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PubMed1988

The diagnostic dilemmas of hyperthyroxinemia and hypothyroxinemia.

It should be apparent that the diagnosis of thyrotoxicosis and hypothyroidism can be correctly made in the majority of ambulatory patients. However, the clinician needs to be extremely careful in reaching such a definitive diagnosis on the hospitalized patient. Both the clinical features and the standard thyroid function tests need careful evaluation and reanalysis before the diagnosis of thyroid dysfunction can be made with confidence.

Humans↗
PubMed1986

Postpartum thyroid disease.

Recent epidemiological studies in Japan and Sweden have disclosed a high prevalence of transient thyroid dysfunction in women following delivery. These changes seem to reflect an immunoregulatory "rebound" following pregnancy-induced immunosuppression. Thyroid microsomal antibody titers characteristically decrease during pregnancy and increase again after delivery to maximum levels around six months postpartum. At this time some microsomal antibody-positive women develop goitrous hypothyroidism. Subsequently, the microsomal antibody titers fall, reaching the early pregnancy values one year postpartum by which time hypothyroidism subsides. The severity of hypothyroidism is closely related to the titer of microsomal antibody, especially the immunoglobulin G1 subclass of microsomal antibody, and partly predictable from the titer in early pregnancy. The HLA-DR4 antigen was observed in 58% of microsomal antibody-positive Swedish women as compared to 33.7% in the general population (relative risk = 2.71). This association was even stronger in microsomal antibody-positive women who developed postpartum hypothyroidism (69%; relative risk = 4.36). Finally, postpartum thyrotoxicosis with a high radioiodine uptake may occur in women with latent Graves' disease. In these cases changes of TSH-receptor-stimulating antibodies analogous to microsomal antibodies seem to occur.

Adolescent↗
PubMed1993

Effect of thyroid function on concentrations of lipoprotein(a)

The effect of thyroid hormones on concentrations of lipoprotein(a) [Lp(a)] was analyzed in 60 patients with active thyroid dysfunction (hyperthyroidism 30 cases, hypothyroidism 32 cases, and 2 cases with opposite changes) and after normalization of the thyroid state. Treatment of hyperthyroidism increased the mean Lp(a) concentrations by 60% (from 73 to 102 mg/L, P < 0.002); at the same time, low-density lipoprotein cholesterol (LDL-C) increased by 53% (from 2.6 to 3.7 mmol/L, P < 0.0001) and apolipoprotein B (apo B) by 35% (from 0.91 to 1.17 g/L, P < 0.0005). In hypothyroidism, the opposite changes were observed: mean Lp(a) decreased from 136 to 114 mg/L (10%, P < 0.02), LDL-C from 4.6 to 3.9 mmol/L (13%, P < 0.01), and apo B from 1.51 to 1.20 g/L (14%, P < 0.01). Although the changes in Lp(a) concentrations did correlate with changes of LDL-C during treatment of hyperthyroidism (r = 0.43, P < 0.05), and with changes in apo B during thyroxine-substitution therapy for hypothyroidism (r = 0.46, P < 0.05), we observed no associations between Lp(a) and LDL-C or apo B in the euthyroid state. These data cannot rule out the possibility that the thyroid hormone-induced increase in LDL-C receptor activity was responsible for the decreased concentrations of Lp(a) in hyperthyroidism. Given that LDL-C is approximately 30% of the Lp(a) molecule but the changes in Lp(a) concentrations are comparable with those in LDL-C (60% vs 53%), and given that Lp(a) is metabolized by an LDL-C-receptor-independent pathway, the present data suggest a direct effect of thyroid hormones on Lp(a) synthesis.

Adult↗
PubMed2007

The spectrum of thyroid disorders in adult type 1 diabetes mellitus.

BACKGROUND: Thyroid disorders such as goiter, nodules, autoimmune thyroid disease and thyroid dysfunction have rarely been investigated in adult type 1 diabetes mellitus. Our aim was to study the spectrum of thyroid disorders in adult type 1 diabetic subjects and compare them with results obtained from a sample of the general adult population. METHODS: The study population comprised 224 type 1 diabetic and 3481 non-diabetic subjects aged 20-69 years. Thyroid function (TSH, FT3 and FT4) and serum autoantibodies to thyroperoxidase (anti-TPO-Ab) were evaluated from blood samples. Thyroid structure and size were measured by ultrasound. RESULTS: Type 1 diabetic subjects had a higher risk of known thyroid disease [odds ratio (OR) 1.78, 95% confidence interval (CI) 1.11-2.85], a lower risk of goiter (OR 0.73; 95%-CI 0.54-0.99) and nodules (OR 0.54; 95%-CI 0.35-0.85), and a higher risk of anti-TPO-Ab >200 IU/mL (OR 1.94; 95%-CI 1.28-2.95) compared to the reference population. Furthermore, diabetic subjects had lower serum FT3 levels than the non-diabetic references (adjusted mean 5.00 pmol/L; 95%-CI 4.88-5.12 pmol/L versus 5.27 pmol/L; 95%-CI 5.24-5.30 pmol/L). CONCLUSIONS: Adult type 1 diabetes mellitus is associated with a decreased risk of goiter and nodules and an increased risk of thyroid autoimmunity. A diabetes-related low T3 syndrome may contribute to the differences in thyroid function between type 1 diabetic and non-diabetic subjects.

Adult↗
PubMed1991

The effects of drugs on tests of thyroid function.

Many drugs affect tests of thyroid function through alterations in the synthesis, transport and metabolism of thyroid hormones, as well as via influences on thyrotrophin (TSH) synthesis and secretion. Despite effects on circulating thyroid hormone and TSH levels, few drugs result in important changes in clinical thyroid state, but difficulty in interpretation of thyroid function tests often results. Commonly prescribed drugs including anti-convulsants, non-steroidal anti-inflammatory drugs, beta-adrenoceptor antagonists, steroid hormones and heparin may result in abnormal thyroid function tests in the absence of clinical features of thyroid dysfunction. In contrast, lithium and iodine containing drugs, including radiographic contrast agents and amiodarone, may result rarely in overt thyroid disease.

Adrenal Cortex Hormones↗
PubMed2001

[High prevalence of subclinical thyroidal disease among individuals attended in health control].

BACKGROUND: There is no information about the prevalence of thyroidal diseases in the general Chilean population. AIM: To assess the prevalence of thyroidal diseases in individuals attended in occupational health examinations. SUBJECTS AND METHODS: Four hundred seventy two individuals were examined between 1998 and 1999. In all, serum levels of thyroid hormones, TSH and anti thyroidal antibodies (anti microsomal, anti thyroid peroxidase and anti thyroglobulin) were measured. RESULTS: Forty four subjects were excluded from the study due to an incomplete medical record and 18 due to a personal history of thyroidal disease. Abnormal serum levels of thyroid hormones or TSH were detected in 28 subjects (6.8%). Four (1%) had hypothyroidism, 23 a subclinical hypothyroidism (5.6%) and one (0.2%) had hyperthyroidism. In 87 subjects (21.2%) at least one of the antibodies was positive. Positive anti thyroid antibodies were found in 14 of 28 subjects (50%) with abnormal thyroid hormone levels, compared with 73 of 382 subjects (19.1%) with normal thyroid hormone levels. Thyroid dysfunction was twice as frequent in women than in men. CONCLUSIONS: In this sample, a 6.8% prevalence of abnormal thyroid function tests was detected.

Adolescent↗
PubMedDate not supplied

[Subclinical thyroid diseases].

The term "subclinical thyroid diseases" describes conditions characterized by low or elevated thyroid-stimulating hormone (TSH), normal levels of circulating thyroid hormones (thyroxine and triiodothyronine), and few or no definite clinical signs or symptoms of thyroid dysfunction. Therefore, it is a diagnosis based on laboratory evaluation, not on clinical criteria. Because the risk of subclinical thyroid disease increases with age, the number of cases should increase as population ages. Their importance lies in the possible adverse effects on the heart, lipids, bone mineral density, quality of life and mortality. Although the subclinical thyroid diseases tend to progress to overt disease, TSH levels in some subjects return to the reference range. However there is controversy about the definition, clinical importance, consequences of untreated disease, whom to screen and when to initiate treatment. We reviewed the literature and our recommendations about screening and treatment are based upon the existing evidence and the author's experience.

Humans↗
PubMed1999

[Down syndrome and hyperthyroidism. Report of 3 cases].

We report three patients with Down syndrome that developed a hyperthyroidism. A 25 years old female and a 18 years old male had Basedow Graves disease and were treated with radioiodine. A 19 years old male had a Hashitoxicosis and is presently being treated with propylthiouracyl. Clinical and subclinical thyroid dysfunction is frequent in patients with Down syndrome and the risk increases with age. Therefore a surveillance with yearly TSH measurements should be done in these patients, since signs and symptoms of thyroid disease are barely detected in them. Hypothyroidism is the most frequent dysfunction but hyperthyroidism is also associated to Down syndrome.

Adolescent↗
PubMedDate not supplied

[Markers of thyroid function (I). Assessment of glandular activity].

Thyroid hormones have a fundamental role in the metabolism, and are active in all organs and systems. Thyroid dysfunction (TD) is an important public health problem that concerns 10% of the general population. Diagnosis of TD is currently carried out on the basis of serum hormone levels determined by laboratory analysis. The results are classified into clinical (TSH and thyroid hormones out of normal range) and subclinical (isolated TSH disorder) dysfunction. The development of third generation assays in the TSH test represents a great step forward in the diagnosis of TD. However, the debate about the pathological significance of subclinical TD has intensified. There is as yet no agreement on the best approach for diagnosis and treatment of this common condition. It is currently impossible to know which subjects with subclinical TD will develop the typical complications of clinical dysfunction. In this setting, it is feasible that a number of subclinical hypothyroid subjects may in some cases be overtreated with thyroxin, while others remain undertreated with increased iatrogenic morbidity as a consequence.

Biomarkers↗
PubMed2004

Chronic autoimmune thyroiditis and rheumatic manifestations.

A variety of rheumatic manifestations have been described in association with autoimmune thyroiditis. In the past, most of these manifestations were attributed to the underlying thyroid dysfunction, in particular hypothyroidism. However, a responsibility of the mechanisms involved in the autoimmunity rather than a direct action of thyroid hormones seems supported by the evidences that some rheumatic manifestations may occur even in euthyroid patients, or that they are more frequent in hypothyroid patient with autoimmune thyroiditis than in those without this disease. Rheumatic manifestations could be sometimes attributable to the autoimmune rheumatic diseases frequently associated with autoimmune thyroiditis, such as Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus, or scleroderma. Among the most important or frequent rheumatic manifestations there are a mild non-erosive variety of arthritis, polyarthralgia, myalgia, and sicca syndrome without a true Sjögren's syndrome. Although the possible pathogenesis of these manifestations is not completely established, some hypotheses may be proposed, including a role of autoantibodies characteristics of autoimmune thyroiditis, a possible overlap between autoimmune thyroiditis and some autoimmune rheumatic diseases, and a systemic inflammatory reaction associated with thyroiditis.

Autoantibodies↗
PubMed2001

Evaluation of the patient with a suspected thyroid disorder.

The principal types of thyroid disorders described herein can be recognized and evaluated clinically and biochemically by the obstetrician/gynecologist. Most patients with diffuse goiter should be referred for further evaluation and an RAI scan arranged while this consultation is awaited. Patients with solitary thyroid nodules should be referred for FNAB. Primary hypothyroidism without significant goiter can be treated without specialist referral, except in patients at high risk for ischemic coronary disease or arrhythmia. Primary hyperthyroidism, apart from subacute and postpartum thyroiditis, should be referred for specialist evaluation and definitive therapy. An RAI scan and uptake should be ordered, and beta-blocker therapy can be initiated as interim therapy in symptomatic patients. Patients with secondary (i.e., hypothalamic- or pituitary-based) thyroid dysfunction should always be referred for evaluation and treatment of the primary intracranial cause. There are several causes of abnormal thyroid function tests in apparently euthyroid patients, and the clinical context often provides important evidence of their nature. Clinical judgment is an important factor in knowing when to arrange specialist consultation.

Diagnosis, Differential↗
PubMed1998

Impaired thyroid function in murine toxoplasmosis.

A decline in serum thyroxine (T4) occurs in Nya: NYLAR female mice infected with Toxoplasma gondii. To ascertain whether the hypothyroxinaemia might be the result of primary thyroid dysfunction, 2 parameters of thyrofollicular cell function were monitored to determine (a) if the cell surface membrane receptors for thyroid-stimulating hormone (TSH) were operative, and (b) whether the cyclic adenosine monophosphate (cAMP)-dependent cascade of intracellular events leading to the release of T4 was responsive to exogenous cAMP. Our results indicated that both parameters were intact and functional in the infected-mouse thyrocytes. However, the elicited T4 responses were distinctly diminished in magnitude, reflecting a lack of readily available thyroidal T4 reserves. Because the continuing synthesis, storage, and release of T4 is dependent on the pulsatile stimulation of the thyroid by TSH, we suggest that the depletion of T4 reserves is likely due to perturbation of the pulsatile release of TSH from the pituitary, rather than to primary thyroid malfunction.

Animals↗
PubMed2005

Thyroid disease and increased cardiovascular risk.

The effects of thyroid dysfunction are thought to be reversible on restoration of euthyroidism, but postmortem and epidemiologic data suggest that subclinical or treated thyroid disease is associated with increased vascular risk. In order to determine the extent of this risk, and to explore whether the nature and/or treatment of thyroid disease are critical in this relationship, we used medical record linkage to match patients with treated thyroid disease of various etiologies with routinely collected national inpatient and daycase hospital discharge records and death records, and assessed the number of hospitalizations from cardiovascular or cerebrovascular disease or death in patients with thyroid disease and control patients. Patients treated for Graves' disease had more hospitalizations from cardiovascular disease than controls (relative risk, 1.42; 95% confidence interval, 1.20 to 1.67; p < 0.001). Toxic multinodular goiter was also associated with significantly higher rates of cardiovascular disease (relative risk, 1.50; 95% confidence interval, 1.11 to 2.02; p = 0.008). Patients with Hashimoto's thyroiditis aged over 50 years had a threefold increase in cardiovascular admissions compared to controls (23.5% and 6.5%, respectively; 95% confidence interval for difference, 6.0% to 27.9%; p = 0.003). Thus, different forms of thyroid disease were associated with increased long-term vascular risk despite restoration of euthyroidism. The mechanisms that mediate this risk are unclear but may not involve thyroid hormone abnormality.

Adult↗
PubMed2006

A differential association of interferon-gamma high-producing allele T and low-producing allele A (+874 A/T) with Hashimoto's thyroiditis and Graves' disease.

Cytokines play a crucial role in the pathogenesis of autoimmune thyroid disease. The aim of this study was to investigate the relationship of the single base change polymorphic variants identified in the first intron of interferon-gamma (IFN-gamma) (+874 T/A) with susceptibility to thyroid dysfunctions. A total of 340 subjects were included in the study comprising of 190 patients (104 patients with Hashimoto's thyroiditis, 26 with non-Hashimoto's hypothyroidism and 60 Graves' disease) and 150 controls. Genotyping was done by amplification refractory mutation system-polymerase chain reaction using a set of sequence-specific primers. Statistical analysis revealed a significant association between high IFN-gamma-producing genotype TT and Hashimoto's thyroiditis compared to controls (P value < 0.001). On the other hand, the frequency of genotype TT was decreased in patients with Graves' hyperthyroidism with a significant increase in low IFN-gamma-producing genotype AA among this group (P = 0.03). To conclude the results of the study suggest a differential association of high- and low-producing alleles of IFN-gamma gene with Hashimoto's thyroiditis and Graves' disease. The high IFN-gamma-producing allele T was observed to be associated with Hashimoto's thyroiditis in the present study where as in Graves' hyperthyroidism the association was observed to be stronger with the low producing allele A.

Adenine Nucleotides↗
PubMed2006

Functional characterization of wild-type and a mutated form of SLC26A4 identified in a patient with Pendred syndrome.

BACKGROUND: Malfunction of the SLC26A4 protein leads to prelingual deafness often associated with mild thyroid dysfunction and goiter. It is assumed that SLC26A4 acts as a chloride/anion exchanger responsible for the iodide organification in the thyroid gland, and conditioning of the endolymphatic fluid in the inner ear. METHODS: Chloride uptake studies were made using HEK293-Phoenix cells expressing human wild type SLC26A4 (pendrin) and a mutant (SLC26A4(S28R)) we recently described in a patient with hypothyroidism, goiter and sensorineural hearing loss. RESULTS: Experiments are summarized showing the functional characterization of wild type SLC26A4 and a mutant (S28R), which we described recently. This mutant protein is transposed towards the cell membrane, however, its transport capability is markedly reduced if compared to wild-type SLC26A4. Furthermore, we show that the SLC26A4 induced chloride uptake in HEK293-Phoenix cells competes with iodide, and, in addition, that the chloride uptake can be blocked by NPPB and niflumic acid, whereas DIDS is ineffective. CONCLUSIONS: The functional characteristics of SLC26A4(S28R) we describe here, are consistent with the clinical phenotype observed in the patient from which the mutant was derived.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2005

X-linked MCT8 gene mutations: characterization of the pediatric neurologic phenotype.

We report a family with X-linked mental retardation that has a novel mutation in the monocarboxylate transporter 8 (MCT8) gene associated with a characteristic neurodevelopmental phenotype with early childhood hypotonia that progresses to spasticity and global developmental delays. Affected patients experience moderate to severe psychomotor delays and congenital hypotonia, develop a myopathic facies, have diminished muscle bulk and generalized muscle weakness, develop progressive spasticity and movement disorders, and have limited speech but alert, affable personalities. Acquired microcephaly and abnormal myelination on brain magnetic resonance imaging can be present. Normal monocarboxylate transporter 8 gene functioning appears to be necessary for normal thyroid-associated metabolism in neurons. Abnormal thyroid function tests appear to be a consistent finding in the absence of typical signs of thyroid dysfunction. Although the phenotype appears to be consistent, and although the neurotoxic effects of abnormal central and peripheral neuromuscular system thyroid metabolism might be partly or wholly responsible for the neurologic phenotype reported, the exact mechanism remains unclear.

Adult↗
PubMed2006

Thyroid hormones, dementia, and atrophy of the medial temporal lobe.

CONTEXT: Thyroid function has been related to Alzheimer disease (AD), but it remains unclear whether thyroid dysfunction results from or contributes to developing AD. OBJECTIVE: The objective of the study was to determine the association between thyroid function and both medial temporal lobe atrophy on brain magnetic resonance imaging (MRI) as putative early sign of AD and risk of dementia. DESIGN AND PARTICIPANTS: This was a population-based cohort study among 1077 elderly subjects aged 60-90 yr and dementia free at baseline (1995-1996). MAIN OUTCOME MEASURES: Nonfasting serum levels of TSH, free T(4) (fT(4)), T(3), and rT(3) were available in 1025 subjects followed up for incident dementia until 2005. In a subset of 489 nondemented elderly, we assessed volumes of the hippocampus and amygdala on brain MRI. Subjects using thyroid medication were excluded. RESULTS: During 5657 person-years of follow-up (mean 5.5 yr), 63 subjects were diagnosed with dementia (46 with AD). TSH and thyroid hormones were not associated with risk of dementia or AD. TSH and T(3) were also not related to brain atrophy, whereas nondemented subjects with higher fT(4) levels had more hippocampal and amygdalar atrophy on MRI. Similar associations were found for rT(3). Excluding subjects with thyroid disorders or incipient AD did not change the results. CONCLUSION: In our study, TSH was related neither to risk of AD nor with early MRI markers thereof, arguing against an important role of thyroid function in the development of AD. Whether the association of higher fT(4) and rT(3) levels with brain atrophy on MRI has functional significance remains to be elucidated.

Aged↗
PubMed1999

[Late complications after treatment of Hodgkin's disease].

Treatment of Hodgkin's disease involves chemotherapy and radiation. Both modalities may cause cardiac, pulmonary and thyroid side-effects. In a cross-sectional study, we aimed to assess the occurrence and severity of such complications. From 1980 to 1989, 129 Norwegian patients (< 50 years old) had curative treatment for Hodgkin's disease 116 (90%) of them participated in the study (follow-up period 5-13 years). Methods included lung function tests, chest X-rays, bicycle exercise tests, echocardiography and thyroid function tests. Nearly 30% of the patients reported dyspnoea on exertion and had associated reductions in lung function. Evidence of fibrosis occurred in 68%, but was associated with reduced lung function in only 12%. Pathological left-sided heart valve regurgitations were detected in 24% of the patients, pericardial thickening in 15%, and coronary artery disease in 5%. Biochemical hypothyreosis was found in 67% of the patients. We conclude that cardiac, pulmonary and thyroid dysfunctions are frequent long-term side-effects after treatment for Hodgkin's disease. We recommend annual screening of thyroid function and echocardiographic examination in patients who have received standard mantle field radiotherapy without cardiac shielding. Lung function testing should be done in individuals who require further radiation, chemotherapy or thoracic surgery.

Adult↗