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PubMed2002

The relationship between the thyroid gland and the liver.

Thyroxine and tri-iodothyronine are essential for normal organ growth, development and function. These hormones regulate the basal metabolic rate of all cells, including hepatocytes, and thereby modulate hepatic function; the liver in turn metabolizes the thyroid hormones and regulates their systemic endocrine effects. Thyroid dysfunction may perturb liver function, liver disease modulates thyroid hormone metabolism, and a variety of systemic diseases affect both organs. We highlight the intricate relations between the thyroid gland and the liver in health and disease.

Chronic Disease↗
PubMed1992

Thyroid peroxidase antibodies in children with autoimmune thyroiditis.

AIMS: To compare the prevalence of thyroid peroxidase antibodies in 25 children with autoimmune thyroid disorders and in 41 children and young adults with type 1 diabetes, and to test the prevalence of thyrotropin receptor antibodies. METHODS: Two commercially available radioimmunoassays for antibodies to thyroid peroxidase, a commercially available agglutination test of particles coated with thyroid microsomal antigens, and a radioimmunoassay for thyrotropin receptor antibodies were used. Patients and controls were studied. RESULTS: One of the radioimmunoassays detected thyroid peroxidase antibodies not only in all children with autoimmune thyroid disorders and children and young adults with type 1 diabetes and thyroid microsomal antibodies, but also in 20% of healthy control children without microsomal antibodies. With this thyroid peroxidase assay and with microsomal agglutination, 94% of the children with autoimmune thyroiditis, 71% of those with Graves' disease, and over 90% of those with type 1 diabetes and thyroid dysfunction tested positive. In the other radioimmunoassay for thyroid peroxidase antibodies thyroid peroxidase antibody titres in half or more of the children with microsomal antibodies failed to reach the level of positivity given by the producers. Eighty five percent of children with Graves' disease and 71% of those with autoimmune thyroiditis had thyrotropin receptor antibodies but so did 35% of children studied for other endocrinological disorders such as delayed growth or puberty. CONCLUSIONS: Testing patients with well characterised disorders of thyroid function and with other endocrine disorders is important in evaluating the efficacy of new diagnostic tests for thyroid autoantibodies.

Adolescent↗
PubMed2001

Coeliac disease in patients with autoimmune thyroiditis.

BACKGROUND AND AIMS: The close association between coeliac disease and autoimmunity prompted us to perform an antibody screening for gluten-sensitive enteropathy in patients with autoimmune thyroid dysfunction. METHODS: Sera from 220 patients with autoimmune thyroiditis, 50 euthyroid subjects with thyroid nodules and 250 blood donors were tested for IgA anti-tissue transglutaminase (anti-tTG) and antiendomysial antibodies (EmA). RESULTS: IgA anti-tTG was positive in 7 patients with autoimmune thyroiditis, whereas IgA EmA was found only in 6 of them. Duodenal biopsy confirmed coeliac disease diagnosis disclosing marked and mild villous atrophy in 6 and 1 of them, respectively. All but 2 of the 7 coeliacs did not show any sign of malabsorption. All euthyroid controls were negative for IgA antibodies, whereas 1 blood donor, positive for both IgA anti-tTG and EmA, was found to be coeliac. The prevalence of coeliac disease in patients with autoimmune thyroiditis (3.2%) was significantly higher than that found in blood donors (0.4%) (p = 0.022, Fisher's exact test). CONCLUSIONS: Antibody screening for coeliac disease should be included in the work-up of patients with autoimmune thyroiditis. Either IgA anti-tTG or EmA may be used, even though the former seems to be slightly more sensitive than the latter.

Adolescent↗
PubMed1993

Reversible inhibition by interferons alpha and beta of 125I incorporation and thyroid hormone release by human thyroid follicles in vitro.

When interferons (IFN-alpha-2a, IFN-alpha-2b, natural IFN-alpha and IFN-beta) were cultured with human thyroid follicles, each IFN inhibited TSH-induced thyroid function (125I incorporation and release of 125I-T4) in a concentration-dependent manner. The minimal inhibitory effect was exerted at 1-10 U/ml. However, the inhibitory effect was reversible, and no inhibitory effect was detected when IFNs were removed from the medium within 12 h. These in vitro findings suggest that each IFN directly inhibits human thyroid function at clinically attainable levels. However, since the inhibitory effect was reversible, IFN therapy would provoke only subtle thyroid dysfunction in a majority of patients without preexisting thyroid autoimmunity.

Culture Techniques↗
PubMed1996

Transient congenital hypothyroidism and hyperthyrotropinemia: normal thyroid function and physical development at the ages of 6-14 years.

Since the introduction of screening programs for congenital hypothyroidism, transient disturbances of thyroid function, especially transient congenital hypothyroidism and hyperthyrotropinemia, mostly due to iodine deficiency or contamination have been observed with variable frequencies. This study was carried out to reevaluate the thyroid function and physical development of 61 schoolchildren with transient congenital hypothyroidism or transient congenital hyperthyrotropinemia. Abnormalities were observed in 3 children. Thyroid function and growth were normal in all children, except 2 with moderately elevated TSH levels at the age of 7.7 and 10 yr in the presence of normal thyroid hormone levels. In 1 child, the TSH elevation was due to an ectopic hemithyroidea; in the other child, an unknown familial cause was suggested. In 1 girl (aged 12 yr), a euthyroid goiter caused by autoimmune thyroiditis was detected. We conclude from our investigation that frequent monitoring of thyroid function in children with transient congenital hypothyroidism or transient congenital hyperthyrotropinemia is not necessary during childhood if, postnatally, thyroid function recovered spontaneously. However, the growth and development of children with neonatal thyroid dysfunction should be followed, and if abnormalities occur, thyroid function tests are essential.

Adolescent↗
PubMedDate not supplied

[Investigations of thyroid function in children and adolescents after treatment of Hodgkin's disease].

Radiotherapy focused on the neck, upper mediastinum or cranium can raise the risk of thyroid dysfunction. The influence of radio- and chemotherapy on thyroid morphology and function after treatment of Hodgkin's disease in 31 children and acute lymphoblastic leucaemia in 36 children was evaluated. Clinical examination, estimation of blood TSH, FT4 levels as well as ultrasonographic scan were performed. In the group of children with Hodgkin s disease the blood level of ATG Antithyreoglobulins andMAB, microsmal antibodies were estimated. The results of clinical examination were normal in all patients. Thyroid function tests were also normal, except for one case with elevated TSH values (22.76 microIU/ml) and decreased FT4 values (0.65 ng/ml). Three patients (9.7%) with Hodgkin s disease and three (8.5%) with ALL (only one had cranial radiotherapy) had an abnormal image of thyroid in ultrasonography (hypoechogenicity, heterogenous ultrasound scan, solid nodule). The results of our investigations indicate that abnormalities found in the ultrasound scan in children and adolescents with Hodgkin's disease in whom treatment has been terminated, can be a first prodrome of thyroid pathology.

Adolescent↗
PubMed2005

Long-term lithium treatment and thyroid antibodies: a controlled study.

OBJECTIVE: Because the role of thyroid autoimmunity in the development of lithium-induced thyroid dysfunction remains controversial, we compared the prevalence of thyroid autoantibodies in patients with affective disorders receiving long-term lithium maintenance therapy with that of age- and sex-matched controls. METHODS: We conducted a cross-sectional study with 100 adult patients with major affective disorders diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, revised (DSM-III-R), who were undergoing lithium therapy for 6 months or more at a specialized lithium university clinic and 100 age- and sex-matched controls with no history of an axis I psychiatric disorder. Serum autoantibodies against thyroid peroxidase (TPOAb), thyroglobulin (TgAb) and TSH receptors (TRAb) were measured. RESULTS: TPOAb were found in 7 patients and 11 controls, and TgAb were found in 8 patients and 15 controls. TRAb were not found in either group. CONCLUSIONS: In this sample of patients with affective disorders, long-term lithium treatment did not increase the prevalence of thyroid autoimmunity.

Adult↗
PubMed1993

Early onset of lithium-associated hypothyroidism.

In general practice, psychiatrists are confronted with the difficulty of structuring a rational design for the early detection of hypothyroidism. To determine the period during which a patient receiving lithium is most at risk of developing hypothyroidism, a retrospective study was conducted on the records of 154 patients at two general hospital lithium clinics from January 1980 to August 1991. Forty-two cases of hypothyroidism (clinical hypothyroidism and/or abnormally elevated levels of TSH) were detected. A significant difference was found between the onset of hypothyroidism and age (older patients developed more thyroid dysfunction), but no significant differences were found between thyroid abnormality and sex or diagnostic category and menopausal status, although trends were observed for the two former variables. This longitudinal study is the first to describe an outline of thyroid functioning in terms of the duration of treatment. Lithium-associated hypothyroidism develops most often during the first two years. Of the 42 cases of hypothyroidism, 16 were diagnosed within six months (38%), 23 within the first year (55%), and 31 two years (74%). Since thyroid functioning is an important parameter in the course of affective disorders, its close and frequent monitoring is mandatory during the first two years of treatment.

Adult↗
PubMed1998

Perchlorate and the thyroid gland.

Perchlorate competitively blocks iodide from entering the thyroid by an effect on the Na+/I- symporter thus preventing the further synthesis of thyroid hormone but has no effect on the iodination process itself. It is concentrated by thyroid tissue in a manner similar to iodide but is not significantly metabolized in the gland or peripherally. What is not settled is whether there are additional perchlorate effects on iodide transport. Perchlorate has a fast turnover in the body and requires frequent daily doses for therapy of thyrotoxicosis. Perchlorate appears to be substantially more effective against large iodide loads than the thionamides, and, with long-term iodide contamination, combined therapy of perchlorate (with < or = 1 g/day) and thionamides is recommended for the more severe cases of thyrotoxicosis that may result from excess iodide or iodide-generating organic compounds, as for example with amiodarone. After approximately 30 days, the perchlorate dosage can be tapered or stopped, continuing with thionamides alone. This markedly increases its safe use. Despite serious side effects during its early use, lower dosages and shorter treatment periods appear to have prevented such reactions in its recent reintroduction, mostly for amiodarone-induced thyroid dysfunction. Perchlorate can also protect against inhibition of thyroid function and the resulting hypothyroidism caused by excess iodide, presumably by reducing the formation of an iodinated inhibitor. The reduction of the iodide pool by perchlorate thus has dual effects--reduction of excess hormone synthesis and hyperthyroidism, on the one hand, and reduction of thyroid inhibitor synthesis and hypothyroidism on the other. Perchlorate remains very useful also as a single dose application in tests measuring the discharge of radioiodide accumulated in the thyroid as a result of many different disruptions in the further metabolism of iodide in the thyroid gland.

Amiodarone↗
PubMed2001

The role of pendrin in iodide regulation.

Recent advances in human genetics have catalyzed the attention on Pendred's syndrome and its disease-gene, PDS. Studies on the expression of the PDS gene and on the function of its encoded protein, which has been named pendrin, are currently in progress. Consistent with the Pendred's syndrome phenotype, which is characterized by thyroid dysfunction associated to deafness, PDS expression has been demonstrated in the thyroid and in the inner ear. Despite its high homology to known sulfate transporters, pendrin has been shown to transport iodide and chloride, but not sulfate. Thus, it is probably devoted to regulate, at the apical membrane where it has been immunolocalized, the flux of iodide from the thyroid cell to the colloid space. The function of pendrin in the inner ear is not well understood, but it seems to function also at this level as an anion transporter. Indeed, a pronounced PDS expression has been detected in structures of the inner ear, such as the membranous labyrinth and the endolymphatic duct and sac. At this level, the possible role of pendrin could be the maintenance of the appropriate ionic composition of the endolymph. Although many questions remain to be answered, these recent achievements concerning the putative role of pendrin aid to better understand the genetic basis of the peculiar phenotype of Pendred's syndrome, which associate the dysfunction of two so different organs such as the thyroid and the inner ear.

Carrier Proteins↗
PubMed1982

Triiodothyronine thyrotoxicosis complicating primary hypothyroidism in a patient with autoimmune thyroiditis.

It is increasingly recognized that autoimmune thyroiditis can have a multifaceted presentation. Documented triiodothyronine thyrotoxicosis developed in a patient with a six-year history of primary hypothyroidism that was left untreated. Serologic and cytologic evidence confirmed the thyroid dysfunction as being on an autoimmune basis. Chronic lymphocytic thyroiditis may be seen with hyperthyroidism, hypothyroidism, or euthyroidism, and in an individual patients, spontaneous progression from one metabolic state to another may occur.

Autoimmune Diseases↗
PubMed1978

Thyroid antibodies in children and adolescents with thyroid disorders.

Thyroid antibodies were determined by three different techniques in the sera of 125 children and adolescents with thyroid disorders and in the sera of 53 short, normal children without thyroid dysfunction. The incidence of antithyroglobulin antibodies in patients with thyroiditis was highest when measured by radioimmunoassay (85%), less than when measured by hemagglutination (24%), and least by antimicrosomal antibodies (7%). No patient who had initially negative serum for RATA subsequently had positive tests during follow-up of five to 24 months, whereas eight of 31 patients with initially negative serum for ATA later developed positive tests. Treatment appeared to have a suppressive effect on RATA, but not on ATA titers, in hypothroid patients with clinical thyroiditis. The incidence of hypothyroidism in the patients with clinical thyroiditis on initial presentation was significant (37%) and suggests that identification of children and adolescents with thyroiditis is important to ensure adequate medical follow-up.

Adolescent↗
PubMed2000

Thyrocyte-interleukin-1 interactions.

Autoimmune thyroid disease is the most common organ-specific autoimmune disease and is a very common cause of thyroid dysfunction such as autoimmune hypothyroidism, Graves' disease and postpartum thyroiditis. The thyroid gland from patients with autoimmune thyroid disease is morphologically characterized by massive infiltration of lymphoid cells. The interleukin-1 (IL-1) family of molecules is together with other cytokines an integral component of the complex intercellular communication required to mount and control an immune response. IL-1alpha/beta in moderate and high concentrations reversibly inhibit thyroid cell function, while IL-1beta in low concentrations stimulates thyroid cell function. The biphasic, non-cytotoxic and reversible influence of IL-1 supports a role of IL-1 in the physiological regulation of thyroid cell function. IL-1 stimulates the guanylate mediated pathways and inhibits the adenylate cyclase mediated pathways. All IL-1 effects are counteracted by IL-1 receptor antagonist indicating that the effects are exerted through activation of specific IL-1 receptors on thyrocytes. Furthermore, IL-1 induces or enhances expression of a number of immunologically active molecules such as adhesion molecules, cytokines, and complement regulatory proteins in thyroid epithelial cells. IL-1 may thus play a role during physiological as well as pathophysiological conditions contributing to for example the euthyroid sick syndrome and development of thyroid autoimmunity. This review summarizes current literature on the phenomenological in vitro influence of IL-1 on the thyroid cell.

Animals↗
PubMed1998

The effects of thyroid status on serum apolipoprotein A-I-containing lipoprotein particles.

Alterations of lipid profile are a well-known phenomenon in thyroid dysfunction. However, little is known about the influence of thyroid hormone on Lp A-I and LpA-I:A-II particles. We have, therefore, studied LpA-I and LpAI:A-II concentrations in a group of 20 patients with hyperthyroidism and in a group of 15 patients with hypothyroidism before and one month after attainment of euthyroidism. In hypothyroid patients, LDL-cholesterol and apo B concentrations decrease significantly after L-T4 replacement treatment (from 4.49+/-2.51 to 2.76+/-0.70 mmol/ L, P=0.036 and from 89.4+/-16.1 to 78.3+/-13.3 mg/dL, P=0.05, respectively), whereas no significant change was observed in the total cholesterol, HDL-C, LpA-I, LpA-I:A-II and apo A-I concentrations. In hyperthyroid patients, total cholesterol (from 3.58+/-0.72 to 4.74+/-1.39mmol/L, P=0.0025), HDL-C (from 1.19+/-0.23 to 1.41+/-0.27mmol/L, P=0.0084), LDL-C (from 1.83+/-0.69 to 2.96+/-1.20 mmol/l, P=0.0025), apo A-I (from 85.6+/-12.5 to 91.7+/-18.1 mg/dL, P=0.05) and apo B (from 52.7+/-8.2 to 65.6+/-16.5 mg/dL, P=0.0013) increased after restoration of euthyroidism while triglycerides, LpA-I and LpA-I: A-II concentrations were unchanged. LpA-I and LpA-I:A-II concentrations were not related to thyroid hormones in both groups. Our study suggests that LpA-I and LpA-I:A-II particles are not under the direct control of thyroid hormones.

Adult↗
PubMed2001

Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study.

OBJECTIVES: Many afflictions have been associated with celiac disease, but chance associations may exists. The aim of this study was to establish, by means of a multicenter prospective study, the prevalence of thyroid impairment among adult patients with newly diagnosed celiac disease and to evaluate the effect of a 1-yr gluten withdrawal on thyroid function. METHODS: A total of 241 consecutive untreated patients and 212 controls were enrolled. In 128 subjects a thorough assessment, including intestinal biopsy, was repeated within 1 yr of dietary treatment. Thyroid function was assayed by measuring the levels of TSH, free T3, free T4, thyroperoxidase, and thyroid microsome antibodies. RESULTS: Thyroid disease was 3-fold higher in patients than in controls (p < 0.0005). Hypothyroidism, diagnosed in 31 patients (12.9%) and nine controls (4.2%), was subclinical in 29 patients and of nonautoimmune origin in 21. There was no difference regarding hyperthyroidism, whereas autoimmune thyroid disease with euthyroidism was present in 39 patients (16.2%) and eight controls (3.8%). In most patients who strictly followed a 1-yr gluten withdrawal (as confirmed by intestinal mucosa recovery), there was a normalization of subclinical hypothyroidism. Twenty-five percent of patients with euthyroid autoimmune disease shifted toward either a subclinical hyperthyroidism or subclinical hypothyroidism; in these subjects, dietary compliance was poor. In addition, 5.5% of patients whose thyroid function was normal while untreated developed some degree of thyroid dysfunction 1 yr later. CONCLUSIONS: The greater frequency of thyroid disease among celiac disease patients justifies a thyroid functional assessment. In distinct cases, gluten withdrawal may single-handedly reverse the abnormality.

Adult↗
PubMed2005

Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation.

The BRAFT1799A mutation is the most common genetic alteration in papillary thyroid carcinomas (PTC). It is also found in a subset of papillary microcarcinomas, consistent with a role in tumor initiation. PTCs with BRAFT1799A are often invasive and present at a more advanced stage. BRAFT1799A is found with high prevalence in tall-cell variant PTCs and in poorly differentiated and undifferentiated carcinomas arising from PTCs. To explore the role of BRAFV600E in thyroid cancer pathogenesis, we targeted its expression to thyroid cells of transgenic FVB/N mice with a bovine thyroglobulin promoter. Two Tg-BRAFV600E lines (Tg-BRAF2 and Tg-BRAF3) were propagated for detailed analysis. Tg-BRAF2 and Tg-BRAF3 mice had increased thyroid-stimulating hormone levels (>7- and approximately 2-fold, respectively). This likely resulted from decreased expression of thyroid peroxidase, sodium iodine symporter, and thyroglobulin. All lines seemed to successfully compensate for thyroid dysfunction, as serum thyroxine/triiodothyronine and somatic growth were normal. Thyroid glands of transgenic mice were markedly enlarged by 5 weeks of age. In Tg-BRAF2 mice, PTCs were present at 12 and 22 weeks in 14 of 15 and 13 of 14 animals, respectively, with 83% exhibiting tall-cell features, 83% areas of invasion, and 48% foci of poorly differentiated carcinoma. Tg-BRAF3 mice also developed PTCs, albeit with lower prevalence (3 of 12 and 4 of 9 at 12 and 22 weeks, respectively). Tg-BRAF2 mice had a 30% decrease in survival at 5 months. In summary, thyroid-specific expression of BRAFV600E induces goiter and invasive PTC, which transitions to poorly differentiated carcinomas. This closely recapitulates the phenotype of BRAF-positive PTCs in humans and supports a key role for this oncogene in its pathogenesis.

Animals↗
PubMed1985

Autoimmune thyroiditis in manic-depressive patients treated with lithium.

To explore whether lithium-induced hypothyroidism is related to an exacerbation of underlying autoimmune processes such as thyroiditis, the authors comprehensively assessed thyroid function in 16 manic-depressive patients. Each of the three patients who showed detectable titers of thyroid microsomal antibodies before treatment manifested a marked increase in antibody titer from 4 to 12 months after lithium treatment was begun. Thus, lithium-induced thyroid dysfunction may not only involve direct effects on the thyroid itself but also involve exacerbation of an underlying indolent autoimmune thyroiditis, possibly by causing shifts in T lymphocyte subpopulations.

Acute Disease↗
PubMed2000

A heterozygous deletion of the autoimmune regulator (AIRE1) gene, autoimmune thyroid disease, and type 1 diabetes: no evidence for association.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare monogenic autoimmune disease with endocrine components including type 1 diabetes, adrenal failure, and thyroid dysfunction, with major autoantibodies directed against adrenal, pancreas, and thyroid tissue. A 13-bp deletion in exon 8 of the autoimmune regulator (AIRE1) gene on chromosome 21q22.3 accounts for more than 70% of mutant alleles in United Kingdom subjects with APECED. To determine whether this polymorphism contributes to disease susceptibility in subjects with autoimmune disease in general, we screened 302 patients with Graves' disease, 154 patients with autoimmune hypothyroidism, 235 patients with type 1 diabetes, and 318 control subjects for the 13-bp deletion of the AIRE1 gene. The mutation was present in only 1 (0.33%) patient with Graves' disease, 1 patient with autoimmune hypothyroidism (0.6%), and 1 (0.315) of the control subjects. No patients with type 1 diabetes were found to carry the mutation. We conclude, therefore, that the 13-bp deletion of the AIRE1 gene is not a susceptibility locus for the more common autoimmune endocrinopathies in the United Kingdom.

Chromosomes, Human, Pair 21↗