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PubMed2006

Optimizing therapy of seizures in patients with endocrine disorders.

Endocrinologic disorders, such as thyroid dysfunction or diabetes, may be comorbidities in patients with epilepsy. The choice of medication should address such comorbidities wherever possible. Enzyme-inducing antiepileptic drugs (AEDs) such as carbamazepine, phenytoin, barbiturates, and oxcarbazepine among the new AEDs, may reduce the levels of free and total thyroxin. However, clinically relevant thyroid dysfunction owing to AED treatment is rare. Nevertheless, there are now better alternative AEDs with similar efficacy to the classic first-line drugs but without their enzyme-inducing properties. Such drugs should be considered in cases of thyroid dysfunction to reduce the likelihood of iatrogenic adverse effects. Sufficient data on some of the new AEDs to support this hypothesis are, however, still lacking and urgently needed. Several reports have pointed out the possible negative impact of valproate on glucose and insulin metabolism and particularly on body weight. The increased risk for development of polycystic ovarian syndrome remains a matter of debate but is certainly another argument for the development of alternative agents. The group of new AEDs offers some potential candidates. Topiramate is the AED that is most likely to lead to weight loss; this may be perceived as a positive side effect in some patients. This review summarizes the data on the possible impact of AEDs in endocrinological disorders, concentrating on thyroid dysfunction, insulin/glucose metabolism, and body weight.

Anticonvulsants↗
PubMed2004

[Mood disorders, psychopharmacology and thyroid hormones].

For more than 40 years thyroid hormones and mood disorders have been associated. Some psychiatric symptoms are produced by thyroid illnesses and there is a frequent association of thyroid dysfunction with mood disorders. Therefore, routine thyroid function assessment in patients with mood disorders and the treatment of sub-clinical thyroid dysfunctions is recommended. The usefulness of adding thyroid hormones to antidepressive treatment in euthyroid patients to obtain a potentiation effect has been probed repeatedly. The most common strategy is potentiation with T3, but high doses of T4 have been also used in patients with resistant depression. Thyroid hormones exert their action in the central nervous system through a variety of mechanisms: modulation of gene expression of several groups of proteins, some of them with known physiopathological implications in mood disorders and the influence over serotonin and noradrenergic neurotransmission, known to be one of the modes of action of antidepressants. Finally, it is also important to stress the complex relationship between psychiatric drugs, deiodinases and thyroid hormones, that can potentially help to understand the mechanisms of action of these drugs.

Central Nervous System↗
PubMed1996

Thyroid function and immune profile in rheumatoid arthritis. A controlled study.

The aim of our study was to determine the prevalence of thyroid dysfunction and autoimmune abnormalities in rheumatoid arthritis (RA) and to further investigate the possible association between D-penicillamine and autoimmune thyroiditis. For this purpose, one hundred and one unselected consecutive patients with RA and 70 age and sex matched controls were studied prospectively. Evaluation included a complete history and physical examination with special attention to symptoms suggestive of thyroid pathology, routine laboratory and serologic immune profile, plus determination of serum levels of thyroxine (T4), triiodothyronine (T3), thyroid stimulating hormone (TSH), antibodies to thyroid peroxidase (AbTPO) and TSH receptor antibodies (TRAB). Serum thyroxine binding globulin (TBG) was measured in all subjects with high thyroid hormone levels, whereas free T3 and T4 concentrations were determined in all individuals with abnormal T3, T4, TSH or TBG. Six patients with hyperhyroidism, 3 with hypothyroidism and 1 with the euthyroid hyperthyroxinemia (EH) syndrome were found, whereas four of the controls had hyperthyroidism. Thirteen patients and 6 controls had high AbTPO levels whereas no one had high TRAB. No association was detected between thyroid abnormalities and any serologic RA finding. Furthermore, no correlation between thyroid dysfunction and elevated AbTPO's was found. A relatively high prevalence of thyroid dysfunction (9,9%) and subclinical autoimmune thyroiditis (12,9%), the latter indicated by elevated AbTPO's, was found in our RA patients. These figures were higher than those in the control group (5,7% and 8,6% respectively), but the difference did not reach statistical significance. Of further interest may be our finding that, despite anecdotal reports blaming D-penicillamine for cases of autoimmune thyroiditis, the incidence of the latter was similar among recipients and nonrecipients of the drug. Similarly, TRAB were not detected in any patient treated with D-penicillamine.

Adult↗
PubMed2000

Long-term interferon beta-1b therapy for MS: is routine thyroid assessment always useful?

BACKGROUND: The authors previously reported on the development of thyroid dysfunction and autoimmunity during 1-year treatment of patients with MS with interferon-beta 1b (IFN beta-1b). OBJECTIVE: To evaluate the evolution of incident thyroid disease and the possible development of more thyroid disease during longer term therapy. PATIENTS: The authors studied 31 patients (aged 34 +/- 7 years; 21 women) with relapsing-remitting MS during 3 years of IFN beta-1b treatment. Systematic thyroid assessment was performed every 3 or 6 months, depending on the development of thyroid disease. RESULTS: After the first year of IFN beta-1b treatment, no further cases of thyroid disease were observed. Among the six patients with early incident subclinical hypothyroidism, thyroid dysfunction persisted only in those with baseline autoimmune thyroiditis (n = 2). The three patients who developed transient hyperthyroidism remained euthyroid throughout the treatment course. A positive autoantibody titer was continually detected in only two out of five patients without baseline autoimmunity. CONCLUSIONS: The risk of thyroid disease seems related to IFN beta-1b treatment during the first year only, particularly in patients with preexisting thyroiditis. Furthermore, incident thyroid dysfunction is generally transient and mild in degree. Indeed, we recommend a routine systematic thyroid assessment only in patients with baseline thyroiditis. During the first year of therapy, serum thyroid-stimulating hormone measurement should suffice as first line test; a systematic thyroid assessment is only useful for those patients with incidental and persistent dysfunction. Further studies with many patients will be necessary to confirm our suggestions as broad clinical guidelines.

Adult↗
PubMed1994

Serum thyroglobulin: an early indicator of autoimmune post-partum thyroiditis.

OBJECTIVE: The aim of this study was to assess whether autoimmune thyroid damage in post-partum thyroiditis was accompanied by a significant rise in the concentration of thyroglobulin in the serum and whether its measurement could be useful in the prediction of the risk and severity of an episode of post-partum thyroid dysfunction. PATIENTS: Fifty-one women, who had taken part in a larger survey of post-partum thyroiditis, were selected at random for this study. Fourteen women without elevated circulating thyroid autoantibodies and 21 with raised thyroid autoantibodies remained euthyroid throughout the post-partum year. A third group of 14 women had raised thyroid autoantibody levels and showed one or more episodes of thyroid dysfunction during the course of the first year post partum. MEASUREMENTS: Thyroid autoantibodies were measured by ELISA, free T3 and free T4 by the Amerlex M method and TSH by an immunoradiometric method. Serum thyroglobulin was measured by a method free from interference by circulating endogenous thyroglobulin autoantibodies. Thyroid ultrasonography was performed using a General Electric RT3600 scanner operating at 7.5 MHz. RESULTS: Fourteen control women had a mean serum thyroglobulin concentration of 3.3 micrograms/l (SD 4.4; range < 1-12 micrograms/l; 95% confidence interval up to 6.0 micrograms/l). Twenty-one thyroid autoantibody positive euthyroid women had a mean serum thyroglobulin level of 5.8 micrograms/l (SD 6.2; range < 1-36 micrograms/l) which was not significantly different from that seen in the control group. Sixteen thyroid autoantibody positive women who showed one or more episodes of thyroid dysfunction during the post-partum period had a mean serum thyroglobulin of 31 micrograms/l (SD 24.8; range up to 88 micrograms/l) and this was significantly elevated compared with both the control and antibody positive groups (P < 0.001). Serum thyroglobulin concentrations at 3 months post partum correlated with the degree of post-partum hypothyroidism (as indicated by the maximum TSH and the minimum free thyroxine concentrations post partum) and, in those cases where thyroid ultrasound examinations were performed, with the degree of lymphocytic infiltration of the thyroid gland. CONCLUSIONS: The data presented in this paper confirm the destructive nature of post-partum thyroiditis and indicate that the measurement of serum thyroglobulin concentration could assist in the identification of those women at risk of post-partum thyroiditis.

Autoantibodies↗
PubMed2002

Postpartum thyroiditis in India: prevalence of postpartum thyroiditis in Kashmir Valley of Indian sub-continent.

Various studies have reported a spectrum of thyroid dysfunction in the postpartum period. Postpartum thyroiditis is a syndrome of thyroid dysfunction that occurs in the first year after parturition. Prevalence of postpartum thyroiditis has been reported to vary from 3 to 6 percent in different regions of the world. Kashmir Valley is inhabited by a relatively homogeneous racial group and the Valley has been documented to have significant iodine deficiency. We studied the prevalence and pattern of postpartum thyroiditis in an urban region of this Valley. 120 women were registered within first month of postpartum period for the study along with one hundred controls. Of these 120 women, 104 reported for follow-up at 3 months postpartum and 106 reported for follow-up at 6 months postpartum. Initial and subsequent clinical details at follow-up were recorded on a pre-determined questionnaire. Overall, postpartum thyroiditis (PPT) was seen in 8 (7%) study subjects. Of these 8 patients with PPT, 4 had biochemical evidence of thyrotoxicosis at first month, 3 developed biochemical thyrotoxicosis at 3-month follow-up while as one study subject developed thyrotoxicosis at 6 months. Most of these subjects were antithyroid antibodies (anti-microsomal and anti-thyroglobulin) positive. We conclude that iodine deficient status of the community doesn't seem to influence the incidence of PPT.

Antibodies, Antinuclear↗
PubMedDate not supplied

[On the method of express-diagnostics of thyroid gland dysfunctions].

The method of express-diagnostics of thyroid diseases on a degree of moisture of the skin integument which is one of clinical attributes of hypothyroidism (a skin is dry, shelled, with sites of keratinization) and hyperthyroidism at which the return picture is observed, i.e. the (increased humidity of a skin is offered. At the same time as a parameter describing a degree of moisture of skin is a relative humidity of the air environment which are taking place above the skin integument in conditions of thermodynamic equilibrium. The instrument is a hermetic glass in which the sensor of humidity is mounted. Studies on the definition of threshold levels of parameter for several groups of patients with clinically confirmed diagnoses of diseases of a thyroid are carried out.

Case-Control Studies↗
PubMed1988

Screening for thyroid disease in a primary care unit with a thyroid stimulating hormone assay with a low detection limit.

In a study at a primary care centre in a predominantly rural area of Sweden the records of all patients with established thyroid disease were scrutinised and 2000 consecutive adult patients screened with an immunoenzymometric thyroid stimulating hormone assay. The aims of the study were fourfold: firstly, to assess the total burden of thyroid disease in primary care centres in Sweden; secondly, to assess the efficacy of clinical diagnosis of the disease in unselected populations of patients; thirdly, to assess the efficacy of clinical evaluation of treatment with thyroxine; and, lastly, to see whether a single analysis of the serum thyroid stimulating hormone concentration by recent methods would be enough to identify an abnormality of thyroid function. Of the roughly 17,400 adults in the study community, 111 women and 10 men were being treated for thyroid disease. Screening detected 68 patients (3.5%) not receiving thyroxine who had a serum thyroid stimulating hormone concentration of 0.20 mU/l or less, all of whom were followed up clinically. Fifty of these patients were also studied biochemically during follow up. Only nine of the 68 patients had thyroid disease (three with thyrotoxicosis requiring treatment), no evidence of the disease being found in the remainder. Sixteen patients had spontaneous hypothyroidism requiring treatment, and neither these nor three patients with thyrotoxicosis had been detected at the preceding clinical examination. Of 35 patients in whom thyroid disease was suspected clinically at screening, none had laboratory evidence of thyroid dysfunction. In this series 1.3% of all women in the study community (2.6% of all 50-59 year olds) and 0.1% of the men were being treated for thyroid disease at the primary care centre, roughly 1.0% of adults subjected to screening were found to have thyroid disease requiring treatment, and most patients with a thyroid stimulating hormone concentration of 0.20 mU/l or less did not have thyroid dysfunction. It is concluded that measuring the basal serum thyroid stimulating hormone concentration by present methods is insufficient for the biochemical assessment of thyroid dysfunction in unselected populations.

Cross-Sectional Studies↗
PubMed2005

Hypothyroidism might be related to breast cancer in post-menopausal women.

An association between breast cancer and thyroid (autoimmune) diseases or the presence of thyroid peroxidase antibodies (TPOAb; a marker of thyroid autoimmune disease) has been suggested. However, little is known about whether women with thyroid (autoimmune) diseases are at increased risk for developing breast cancer. This cross-sectional and prospective cohort study investigated whether the presence of TPOAb or thyroid dysfunction is related to the presence or development of breast cancer. An unselected cohort of 2,775 women around menopause was screened for the thyroid parameters thyrotropin (TSH), free thyroxine (FT(4)), and TPOAb during 1994. Detailed information on previous or actual thyroid disorders and breast cancer, and on putative factors related to breast cancer and thyroid disorders, was obtained. Clinical thyroid dysfunction was defined by both abnormal FT4 and TSH, and subclinical thyroid dysfunction by abnormal TSH (with normal FT4). A TPOAb concentration >or= 100 U/ml was defined as positive (TPOAb(+)). The study group was linked with the Eindhoven Cancer Registry to detect all women with (in situ) breast cancer (ICD-O code 174) diagnosed between 1958 and 1994. Subsequently, in the prospective study, all women who did not have breast cancer in 1994 (n = 2,738) were followed up to July, 2003, and all new cases of (in situ) breast cancer and all cancer-related deaths were registered. Of the 2,775 women, 278 (10.0%) were TPOAb(+). At the 1994 screening, 37 women (1.3%) had breast cancer. TPOAbs were (independently) related to a current diagnosis of breast cancer (OR = 3.3; 95% CI 1.3-8.5). Of the remaining women, 61 (2.2%) developed breast cancer. New breast cancer was related to: (1) an earlier diagnosis of hypothyroidism (OR = 3.8; 95% CI 1.3-10.9); (2) the use of thyroid medication (OR = 3.2; 95% CI 1.0-10.7); and (3) low FT4 (lowest tenth percentile: OR = 2.3; 95% CI 1.2-4.6). In the first 3 years follow up, the relationship between FT4 and log-TSH was disturbed in women with a new breast cancer diagnosis. The presence of TPOAb was not related to breast cancer during follow-up. A direct relationship between thyroid autoimmunity and breast cancer is unlikely. Hypothyroidism and low-normal FT4 are related with an increased risk of breast cancer in post-menopausal women. Studies are needed to clarify the origins of this possible association.

Breast Neoplasms↗
PubMed2003

A prospective study of thyroid function, morphology and autoimmunity in young patients with type 1 diabetes.

OBJECTIVE: Thyroid autoantibodies (TA) and thyroid ultrasonography are widely used in the diagnosis of autoimmune thyroid disease (AITD). However, we know little of the significance of having ultrasonographic abnormalities (USabn) without having any other signs of AITD. In a previous population-based study of 105 young patients with type 1 diabetes (T1DM) we found a high prevalence (42%) of USabn. In the present study we evaluate the development of both USabn and TA in a 3-Year follow-up of this cohort. DESIGN: Of the 105 previously investigated children and adolescents with T1DM (aged 5-21 Years), 101 were re-examined. Serum concentrations of tri-iodothyronine (T(3)), thyroxine (T(4)), TSH, thyroid peroxidase antibodies (TPOab) and thyroglobulin antibodies (Tgab), as well as thyroid size and morphology were determined in all patients. RESULTS: During the 3 Years follow-up period, the prevalence of thyroid dysfunction increased from 5 to 8%, the prevalence of TPOab was unchanged at 13%, while the prevalence of Tgab decreased from 14 to 7%. The prevalence of USabn increased from 42 to 49%. Most patients presented USabn at both examinations. Patients with USabn had a higher prevalence of TA than those without USabn (P=0.038) and higher serum levels of TSH (P=0.027). All patients with thyroid dysfunction presented with USabn. However, many patients with USabn had no other signs of AITD. CONCLUSIONS: A high prevalence of thyroid dysfunction, TA and thyroid USabn were found in young patients with T1DM. Thyroid USabn was a sensitive but non-specific marker of AITD and is therefore unsuitable for screening purposes. Instead, we recommend regular screening using serum TSH in the follow-up of young diabetic patients.

Adolescent↗
PubMed1996

Cytokines and thyroid function.

Cytokines play a crucial role in autoimmune thyroid disease (ATD) through various mechanisms. They are produced in the thyroid by intrathyroidal inflammatory cells, in particular lymphocytes, as well as by the thyroid follicular cells (TFC) themselves and may thus act in a cascade to enhance the autoimmune process (Fig. 1). Cytokines upregulate the inflammatory reaction through stimulation of both T and B cells, resulting in antibody production and tissue injury. In addition, intrathyroidal cytokines induce immunological changes in TFC including enhancement of both major histocompatibility complex (MHC) class I and class II molecule expression, and upregulation of adhesion and complement regulatory molecule expression. Cytokines can also modulate both growth and function of TFC and have a role in extrathyroidal complications of ATD, most importantly thyroid-associated ophthalmopathy (TAO), where they induce fibroblast proliferation and enhance the production of glycosaminoglycans (GAG), resulting in proptosis and the other clinical features of the disease. In addition to these effects, exogenous administration of cytokines has been associated with impairment of thyroid function ranging from the appearance of autoantibodies alone to the development of frank thyroid dysfunction. Cytokines have also been implicated in subacute thyroiditis (SAT) and amiodarone-induced thyroid dysfunction, as well as in thyroid function abnormalities occurring in patients with non-thyroidal illnesses (NTI). Genetic variations in cytokine genes represent potential risk factors for ATD, and disease associations have been described for polymorphisms in IL-1ra and TNF beta genes. Recent experimental evidence suggests the possibility of novel cytokine-based therapeutic approaches for ATD and its complications, in particular TAO.

Animals↗
PubMed1992

The fetal thyroid: normal and abnormal sonographic measurements.

The thyroid of 31 fetuses at low risk for perinatal thyroid disease were evaluated sonographically. The transverse width and circumference of the fetal thyroid was measured prospectively to provide normative values for each gestational age. In addition, the thyroid of 23 fetuses at risk for thyroid disease were examined sonographically and compared to the control group. At birth, 18 of the neonates had no evidence of thyroid dysfunction, whereas 5 newborns had goiters and abnormal thyroid function. The fetal thyroid measurements for these 5 neonates were above the upper limit of the 95% confidence interval compared to the control group. The other 18 fetuses in the group at risk for thyroid disease but without evidence of thyroid dysfunction at birth had fetal thyroid measurement within the normal range.

Female↗
PubMed2004

Adverse effects of mercuric chloride on thyroid of mice, Musculus albinus and pattern of recovery of the damaged activity.

The protective role of "essentiale phospholipids" (EPL) on mercury induced thyroid dysfunction with special reference to cholesterol, thyroid peroxidase and thyroxine activity in mice were investigated. The animals were treated with 0.5 ml/day of 0.5 ppm aqueous mercuric chloride for a period of 7, 14 and 21 days. For the recovery 175 mg of EPL was given to mice (already treated with HgCl2) for a period of 7, 14 and 21 days. Daily treatment of HgCl2 for 7, 14 and 21 days decreased serum cholesterol, TPO and T4 activity. Simultaneous administration of EPL (25 mg/mice) restored thyroid function in mice by maintaining serum thyroid hormone concentration almost normal. It increased serum cholesterol, TPO and T4 activity. It appears that the protective effect of EPL against HgCl2 induced thyroid dysfunction is mediated through its antioxidative action.

Animals↗
PubMed1999

[Autoimmune thyroid disease induced by interferon therapy].

Interferon therapy, widely used in chronic viral hepatitis and in various malignant diseases, has been known to induce autoimmune phenomena, the most frequent being autoimmune thyroid disease. We have studied the human leukocyte antigen (HLA) in patients who developed autoimmune thyroid dysfunction after interferon-alpha therapy for chronic hepatitis C. Seventeen of 439 patients (3.9%) developed symptomatic autoimmune thyroid dysfunction after interferon-alpha therapy, including nine cases of hyperthyroidism and eight cases of hypothyroidism. The incidence of HLA-A2 in those patients was significantly higher than that in general population in Japan. The present results suggest that HLA-A2 is associated with interferon-alpha therapy-induced autoimmune thyroid dysfunction in patients with chronic hepatitis C.

Autoimmune Diseases↗
PubMed2005

Thyroid autoimmunity in chronic urticaria.

BACKGROUND: Chronic urticaria (CU) is an autoimmune process in some patients. An association between CU and autoimmune thyroid disease has also previously been proposed. Our group has identified functionally significant histamine-releasing autoantibodies in one subset of CU patients (subset 1), predicted by positive autologous intradermal serum tests and positive histamine release from donor basophil leucocytes in vitro. Sera from a second subset of patients (subset 2), all of whom had positive autologous intradermal serum tests, failed to release histamine from donor basophils. A final disease subset (subset 3) has no identifiable skin reactivity (negative autologous serum skin test) or in vitro histamine releasing activity. OBJECTIVES: In order to examine further the possible relationships between thyroid autoimmunity, thyroid dysfunction and CU, we have examined thyroid autoantibodies and thyroid-stimulating hormone (TSH) levels (an indirect measure of thyroid dysfunction) in the three CU subsets. PATIENTS/METHODS: We studied 182 patients (69% female), of whom 90 had a positive autologous intradermal serum test. RESULTS: Eighteen skin test-positive and four skin test-negative patients had thyroid microsomal antibodies (TMA). TSH outside the normal range was found in 13 skin test-positive and one skin test-negative patient. These findings represent clustering of TMA positivity [risk ratio (RR) 4.06, 95% confidence interval (CI) 1.56-10.6] and of abnormal thyroid function (RR 15.5, CI 2.07-11.6) among the skin test-positive patients. However, in the overall study group an elevated TSH was present in seven patients (3.8%, CI 1.6-7.8) comparable to the 5% expected prevalence in the community. Thyroglobulin antibodies (TGA) were present in two of 182 patients. CONCLUSIONS: There were significant differences between skin test-positive and skin test-negative patients with regard to autoimmune thyroid disease. Evidence for autoimmune thyroid disease and abnormal thyroid function was largely found among the skin test-positive patients, supporting the theory of an autoimmune aetiology in this group.

Adolescent↗
PubMed1983

[The effect of nonthyroidal diseases on the serum hormone level of the thyroid gland function regulation cycle].

Thyroid hormone serum concentrations were measured in clinically apparently euthyroid patients suffering from diseases that have symptoms in common with thyroid dysfunction. The diseases investigated were: anorexia nervosa (n = 13), myocardial infarction (n = 13) cirrhosis of the liver (n = 19), terminal renal insufficiency (n = 30) and rheumatoid arthritis (n = 14). In each group, the patients were divided into groups according to the degree of their disease. A relative decrease in 3,5,3'-triiodothyronine (TT3) serum levels is the most pronounced effect of all the non-thyroidal ailments investigated. Individual observations show that total and free thyroxine levels can also be lowered by some acute illnesses. Moreover, the extent of the decrease in TT3 serum levels depends significantly on the severity of the non-thyroidal illness. This phenomenon was observed in all ailments investigated. Based on our findings it is concluded that the diagnosis of thyroid dysfunction may be extremely difficult in many non-thyroidal illnesses. This study should help the clinician to evaluate laboratory hormone data correctly in respect to the diagnosis of thyroid dysfunction in patients with non-thyroidal illnesses.

Adolescent↗
PubMed1995

Effects of interleukin-1 alpha administration on pituitary-adrenal and pituitary-thyroid axes function of patients with ovarian cancer.

We monitored pituitary, adrenal, and thyroid function in 21 women who had recurrent ovarian cancer and who received interleukin-1 alpha (IL-1 alpha) before and after carboplatin. Serum cortisol, corticotropin, thyroxine, and thyrotropin were measured in the morning before and at the end of each treatment cycle. Serum corticotropin levels were suppressed in many patients despite a normal simultaneous serum cortisol; thyrotropin tended to rise with declining thyroxine levels after prolonged IL-1 alpha administration. However, serum cortisol and thyroxine remained within the normal range at all times, in all patients. Thyroid dysfunction consistent with thyroiditis was seen in one patient. We conclude that administration of IL-1 alpha as currently used in clinical studies does not create significant thyroid or adrenocortical dysfunction.

Female↗
PubMed2002

Serum concentrations of tumour necrosis factor-alpha (TNF-alpha) and soluble TNF-alpha receptor p55 in patients with hypothyroidism and hyperthyroidism before and after normalization of thyroid function.

BACKGROUND: Tumour necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. Receptors for TNF-alpha have been demonstrated in thyroid follicular cells and TNF-alpha and its receptors have been implicated in the cytotoxic mechanisms that characterize the thyroid destruction in autoimmune thyroid disease. In patients with Graves' disease, serum levels of TNF-alpha have been reported to be elevated and administration of TNF-alpha to humans has been shown to induce hormonal alterations resembling those seen in the nonthyroidal illness syndrome. OBJECTIVE: To evaluate serum concentrations of TNF-alpha and the soluble receptor for TNF-alpha (sTNFR-I) in a group of patients with thyroid dysfunction before and after normalization of thyroid function with appropriate therapy. DESIGN: We studied 20 patients with hypothyroidism (18 women and 2 men, mean age +/- SD, 48.8 +/- 16.1 years) and 20 patients with hyperthyroidism (14 women and 6 men, age 44.6 +/- 15.9 years). Patients were assessed at the time of diagnosis and again after normalization of thyroid function tests with appropriate therapy. A group of 20 healthy subjects (15 women and 5 men, age 44.9 +/- 15.1 years) were also studied as a control group. SETTING: All subjects were ambulatory and were studied as outpatients during visits to the endocrinology clinic. MEASUREMENTS: Serum concentrations of free T4 (FT4), total T3, TSH, TNF-alpha and sTNFR-I were measured in all subjects. TNF-alpha and sTNFR-I were measured using a quantitative enzyme immunoassay. RESULTS: In patients with hypothyroidism serum concentrations of TNF-alpha (3.17 +/- 1.18 pg/ml) and sTNFR-I (1273 +/- 364 pg/ml) were significantly higher than those found in controls (2.42 +/- 0.76 pg/ml, P < 0.05, and 971 +/- 235 pg/ml, P < 0.01, respectively). Normalization of thyroid function with l-thyroxine therapy did not significantly modify TNF-alpha or sTNFR-I levels. There were no differences in pre- and post-therapy values of TNF-alpha and sTNFR-I in patients with autoimmune (n = 14) or nonautoimmune (n = 6) hypothyroidism. Before therapy, patients with hyperthyroidism showed elevated serum concentrations of TNF-alpha (3.36 +/- 1.21 pg/ml; P < 0.01) and sTNFR-I (2274 +/- 579 pg/ml; P < 0.001) in relation to the control group. Treatment of hyperthyroidism was accompanied by a normalization of TNF-alpha levels (2.46 +/- 0.89 pg/ml; P < 0.001) and by a significant decrease in sTNFR-I concentrations (1369 +/- 475 pg/ml; P < 0.001). Post-therapy levels of TNF-alpha and sTNFR-I showed a significant correlation with loss of weight (r = 0.674, P < 0.01, and r = 0.629, P < 0.01, respectively) in hypothyroid patients. No correlation between these parameters was found in the group of patients with hyperthyroidism. CONCLUSIONS: In summary, these results confirm the relevance of activation of the TNF-alpha system in patients with thyroid dysfunction, as high plasma concentrations of TNF-alpha and sTNFR-I have been demonstrated in patients with hypothyroidism or hyperthyroidism. Treatment of hyperthyroidism is accompanied by a significant reduction in the previously elevated concentrations of both TNF-alpha and sTNFR-I. However, these changes are not seen when normalizing thyroid function in patients with hypothyroidism.

Adult↗