[Concentration of cyclic AMP in cultured thyroid cells isolated from the thyroids of patients with various thyroid diseases].
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Culture Techniques↗
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Thyroid peroxidase antibodies in children with autoimmune thyroiditis.
AIMS: To compare the prevalence of thyroid peroxidase antibodies in 25 children with autoimmune thyroid disorders and in 41 children and young adults with type 1 diabetes, and to test the prevalence of thyrotropin receptor antibodies. METHODS: Two commercially available radioimmunoassays for antibodies to thyroid peroxidase, a commercially available agglutination test of particles coated with thyroid microsomal antigens, and a radioimmunoassay for thyrotropin receptor antibodies were used. Patients and controls were studied. RESULTS: One of the radioimmunoassays detected thyroid peroxidase antibodies not only in all children with autoimmune thyroid disorders and children and young adults with type 1 diabetes and thyroid microsomal antibodies, but also in 20% of healthy control children without microsomal antibodies. With this thyroid peroxidase assay and with microsomal agglutination, 94% of the children with autoimmune thyroiditis, 71% of those with Graves' disease, and over 90% of those with type 1 diabetes and thyroid dysfunction tested positive. In the other radioimmunoassay for thyroid peroxidase antibodies thyroid peroxidase antibody titres in half or more of the children with microsomal antibodies failed to reach the level of positivity given by the producers. Eighty five percent of children with Graves' disease and 71% of those with autoimmune thyroiditis had thyrotropin receptor antibodies but so did 35% of children studied for other endocrinological disorders such as delayed growth or puberty. CONCLUSIONS: Testing patients with well characterised disorders of thyroid function and with other endocrine disorders is important in evaluating the efficacy of new diagnostic tests for thyroid autoantibodies.
Adolescent↗
Altered thyroidal responsivity to thyrotropin induced by circulating thyroid hormones. A "short-loop" regulatory mechanism?
We studied the effect of thyroid hormone administration on responsivity of murine thyroid to exogenous thyrotropin (TSH) in order to explore the possibility that the thyroid gland might be directly inhibited by its own hormones. In the rat both L-thyroxine (T4) and 3,5,3'-L-triiodothyronine (T3) pretreatment inhibited TSH-induced thyroidal ornithine decarboxylase (ODC) activity in vivo in a dose-related manner (half-maximal inhibition, 1.7 mug/rat and 0.6 mug/rat, respectively). Other structurally related compounds exhibited the following inhibitory potencies compared to T4: T3, 283%; triiodothyroacetic acid, 40%; D-T4, 18%; 3,5-L-diiodothyronine, 9%. Monoiodotyrosine, diiodotyrosine, and iodide were not inhibitory. The full inhibitory effect of T4 or T3 was observed when thyroid hormone was administered from 96 to 12 h before TSH and was also seen in hypophysectomized animals. Pretreatment with T4 or T3 in divided doses over 2 1/2 days inhibited TSH-induced increase in [1-14C]glucose oxidation to 14C02 and [3H] leucine incorporation into protein in rat thyroid. In the mouse T4 or T3 pretreatment (0.25-25 mug daily) caused dose-related inhibition of both thyroidal ODC activity and 131I release induced by TSH in vivo. In mice on a low-iodine diet (LID) but not in animals on a regular diet (RD) NaI pretreatment also blunted TSH-induced thyroidal ODC activation and 131I release. When LID or RD mice were pretreated with 12.5-125 mug of T4 or T3 over 2 1/2 days, TSH-induced in vitro stimulation of thyroid cyclic 3',5'-adenosine monophosphate formation was inhibited in a dose-related manner; NaI pretreatment was inhibitory in the LID mouse only. Prior administration of exogenous TSH blunted the activation of thyroid ODC and thyroid hormone release induced by subsequent TSH administration in rat and mouse. These studies indicate altered thyroid responsivity to TSH under the influence of circulating thyroid hormones and suggest the existence of a "short-loop" negative feedback regulating thyroid function.
Animals↗
Effect of adrenal hormones on thyroid secretion and thyroid hormones on adrenal secretion in the sheep.
1. Previous work has shown that after stressful stimuli, sheep initially secrete increased amounts of thyroid hormone, at a time when adrenal secretion is also elevated. 2. This study was designed to evaluate (a) any short-term activation or inhibition of thyroid secretion by exogenous cortisol or ACTH administered in quantities comparable to those secreted after stress in sheep and (b) any short-term effect that exogenous thyroxine or triiodothyronine may have on the concentration of plasma cortisol in the sheep. 3. Thyroid activity was measured by determination of plasma protein bound 125I (PB125I) and total 125I in thyroid vein and mixed venous (jugular) blood. Plasma cortisol and thyroxine concentrations were measured by a competitive protein-binding assay at intervals for up to 5 hr after commencement of the experiment. 4. No evidence of an activation of thyroid secretion was found during cortisol or ACTH infusion, as monitored by thyroid vein PB125I. Similarly there was no evidence of any inhibition of thyroid function, as measured by continued secretion of thyroid hormones into thyroid vein blood. 5. No effect on plasma cortisol concentration due to thyroid hormone treatment was observed. 6. It was concluded that (a) elevated circulating corticosteroids in physiological concentrations have no short-term effects on thyroid activity in the sheep and (b) the short-term alterations in thyroid and adrenal cortical secretion observed during stress in the sheep could not be attributed to direct interaction of elevated thyroid hormone concentrations with adrenal cortical secretion.
Adrenal Glands↗
Thyroid-joint crosstalk: a systematic review and meta-analysis of thyroid autoimmunity and dysfunction in juvenile idiopathic arthritis.
BACKGROUND: Recent observational studies outlined the concomitant presence of autoimmune diseases in children with juvenile idiopathic arthritis (JIA), including endocrine autoimmunity. Despite the growing evidence of thyroid involvement in JIA, available data are heterogeneous and fragmented. We aimed to systematically review the available evidence on the prevalence of thyroid autoantibody positivity and thyroid dysfunction in patients with JIA. METHODS: PubMed/Medline, Cochrane, and Scopus databases were approached to identify studies reporting data on thyroid autoantibody positivity and dysfunction in children with JIA. RESULTS: A total of 15 studies were included in the final analysis, encompassing 19 015 children with JIA (13 225 females, 69.6%) with a weighted mean age of 8.0 years (range 1.8-21 years). The pooled prevalence estimates of antithyroid antibody positivity and thyroid dysfunction were 0.04 (95% CI: 0.03-0.05) and 0.04 (95% CI: 0.03-0.08), respectively. The risk difference for thyroid autoantibody positivity between children with JIA and controls was 0.08 (95% CI: 0.02-0.14). Possible risk factors were analyzed: the presence of family history for thyroid autoimmune disease (odds ratio - OR 3.91, 95% CI 1.86-8.25), concurrent Antinuclear Antibodies (ANA) positivity (OR 1.62, 95% CI 1.13-2.31), and older age (MD 2.10 years, 95% CI 1.32-2.89) were associated with thyroid autoantibody positivity and/or thyroid dysfunction in children with JIA. No significant difference emerged for the specific JIA form. CONCLUSION: Thyroid dysfunction may be detected in children with JIA, with a significant risk difference in comparison to healthy controls. Specific clinical characteristics, such as family history, ANA positivity, and older age at JIA onset, may suggest which patients should benefit from thyroid autoantibody screening.
Humans↗
[Studies on hypophyseo-thyroid function in patients with chronic thyroiditis (author's transl)].
It is well known that serum TSH levels are elevated in most patients with chronic thyroiditis, even if the patient exhibits normal thyroid function tests. The determination of serum TSH levels in these patients is thought to be the most sensitive indicator of subclinical hypothyroidism. In this study, the hypophyseo-thyroid functions of untreated euthyroid patients with chronic thyroiditis were evaluated. Serum T3 levels in most of these patients were raised or at high normal levels, although serum T4 levels were in the low normal range. Serum T4 levels in patients with raised basal TSH were distributed in the low normal range. Hence, it is suggested that the decreased serum T4 stimulates TSH secretion which in turn stimulates T3 (and T4) secretion from the thyroid and the elevated T3 maintains the patient's euthyroid condition. Basal TSH levels in these patients varied from 2.5 to 37.0 muU/ml and mean +/-SD was 12.9+/-9.6 muU/ml. Thirteen out of 30 patients (43%) with normal free T4 indices showed elevated basal TSH levels. TSH responses to TRH injection were exaggerated in all euthyroid patients with raised basal TSH levels, as well as in 11 out 14 patients (78.6%) with normal basal TSH levels as well. But the maximum TSH responses after TRH injection were well correlated with basal TSH levels (gamma=0.79). The percent increases of serum T3 after TRH injection in those patients were less than those of the normal person, and there was no difference in T3 response between the normal TSH group and the group with raised TSH. Eight patients who suffered from collagen diseases (SLE:6, RA:1, PSS:1) without any evidence of thyroid disease also exhibited exaggerated TSH responses to TRH. In five out of these eight patients (62.5%) antithyroglobulin antibody was positive. This may indicate the presence of the so-called asymptomatic autoimmune thyroiditis in these patients. It is suggested that the elevated basal TSH levels in euthyroid patients with chronic thyroiditis are a much more sensitive indicator of thyroid failure than any other routine thyroid function tests. Moreover, the exaggerated TSH responses to TRH in patients with normal basal TSH levels indicated that the TRH-test is more useful for the detection of minimal thyroid failure, especially in patients having such conditions as asymptomatic automimune thyroiditis.
Collagen Diseases↗
Medullary thyroid carcinoma--an uncommon cause of thyroid nodules but an important cause of thyroid neoplasms.
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Carcinoma↗
Thyroid hormone concentrations and inhibition of thyroid stimulating hormone secretion in euthyroid subjects wit autonomous thyroid nodules.
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Adult↗
Thyroid function and polyamines. III. Changes in ornithine decarboxylase activity and polyamine contents in the rat thyroid during hyperplasia and involution.
Changes in ornithine decarboxylase (ODC) activity and in polyamine contents of the rat thyroid were studied under various experimental conditions. Methylthiouracil (MTU) treatment produced several-fold increases in the thyroid ODC activity and in the content of putrescine, spermidine and spermine within a week. While serum thyrotropin (TSH) levels increased gradually up to 3 weeks, the content of both putrescine and spermidine tended to reach a plateau after 2 weeks of the goitrogen treatment; spermine content continued to increase progressively for 3 weeks. Discontinuance of MTU at 7 days resulted in a rapid decline in the elevated thyroid ODC activity, followed by a diminution of putrescine, spermidine and RNA contents. Thyroidal putrescine, spermidine and RNA responded more sensitively to both introduction and withdrawal of TSH stimulation than thyroidal spermine and DNA. Excess iodide, having no effect on the basal level of thyroid ODC, suppressed the MTU-induced increase in this enzyme activity without affecting circulating TSH, thyroxine (T4) and triiodothyronine (T3) levels. There was a significant negative correlation between the ODC activity and intrathyroidal concentration of iodine in MTU-pretreated rats. Theophylline increased the thyroid weight and ODC activity when given to rats fed with a subeffective dose of MTU. Analyses of serum TSH, T4, T3 and of thyroidal iodine revealed that TSH-induced thyroid ODC activity was suppressed by increased circulating thyroid hormones and/or intrathyroidal iodine. Furthermore, it was suggested that thyroid hormones and excess iodide acted directly on the thyroid to alter polyamine biosynthesis, possibly by changing the responsiveness of the gland to TSH.
Animals↗
Evidence for thyroid antigen-reactive T lymphocytes infiltrating the thyroid gland in Graves' disease.
We have investigated the relative distribution and some in vitro functions of thyroid-infiltrating immunocompetent cells obtained at fine-needle aspiration biopsy in twelve patients with Graves' disease and thirteen patients with Hashimoto's thyroiditis. In both disorders the predominant (57--59%) thyroid-infiltrating cell was a small lymphocyte. Significant numbers of plasma cells (10%) were seen only in Hashimoto's thyroiditis. Mononuclear phagocytes (monocytes plus macrophages) were present in similar numbers (12--18%) in both disorders. In both Graves' and Hashimoto's disease there was a relative reduction of (thymus-dependent) lymphocytes in the thyroid gland as compared to the blood. Blood and thyroid-infiltrating T lymphocytes were tested for in vitro cell-mediated immunity (CMI) to thyroid antigen in the leucocyte migration inhibition test (LMT). CMI was readily demonstrated in the blood of most patients with Graves' and Hashimoto's disease. When the thyroid-infiltrating lymphocytes were tested for CMI in the LMT, only the infiltrating cells from patients with Graves' disease displayed CMI, whereas the thyroid-infiltrating lymphocytes in Hashimoto's disease were negative. Fractionation of the immunocompetent cells demonstrated that the thyroid antigen-induced LMT response of blood and thyroid-infiltrating lymphocytes in Graves' disease is a T lymphocyte-dependent phenomenon.
Adolescent↗
[Acute suppurative thyroiditis in a patient with prior subacute thyroiditis].
Acute suppurative thyroiditis is an uncommon thyroid disorder usually caused by bacterial infection. The most common route of infection is a fistula that originates from the fundus of the pyriform sinus. Pre-existing thyroid disease, most commonly nodular goiter, has been reported to be present in acute suppurative thyroiditis. A 44 year old man presented a subacute thyroiditis, resolved by nonsteroidal antiinflammatory treatment. One year later, the patient abruptly complained of fever and painful swelling in the thyroid region. A relapse subacute thyroiditis was diagnosed and prednisone treatment was started. A few days later owing to a worsening of the pain and of the clinical features the patient was referred to our department. He presented dysphagia and he was feverish, the overlying skin of the neck swelling was erythematous and warm. There was a neutrophilia (83.7%). Plasma FT4, FT3 and TSH were normal. Anterior neck region ultrasonography showed an enlargement of the left thyroid lobe with poorly defined shapes and inhomogeneous parenchyma while the right lobe of the gland was normal. The 131-I thyroid scan showed a large cold area in the upper part of the left thyroid lobe and preserved radionuclide uptake in the residual parenchyma. The RAIU was normal. We diagnosed acute suppurative thyroiditis and started antibiotics treatment. The day after the patient was still feverish and he gave out from the mouth a great quantity of sero-purulent material with a swelling reduction and improvement of the neck pain. Barium swallow examination did not show any fistula in the cervical esophagus. The fistula opening was demonstrated by indirect laryngoscopy in the postero-lateral side of hypopharynx.(ABSTRACT TRUNCATED AT 250 WORDS)
Abscess↗
[Latent pathology of the thyroid: an epidemiological and statistical study of thyroids sampled during 507 consecutive autopsies].
In order to highlight the occult pathology of the thyroid in the aged, the authors examined all the glands withdrawn from 507 consecutive autopsies on subjects of 67.10 years of median age. In 10 tables there are weight and measurements of the thyroids, macro and microscopic details and pathologic appearances. Adenomas were found in 17.1% of cases and histologically besides the known cases referred also to the Hürtle cells type, 4 clear cells adenomas and 5 adenolipomas were found. In 27.42% the subjects were affected or were dead for a malignant extrathyroidal neoplasm, and in 26% of these there was a metastasis in the thyroid. Never a primitive thyroid carcinoma, macroscopically and clinically evident, but in 53 thyroid glands, 54 occult carcinomas (OC) were found, particularly 37 papillary and 17 medullary. IN 57% of 165 histologically treated thyroids, to evidence C-cells, hyperplasia of these cells was found associated with various pathologic conditions, more in aged subjects. In 147 glands were found 170 nodules of various number of cells, at times positive for calcitonin. These solid cellular nodes (SCN) were evaluated as nodular C-cells hyperplasia. Besides isolated cases of acute thyroiditis (also the mycotic type), of tubercular thyroiditis and Hashimoto's, in 12% of the glands a lymphocytic chronic thyroiditis was found, frequently with Hürtle cells. Others observations were: basophilic thickening of colloid also with calcium oxalate crystals, lipoid degeneration of follicular cells and fat interfollicular and interlobular infiltration, thyroid amyloidosis, inner and media elastic calcification of thyroid arteries, presence of cysts with squamous cells coating, parathyroid glands and cartilage intrathyroidal plaques.
Adolescent↗
Influence of histamine- and 5-hydroxytryptamine-containing thyroid mast cells on thyroid blood flow and permeability in the rat.
The possible significance of thyroid mast cells in the regulation of thyroid blood flow and capillary permeability was investigated in rats whose TSH secretion had been eliminated by exogenous T4. Mast cells were identified by their abundance of metachromatic granules, and their content of histamine and 5-hydroxytryptamine (5-HT) was examined by fluorescence histochemistry. Thyroid histamine levels were determined by fluorometry. The tissue uptake of 86Rb was used as an indicator of blood flow and permeability. Numerous histamine- and 5-HT-containing mast cells were found within the thyroid and in connective tissue adjacent to the thyroid, whereas juxtathyroidal muscle tissue was virtually devoid of mast cells. Administration of compound 48/80 evoked a prompt depletion of 5-HT, histamine and metachromatic granules from thyroid mast cells, and a concomitant increase in the thyroidal uptake of 86Rb. The 86Rb uptake by juxtathyroidal muscle tissue was unaffected. Exogenous 5-HT and histamine both induced prompt increments in thyroidal 86Rb uptake, and 5-HT also stimulated 86Rb uptake in juxtathyroidal muscle tissue. TSH, previously shown to induce a gradual amine release from mast cells within, but not outside, the thyroid, evoked a gradual increase in thyroidal, but not in muscular, uptake of 86Rb. The findings support the concept that, in the rat, histamine and/or 5-HT, released from intrathyroidal mast cells by TSH, stimulate thyroid blood flow and/or permeability.
Animals↗
Thyroid antigen stimulates lymphocytes from patients with Graves' disease to produce thyroid-stimulating immunoglobulin (TSI).
Circulating lymphocytes from patients with Graves' disease and from control subjects were cultured in vitro alone, with normal human thyroid tissue homogenates, and with other nonthyroid human tissue homogenates. The supernatants of these cultures were assayed for human thyroid-stimulating activity by incubation with human thyroid slices in which increases in cAMP levels were then measured. Human thyroid stimulator activity was demonstrated in 16 out of 20 experiments in which lymphocytes from patients with active untreated Graves' disease (with hyperthyroidism) were cultured with normal thyroid homogenate, in 4 out of 17 experiments when control lymphocytes were similarly cultured, and in one out of 12 experiments in which the lymphocytes from the patients with Graves' disease were cultured with liver or gastric mucosa homogenate. Thyroid-stimulating activity was abolished by precipitation of the globulin from the supernatant by goat anti-human globulin serum. These results demonstrate that normal human thyroid tissue homogenates can specifically stimulate most lymphocytes from patients with Graves' disease and lymphocytes from a few normal subjects to produce human thyroid-stimulating immunoglobulins in vitro. This suggests that the human thyroid-stimulating immunoglobulins are auto-antibodies to normal thyroid constituents, but the possiblity that an antigenic change in the thyroid initiates the disease cannot be entirely excluded. The findings suggest that the prime change in Graves' disease is immunologic, perhaps a failure of immunological suppression.
Antigens↗
The Thyroid-Brain Network: Exploring Inflammation, Immune Mechanisms and Common Triggers in Thyroid-Related Neurological Dysfunction.
Autoimmune thyroid diseases (AITD), including Hashimoto's thyroiditis and Graves' disease, represent the most prevalent endocrine disorders worldwide, affecting hundreds of millions with profound but often under recognized neurological consequences. There are emerging lines of evidence establishing inflammation and immunity as the critical missing link connecting peripheral thyroid dysfunction to central nervous system manifestations. Thyroid hormones function as essential neuromodulators governing neurodevelopment, synaptic plasticity, and cognitive processing through integrated genomic and non-genomic mechanisms, with region-specific cerebral metabolic disturbances correlating with distinct neuropsychiatric symptoms. The immunological perspective reveals that AITD propagates neuroinflammation through convergent pathways: molecular mimicry enabling cross-reactivity between thyroid and neural antigens, cytokine-mediated disruption of neurotransmitter metabolism, HMGB1-driven glial activation, and blood-brain barrier compromise facilitating immune cell infiltration. The thyroid-gut-microbiota axis emerges as a critical mediator wherein dysbiosis perpetuates both thyroid autoimmunity and neuroinflammation through impaired serotonin precursor availability and increased intestinal permeability. Mitochondrial dysfunction represents an energetic common denominator, as thyroid hormone dysregulation directly impairs oxidative phosphorylation, producing region-specific cerebral metabolic disturbances. Simultaneous compromise of monoamine systems, cholinergic signaling abnormalities, and glutamate excitotoxicity creates a particularly toxic neurochemical state in untreated thyroid dysfunction. Common triggers such as psychological stress, gut dysbiosis, and mitochondrial impairment may activate interconnected pathways that simultaneously compromise thyroid and brain function, revealing that these disorders share fundamental mechanistic origins. These insights have been discussed in the current review to enhance the understanding of thyroid-brain function, the core mechanisms and consequences of functional deficits.
Journal Article↗
Thyroid cells in Graves' disease and Hashimoto's thyroiditis stimulate allogeneic T cells when pretreated with phorbol ester.
OBJECTIVE: To assess the capacity of thyroid follicular cells to function as antigen presenting cells, we have examined their ability to stimulate allogeneic T cells. DESIGN: Thyroid follicular cells were pretreated with interferon-gamma or phorbol myristate acetate, washed thoroughly, and their capacity to induce allogeneic T cell proliferation was determined. PATIENTS: Thyroid cells were prepared using thyroidectomy specimens from eight patients with Graves' disease, one with Hashimoto's thyroiditis and two with non-toxic multinodular goitre. MEASUREMENTS: T cell 3H-thymidine incorporation was measured after a 16-hour incubation period with the isotope, 3 days after co-culture of T cells and thyroid cells. RESULTS: Four of the eight thyroid cell preparations from thyroid autoimmunity patients failed to stimulate T cells, although there was a significant, weak stimulation for the whole group (P < 0.05): interferon-gamma pretreatment had no effect on this. Phorbol myristate acetate pretreatment significantly increased the ability of thyroid cells (from both autoimmune and multinodular glands) to stimulate T cells (P < 0.05); this was time and concentration dependent. Cell fixation after PMA treatment did not abolish this stimulatory activity, which could be transferred by supernatants from unfixed cells; exogenous interleukin-1 did not mimic the activity. CONCLUSIONS: Thyroid cells expressing major histocompatibility complex class II molecules only weakly and inconsistently stimulate allogeneic T cells, compared to thyroid cells pretreated with phorbol myristate acetate, a difference which may be due to the expression of an unidentified co-stimulatory signal induced by phorbol ester.
Antigen-Presenting Cells↗
Free diiodotyrosine effects on protein iodination and thyroid hormone synthesis catalyzed by thyroid peroxidase.
Free diiosotyrosine exerts two opposite effects on the reactions catalyzed by thyroid peroxidase, thyroglobulin iodination and thyroid hormone formation. 1. Inhibition of thyroglobulin iodination catalyzed by thyroid peroxidase was observed when free diiodotyrosine concentration was higher than 5 muM. This inhibition was competitive, suggesting that free diiodotyrosine interacts with the substrate site(s) of thyroid peroxidase. Free diiodotyrosine also competively inhibited iodide peroxidation to I2. 2. Free diiodotyrosine, when incubated with thyroid peroxidase in the absence of iodide was recovered unmodified; in the presence of iodide an exchange reaction was observed between the iodine atoms present in the diiodotyrosine molecule and iodide present in the medium. Using 14C-labelled diiodotyrosine, 14C-labelled non-iodinated products were also observed, showing that deiodination occurred as a minor degradation pathway. However, no monoiodo[14C]tyrosine or E114C]tyrosine were observed. Exchange reaction between free diiototyrosine and iodide is therefore direct and does not imply deiodination-iodination intermediary steps. Thyroglobulin inhibits diiodotyrosine-iodide exchange and vice versa, again suggesting competition for both reactions. These results support, by a different experimental approach, the two-site model for peroxidase previously described by us in this journal. 3. Free diiodotyrosine when present at a very low concentration, 0.05 muM, exerts a stimulatory effect on throid hormones synthesis. The relationship between diiodotyrosine concentration and thyroid hormone synthesis give an S-shaped curve, suggesting that free diiodotyrosine acts as a regulatory ligand for thyroid peroxidase. Evidence is also presented that free diiodotyrosine is not incorporated into thyroid hormones. Therefore, thyroid peroxidase catalyzes only intra-molecular coupling between iodotyrosine hormonogenic residues. 4. Finally, although no direct proof exists that these free diiodotyrosine effects upon thyroglobulin iodination and thyroid hormone synthesis are physiologically significant, such a possibility deserves further investigation.
Animals↗
Lymphocyte transformation in response to human thyroid extract in patients with subacute thyroiditis.
Seven patients with subacute thyroiditis were studied for evidence of cell-mediated immunity (CMI) to human thyroid extract, as judged from lymphocyte transformation responses, measured by the increase in labeled thymidine uptake in vitro. Significant transformation was observed in lymphocytes from five of the seven patients with active subacute thyroiditis, and in the lymphocytes from only three of 15 patients with Graves disease (x2, P EQUALS 0.036). Repeated studies of lymphocyte transformation were done in four of the patients with subacute thyroiditis, three of whom initially showed abnormal responses. By eight weeks after initial studies, when all patients were in clinical remission without treatment, transformation responses were within the normal range. Thyroid antibodies were absent or present in low titer (is less than 1:100) in sera of patients with subacute thyroiditis, and became undetectable by eight weeks in those patients initially positive. In contrast, significant titers of antithyroid antibodies were frequently present in patients with Graves' disease. The present studies have shown the occurence of CMI to thyroid antigens during the active phase of subacute thyroiditis. The abnormality was transient, however, since it disappeared when the disease had resolved. These findings strongly suggest that the release of thyroid antigen leading tothe development of a cell-mediated immune responses is not in itself sufficient to initiate chronic immunological disease of the thyroid. If, as some have suggested, Hashimoto's disease or Graves' disease are characterized by a permanent disorder of CMI, then in these diseases either the antigenic stimulus is persistent or there exists an intrinsic disorder of immune surveillance.
Acute Disease↗