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At least 19 recordsLinked to original sources
PubMed1996

Associations between lymphocytic thyroiditis, hypothyroidism, and thyroid neoplasia in beagles.

The thyroids were evaluated in 276 control Beagles that were allowed to live out their full life span (mean = 12 years) in a closed breeding colony. Lymphocytic thyroiditis was found in 26.3% of the dogs. This lesion was characterized by lymphoplasmacytic inflammation accompanied by follicular destruction. The thyroiditis was progressive, resulting in severe atrophy of follicular tissue, and 44 dogs (15.9%) were diagnosed as hypothyroid at the time of death. In accordance with the experimental protocol, hypothyroid dogs were not given thyroxine replacement therapy. There was a high degree of heritability for the hypothyroidism. Hypothyroid dogs had an increased risk for thyroid follicular epithelial neoplasia and, in particular, for follicular adenocarcinomas. Twenty-four of the 44 hypothyroid dogs (54.5%) had one or more follicular thyroid neoplasms, whereas only 53 of the 232 (22.8%) clinically euthyroid dogs had similar tumors. Multiple thyroid tumors were present in 14 of the 44 (31.8%) hypothyroid dogs but in only 12 of the 232 (5.2%) euthyroid dogs. One or more follicular adenocarcinomas were present in 15 of the 44 (34.1%) hypothyroid dogs but in only 16 of the 232 (6.9%) euthyroid dogs. There was no difference in prevalence of hypothyroidism or tumors between the sexes. The strong association between progressive lymphocytic thyroiditis, hypothyroidism, and thyroid follicular neoplasia in these Beagles probably relates to promotion of residual follicular epithelium by chronic excess thyrotropin stimulation.

Adenoma↗
PubMed1978

Riedel's struma associated with subacute thyroiditis, hypothyroidism, and hypoparathyroidism.

Riedel's struma with dense fibrous invasion of surrounding muscle and fat was found in a patient who had clinical subacute thyroiditis superimposed on primary hypothyroidism. Riedel's struma may sometimes be an uncommon stage in the more common subacute form of thyroiditis, although in our patient an unusual coincidence of subacute thyroiditis and Riedel's struma is also possible. Of interest in our patient was the development of spontaneous primary hypoparathyroidism; parathyroid function returned to normal concomitant with the spontaneous resolution of the goiter after partial resection. This patient also represents another instance of hyperthyroidism developing in a previously hypothyroid patient.

Female↗
PubMed2002

A novel loss-of-function mutation in TTF-2 is associated with congenital hypothyroidism, thyroid agenesis and cleft palate.

Thyroid dysgenesis is the most common cause of congenital hypothyroidism (CH) and its genetic basis is largely unknown. Here, we describe the second homozygous missense mutation in TTF-2 (or FOXE1), a transcription factor that has been implicated in thyroid development. Two male siblings, born to consanguineous parents, presented with CH, athyreosis and cleft palate and were found to be homozygous for a mutation corresponding to a serine to asparagine substitution at codon 57 (S57N) in the forkhead DNA binding domain of TTF-2. Their heterozygous parents were unaffected and this mutation was not found in 31 unrelated cases of athyreosis or normal controls. Consistent with its location, the S57N TTF-2 mutant protein showed impaired DNA binding and partial loss of transcriptional function. Such incomplete loss of TTF-2 function may account for the absence of choanal atresia and bifid epiglottis in our patients, anomalies which were present together with CH and cleft palate in two other individuals with the only other, more deleterious, TTF-2 mutation (A65V) described previously. Our observations support the role of TTF-2 in both thyroid and palate development but suggest phenotypic heterogeneity of this syndromic form of CH.

Adolescent↗
PubMed2006

Thyroid disorders. Part II: hypothyroidism and thyroiditis.

Part II of the series on thyroid disorders discusses hypothyroidism and thyroiditis that may be found in dental patients. An overview of the conditions is presented. Presenting signs and symptoms, laboratory tests used to diagnose hypothyroidism and thyroiditis, and their medical management is discussed. The dental management of patients with hypothyroidism is discussed in detail. The dentist by detecting the early signs and symptoms of hypothyroidism and thyroiditis can refer the patient for medical diagnosis and treatment and avoid potential complications of treating patients with uncontrolled disease. Patients with thyroiditis may have a short period of being hyperthyroid and it may be best to avoid routine dental treatment during that period. Patients with suppurative thyroiditis should not receive routine dental treatment during the acute stage of the disease. The end stage of Hashimoto's thyroiditis results in hypothyroidism. Central nervous system depressants, sedatives, or narcotic analgesics must be avoided in patients with severe hypothyroidism because significant respiratory depression may occur. In addition, myxedematous coma, particularly in elderly hypothyroid patients, can be precipitated by central nervous system depressants, infection, and possibly stressful dental procedures. In medically well-controlled patients the dental treatment plan is not affected and most dental procedures can be offered to these patients.

Adult↗
PubMed1986

Compensated 131I-therapy of solitary autonomous thyroid nodules: effect on thyroid size and early hypothyroidism.

Thyroid function and thyroid gland volume, ultrasonically determined, were investigated in 27 hyperthyroid patients with solitary autonomous thyroid nodules before and during one year after 131I-treatment. Total thyroid volume decreased gradually from 40.9 +/- 3.5 ml (mean +/- SEM) before treatment to 23.9 +/- 1.8 ml (P less than 0.001) at 3 months after 131I-treatment. No further change was observed. All but two patients received only one dose of 131I, and in spite of a significant decrease also of the non-adenoma side of the gland, none became hypothyroid. We conclude that 131I-therapy has an important place in the treatment of solitary autonomous thyroid nodules since all our patients became euthyroid within 3 months, only 2 of 27 patients needed more than one dose of 131I, no cases of hypothyroidism occurred, and thyroid volume was substantially decreased.

Adenoma↗
PubMed1994

Circulating soluble IL-2 receptor levels are low in patients with hypothyroid autoimmune thyroiditis.

In hypothyroid patients serum soluble IL-2 receptor levels showed scattered and conflicting results. In our report we studied circulating soluble interleukin 2 receptors in 22 patients with hypothyroid autoimmune thyroiditis before L-thyroxine treatment and when the patients became euthyroid. The mean of soluble Interleukin 2 receptor levels in the hypothyroid state was 48.6 pmol/l (95% confidence interval, 45.6-51.5) statistically lower than in the controls (95% confidence interval, 86.4 pmol/l, 83.3-89.4) (p < 0.0001). When the patients became euthyroid during L-thyroxine treatment, soluble Interleukin 2 receptor levels increased, showing mean values comparable to the controls. A positive high correlation (p < 0.001) was observed between soluble Interleukin 2 receptor levels and thyroxine free levels in the hypothyroid as well as in the euthyroid state and between soluble Interleukin 2 receptors and the mean weekly L-thyroxine dose. Our study confirmed that in the hypothyroid state, the behaviour of soluble Interleukin 2 receptors is anomalous as compared to other autoimmune diseases. In fact a strict relationship exists between the levels of thyroid hormones and soluble Interleukin 2 receptors but not between the latter and antithyroid antibodies. These results agree with those supporting a role for thyroid hormones in the regulation of the immune system. They also suggest that the measurement of soluble Interleukin 2 receptors could be used as a marker of the peripheral action of thyroid hormones.

Adolescent↗
PubMed1990

Test for recovery from hypothyroidism during thyroxine therapy in Hashimoto's thyroiditis.

Hypothyroid patients with Hashimoto's thyroiditis usually receive lifelong thyroxine therapy. Some are known to recover thyroid function, but identification of these patients during continued thyroxine therapy has been impossible. 92 patients with hypothyroidism after Hashimoto's thyroiditis and 70 normal controls were studied. All controls but not patient before thyroxine was started had a normal thyroid response to thyroid stimulating hormone (TSH), circulating concentrations of which were increased by administration of 500 micrograms thyrotropin releasing hormone (TRH). During treatment with thyroxine, 22 patients recovered thyroid responsiveness to TSH, and when treatment was stopped these patients have remained euthyroid for 1-8 years, whereas all 70 who did not recover thyroid TSH responsiveness became hypothyroid within 3 months. Over 20% of patients with hypothyroidism after Hashimoto's thyroiditis may recover satisfactory thyroid function, and can be identified during thyroxine treatment by their thyroid response to TSH in a TRH test.

Adolescent↗
PubMed2003

Additional phenotypic abnormalities with presence of cysts within the empty thyroid area in patients with congenital hypothyroidism with thyroid dysgenesis.

Congenital hypothyroidism (CH) is most frequently caused by thyroid developmental abnormalities, and it has recently been shown to have a familial component with members affected by either CH or asymptomatic thyroid developmental abnormalities. The pathogenesis of the disease is unknown, but it seems possible that a common genetic mechanism underlies these heterogeneous phenotypic expressions. Associations among these anomalies in the same individuals have occasionally been described. The aim of this study was to investigate whether cysts of the thyroglossal duct could be shown by ultrasonography in patients with CH caused by thyroid dysgenesis. Children with CH (n = 57) who were diagnosed by newborn TSH screening were prospectively evaluated by ultrasonography at the age of 10.5 +/- 4.5 yr. The etiology of CH (ectopic thyroid tissue, n = 42; athyreosis, n = 15) was established before treatment initiation on the basis of thyroid radioiodine scanning and the absence of any thyroid tissue in the normal location confirmed by ultrasonography. Cysts were found in 39 patients (68% of cases) with either ectopic thyroid tissue (n = 29) or athyreosis (n = 10). All cysts were located in the empty thyroid area in the left (57%) or right (43%) side and were mostly closer to the midline. Patients had either a single cyst (n = 16 patients) or multiple cysts (n = 23 patients). The cysts were bilateral in 17 of the 39 patients. Most of them were vertically oval or round, with a size ranging in diameter from 2-21 mm (mean, 3.5 +/- 2). In conclusion, the presence of cysts within the empty thyroid area in 68% of patients with CH due to thyroid dysgenesis is a novel observation that is part of the developmental anomaly of this disease. Several explanations can be put forward to explain the presence of these cysts. They might be due to the persistence of the ultimobranchial bodies as a cystic structure or part of the thyroid-forming material, which may migrate along the normal pathway of the usual course of the thyroglossal duct, giving rise to cell residues within the empty thyroid area.

Adolescent↗
PubMed1987

[Surgical hypothyroidism].

Thyroid hormone secretion is often modified after thyroidectomy and is not always assessed correctly. The condition is revealed less by the drop in hormonal immune reactivity than by the rapid increase in TSH and the appearance of a clinical syndrome consisting essentially of weight gain and the onset of psychological symptoms; alterations in calcium balance are not examined here. The study confirmed the behalf that these phenomena affect a large number of thyroidectomized patients and derive from a particular form of thyroid deficiency: surgical hypothyroidism. This condition should always be borne in mind after thyroid surgery and should be treated appropriately, which is only possible if hormone functions and clinical symptoms are correctly monitored.

Body Weight↗
PubMed1994

Relationship between thyroid functions and urinary growth hormone secretion in patients with hyper- and hypothyroidism.

Thyroid hormone plays an important role in growth hormone (GH) synthesis and secretion. To study the relationship between thyroid function and urinary GH secretion in the hyperthyroid and hypothyroid states, we measured thyroid hormones, simultaneously with serum and urinary GH levels, in 54 patients with thyroid diseases. GH-releasing hormone (GRH) test was performed in 18 patients in order to evaluate serum and urinary GH responses to GRH in hyper- and hypothyroid states. Serum thyroid hormone levels were strongly correlated with the urinary GH levels in the patients, and the correlation was greater than that between serum thyroid hormone and serum GH levels. Urinary GH levels were significantly higher in the hyperthyroid patients than in the euthyroid and hypothyroid patients, although serum GH levels were not significantly different among these three groups. Serum GH response to GRH was significantly decreased in hyperthyroid patients as compared to euthyroid patients. However, urinary GH levels after GRH administration were not decreased in the hyperthyroid patients. These results suggest that hyperthyroid states increase GH in urine and may accelerate the urinary clearance of GH.

Adult↗
PubMed1992

Disappearance of thyrotropin-blocking antibodies and spontaneous recovery from hypothyroidism in autoimmune thyroiditis.

BACKGROUND: Hypothyroidism may result from the production of antibodies that block the actions of thyrotropin. How often these thyrotropin-blocking antibodies are a cause of hypothyroidism and whether their production may cease, causing hypothyroidism to disappear, have not been extensively studied. METHODS: We determined the frequency with which thyrotropin-blocking antibodies were present in 172 hypothyroid patients with goitrous autoimmune thyroiditis (Hashimoto's disease) and 64 hypothyroid patients with atrophic autoimmune thyroiditis (idiopathic primary hypothyroidism). For 6 to 11 years we then followed 21 of these patients who were found to have thyrotropin-blocking antibodies. They received levothyroxine therapy for 3.5 to 8 years, after which it was discontinued. At frequent intervals during this time we measured the patients' serum concentrations of thyroxine, triiodothyronine, thyrotropin, and thyrotropin-blocking antibodies (measured as immunoglobulins that inhibit thyrotropin binding and immunoglobulins that inhibit thyrotropin bioactivity). RESULTS: Thyrotropin-blocking antibodies were detected in 9 percent of the patients with goitrous autoimmune thyroiditis and in 25 percent of those with atrophic autoimmune thyroiditis. Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially. Levothyroxine therapy was subsequently discontinued in these 21 patients. Six of those in group 1 (four with goiter) remained euthyroid (mean follow-up after discontinuation of therapy, 2.1 years), and nine became hypothyroid again within 3 months. All six patients in group 2 remained hypothyroid. CONCLUSIONS: Hypothyroidism in some patients with autoimmune thyroiditis may be due to thyrotropin-blocking antibodies. The production of thyrotropin-blocking antibodies may subside, producing remissions of hypothyroidism. Chronic autoimmune thyroiditis may therefore cause transient as well as permanent hypothyroidism.

Adult↗