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PubMed2001

Increased risk for nonmedullary thyroid cancer in the first degree relatives of prevalent cases of nonmedullary thyroid cancer: a hospital-based study.

The genetic basis for nonmedullary forms of thyroid cancer (NMTC) is less well established than that of medullary thyroid cancer. However, epidemiological and family studies suggest that a proportion of NMTC may be due to inherited predisposition. To estimate the familial risk of thyroid cancer, we conducted a hospital-based case-control study at the Princess Margaret Hospital in Toronto, Ontario, Canada, and at 2 university hospitals in Montréal, Québec, Canada. We obtained pedigrees from 339 unselected patients diagnosed with NMTC and from 319 unaffected ethnically matched controls. Family histories of cancer were obtained from the cases and controls for 3292 first degree relatives of cases and controls. Seventeen cases (5.0%) and 2 controls (0.6%) reported at least one first degree relative with thyroid cancer. In relatives of patients with thyroid cancer, the incidence of any type of cancer (including NMTC) was 38% higher than in relatives of controls (incidence rate ratio, 1.4; 95% confidence interval, 1.1-1.7). The relative risk for thyroid cancer was 10-fold higher in relatives of cancer patients than in controls (incidence rate ratio, 10.3; 95% confidence interval, 2.2-47.6). Our findings suggest that hereditary or other familial factors are important in a small proportion of NMTC. Molecular studies are needed to determine the genetic basis of cancer susceptibility in these families.

Adolescent↗
PubMed2002

Endogenous excitatory amino acid neurotransmission regulates thyroid-stimulating hormone and thyroid hormone secretion in conscious freely moving male rats.

The role of neurotransmission of endogenous excitatory amino acid (EAA) on serum thyroid hormones and thyroid-stimulating hormone (TSH) levels was examined in conscious and freely moving adult male Sprague-Dawley rats. The rats were cannulated at the third ventricle 2 d before the experiments. Several glutamate receptor agonists, such as kainic acid and domoic acid, and antagonists, such as 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and dizocilpine (MK-801) were administered into the third ventricle. Serum TSH levels were assesed by radioimmunoassay, and serum thyroid hormone levels were assessed by enzyme immunoassay. The results showed that the administration of CNQX and MK-801 produced a decrease in serum levels of TSH and thyroid hormones. The administration of kainic acid and domoic acid increased TSH concentrations, whereas CNQX completely blocked the release of TSH induced by kainic acid and domoic acid. These results suggest the importance of endogenous EAA in the regulation of hormone secretion from the pituitary-thyroid axis, as well as the role of the N-methyl-D-aspartate (NMDA) and non-NMDA receptors in the stimulatory effect of EAAs on the pituitary-thyroid axis.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1987

[Circulating HLA-DR (Ia) positive T cells and T cell activation by thyroglobulin, thyroid microsome and TSH-receptor in autoimmune thyroid diseases].

HLA-DR antigens are not expressed on normal circulating T lymphocytes, but recently it has become apparent that HLA-DR antigens are expressed on immunologically activated T lymphocytes, as well as monocytes, macrophages, and B lymphocytes. Namely, the HLA-DR antigens are considered to be one of the activated T cell antigens. It is apparent from the previous studies that increased numbers of HLA-DR positive T cells frequently appear in the circulation in systemic autoimmune diseases, such as RA and SLE. Furthermore, in such diseases, it is reported that the variations in circulating HLA-DR positive T cells are related to the activity of the diseases. In this communication, we examined the variations in HLA-DR positive T cells in the peripheral blood of the patients with autoimmune thyroid diseases. HLA-DR positive T cells were detected by cytotoxicity test using anti HLA-DR mouse monoclonal antibody (Leu-HLA-DR antibody) and rabbit complement. The results indicate that; 1) The percentage of HLA-DR positive T cells were increased in the patients with autoimmune thyroid diseases. 2) The changes of HLA-DR positive T cells accompanied with the stimulation by non-specific mitogens in vitro in autoimmune thyroid diseases did not differ from those in the normal controls. 3) The percentage of HLA-DR positive T cells increased by the stimulation of TSH-receptor and thyroid microsome in Graves' disease, on the other hand, it occurred by the stimulation of thyroglobulin and thyroid microsome in Hashimoto's thyroiditis. 4) The percentage of HLA-DR positive T cells were correlated with TRAb (TSH receptor Ab assayed by Smith's kit) in Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Cancer-specific mRNAs in thyroid carcinomas: detection, use, and their implication in thyroid carcinogenesis.

Molecular-based diagnosis ofthyroid carcinomas can be more easily establishedby utilizing specific mRNAs that are expressed in a restricted manner in cancer tissues. Accordingly, several cancer-specific mRNAs in thyroid carcinomas have been identified by means of sequence specific-differential display (SS-DD), serial analysis of gene expression (SAGE) and other new techniques. By using these cancer-specific mRNAs, some new methods of preoperative diagnosis of thyroid carcinomas have been developed. In one such method, Aspiration Biopsy-Reverse Transcription-Polymerase Chain Reaction (ABRP), RNA is extracted from leftover cells within the needle used for fine needle aspiration biopsies (FNABs), thereby allowing cytological and molecular-based diagnoses to be performed simultaneously. ABRP provides both RNA information and a cytological diagnosis without further invasion to the patient. By ABRP detection of cancer-specific mRNAs, papillary, anaplastic and medullary carcinomas and a part of malignant lymphomas can be accurately diagnosed preoperatively. It remains to be clarified why cancer-specific mRNAs, especially those that are overexpressed in fetal tissues, can clearly distinguish benign tissues from carcinomas, while genomic alternations, such as mutations in the RAS or P53 gene cannot. Further, the widely accepted hypothesis of multi-step carcinogenesis cannot explain some of the clinical and experimental findings of thyroid carcinomas. Considering these facts, we propose a novel hypothesis of thyroid carcinogenesis, the "germ-cell carcinogenesis" hypothesis, in which cancer cells derive from the remnants of fetal thyroid germ cells (thyroblasts) instead of normal thyroid follicular cells.

Carcinoma↗
PubMed1975

Alteration of thyroidal responsiveness to TSH under the influence of circulating thyroid hormone: short feed-back regulatory effect.

In order to examine the hypothesis that the thyroidal responsiveness to TSH is under the influence of thyroid hormone, following the T3 injection to the mice, serum T3 concentrations and the response of thyroid tissue to a fixed dose of TSH in terms of intracellular colloid droplet formation was studied. The colloid droplets induced by TSH was significantly reduced when serum T3 was decreasing, while it was significantly increased when serum T3 was increasing. This results demonstrate for the first time the existence of short feed-back loop regulating intra-thyroidal function by circulating T3. To delineate the possible mechanism of action of T3, the thyroid gland of mouse whose serum T3 concentration was elevated by injecting 50 mug T3, was incubated with TSH in vitro. TSH-induced cyclic AMP generation was not inhibited at all but colloid droplet formation was significantly inhibited in the thyroid tissue of the animal whose serum T3 concentration was enormously high. Thus, it was demonstrated that the site at which T3 affects is beyond cylcic AMP generation but prior to endocytosis, being consistent with our previous results.

Animals↗
PubMed1987

The inhibitory effects of calmodulin antagonists on TSH-stimulated thyroid hormone release by mouse thyroid lobes.

Calcium ions have been shown to play a mojor regulatory role in the release of various hormones from a wide variety of endocrine organs. More recently, in vitro evidence suggests that a calcium-binding protein, calmodulin, is also involved in the release of many hormones. So we examined the effects of several types of calmodulin antagonists on TSH-stimulated thyroid hormone release in vitro. Mouse thyroid lobes (one thyro-tracheal unit/tube) were incubated in Krebs-Ringer bicarbonate buffer at 37 degrees C for 4h. Free thyroxine (fT4) released in the incubation medium, thyroidal cAMP and calmodulin content were measured by RIA. TSH (5 mU/ml) and dibutyryl cAMP (DBC) (200 micrograms/ml) caused a 2-4 fold increase in thyroidal release of fT4. The stimulatory effects of TSH on fT4 release were significantly inhibited by trifluoprazine and prenylamine lactate at the concentration of 5 X 10(-5) M. More specific calmodulin antagonists, W-7 and W-13, were also shown to inhibit TSH stimulation of fT4 release at the concentration of 5 X 10(-5) M. In contrast, TSH stimulation of fT4 release was not depressed by non-specific antagonists, W-5 or W-12, at the same concentration as 5 X 10(-5) M. Further, W-13 also markedly inhibited DBC-stimulated fT4 release. Neither TSH nor PGI2 altered the thyroidal calmodulin content, dissociating with a marked increase in the cAMP concentration. These results suggest that calmodulin plays an important role in TSH-stimulated thyroid hormone release and further that this mechanism exists, at least in part, at the site subsequent to the generation of cAMP.

Animals↗
PubMed1990

Trial of thyroid autotransplantation in patients with Graves' disease whose remnant thyroid has unintentionally been made too small at subtotal thyroidectomy.

Autotransplantation of thyroid tissue was carried out in 5 patients with Graves' disease in order to prevent postoperative hypothyroidism, because the amount of remnant thyroid tissue was estimated to be too small, i.e. from 3 to 5 g. Approximately 0.5 to 2 g of thyroid tissue was cut into small pieces and transplanted into the sternocleidomastoid muscles or the strap muscles. Although the postoperative serum TSH levels were normal or slightly elevated, the serum concentrations of triiodothyronine were within the normal range in these 5 patients at a follow-up study carried out 2 to 7 years after surgery. Thyroid scanning with I-123 or 99mTc-pertechnetate (Tc-99m) revealed radioisotope uptake at the sites of transplantation in 4 of the 5 patients. These findings verify that the implanted thyroid tissues were alive and functioning and that autotransplantation may be a way of preventing postoperative hypothyroidism in patients whose remnant thyroid tissue has unintentionally become too small.

Adult↗
PubMedDate not supplied

Thyroid dysfunction and high thyroid stimulating hormone levels in children with Down's syndrome.

UNLABELLED: In order to delineate the spectrum of thyroid abnormalities in children with Down's syndrome (DS), first visit height data (SDS) and serum TSH, T4 and antiperoxidase antibodies concentrations were retrospectively evaluated in 137 children (71 girls) with DS (0.04-16 years). RESULTS: Congenital hypothyroidism was detected in 2.9% of patients. Thyroid disease occurred in 9%: four hyperthyroidism and eight hypothyroidism. Overt thyroid disease was always related to thyroid autoimmunity. The remaining 121 patients had normal T4 levels but increased mean TSH compared with controls (4.7 +/- 2.8 vs 2.3 +/- 1.3 mU/l). According to TSH levels, they were divided into two groups: G1 (n = 68) with normal TSH (<5 mU/l), and G2 (n = 53) with high TSH (> 5 mU/l). T4 levels were significantly lower in G2 (p < 0.01 vs G1 and controls). Height SDS was not different. CONCLUSIONS: Thyroid disorders are frequent in children with DS. Subtle thyroid abnormalities found in patients with DS with no evidence of clinical dysfunction need further investigation to demonstrate whether there is a need for therapeutic intervention.

Adolescent↗
PubMed1979

Effect of endogenous thyroid stimulating hormone levels on the secretion of thyroid hormones in man.

The effect of endogenous thyroid stimulating hormone (TSH) on the thyroid secretion of triiodothyronine (T3) and thyroxine (T4) was evaluated by serial determinations of serum T3. T4 and TSH concentrations in the following groups of patients: a) three patients submitted to surgical removal of a solitary, autonomous thyroid nodule which had completely inhibited the extranodular tissue; b) five subjects, with the same disease, in whom functional recovery of the extranodular tissue was induced by increased circulating TSH levels, produced by treatment with methimazole; c) one patient submitted to hemithyroidectomy for multinodular goitre; d) two hyperthyroid patients who had been treated with methimazole. In all these patients serum T3 and T4 levels progressively decreased, with a consequent progressive increase in serum TSH concentrations, leading to stimulation of the thyroid gland. During this TSH-induced stimulation of thyroid tissue, a significant positive correlation was found between the serum TSH concentrations and the corresponding ratio between the serum levels of T3 and T4 (T3/T4), both within each patient group (P less than 0.001) and among all patients (P less than 0.001). The same correlation also governs the relationship between the TSH and the T3/T4 values of 34 euthyroid control subjects and one patient with incipient hypothyroidism. These data strongly suggest that endogenous TSH can induce a preferential secretion of T3 over T4 by the human thyroid.

Goiter↗
PubMed1996

Activated and interferon-gamma producing thyroid-derived T cells are detected in Graves' disease, thyroid autonomy as well as in non-toxic multinodular goiter.

The relative numbers of activated and interferon gamma (IFN-gamma)-producing peripheral blood lymphocytes (PBL) and thyroid-derived lymphocytes (TL) were determined using double surface and intracellular labeling techniques in flow cytometry. Cells were analyzed from 10 patients with Graves' disease (GD), eight patients with thyroid autonomy (TA) and five patients with non-toxic multinodular goiter (NTG). A maximum of 1% IFN-gamma+ cells were detected both in unstimulated PBL and TL. Stimulation caused a two- to threefold higher number of IFN-gamma+ cells in TL (GD, 48 +/- 12%; TA, 48 +/- 11%; NTG, 50 +/- 15%) as compared to PBL (GD, 15 +/- 7%; TA, 16 +/- 8%, NTG, 18 +/- 10%) of the same patients. Nearly all IFN-gamma+ TL in GD were CD3+ T cells, whereas 10-20% of IFN-gamma+ TL in TA and NTG were NK cells. In PBL 80% and in TL almost 100% of IFN-gamma+ cells were antigen-primed CD45RO+ cells. Only 25-35% of IFN-gamma+ thyroid-derived T cells expressed the CD4 antigen. About 42 +/- 10% thyroid-derived T cells in GD, 33 +/- 11% in TA and 34 +/- 13% in NTG expressed the HLA-DR molecule but not the interleukin 2 (CD25) or the transferrin receptor (CD71). Forty per cent of these HLA-DR+ T cells showed an intracellular staining for IFN-gamma and half of them co-expressed the activation antigen CD69. Immunofluorescence double labeling on thyroid cryostat sections demonstrated that HLA-DR+ T cells were also present in situ. The presence of activation antigens on thyroid-derived T cells not only in patients with GD but also in TA and NTG suggests failsafe mechanisms such as anergy, suppression or cytokine regulation in so-called non-immunogenic goiter.

Adult↗
PubMed2006

Graves' disease and Hashimoto's thyroiditis in monozygotic twins: case study as well as transcriptomic and immunohistological analysis of thyroid tissues.

OBJECTIVE: To report on the rare simultaneous occurrence of Graves' disease (GD) and Hashimoto's thyroiditis (HT) in monozygotic twins. DESIGN: We compared the pattern of thyroid tissue-derived cDNAs to gain insight into previous and ongoing immune destruction and reconstruction processes using microarrays. The results were confirmed by immunohistology and real-time PCR. RESULTS: Destruction of thyroid tissue in HT reduced levels of thyrocyte-related cDNAs and cDNAs encoding extracellular matrix components, but increased levels of proteases involved in extracellular matrix degradation compared with GD. Lymphocytic infiltrates forming ectopic follicles replaced the thyroid tissue almost completely in HT. Thus, lymphocyte-related cDNA levels were higher in HT than in GD. The same was true for many chemokines and their receptors, which not only enable migration towards the thyroid but also maintain the lymphocytic infiltrate. HT also showed increased levels of cDNAs encoding molecules related to apoptosis than did GD. Surprisingly, the Th1- and Th2-specific cytokine profiles suggested for HT and GD respectively could not be confirmed. cDNAs encoding factors and receptors involved in angiogenesis were increased in GD compared with HT. CONCLUSIONS: Comparison of gene expression reflects the cellular differences between the two types of autoimmune thyroid disease in twins with identical genetic and similar environmental background.

Adolescent↗
PubMed1989

Relationship between serum free thyroid hormone concentrations and target organ responsiveness in thyroid disease patients before and after treatment.

Relationship between serum free thyroid hormone concentrations and several markers of peripheral tissue response to thyroid status was studied in 24 patients with hyperthyroidism, 17 with euthyroidism with goiter and 10 with primary hypothyroidism before and after the initiation of standard forms of treatment. Before treatment, serum free T4 correlated significantly, either positively or negatively, with the basal metabolic rate (BMR), duration of the achilles tendon reflex (ATR), resting pulse rate (RPR), serum total cholesterol (T-cholesterol), ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET), serum high density lipoprotein (HDL) and creatine phosphokinase (CPK) in the descending order. Serum free T3 also correlated significantly all the these parameters. After treatment, changes in both serum free T4 and free T3 correlated well with those of the BMR and ATR in the patients with hyperthyroidism, and with those of the ATR, serum CPK and T-cholesterol in the patients with hypothyroidism. These results indicate that these peripheral parameters correlated well with serum free thyroid hormone concentrations in thyroid disease patients. Therefore, these parameters can be used to assess thyroid functions in patients with thyroid hormone resistance.

Adult↗
PubMedDate not supplied

Hyalinizing trabecular carcinoma of the thyroid gland: report of two cases of follicular cell thyroid carcinoma with hyalinizing trabecular pattern.

Recently tumors have been reported that have an architectural pattern and cellularity similar to hyalinizing trabecular adenoma and show either parafollicular differentiation or histological findings suggestive of malignant neoplasm of the follicular cells. This study describes two cases of thyroid carcinoma of follicular cells that displayed a hylinizing trabecular pattern. The first case was a 25-year-old euthyroid woman with a cold thyroid nodule in the right lobe. On fine needle aspiration a diagnosis of papillary carcinoma was rendered. The thyroidectomy disclosed a 2-cm, firm, brown, encapsulated tumor in the right lobe. The tumor had a growth pattern and cytologic features similar to those described in hyalinizing trabecular adenoma. The differences between these neoplasms were the presence of mitotic figures, prominence of the nucleolus, capsular blood vessel invasion, and microtubule groups in the endoplasmic reticulum. The second case was a 19-year-old euthyroid woman with a cold thyroid nodule in the left lobe. A cytologic diagnosis of follicular proliferation was rendered. A 4-cm, firm, whitish, encapsulated nodule was found in the left lobectomy. The tumor cells were arranged in two clear-cut patterns: a trabecular hyalinizing pattern with a small focus of papillary growth, and a follicular pattern. These findings confirm the existence of malignant thyroid tumors with a hyalinizing trabecular pattern and illustrate the nonspecificity of this peculiar pattern, since it may also be seen in papillary carcinomas of the thyroid. The relationship between hyalinizing trabecular adenoma and papillary carcinoma of the thyroid is commented on.

Adenocarcinoma, Follicular↗
PubMed2000

Autoimmune response to the thyroid in humans: thyroid peroxidase--the common autoantigenic denominator.

Autoimmunity to thyroid peroxidase (TPO), manifest as high affinity IgG class autoantibodies, is the common denominator of human thyroid autoimmunity, encompassing patients with overt hyper- or hypothyroidism as well as euthyroid individuals with subclinical disease. The identification and cloning of TPO (the "thyroid microsomal antigen") provided the critical tool for analyzing B and T cell reactivity to this major thyroid autoantigen. In particular, the availability of immunoreactive TPO permitted the isolation of essentially the entire repertoire of human monoclonal antibodies, a feat unparalled in an organ-specific autoimmune disease. These recombinant autoantibodies (expressed as Fab) provide insight into the genes encoding their H and L chains as well as the conformational epitopes on TPO with which serum autoantibodies interact. Analyses of TPO autoantibody epitopic "fingerprints" indicate a lack of epitope spreading as well as a genetic basis for their inheritance. Limited data are available for the responses and cytokine profiles of T cells to endogenously processed TPO. Moreover, the role of thyroid cells in initiating the autoimmune response to TPO, and of B cells in expanding and/or modulating the response of sensitized T cells, has yet to be established. Finally, because autoantibody (and likely T cell) responses to TPO parallel those to TSH receptor and thyroglobulin, manipulation of T and B cell responses to TPO may provide the basis for the development of immunospecific therapy for autoimmune thyroid disease in general.

Animals↗
PubMed2005

[Thyroid ophthalmopathy: clinical activity determination of thyroid ophthalmopathy as a prognostic factor of immunosuppressive treatment response].

OBJECTIVE: To determine the usefulness of the clinical, biochemical and thyroid imaging parameters in patients with thyroid-associated ophthalmopathy, in predicting their response to immunosuppressive treatment. METHODS: This retrospective study of 16 patients with thyroid ophthalmopathy considered a number of variables including sex, age, thyroid hormone levels, treatment of the thyroid dysfunction, clinical activity score (CAS), severity (NOSPECS) of the ophthalmopathy, signs in standardized A-mode ultrasonography, in CAT and/or NMR, and previously used treatments and their effectiveness. RESULTS: The average age of the patients was 50.81 (S.D: 11.89) years; there were 5 males (31.3%) and 11 females (68.8%). The ophthalmopathy was classified as active in 10/16 patients (62.5%) and inactive in 6/16 (37.5%); and as moderate in 9/16 (56.25%) and severe in 7/16 (43.75%) according to the severity defined in NOSPECS. Ultrasonography was diagnostic in 100% of the cases. The severity decreased significantly (p < or =0.05), however the clinical activity decrease did not reach significance (p=0.38) during immunosuppressive therapy. Better results were obtained during treatment of patients with a higher CAS (p=0.04) and in those with more severe ophthalmopathy (p=0.02). There was a tendency for the patients with higher levels of TSI to respond better to the treatment (p=0.06). CONCLUSIONS: The CAS is the best parameter to quantify the activity of the disease and predicting the response to treatment. The higher the CAS and the more severe the ophthalmopathy, the better the response to treatment. No association existed between thyroid function and the activity or severity of the ophthalmopathy; or the effectiveness of treatment.

Adult↗
PubMed2003

Two cases of epithelioid angiosarcoma involving the thyroid and a brief review of non-Alpine epithelioid angiosarcoma of the thyroid.

Epithelioid angiosarcoma involving the thyroid is a rare entity, more often described in the Alpine region. Two cases of epithelioid angiosarcoma that affected the thyroid in patients from a non-Alpine location were diagnosed during a 10-year period in our department. The first case occurred in an 89-year-old Chinese man with a history of longstanding goiter, whereas the second case involved a 74-year-old Chinese man with a history of angiosarcoma of the scalp. On histologic examination, both thyroid tumors were composed of plump epithelioid cells with vesicular chromatin and prominent nucleoli, forming vascular structures and solid sheets. Positive staining for CD31 and factor VIII-related antigen confirmed endothelial differentiation in both cases. Both patients died within 5 months following the diagnosis of thyroid disease. The relationship of the scalp angiosarcoma and thyroid disease of the second patient is unclear. A brief review of non-Alpine primary thyroid epithelioid angiosarcoma is presented.

Aged↗
PubMed2006

Indication and timing of thyroid surgery for patients with hereditary medullary thyroid cancer syndromes.

Hereditary medullary thyroid cancer syndromes comprise familial medullary thyroid cancer (FMTC) and multiple endocrine neoplasia types 2A and 2B. Hereditary medullary thyroid cancers have an autosomal dominant pattern of inheritance and are caused by activating germline point mutations in the RET proto-oncogene. Evaluation of the onset, extent, and progression of hereditary medullary thyroid cancer associated with specific RET mutations has enabled clinicians to treat patients based on the level of risk associated with their specific mutation. Children identified by RET screening to be at risk for the development of medullary thyroid cancer can be treated with prophylactic thyroidectomy before developing the disease. This review covers the diagnosis, evaluation, timing of surgical management, and optimal follow-up of patients with hereditary medullary thyroid cancer syndromes.

Biopsy, Needle↗
PubMed2000

Influence of thyroid-stimulating hormone levels on uptake of FDG in recurrent and metastatic differentiated thyroid carcinoma.

UNLABELLED: The objective of this prospective study was to determine the extent to which the levels of thyroid-stimulating hormone (TSH) influence the uptake of FDG by thyroid carcinoma tumors METHODS: Ten patients with follicular (n = 7) or papillary (n = 3) thyroid carcinoma underwent FDG PET during TSH suppression (<0.05 microU/mL) and TSH stimulation (>22 microU/mL) within an average interval of 42 d (range, 28-73 d). The findings were evaluated by visual criteria. In addition, a tumor-to-background ratio (TBR) was determined for 17 lesions that were visualized. RESULTS: In 15 of 17 lesions with positive FDG uptake, TSH stimulation was associated with an increase in the TBR from 3.85 +/- 2.53 (mean +/- SD) to 5.84 +/- 4.84, corresponding to an average increase of 63.1% (P < 0.001). Determination of absolute counting rates indicated that this increase was the result of a decrease in FDG metabolism in the background together with an increase in the tumor tissue. No relationship was found between the presence or absence of iodine storage capacity (5 versus 12/17 lesions) and increase in FDG accumulation. Seven of 10 patients had additional iodine-positive metastases that showed no accumulation of FDG. CONCLUSION: Most locally recurrent and metastatic follicular and papillary thyroid carcinomas exhibited a significant increase in FDG uptake on TSH stimulation. In 3 of 10 patients, TSH stimulation resulted in either detection of new lesions or classification of the FDG uptake pattern as typical for malignancy. These findings suggest that FDG uptake in recurrent and metastatic thyroid carcinoma depends on the TSH level. Therefore, we recommend that PET examinations be performed in patients with thyroid carcinoma under TSH stimulation and follow-up examinations be performed under identical TSH conditions to prevent erroneous interpretation.

Adenocarcinoma, Follicular↗