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PubMed1992

Prevalence and characteristics of post-partum thyroid dysfunction: results of a survey from Toronto, Canada.

In order to determine the prevalence of post-partum thyroid dysfunction in our region, 1,376 randomly selected mothers were enrolled immediately post-partum and followed prospectively over a 2 year period in a large single-center survey. Beginning at delivery, sequential clinical and laboratory assessments were conducted at 6-8 week intervals up to 1 year post-partum and a questionnaire was administered at 3 months post-partum. Among the 1,376 mothers who qualified for entry into this study, 495 (36%) completed at least 3 months follow-up and 300 (22%) completed at least 1 year of follow-up. Abnormalities in post-partum thyroid function (PTD) were detected in 82 of the 1,376 enrolled mothers for an overall minimum prevalence rate of 6.0%. Hyperthyroidism confirmed to be associated with a low 24h radioactive iodine thyroid uptake (RAIU), compatible with the post-partum painless thyroiditis syndrome (PPT) was documented in 44 (3.2% minimum prevalence of typical PPT) of which 39 (89%) had a typical biphasic (hyperthyroid to hypothyroid) PTD while 5 (11%) had only a hyperthyroid phase with a suppressed RAIU without a subsequent hypothyroid phase. Another 17 (1.2%) had transient hyperthyroidism likely due to PPT but were not confirmed by an RAIU test and did not evolve to a detectable hypothyroid phase; and, 17 mothers (1.2%) had hypothyroidism between 5-7 months post-partum without preceding hyperthyroidism, resulting in an overall minimum prevalence of 5.7% for all variants of PPT. Graves' hyperthyroidism occurred in 3 (0.2%) and toxic nodular goiter was present in 1 (0.07%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Thyroid dysfunction in Down's syndrome.

One hundred and sixteen children with Down's syndrome, living in the community, were examined for clinical or laboratory evidence of thyroid dysfunction. Three were hypothyroid and one was hyperthyroid. Twenty eight (29%) had thyroid autoantibodies. Autoimmune conditions were present in first or second degree relatives of 35 (30%) of the children, and in 17 (15%) this was a thyroid disorder. The families of normal control children also showed a 30% incidence of overt autoimmune conditions, and 19 (16%) families showed overt thyroid disease.

Adolescent↗
PubMed1988

Radioactive iodine thyroid uptake in patients with amiodarone-iodine-induced thyroid dysfunction.

Amiodarone, an iodine-rich drug, represents at the present, at least in Europe, one of the most common sources of iodine-induced thyroid dysfunction. The drug may induce both hypothyroidism and thyrotoxicosis. In spite of the large iodine intake occurring during amiodarone therapy, 131I thyroid uptake is detectable in patients with amiodarone-iodine-induced hypothyroidism, irrespective of the presence or absence of underlying thyroid disease. In contrast, in patients with amiodarone-iodine-induced thyrotoxicosis, 131I thyroid uptake is normal or even elevated in those with co-existent underlying thyroid disorders, whereas it is very low in those with an apparently normal thyroid gland. Perchlorate discharge test was performed in 8 patients with hypothyroidism and in 5 patients with hyperthyroidism induced by amiodarone: a positive test was found in all hypothyroid patients and a negative test in all hyperthyroid patients.

Adult↗
PubMed1990

[The role of TSH psychological and somatic changes in thyroid dysfunctions].

The characteristic psychic and somatic features found in patients with overt hyper- or hypothyroidism are usually attributed to elevated or diminished levels, respectively, of thyroid hormones. This concept does not sufficiently explain our previous investigations in which the same symptoms, albeit attenuated, were also seen in patients suffering from so-called latent disturbances of thyroid function. This state of disorder, however, exhibits normal concentrations of peripheral thyroid hormones. Only the response of thyroid-stimulating hormone (TSH) to thyrotropin-releasing hormone (TRH) stimulation is in accordance with the behaviour of the overt thyroid dysfunction and enables its differentiation from the euthyroid state. In this context, we investigated the question as to whether pathologic signs in thyroid disorders are correlated to alterations of peripheral thyroid hormones or to changes in the hypothalamus pituitary axis. Therefore, we investigated two groups of ten patients each who suffered from latent hyper- or hypothyroidism, respectively, and ten euthyroid controls. All were matched from sex and age. Endocrine function was estimated by TRH testing, TT3, TT4 and thyroxine binding globulin (TBG). Psychologic testing was performed by questionnaires concerning subjective somatic symptoms, emotional disturbances, psychomotoric performance, cognitive impairment and personality. Patients with latent hyperthyroidism were more subject to somatic symptoms and affective complaints than were those who had latent hypothyroidism. As compared with controls, there were significant differences in exhaustion and pain in the limbs and heart. In terms of affective complaints, patients were more depressive, anxious, touchy and irritable; their personalities showed a higher degree of emotional lability, excitement and irritability.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Thyroid dysfunction in individuals with Down syndrome.

A group of 138 community-based patients with Down syndrome were examined for evidence of autoimmune thyroid dysfunction at the time of their referral for routine health care services provided as part of a model program. Twenty-eight patients (20.3%) were found to have previously unrecognized hypothyroidism, and 2 patients (1.4%) had previously unrecognized hyperthyroidism. In addition, 66 patients were tested for thyroid autoantibodies, and 26 were found to have positive antimicrosomal and/or antithyroglobulin antibody test results. There was no statistically significant association between age or sex and the mean thyrotropin value or the presence of thyroid autoantibodies. The relationship between the mean thyroxine level and sex was mildly significant. Of the patients with hypothyroidism, 78.5% were female, and most were between the ages of 30 and 50 years. However, a higher-than-expected number of patients with autoimmune hypothyroidism were under age 30 years. These findings highlight the lack of adequate health care services available to persons with Down syndrome who live in the community. All persons with Down syndrome must undergo regular clinical and laboratory screening for the presence of thyroid disease.

Adolescent↗
PubMed1991

Elastase inhibitory activity in serum of patients with thyroid dysfunction.

Dermal elastic fiber fragmentation and decreased fiber density are characteristic cutaneous abnormalities in myxedema. We therefore evaluated elastase inhibitory activity in serum in thyroid dysfunctional states by measuring the protease inhibitor alpha 1-antitrypsin (A-1-AT), as well as by directly determining the inhibition of porcine pancreatic elastase activity. Overall there was a strong correlation between A-1-AT concentration and elastase inhibitory activity in serum (r = 0.95, P less than 0.001). Mean (+/- SE) A-1-AT concentrations were greatest in hyperthyroidism (39 +/- 3 mumol/L, n = 13), followed by normal controls (29 +/- 1, n = 11), subclinical hypothyroidism (27 +/- 2, n = 7), and hypothyroidism (25 +/- 1, n = 12). Concentrations of both A-1-AT and porcine pancreatic elastase inhibitory activity were significantly greater in subjects with hyperthyroidism than in the other groups (P less than 0.01). The correlations (r) between the overall free thyroxin (T4) index and A-1-AT and elastase inhibitory activity were 0.68 and 0.61, respectively (P less than 0.01), implying that free T4 variations account for 46% of the variance in A-1-AT concentrations and 37% of the variance in elastase inhibitory activity. We conclude that serum elastase inhibitory activity is increased in hyperthyroid patients.

Adult↗
PubMed1984

Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy.

Amiodarone, an iodine-containing drug used frequently in the treatment of cardiac arrhythmias and angina pectoris, has many effects on thyroid hormone metabolism, including decreasing the production of triiodothyronine (T3) and decreasing the clearance of thyroxine and reverse T3. These effects result in elevated serum thyroxine and reverse T3 concentrations and decreased serum T3 concentrations. In addition, iodine-induced hyperthyroidism or hypothyroidism may occur in patients chronically treated with amiodarone. This study is a retrospective analysis of the incidence of thyroid dysfunction in Lucca and Pisa, West Tuscany, Italy, and in Worcester, Massachusetts. Hyperthyroidism was a more frequent (9.6%) complication of amiodarone therapy in West Tuscany, where iodine intake is moderately low; hypothyroidism was more frequent (22%) in Worcester, where iodine intake is sufficient. In patients receiving chronic amiodarone therapy, clinically suspected hyperthyroidism is best confirmed by showing elevations in serum T3 or free T3 concentrations; hypothyroidism is best diagnosed by showing an elevated serum thyrotrophin concentration. Thyroid function should be carefully monitored in patients receiving amiodarone chronically, especially if they have goiter or Hashimoto's thyroiditis.

Adult↗
PubMed1987

Performance of direct equilibrium dialysis and analogue-type free thyroid hormone assays, and an immunoradiometric TSH method in patients with thyroid dysfunction.

Direct equilibrium dialysis and analogue-type radio-immunoassays for free triiodothyronine (FT3) and free thyroxine (FT4) in serum were compared in 168 subjects with various states of thyroid function. A good diagnostic efficacy for FT3 and FT4 by either type of assay was observed in hyperthyroidism. In hypothyroidism the free thyroid hormone assays, particularly the FT3 assays, performed diagnostically less well, partly because patients with mild disease were included in the study. No significant differences in the percentages of misclassifications of thyroid dysfunction patients by corresponding dialysis and analogue assays were found. We observed a good linear correlation between dialysis and analogue methods for FT3 (r = 0.98) and FT4 (r = 0.97) in this study comprising out-patients not suffering from severe non-thyroidal disease, known from earlier studies in this and other laboratories to interfere in these assays. It is concluded that analogue assays may be used on out-patients in whom severe systemic diseases are less frequent than in hospitalized patients. There are, however, other limitations to the use of analogue assays than systemic diseases. We observed two euthyroid patients with thyroxine auto-antibodies causing very high FT4 concentrations as determined by analogue assay; their dialysable FT4 concentrations were normal. We also tested a recently developed immunoradiometric serum TSH assay, which was found to perform well in primary hypo- and hyperthyroidism. Serum TSH was elevated in one patient hyperthyroid because of a TSH-producing pituitary adenoma, and within the reference limits in a patient with secondary hypothyroidism.

Adult↗
PubMed1988

Expression and regulation of c-erb-A mRNA from lymphocytes in patients with thyroid dysfunction.

To investigate the expression and the regulation of nuclear triiodothyronine (T3) receptor at the gene level, cellular(c)-erb-A mRNA isolated from lymphocytes in patients with thyroid dysfunction was examined by Northern gel analysis and dot blot hybridization using viral (v)-erb-A cDNA probe. Human lymphocytes contained c-erb-A mRNA (approximately 2.0 kilobase (kb) in length), and c-erb-A mRNA, which was determined by dot blot hybridization, was observed to be increased in hypothyroid patients but unaltered in hyperthyroid patients. The high level of c-erb-A mRNA may contribute in part to the increase in nuclear T3 receptor and these results suggest the presence of up-regulation of nuclear T3 receptor at the gene level in the lymphocytes of hypothyroid patients.

Cell Nucleus↗
PubMed1980

Postpartum lymphocytic thyroiditis in American women: a spectrum of thyroid dysfunction.

Six episodes of primary hypothyroidism followed pregnancy in five women. Within 6 months post partum, all were clinically hypothyroid, with a diffuse goiter of two or three times normal size, altered thyroid function tests (average thyroxine [T4] = 2.6 micrograms/dl, thyroid-stimulating hormone [TSH] = 58.2 microunits/ml), and elevated antithyroid antibodies. (All had antimicrosomal antibody titers of 1:6,400 or more.) After 5 more months, all patients had a decrease in antibody titer, resolution of symptoms, and recovery of thyroid hormone levels (average T4 = 7.3 micrograms/dl), although two patients had compensated hypothyroidism (their average TSH = 9.3 microunits/ml). Four patients had lymphocytic thyroiditis diagnosed by fine-needle aspiration biopsy. Despite the apparent transience of postpartum hypothyroidism, all five patients have chronic thyroid dysfunction: three women have persistent goiters (all less than twice normal size) and two have compensated hypothyroidism; one patient had previous Graves' hyperthyroidism, and two had recurrent transient hypothyroidism (at 21 months postpartum in one patient, and 5 months after another pregnancy in the other). Three women had transient, painless hyperthyroidism (average T4 = 16.1) before becoming hypothyroid: two patients within 8 weeks post partum, and the third patient at 20 months (preceding an episode of recurrent hypothyroidism). Previous reports of postpartum hypothyroidism have come from scattered locales abroad, and it is unclear whether local environmental factors are pathogenic. Nevertheless, this syndrome may, in general, have gone unrecognized and may be a significant cause of illness in postpartum women.

Adult↗
PubMed1991

Natural course of Graves' disease after subtotal thyroidectomy and management of patients with postoperative thyroid dysfunction.

The Natural course of Graves' disease after subtotal thyroidectomy was studied in 67 patients who had subtotal thyroidectomy for Graves' disease and did not receive any medical treatment for 8 to 12 years after surgery. Postoperative thyroid status was determined by serum free thyroxine (T4), free triiodothyronine (T3), and thyrotropin (TSH) levels in the first period (1 year after surgery), second period (3.9 +/- 1.0 years), and third period (8.8 +/- 1.5 years). Serum thyroid stimulating antibody (TSAb) and TSH binding inhibitor immunoglobulin (TBII) activities were also measured. A total of 53 patients (79%) changed thyroid status during the observation period. One year after surgery, 50 percent of euthyroid subjects developed abnormal thyroid function in the next period. Reversible latent hypothyroidism was the most common type of thyroid dysfunction seen in up to 46% of patients. Interestingly, hyperthyroidism and hypothyroidism that developed in the postoperative period were temporary disorders in most cases. Serum TSAb and TBII activities did not help predict the postoperative changes of thyroid status. Our study indicates that the instability of the thyroid function is common after subtotal thyroidectomy.

Adult↗
PubMed1984

[The conversion of thyroxine to triiodothyronine (T3) or to reverse T3 in patients with thyroid dysfunction].

In order to clarify the conversion of thyroxine (T4) to triiodothyronine (T3) or to reverse T3 (rT3), serum concentrations of T4, T3, rT3, thyrotropin (TSH), thyroxine-binding globulin (TBG) and values of T3 uptake (T3 U) were measured in 61 hyperthyroid and 31 hypothyroid patients, 8 patients with subacute thyroiditis, and 40 normal subjects. Then, free T4 index (FT4I), T3/T4, rT3/T4, and rT3/T3 ratio were calculated. The rT3/T3 ratio was high in the hyperthyroid patients and low in the hypothyroid patients compared with that in the normal subjects. The ratio was positively related to serum T4, T3, rT3 levels, and FT4I in the patients and normal subjects. The regression equation was represented by rT3/T3 = 0.015[T4] + 0.083. No influences of serum TBG and age on the rT3/T3 ratio were observed. Our results indicated that thyroid hormones themselves could regulate the conversion of T4 to T3 or rT3 by activating 5-monodeiodinase in hyperthyroidism and by activating 5'-monodeiodinase and suppressing 5-monodeiodinase in hypothyroidism. Serum rT3 level was a more sensitive parameter than serum T4 or T3 for evaluating thyroid dysfunction. During the treatment with methimazole (MMI) or L-thyroxine and the natural course of subacute thyroiditis, serum T4 levels and rT3/T3 ratios changed parallel to the regression line. However, once adverse effects of MMI occurred, those changed out of the line. From these results, we concluded that the relationship between serum T4 level and rT3/T3 ratio should be examined for adequate information concerning the peripheral conversion of thyroid hormones under various thyroid diseases.

Adolescent↗
PubMed1991

Malabsorption in thyroid dysfunctions.

Studies of intestinal absorptive functions in 11 hyperthyroid and 14 hypothyroid patients showed that steatorrhoea was common in hyperthyroid patients and rare in hypothyroid patients. D-xylose malabsorption was present in both the groups of thyroid disorders being more common in hypothyroid one. Occasionally vitamin B12 malabsorption was found in 2 hypothyroid patients. Jejunal mucosal changes were almost unremarkable. Both fat and carbohydrate malabsorption in both groups of patients appeared to be casually related to the thyroid dysfunction.

Adult↗
PubMed1990

[Problems in the diagnosis of thyroid dysfunction of the elderly adult].

Thyroid disfunction in the aged is often misdiagnosed either due to scanty symptoms, masking by other ailments or because function tests can be altered by extrathyroid causes such as chronic diseases, drugs or undernutrition. We surveyed 93 patients from 60 to 104 years old (73 females) living in geriatric homes. Most received at least 2 drugs for control of hypertension, coronary artery disease, diabetes, parkinsonism or psycho-organic deterioration. No clinical evidence of thyroid disfunction was found in 75 patients. T3 was 73.6 +/- 25.5 ng/dl, T4 7.3 +/- 1.8 micrograms/dl, TSH 2.8 +/- 0.9 uU/ml and rT3 32.2 +/- 16.3 ng/dl. Antimicrosomal antibodies were negative in all. Significant differences were found comparing these values with those obtained in 26 normal adults with mean age 39.9 years: T3 was lower and TSH and rT3 were higher in the elderly (p less than 0.0001). T3 decreased and rT3 increased in relation to age and males had significantly lower values of T3, T4 and TSH than females. Some evidence of thyroid disfunction was present in the remaining 18 patients: 9 had multinodular and/or positive antimicrosomal antibodies with euthyroid hormone levels; 6 had elevated T3, T4 and fT4 so hyperthyroidism was suspected; the remaining 3 patients had TSH levels above 20 uU/ml indicating the presence of hypothyroidism of which only one had some clinical manifestation. Thus, thyroid disfunction in the elderly + is not uncommon (3.2% of hyperthyroidism and 2.6% hypothyroidism in this series) in the absence of clinical manifestation. Treatment may improve the quality of life in these patients.

Aged↗
PubMed1987

Lipid peroxidation and free radical scavengers in thyroid dysfunction in the rat: a possible mechanism of injury to heart and skeletal muscle in hyperthyroidism.

This study was designed to determine if peroxidation of biomembrane lipid and the protective system can be modified by the change in oxidative metabolism induced by thyroid dysfunction. The free radical scavengers (i.e. cuprozinc cytosolic and mangano mitochondrial superoxide dismutases, glutathione peroxidase, and catalase), mitochondrial oxidative marker enzymes (cytochrome c oxidase and fumarase), and lipid peroxide were measured in liver, heart, soleus (slow oxidative), and extensor digitorum longus (fast glycolytic) muscles. Rats were rendered hyper- or hypothyroid for 4 weeks and then killed. Superoxide dismutases were detected by specific RIAs: catalase by polarography, and lipid peroxide by fluorimetry. Hypothyroid rats failed to grow, while hyperthyroid rats had hypertrophied hearts but no growth failure. An increase in lipid peroxide was observed in the soleus and heart muscles of hyperthyroid rats. This was accompanied by an increase in mitochondrial superoxide dismutase and oxidative markers. No such change was observed in either fast glycolytic muscle or liver. Glutathione peroxidase decreased in all tissues of hyperthyroid rats, and there was a parallel decrease in catalase in most tissues. On the other hand, hypothyroidism induced a reduction in oxidative markers and mitochondrial superoxide dismutase in heart and skeletal muscles, but only a marginal change in lipid peroxidation. The cytosolic superoxide dismutase did not change in relation to either oxidative metabolism or lipid peroxidation. These results suggest that the enhanced oxidative metabolism and decreased glutathione peroxidase in hyperthyroidism result in an increase in lipid peroxidation and, in slow oxidative and heart muscle, possible organ damage. No adverse reaction mediated by active oxygen species was found in hypothyroid rat tissues.

Animals↗
PubMed1984

A search for the mechanism underlying the altered MCV in thyroid dysfunction: a study of serum and red cell membrane lipids.

The mean red cell volume (MCV) is increased in hypo- and decreased in hyperthyroidism but the underlying cause(s) is unknown. In view of the well recognised alterations in serum lipids in thyroid dysfunction, we have examined the possibility that a corresponding alteration in the amount or distribution of lipids in the red cell membrane may account for the red cell volume changes. Our findings however do not support this hypothesis.

Adult↗
PubMed1990

Screening of geriatric patients for thyroid dysfunction with thyrotropin-releasing-hormone test, sensitive thyrotropin and free thyroxine estimation.

Hospitalized geriatric patients (N = 354) from an iodine-deficient area were screened with sensitive thyrotropin (TSH), free and total thyroxine (FT4, T4) and total triiodothyronine (T3) to determine the occurrence rate of clinical and subclinical thyroid dysfunction. The diagnostic value of the tests was compared to each other and to that of the thyrotropin-releasing-hormone test (TRH-test) in order to find the optimal first line screening test in geriatric patients. Clinical hyperthyroidism was found in 13, subclinical hyperthyroidism in 10, overt hypothyroidism in 6 and subclinical hypothyroidism in 8 cases. 20.6% of the patients were euthyroid but had subnormal TSH response to TRH, as a sign of possible thyroid autonomy. The low occurrence rate of clinical thyroid disorders (4.8%) does not justify the screening of geriatric patients in general, but the high probability of thyroid autonomy makes reasonable the investigation of every geriatric patient before iodine administration. Suppressed basal TSH and high FT4 were found to be both sensitive and specific in diagnosing clinical hyperthyroidism, but the predictive value was insufficient; elevated T4 and T3 are specific, but not sensitive. Basal TSH is sensitive, specific and has a good predictive value in diagnosing euthyroidism, whereas normal T4, FT4 or T3 are not specific enough for euthyroidism. Basal TSH is better as a first line test of thyroid function than FT4. A normal basal TSH confirms euthyroidism by itself. Other tests (TRH test, T4, FT4, T3) are necessary to elucidate the clinical importance of a subnormal or suppressed basal TSH.

Aged↗
PubMed1992

A prospective study of lymphocyte-initiated immunosuppression in normal pregnancy: evidence of a T-cell etiology for postpartum thyroid dysfunction.

Immune function in normal pregnancy and the postpartum period remains poorly defined. We hypothesized that a comparative study between pregnant women with normal and abnormal immune function would further our understanding of the immune mechanisms of pregnancy. We chose to study a cohort of pregnant women at risk for the development of postpartum thyroid dysfunction (PPTD) as well as a group of normal controls. We chose PPTD as the model for abnormal immune function because of the relative ease of monitoring disease development and the relatively high prevalence for PPTD reported in earlier studies. Five hundred and fifty-two women were screened for the presence of thyroid autoantibodies in the first trimester of pregnancy. Thirty-three thyroid autoantibody-positive women and 28 thyroid autoantibody-negative women were followed prospectively throughout pregnancy and 6 months into the postpartum period. Lymphocyte subset analyses, thyroid function tests, and thyroid autoantibodies (antihuman thyroglobulin and antithyroid peroxidase) were performed at defined intervals. All patients were HLA serotyped. Normal pregnancy was principally characterized by decreased CD4+ T-cells and increasing CD8+ T-cells, causing a significant fall in the CD4+/CD8+ ratio in late pregnancy and into the postpartum period. Women who developed PPTD had 1) a higher CD4+/CD8+ ratio (P = 0.04), 2) activation of T-cells in the postpartum period (P = 0.02), and 3) significantly higher thyroid autoantibody titers (antihuman thyroglobulin, P = 0.02; antithyroid peroxidase, P = 0.0018). We found an overall incidence for PPTD of 8.8%. These data demonstrated that women who were thyroid autoantibody positive in the first trimester of pregnancy had a one in three chance of developing PPTD. We observed a significant fall in the T-cell helper/suppressor ratio in normal pregnant women, which was associated with distinct T-cell subset changes. This pregnancy-initiated T-cell regulation reflected an overall suppression of immune function. The development of PPTD was a frequent postpartum event in our population and was associated with a triad of immune markers: a reduction in the normal immune suppression of pregnancy (as indicated by higher T-cell helper/suppressor ratios), enhanced postpartum T-cell activation, and elevated thyroid autoantibodies. The reduction in the degree of immune suppression was, therefore, a major factor in the development of PPTD. Our results define immunological changes that occur in normal pregnancy and distinct immunological abnormalities necessary for the development of PPTD.

Autoantibodies↗