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PubMed2006

Serum thyrotropin concentration as a novel predictor of malignancy in thyroid nodules investigated by fine-needle aspiration.

CONTEXT: Thyroid nodules and goiter are common, and fine-needle aspiration biopsy (FNAB) is the first investigation of choice in distinguishing benign from malignant disease. OBJECTIVE: The objective of the study was to assess whether simple clinical and biochemical parameters can predict the likelihood of thyroid malignancy in subjects undergoing FNAB. DESIGN: The design was a prospective cohort. SETTING: The study was conducted at a single secondary/tertiary care clinic. PARTICIPANTS: One thousand five hundred consecutive patients without overt thyroid dysfunction (1304 females and 196 males, mean age 47.8 yr) presenting with palpable thyroid enlargement between 1984 and 2002 were evaluated by FNAB of the thyroid. INTERVENTION(S): There were no interventions. MAIN OUTCOME MEASURES: Goiter type was assessed clinically and classified as diffuse in 183, multinodular in 456, or solitary nodule in 861 cases. Serum TSH concentration at presentation was measured in a sensitive assay in patients presenting after 1988 (n = 1183). The final cytological or histological diagnosis was determined after surgery (n = 553) or a minimum 2-yr clinical follow-up period (mean 9.5 yr, range 2-18 yr). RESULTS: The overall sensitivity and specificity of FNAB in predicting malignancy were 88 and 84%, respectively. The risk of diagnosis of malignancy rose in parallel with the serum TSH at presentation, with significant increases evident in patients with serum TSH greater than 0.9 mU/liter, compared with those with lower TSH. Binary logistic regression analysis revealed significantly increased adjusted odds ratios (AORs) for the diagnosis of malignancy in subjects with serum TSH 1.0-1.7 mU/liter, compared with TSH less than 0.4 mU/liter [AOR 2.72, 95% confidence interval (CI) 1.02-7.27, P = 0.046], with further increases evident in those with TSH 1.8-5.5 mU/liter (AOR 3.88, 95% CI 1.48-10.19, P = 0.006, compared with TSH < 0.4 mU/liter) and greater than 5.5 mU/liter (AOR 11.18, 95% CI 3.23-8.63, P < 0.001, compared with TSH < 0.4 mU/liter). Males (AOR 1.8, 95% CI 1.04-3.1, P = 0.04), younger patients (AOR 1.1, 95% CI 1.01-1.15, P = 0.025), and those with clinically solitary nodules (AOR 2.53, 95% CI 1.5-4.28, P = 0.001) were also at increased risk. Based on these findings, a formula to predict the risk of the diagnosis of thyroid malignancy in individual patients, taking into account their gender, age, goiter type determined clinically, and serum TSH, was calculated. CONCLUSIONS: The risk of malignancy in a thyroid nodule increases with serum TSH concentrations within the normal range. In addition to patient's gender, age, and goiter type, the serum TSH concentration at presentation is an independent predictor of the presence of thyroid malignancy. We propose that these simple clinical and biochemical factors can serve as an adjunct to FNAB in predicting risk of malignancy.

Adolescent↗
PubMed1986

Free thyroxine estimation for the screening of hyper- and hypothyroidism in an adult population.

Serum free thyroxine (FT4), total T4 (T4) and total T3 (T3) were determined by radioimmunoassay in 1,114 adults during a periodic health evaluation to detect unsuspected thyroid dysfunction. As a result, 3 patients with hyperthyroidism, 4 with hypothyroidism, 3 taking thyroid medication, 4 with chronic thyroiditis, 1 with simple goiter and 3 women under estrogen administration were found. Free T4 values were within the normal limits in the present four subjects taking estrogens, but all of them showed high T4 and one high T3 values. FT4 and T4 were low in four patients with hypothyroidism, but two of them showed normal T3 values. For the screening of hyperthyroidism, FT4 was the most reliable measurement and determination of either FT4 or T4 was suitable for the screening of hypothyroidism, but T3 measurement did not diagnose all patients with hypothyroidism, but T3 measurement did not diagnose all patients with hypothyroidism.

Adult↗
PubMed2000

Disclosing subclinical thyroid disease. An approach to mild laboratory abnormalities and vague or absent symptoms.

Patients with subclinical thyroid disease often have no apparent symptoms or only nonspecific complaints. However, increasing evidence that early disease is associated with behavioral, psychiatric, biochemical, and organ-specific abnormalities has led several specialty organizations to publish or modify position papers. Serum TSH testing is the most sensitive method of identifying early thyroid dysfunction. It should be considered in patients who have risk factors for mild thyroid failure, have symptoms that could be related to thyroid disease, or are taking exogenous thyroid hormone. T4 therapy should be strongly considered in patients with a TSH level of 10 mIU/L or more. If observation is elected in asymptomatic patients with lesser TSH elevation, periodic measurements are advised. In patients with TSH suppression who are taking thyroid hormone, the dose should be lowered. If the TSH level is decreased because of endogenous suppression and free-T4 and T3 levels are normal, options include observation and treatment with an antithyroid drug or thyroid ablation. Early therapy should be considered in older patients and those with heart disease or nodular thyroid disease. The goal of all treatment methods should be to keep the TSH level in the normal range.

Humans↗
PubMed2002

Thyroid hypoechogenicity in patients with chronic hepatitis receiving interferon-alpha therapy: evaluation by standardized grey scale ultrasonography.

BACKGROUND: Recombinant human interferon-a therapy of chronic hepatitis B and C is associated with the induction of thyroid dysfunction in up to 15%. Little is known about morphological changes of the thyroid gland, especially about its tissue echogenicity under this immunomodulative drug treatment. METHODS: 116 patients with chronic hepatitis B or C were consecutively investigated. 53 patients qualified for treatment with interferon-a alone or in combination with ribavirin. Patients with normal serum aminotransferase levels, advanced liver cirrhosis, hepatocellular carcinoma, active intravenous drug or alcohol abusus and with focal thyroid lesions (nodes, cysts, calcifications) were excluded. Thyroid function was determined by measurements of FT4, TSH and thyroidal autoantibodies. Ultrasonography was performed before, during and after interferon-a therapy including volumetry and standardized grey scale analysis. The data were compared with values of 100 euthyroid volunteers as control group. RESULTS: After six months of therapy patients differed from controls by significant TSH elevation (12.8 +/- 9.34 vs. 2.8 +/- 1.1 microU/ml, p<0.02). Six patients (11%) developed overt hypothyroidism with detectable thyroidal autoantibodies. Thyroid volume in patients was similar (13.0 +/- 4.1 ml) to that in the control group (12.6 +/- 4.7 ml). However, thyroid echogenicity of the patients was significantly lower after 6 months of therapy (21.9 +/- 2.5 grey scales) compared to the status before (25.6 +/- 2.3 grey scales) and compared to the values of controls (25.4 +/- 2.1 grey scales, p <0.002). CONCLUSION: Beside of functional disorders interferon-alpha leads to thyroid hypoechogenicity suggesting relevant morphological changes of the organ.

Adult↗
PubMedDate not supplied

[Thyroid diseases in pregnancy].

The thyroid diseases are more frequent in women, which is probably related to the fact that many thyroid diseases are of the autoimmune type, secondary to the effects of sexual steroids in the immunological system; although it had never been completely cleared up, it seems that estrogens and progestogens may modulate the lymphocyte differentiation as well as the induction of the autoimmune response. After delivery, the thyroid dysfunction of autoimmune type often occurs, even in women without previous history of thyroid disease. Some authors assume that the cytokines, produced by the mother, fetus or placenta, inhibit the autoimmune reaction during pregnancy. The subsequent reduction in the inhibiting cytokines, after delivery, allows the aggravation or the beginning of the autoimmune disease. Although autoimmunity is traditionally considered as a major cause for thyroid disease during pregnancy, recent studies indicate that the most common aetiology of disturbance of thyroid tests during pregnancy is the hyperthyroidism due to the inadequate production of human chorionic gonadotropin (hCG). However, from the clinical point of view, the hyperthyroidism caused by Graves' disease is the most important cause for maternal and fetal morbidity.

Female↗
PubMed2006

[Thyroid and hemostasis].

Several studies have reported hemostatic abnormalities, both in terms of bleeding or thrombosis, in patients with various thyroid dysfunctions. The aim of this paper is to briefly discuss the relationship between thyroid disorders and hemostasis (i.e., primary hemostasis, coagulation factors and fibrinolytic system). From the analysis of the more recent literature data, it is evident that most of the coagulation abnormalities, associated with thyroid disorders, are a consequence of a direct action of thyroid hormones on the synthesis of various hemostatic factors or a derangement of immune function. On the whole, these data suggest that a hypercoagulable state is present in hyperthyroid patients, while patients suffering from moderate hypothyroidism are at increased risk of thrombosis, contrasting with the bleeding tendency of those presenting severe hypothyroidism.

Blood Coagulation Disorders↗
PubMed2006

[Gynecological aspects of thyroid disorders. A review].

OBJECTIVE: The most frequent thyroid syndromes--hypothyroidism and thyrotoxicosis--are often accompanied with menstrual disturbances. The aim of this study was to summarize knowledge of physiology, pathology and clinical aspects of both thyroidal and gonadal axis interactions. SUBJECT: A review. SETTING: Department of Pathological Physiology, 1st Faculty of Medicine, Charles University, Prague. CONCLUSION: About 25% female infertility and 15% menstrual cycle disorders result from thyroid dysfunction. Particularly, the subclinical hypothyroidism has a high prevalence in the population; therefore, thyroid function must be examined in female with unclear infertility or menstrual disturbances. The next overlap of thyroid disorders and gynaecology represents iodine-131 use for differentiated thyroid carcinoma in fertile age with aspects to ovarian failure and gestational risk.

Female↗
PubMed2006

[Postparum thyroiditis].

Postpartum thyroiditis is one of the most common endocrinological disorders annually affecting millions of women world-wide. It is is defined as a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery. A thyrotoxic phase of postpartum thyroiditis may be brief and unnoticed before a more long-lasting (permanent in up to 30%) hypothyroid phase occurs. The disease, found in approximately 5-10% of mothers in the general population, is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Women suffering from other autoimmune conditions, or having a previous or family history of thyroid disease are at increased risk of its development. In this paper we present an overview of the pathogenesis, clinical aspects, diagnosis, and treatment options for postpartum thyroiditis with putting special emphasis on the results of recently published studies.

Diagnosis, Differential↗
PubMed1987

Diagnostic value of a modified assay of free triiodothyronine in serum.

The performance of a modified commercial (Diagnostic Products Corp.) assay for free triiodothyronine in serum was evaluated, and its diagnostic value was compared with two other methods for free triiodothyronine estimation in euthyroid subjects and in patients with thyroid dysfunction. No advantage was demonstrated for the modified assay as an index of thyroid status. In conditions involving thyroxin-binding globulin excess the modified assay produced misleading results more frequently than did the comparison methods.

Female↗
PubMed1987

Past and current thyroid function in subjects with panic disorder.

Disturbances in thyroid function can result in symptoms similar to those occurring in patients with anxiety disorders, especially panic disorder. An association between thyroid illness and panic and phobic disorders has been suggested, but few studies have directly investigated this issue. To assess this possible relationship, the authors measured indices of thyroid function in 165 subjects who had a current DSM-III diagnosis of panic disorder, either with or without phobic avoidance. These subjects reported a higher prevalence of thyroid illness by history compared with the prevalence of thyroid illness in the general population; however, less than 1% of all subjects had current thyroid dysfunction. The presence of a major depressive episode (MDE) was unrelated to current thyroid function, although subjects with MDE reported a higher prevalence of thyroid disease by history. Indices of thyroid function were not correlated with the severity of panic attacks or phobias.

Adult↗
PubMed1994

Routine thyroid function tests in infertile women: are they necessary?

To investigate the yield of routine thyroid function testing in infertile women, the records of 444 infertile women were categorized to standard infertility groups. Thyroid function was evaluated by measuring plasma free thyroxine and thyroid-stimulating hormone. All free thyroxine values were in the normal range (0.8 to 1.8 ng/ml), and only three thyroid-stimulating hormone values were higher than the normal range (0.15 to 4.5 mIU/L). The three women had ovulatory dysfunction. Thyroid function testing is more prudent in screening the subset of infertile women with ovulatory dysfunction and not as a routine measure in the infertile population.

Female↗
PubMed1991

Age-related patterns of thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation in Down syndrome.

Thyroid function in subjects with Down syndrome was studied using the thyrotropin-releasing hormone test. Forty-seven infants and children with Down syndrome were investigated. Ages ranged from 1 month to 7 years; there were 26 boys and 21 girls. Fourteen of the subjects with Down syndrome who had an exaggerated thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation had two or more annual follow-up tests. The remaining 33 subjects who only underwent one thyrotropin-releasing hormone test were compared with 22 age-matched controls (11 boys and 11 girls). Mean basal thyroxine 4 and triiodothyronine 3 values were in the normal ranges. All thyroid antibody titers were negative. Mean basal thyroid-stimulating hormone levels of subjects with Down syndrome were significantly higher than those of controls for all ages, even though there was a decline in thyroid-stimulating hormone levels in both groups. Peak thyroid-stimulating hormone response levels were significantly greater in the subjects with Down syndrome than in the controls. Longitudinal study of the 14 children with Down syndrome with an exaggerated thyroid-stimulating hormone response showed that the response remained exaggerated until the third year of life, when it declined to normal levels. Thyroid dysfunction during the growth spurt of infancy or delayed maturation of the hypothalamic pituitary thyroid axis are proposed mechanisms.

Analysis of Variance↗
PubMed2004

Graves' ophthalmopathy and atrophic thyroiditis: a case report.

Graves' ophthalmopathy (GO)--also known as thyroid-associated orbitopathy or ophthalmopathy--usually affects patients with Graves' disease. Antibodies stimulating the TSH receptor are thought to be involved in the pathogenesis of this important and disabling extra-thyroidal manifestation of Graves' disease. Less frequently, GO occurs in subjects who neither have nor have ever shown evidence of thyroid dysfunction ("euthyroid GO"), while the occurrence of GO in patients with autoimmune Hashimoto's thyroiditis is thought to be quite rare and has sporadically been reported. The late and abrupt occurrence of severe GO without hyperthyroidism in an 88-yr-old woman with primary myxedema due to atrophic thyroiditis must be considered as an exceptional event. In this patient, GO was combined with elevated titres of serum auto-antibodies directed against the TSH receptor, while serum levels of anti-thyroglobulin and thyroperoxidase antibodies were within the normal range or only occasionally slightly above the normal values.

Aged↗
PubMed1992

Transient thyrotoxicosis and persistent hypothyroidism due to acute autoimmune thyroiditis after interleukin-2 and interferon-alpha therapy for metastatic carcinoma: a case report.

A 59-year-old man with metastatic renal cell carcinoma developed symptomatic thyroid dysfunction following interleukin-2 (IL-2) and interferon-alpha (IFN-alpha) therapy. Thyroid evaluation prior to this therapy revealed evidence of subclinical Hashimoto's thyroiditis. Symptomatic thyrotoxicosis, including atrial fibrillation, developed after the initial two courses of intermittent intravenous bolus therapy with human recombinant IL-2 and IFN-alpha. At 4 weeks after initiation of immunotherapy, the thyroid antimicrosomal antibody (AMA) titer rose from 1:6,400 to 1:25,600; thyroid-stimulating immunoglobulin was negative. A technetium 99m-pertechnetate thyroid scan obtained while the patient was thyrotoxic showed diminished uptake in a symmetrically enlarged gland. The patient was temporarily treated with propranolol, digoxin, and quinidine. The atrial fibrillation quickly resolved, and thyrotoxicosis abated over the following 5 weeks, while the AMA titer rose further to 1:102,400. By 11 weeks after initiation of immunotherapy, hypothyroidism developed and persisted through two subsequent courses of cytokine therapy at Weeks 16 and 18. The tumor metastases partially responded to the immunotherapy. The patient has remained hypothyroid up to 27 weeks of follow-up. This case history suggests that IL-2 and IFN-alpha therapy may precipitate a fulminant autoimmune thyroiditis syndrome in a vulnerable patient with preexisting autoimmune thyroid disease.

Carcinoma, Renal Cell↗
PubMed2006

Pathology of the thyroid in severe acute respiratory syndrome.

The severe acute respiratory syndrome (SARS) epidemic started in November 2002 and spread worldwide. The pathological changes in several human organs of patients with SARS have been extensively described. However, to date, little has been reported about the effects of this infection on the thyroid gland. Femoral head necrosis and low serum triiodothyronine and thyroxine levels, commonly found in patients with SARS, raise the possibility of thyroid dysfunction. We have undertaken this study to evaluate for any potential injury to the thyroid gland caused by SARS on tissue samples obtained from 5 SARS autopsies. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay was performed to identify apoptotic cells. The follicular epithelium was found to be damaged with large numbers of cells exfoliated into the follicle. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay demonstrated many cells undergoing apoptosis. Follicular architecture was altered and showed distortion, dilatation, and collapse. No distinct calcitonin-positive cells were detectable in the SARS thyroids. In conclusion, both parafollicular and follicular cells were injured. This may provide an explanation both for low serum triiodothyronine and thyroxine levels and the osteonecrosis of the femoral head associated with patients with SARS. Apoptosis may play a role in the pathogenesis of SARS associated coronavirus infection in the thyroid gland.

Adult↗
PubMed1985

Thyroiditis: a clinical update.

Thyroiditis may be categorized as acute (suppurative), subacute (granulomatous or lymphocytic), or chronic (invasive fibrous or lymphocytic). Acute suppurative thyroiditis is typically caused by a bacterial infection and resolves with appropriate antibiotic treatment. The subacute thyroiditides are characterized by spontaneously resolving hyperthyroidism associated with low radioiodine uptake, often followed by transient hypothyroidism. Neck pain is the initial symptom in subacute granulomatous thyroiditis, and the disorder recurs only in a minority of patients. Subacute lymphocytic thyroiditis is typically painless, often occurs in the postpartum period, and is being increasingly recognized in the Great Lakes area of the United States. Invasive fibrous thyroiditis (Riedel's struma) is exceedingly rare, often mimics carcinoma, and is associated with extracervical foci of fibrosclerosis. Chronic lymphocytic (Hashimoto's) thyroiditis, an organ-specific autoimmune disease, occurs in at least 2% of women. Although the disorder often produces hypothyroidism, the type of thyroid dysfunction present in patients with Hashimoto's disease reflects the character of the dominant thyroid autoantibody--that is, destructive, blocking, or stimulatory.

Acute Disease↗
PubMed1999

Prevalence and significance of thyroid autoantibodies in patients with chronic hepatitis C virus infection: a prospective controlled study.

OBJECTIVE: To clarify controversies on the prevalence and clinical significance of thyroid autoimmunity in hepatitis C virus (HCV) infection. DESIGN: A prospective controlled and follow-up study. PATIENTS AND MEASUREMENTS: Serum thyroid microsomal antibody (TMA) and thyroid stimulating hormone were assayed and compared in a consecutive, unselected series of 130 patients with chronic HCV infection, 130 sex/age (+/- 2 years)-matched patients with chronic hepatitis B virus (HBV) infection and 260 matched normal controls. RESULTS: The prevalence of thyroid autoantibodies in male patients with chronic HCV was < 2%. The prevalence of TMA (< 1:400) in female patients with chronic HCV infection was significantly higher than that of HBV controls (22.1 vs. 1.6%; P < 0.001), and higher but not significant compared with normal controls (13.5%). However, the trend of increasing prevalence with age in normal controls was not observed in HCV patients. TMA seropositive female HCV patients were not different from seronegative counterparts in age, duration of infection, HLA haplotype, associated autoantibodies and liver histology but had a significantly higher prevalence of genotype 1b/2b mixed infection (P < 0.01) and anti-GOR (P < 0.05). Of the 23 HCV patients seropositive for thyroid autoantibodies, seven had Hashimoto's thyroiditis, two had Graves' disease and three had received subtotal thyroidectomy. During follow-up, four of 15 female patients showed a 14-16-fold increase in TMA titre and one developed hyperthyroidism. Patients with thyroid autoantibodies did not show a propensity to develop thyroid dysfunction during interferon therapy. CONCLUSIONS: These results suggest a weak association between HCV and thyroid autoimmunity in females. As in the ordinary population with thyroid autoantibodies, they should be evaluated for thyroid status and be followed-up if thyroid autoimmunity is evident. However, seropositivity of thyroid autoantibodies is not a contraindication to interferon therapy.

Adult↗
PubMed2002

Complement activation in postpartum thyroiditis.

BACKGROUND: Postpartum thyroid dysfunction (PPTD) develops in 50% of pregnant women who have raised levels of circulating thyroid peroxidase autoantibodies (TPOAb) at booking. Although these antibodies are able to activate the complement cascade in vitro, it is not known whether complement activation plays any role in the pathogenesis of this disease. AIM: To investigate potential and actual activation of the complement system in women with postpartum thyroiditis. DESIGN: Complement activation was monitored on a weekly basis in 24 postpartum women who had raised TPOAb at 16 weeks gestation, attending an antenatal clinic in Mid-Glamorgan, Wales. METHODS: ELISA procedures were used to measure both in-vitro complement C3 activation by TPOAb and circulating terminal complement complexes (TCC) in serum. RESULTS: Higher levels of bioactive TPOAb activity were seen in women who developed PPTD when compared to those who did not. However, TCC remained undetectable in serum throughout the period of study. CONCLUSIONS: In PPTD, despite the presence of circulating bioactive TPOAbs, the extent of complement activation is inadequate to cause detectable increases in peripheral blood TCC, suggesting that the complement system may not play a major role in PPTD pathogenesis.

Autoantibodies↗