rate (BMR) mean values were significantly lower in patients with subacute thyroiditis than in patients with thyrotoxicosis. The serum T4 determination based on competitive protein-binding was not influenced by other organic iodinated products, and our results indicate that the elevated serum PBI in subacute thyroiditis is largely due to T4. The lower BMR in patients with subacute thyroiditis is possibly explained by a difference in the thyroxine binding protein (TBP) binding capacity and free T4 in the serum between patients with subacute thyroiditis and those with thyrotoxicosis.

Restricted access

Jan H. Solem and Helge Svaar

Abstract. Documented thyrotoxicosis developed in a 12 year old girl with chronic autoimmune thyroiditis. During the following 3 years there was a spontaneous progression from hyperthyroidism to hypothyroidism and vice versa fluctuating from one metabolic state to another. The diagnosis of Hashimoto's thyroiditis was based upon thyroid function tests, elevated titres of antibodies against thyroid constituents, and upon thin-needle biopsy of the enlarged thyroid gland.

Free access

F Bogazzi, L Bartalena, S Brogioni, A Burelli, L Manetti, ML Tanda, M Gasperi, and E Martino

OBJECTIVE: Thyroid blood flow is greatly enhanced in untreated Graves' disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). SUBJECTS AND METHODS: We investigated 24 normal subjects, and 78 patients with untreated hyperthyroidism (49 with Graves' hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto's thyroiditis, and 21 untreated hypothyroid patients with Hashimoto's thyroiditis. RESULTS: Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8+/-1.2cm/s. Patients with spontaneous hyperthyroidism due to Graves' disease, TSHoma, and toxic adenoma had significantly increased PSV (P<0.0001, P=0.0004, P<0.0001 respectively vs controls) and CFDS pattern. Patients with Graves' disease had CFDS pattern II (mild increase of color flow doppler signal) in 10 (20%) and pattern III (marked increase) in 39 cases (80%). Mean PSV was 15+/-3cm/s. Patients with toxic adenoma had CFDS pattern I (presence of parenchymal blood flow with patchy uneven distribution) in 2 (8%), pattern II in 16 (70%) and pattern III in 5 (22%). Mean PSV was 11+/-2.4cm/s. Patients with TSHoma showed CFDS pattern I in one case (20%) and pattern II in 4 (80%). Mean PSV was 14.8+/-4.2cm/s. Patients with thyrotoxicosis had normal PSV (4.2+/-1. 1cm/s in subacute thyroiditis, 4+/-0.8cm/s in thyrotoxicosis factitia, P=not significant vs controls) and CFDS pattern 0. Untreated euthyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern 0, and mean PSV (4.3+/-0.9cm/s; P=not significant vs controls). Untreated hypothyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern I in 14 cases (67%), pattern II in 4 (19%) and pattern 0 in 3 (14%) and mean PSV (5.6+/-1. 4cm/s) was higher than that of controls (P=0.026). CONCLUSIONS: An increase in both intrathyroidal vascularity and blood velocity was observed in patients with spontaneous hyperthyroidism but not in thyrotoxicosis due to either ingestion of thyroid hormones or to a thyroidal destructive process. The slightly increased vascularity and blood velocity observed in patients with hypothyroid Hashimoto's thyroiditis suggests that thyroid stimulation by either TSH-receptor antibody or TSH is responsible for the increased thyroid blood flow.

Restricted access

Per Anders Dahlberg and Rolf Jansson

Abstract. During a 4 year period 19 women with post-partum onset of thyroid dysfunction have been seen in our clinic. Five women had high radioiodine uptake thyrotoxicosis (Graves' disease). Twelve women had hypothyroid symptoms starting within 3–6 months of delivery. All of these women had thyroid microsomal and/or cytoplasmic autoantibodies and thyroid lymphocytic infiltration suggesting aggravation of pre-existing subclinical autoimmune thyroiditis (Hashimoto's disease). At follow-up thyroid function gradually improved in all but signs of persistent thyroid hypofunction remained in seven. Thus women developing symptomatic postpartum hypothyroidism should be followed regularly and when thyroxine treatment is commenced in the post-partum period, it has to be continued indefinitely in many cases.

Two women presented with transient low radioiodine uptake thyrotoxicosis and a small painless goitre. Thyroid cytology revealed thyroiditis but they had no thyroid autoantibodies. When followed after a succeeding delivery none of these women developed post-partum thyroid dysfunction in contrast to women in the autoimmune group. Probably the aetiology of thyroid dysfunction in these 2 women was different.

Restricted access

Rajata Rajatanavin, La-or Chailurkit, Kanokporn Tirarungsikul, Wirawat Chalayondeja, Uraiwan Jittivanich, and Winit Puapradit


To determine the prevalence of thyroid dysfunction in Thai postpartum women, we evaluated thyroid function and thyroid autoantibodies in 812 consecutive unselected women at 1.5 months post partum. At 3.5 months post partum 570 women without previous thyroid abnormality returned for a second set of thyroid function test. The prevalence of thyroid dysfunction was 1.1%, which was less than that reported from other countries. Various types of postpartum thyroid dysfunction, namely, transient thyrotoxicosis followed by transient hypothyroidism, transient thyrotoxicosis or hypothyroidism occurring alone or permanent hypothyroidism were encountered. Eight out of 9 patients with thyroid dysfunction had thyroid autoantibodies. Fine needle aspiration biopsy of the thyroid was done in 4 patients and all showed lymphocytic thyroiditis. Even though Bangkok is an iodine surfeit area, iodine intake is relatively lower than in other areas where the prevalence of postpartum thyroid dysfunction is much higher. The discrepancy in geographic prevalence of postpartum thyroid dysfunction may result from the interaction of immunogenetic heterogeneity of different ethnic background, environmental iodine intake, and other unidentified environmental factors.

Restricted access

ståle Skare and Harald M. M. Frey


Two male patients aged 36 and 52 years with thyrotoxicosis revealed a serum T3 of 2.8 and 6.5 nmol/l and a serum T4 of 166 and 238 nmol/l, respectively. Both had been exposed to iodine (2–10 mg daily) for 2–12 months before thyrotoxicosis was diagnosed. Urinary iodine excretion was high, 5000 and 10000 nmol/24 h (624–1250 μg). The uptake of 131I in the thyroid glands were low, none had goitre.

Their iodine intake was interrupted, urinary iodine excretion gradually decreased, and T3 and T4 in serum concomitantly normalized. They were clinically and biochemically euthyroid 9 and 11 weeks after withdrawal. After 14 and 22 weeks they had normal thyroid uptake of 131I, and thyroid scans showed glands of normal size and configuration, TRH-stimulation and a T3-suppression tests became normal. ESR was not elevated in any of the cases, thyroid antibodies against thyroglobulin and follicular cell microsomes were absent and TSAb was undetectable during the thyrotoxic stage.

Thus no evidence of any pre-existing and/or pre-disposing pathological condition in the thyroid glands were found. The mechanism for the iodine-induced thyrotoxicosis in such cases remains obscure.

Restricted access

Irene Gavras and John A. Thomson


The cases of 2 women who had clinical and biochemical evidence of autoimmune thyroiditis, who progressed to develop hypothyroidism and who then, some years later, developed thyrotoxicosis are described. Possible mechanisms for the production of this unusual clinical course are discussed.