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At least 721 records · Page 40Linked to original sources
PubMed2006

Dose selection for radioiodine therapy of borderline hyperthyroid patients according to thyroid uptake of 99mTc-pertechnetate: applicability to unifocal thyroid autonomy?

PURPOSE: The aim of this study was to evaluate the feasibility of applying a previously described dose strategy based on (99m)Tc-pertechnetate thyroid uptake under thyrotropin suppression (TcTU(s)) to radioiodine therapy for unifocal thyroid autonomy. METHODS: A total of 425 consecutive patients (302 females, 123 males; age 63.1+/-10.3 years) with unifocal thyroid autonomy were treated at three different centres with (131)I, using Marinelli's formula for calculation of three different absorbed dose schedules: 100-300 Gy to the total thyroid volume according to the pre-treatment TcTU(s) (n=146), 300 Gy to the nodule volume (n=137) and 400 Gy to the nodule volume (n=142). RESULTS: Successful elimination of functional thyroid autonomy with either euthyroidism or hypothyroidism occurred at a mean of 12 months after radioiodine therapy in 94.5% of patients receiving 100-300 Gy to the thyroid volume, in 89.8% of patients receiving 300 Gy to the nodule volume and in 94.4% receiving 400 Gy to the nodule volume. Reduction in thyroid volume was highest for the 100-300 Gy per thyroid and 400 Gy per nodule strategies (36+/-19% and 38+/-20%, respectively) and significantly lower for the 300 Gy per nodule strategy (28+/-16%; p<0.01). CONCLUSION: A dose strategy based on the TcTU(s) can be used independently of the scintigraphic pattern of functional autonomous tissue in the thyroid.

Adult↗
PubMed1993

Mechanisms of thyroid hormone action on the insulin-like growth factor system: all thyroid hormone effects are not growth hormone mediated.

Normal somatic growth requires that both the thyroid hormone axis and GH axis be intact. Thyroid hormone stimulates GH secretion, and many thyroid hormone actions on the insulin-like growth factor (IGF) system can be explained by this mechanism. We have previously described distinct changes in IGF binding protein (IGFBP) expression in experimental hypothyroidism in the rat; these changes could be completely corrected by thyroid hormone replacement. To see if the effects of thyroid hormone on IGFBP expression are, in fact, indirect GH effects, we rendered both newborn and adult rats hypothyroid with methimazole treatment, and investigated whether we could correct the resulting IGF and IGFBP changes with GH replacement. The prolonged high expression of serum IGFBP-2 and liver IGFBP-2 messenger RNA (mRNA) during the perinatal period in hypothyroid rat pups could not be normalized by GH therapy, although serum IGF-I values (reduced to 54% of control levels in the hypothyroid animals) were brought up to control level. In adult hypothyroid rats, serum IGF-I concentrations (51% of control levels), were increased up to 79% of control levels, but not totally corrected, by GH therapy. Reduced IGFBP-3 expression (80% of control serum and 50% of control liver mRNA levels) in adult hypothyroid animals was normalized by GH, but there was no correction of the reduced IGFBP-4 serum levels (50% of control levels). Hepatic mRNA levels for the type 1 and 2 IGF receptors were not altered by hypothyroidism, or by thyroid or GH replacement. Somatic growth in hypothyroid pups and adults was only partially corrected by GH therapy. We conclude that GH treatment of hypothyroid animals normalized serum IGF-I levels in the hypothyroid rat pup, but did not correct their prolonged IGFBP-2 expression. In the mature animal, serum IGF-I levels were partially corrected and IGFBP-3 levels were normalized by GH, but no change could be induced in the reduced serum IGFBP-4 levels. All the above changes were normalized by thyroid hormone replacement. Thus, the effects of thyroid hormone on serum IGF levels and IGFBP-3 expression seem to be mediated indirectly via GH. The effects on IGFBP-2 ontogeny, and IGFBP-4 expression in the mature animal, however, are either direct thyroid hormone effects, or mediated by some other route, independent of GH, IGFs, or IGF receptors.

Aging↗
PubMedDate not supplied

Thyroid ultrasonography with fine-needle aspiration cytology for the diagnosis of thyroid cancer.

This series retrospectively reviewed 3657 patients who received thyroid ultrasonography with fine-needle aspiration cytological (FNAC) examinations at Chang Gung Memorial Hospital during the period from January 1, 1993 to December 31, 1993. Thyroid ultrasonography studies were performed using a real-time ultrasonographic machine with a 10 MHz transducer. The aspirates were air dried and stained by the Romanowsky-based Liu method. Three hundred seventy-eight cases (10.3%) received surgical treatment after the ultrasonographic and FNAC examinations. Benign lesions were diagnosed in 269 patients. Thyroid malignancy was confirmed histopathologically in 109 cases including 76 papillary thyroid carcinomas, 17 follicular carcinomas, 5 medullary thyroid carcinomas, 3 anaplastic carcinomas, 3 Hürthle cell carcinomas, and 3 lymphomas. Another 2 cases were metastatic cancer to thyroid. The results demonstrated that 28.8% of the surgically treated patients had histopathologically proven malignancies. The incidence of thyroid malignancy was 2.98% in this study. The sensitivity of the cytological diagnosis was 79.80% and the specificity was 98.66%. The positive predictive value was 96.34%. Negative predictive value was 91.70%. The false negative index was 20.20%. The diagnostic accuracy was 92.89%. Thyroid ultrasonography with the FNAC can provide high specificity and sensitivity in differentiating malignant lesions from benign.

Biopsy, Needle↗
PubMed1996

Evidence of HTLV-I in thyroid tissue in an HTLV-I carrier with Hashimoto's thyroiditis.

Human T-lymphotropic virus type l (HTLV-I) protein and messenger RNA (mRNA) for HTLV-I were examined in thyroid tissues from two patients with Hashimoto's thyroiditis and serum anti-thyroid antibody. The virus envelope protein and signals for the mRNA were detected in many of the follicular epithelial cells of the thyroid tissue from one of the patients, respectively, by immunohistochemistry and in situ hybridization. PCR-Southern blotting revealed the presence of HTLV-I DNA in the thyroid tissue, in which the viral protein and mRNA were detected, although no virus particles were found in the epithelial cells by electron microscopy. HTLV-I virus was not present in the thyroid tissue from the second patient. The present findings suggest that infection of thyroid tissue with HTLV-I is associated with the pathogenesis of Hashimoto's thyroiditis in some patients.

Base Sequence↗
PubMed1983

Peroperative studies of S-calcitonin in thyroid and peripheral venous samples from patients with normal C-cells, C-cell hyperplasia, and medullary carcinoma on the thyroid.

The calcitonin (Ct) secretion was studied during surgery in 11 patients with benign thyroid and/or parathyroid disorders and in six patients with familial medullary carcinoma of the thyroid (MCT) and C-cell hyperplasia (CCH). The preoperative diagnosis of MCT and CCH was established by S-Ct determinations before and after pentagastrin provocation. During surgery blood samples were collected from thyroid and peripheral veins before and after injection of 0.6 micrograms pentagastrin . kg-1 in the inferior thyroid artery. In the control group the thyroid venous concentration of S-Ct increased from 395 +/- 42 pmol . l-1 to 2,692 +/- pmol . l-1 after intra-arterial (i.a) pentagastrin. The basal value for S-Ct in thyroid venous samples from patients with MCT and CCH was distinctly elevated in five of six patients. After pentagastrin stimulation a very prompt and striking S-Ct peak in thyroid venous samples was demonstrated (range 11,500-2,700,000 pmol . l-1), which in all cases widely exceeded that in the control group. Varying responses were registered in peripheral vein samples. S-Ct values obtained in the present investigation constitute valuable information for the interpretation of S-Ct values obtained in thyroid venous catheterization studies.

Adult↗
PubMed2002

Autoimmune thyroid disease accompanied by recurring episodes of painful thyroid ameliorated by thyroidectomy.

A 71-yr-old female initially presented with clinical and biochemical hyperthyroidism with high TSH binding inhibitory immunoglobulin (TBII) and anti-thyroid peroxidase antibody (TPOAb) titers. Histological findings of the thyroid revealed hyperplasia with a focal germinal center, indicating Graves' disease and mild focal chronic thyroiditis. Four episodes of painful and tender thyroid occurred over the next 2 yr accompanied by acute inflammatory reactions. The first episode that developed while the patient was in a hyperthyroid state was soon followed by hypothyroidism associated with further increases in anti-thyroglobulin antibody (TGAb) and TPOAb titers. The subsequent 3 episodes occurred during the hypothyroid state, when the TGAb titer progressively increased with each episode. We performed subtotal thyroidectomy to prevent further episodes. Specimens obtained at thyroidectomy showed that extreme fibrosis had replaced the thyroid parenchyma with collapsed follicles and moderate lymphocyte infiltration. No further episodes occurred after thyroidectomy, and during a 3-yr follow-up period, TBII and thyroid-stimulating antibody (TSAb) disappeared and TGAb and TPOAb titers decreased. This case report provides further evidence supporting the notion that thyroid epithelial destruction progresses during relatively short periods of recurrent painful thyroid and that thyroidectomy helps patients affected by this condition that are unresponsive to other treatment strategies.

Aged↗
PubMed1994

The presence of higher levels of thyroglobulin, but not thyroid autoantibodies, in the thyroid vein in Graves' disease.

To investigate the possible major source of thyroid autoantibodies production, blood samples were obtained from thyroid vein, jugular vein and peripheral vein during subtotal thyroidectomy in 12 patients with Graves' disease (11F, 1M; age 16-39 yr). Among them, 7 were treated preoperatively by methimazole, 4 by iopanoic acid and 1 by propranolol. All blood samples were assayed for thyroglobulin (Tg), thyrotropin binding inhibition immunoglobulin (TBII), antithyroglobulin antibody (TgAb) and antimicrosomal antibody (McAb). Tg, a native product of thyroid gland, was markedly elevated in the thyroid veins, over 4 to 6 folds that of jugular veins or peripheral veins. However, the level of thyroid autoantibodies including TBII, TgAb and McAb in the thyroid veins were not significantly different from that in the jugular or peripheral veins. Our preliminary data suggest that it is thyroglobulin, and not thyroid antibodies that is present at higher level in the thyroid vein than the periphery.

Adolescent↗
PubMed1986

L-thyroxine therapy induces a fall of thyroid microsomal and thyroglobulin antibodies in idiopathic myxedema and in hypothyroid, but not in euthyroid Hashimoto's thyroiditis.

Thyroid microsomal (MAb) and thyroglobulin (TgAb) antibodies were sequentially measured by sensitive and quantitative radioassays in 17 patients with goitrous Hashimoto's thyroiditis (9 hypothyroid, 8 euthyroid) and in 19 patients with idiopathic myxedema before and at various time intervals up to 24-48 months after the institution of L-thyroxine therapy. Thyroid antibodies were also determined in 5 euthyroid subjects with Hashimoto's thyroiditis maintained without treatment for a similar period. During L-thyroxine administration a reduction of MAb with respect to the pretreatment level was found in 6 of the 9 (67%) hypothyroid patients with Hashimoto's thyroiditis and in 16 of the 19 (84%) patients with idiopathic myxedema. The decrease of MAb was highly significant in both groups (p less than 0.001 and p less than 0.0001, respectively). A fall of TgAb occurred in 2 of the 3 patients (75%) with hypothyroid Hashimoto's thyroiditis and in 9 of the 10 (90%, p less than 0.001) patients with idiopathic myxedema having abnormally elevated pretreatment TgAB levels. No consistent pattern of MAb and TgAb changes was observed in the euthyroid subjects with Hashimoto's thyroiditis, whether treated or untreated. In the hypothyroid patients with Hashimoto's thyroiditis a significant association was found between the decrease of MAb and the reduction of goiter size (p less than 0.05) occurring during L-thyroxine administration. Moreover, the decrease of MAb and TgAb in idiopathic myxedema was greater (p less than 0.05) in the patients with normalized serum TSH (less than or equal to 4 microU/ml) than in those showing only a partial reduction of serum TSH (greater than 4 microU/ml) under L-thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Analysis of genetic regulation of chicken spontaneous autoimmune thyroiditis, an animal model of human Hashimoto's thyroiditis.

We analyzed the genetic regulation of spontaneous autoimmune thyroiditis (SAT) by means of crosses between Obese strain (OS) chickens with the disease, and healthy inbred chicken of line CB. Mononuclear cell infiltration of the thyroid was used as a criterion for the disease. We confirmed the existence of one recessive gene, regulating the susceptibility of the thyroid gland to autoimmune attack. From the frequency of progeny with the thyroid infiltration in backcross and F2 generations, we presume the existence of one or two additional dominant genes coding for abnormal reactivity of the immune system. The total number of genes regulating SAT is therefore a maximum of three. We attempted to identify disease-specific transcripts responsible for the initiation of the disease using suppression subtractive hybridization of RNA prepared from OS and CB thyroid lobes, obtained from 3-day-old chicks. From forward and reverse subtractions, we recovered a fragment mixture in the range of 300 bp to 1.5 kb. In total, 768 clones were screened and 9 were sequenced. Four of them represent unknown sequences. Two, specific for OS thyroid, correspond to envelope genes of avian endogenous viruses (ev)-1, -3 and -6. The expressed product of an env gene could be iodinated in the thyroid gland and become involved in thyroglobulin metabolism. This may be another possible mechanism driving SAT, as iodine modulates SAT in the chicken. Further experiments will be required to prove this hypothesis. Two thyroid-specific clones had significant alignment to human thyroglobulin, and one clone to human coatomer protein. We analyzed, by RFLP and RNA dot blots, cosegregation between clones for the env gene of endogenous viruses as the most promising candidate for involvement in driving SAT; we did not find differences at the DNA and RNA levels. We can possibly therefore rule out a simple involvement of env genes with the initiation of disease.

Animals↗
PubMed1999

Thyroid antibodies in children of mothers with auto-immune thyroid disease.

UNLABELLED: In a cross-sectional study, 29 children aged between 1 month and 15.3 years (average age 6.8 years) born to mothers with Graves disease or Hashimoto thyroiditis were examined clinically, biochemically, and by sonography of the thyroid gland. At the time of examination all children were clinically euthyroid. Tests of thyroid peroxidase antibody, thyroglobulin antibody, TSH receptor antibody and free thyroxine (fT4) gave normal results. In 3 children subclinical hypothyroidism with elevated TSH and normal fT4 concentrations were found; one of these children had a minor decrease of total thyroxine. Three children with otherwise normal test results had marginally elevated triiodothyronine concentrations. Increased antibody titres were present in 8 out of 29 children. TSH function-blocking antibodies were elevated in 8 cases. In addition, cytotoxic antibodies were found in one of the children. The distribution pattern of antibodies was different in each child and unrelated to the type of maternal thyroid disease. CONCLUSION: Children of mothers with auto-immune thyroid disease often have thyroid antibodies without signs of thyroid disease. Whether antibody-positive children have an increased risk of developing thyroid disorders later in life must be examined in a longitudinal study.

Adolescent↗
PubMed1984

T-cell subsets in the thyroids of mice developing autoimmune thyroiditis.

To examine the role of T-cell subsets in the development of thyroid lesions, female CBA/J mice were immunized with 60 micrograms mouse thyroglobulin (MTg) in 0.1 ml complete Freund's adjuvant in both hind footpads. The thyroids were removed 12-21 days later, pooled, and dispersed. The cell suspension was examined by membrane immunofluorescence for the distribution of Thy-1+, Lyt-1+, Lyt-2+, and sIg+ lymphocytes. For comparison, peripheral blood leukocytes (PBL) from the same animals were similarly examined. Throughout this 10-day interval, B cells in the thyroid were consistently below 5%, whereas B cells represented 19-24% of PBL. Thy-1+ cells in PBL ranged from 45 to 59%, whereas Thy-1+ cells in the thyroid were 37-50%. However, only thyroidal T cells showed a consistent decline with time and were replaced gradually by cells without T or B cell markers. In particular, there was a clear shift in the Lyt-1+:Lyt-2+ ratio from about 7 down to 2 in the thyroid as the early predominance of Lyt-1+ cells was followed by a relative increase in Lyt-2+ cells. Our results show that there is an accumulation of Lyt-1+ and Lyt-2+ cells in the infiltrated thyroid. These cells may include MTg-reactive, helper, and cytotoxic T cells which localize (or differentiate) in the thyroid and initiate the lesions.

Animals↗
PubMed1982

A microcytotoxicity assay for thyroid-specific cytotoxic antibody, antibody-dependent cell-mediated cytotoxicity and direct lymphocyte cytotoxicity using human thyroid cells.

A microcytotoxicity assay for detection of thyroid-specific complement-dependent cytotoxic antibody (cytotoxic antibody), antibody-dependent cell-mediated cytotoxicity (ADCC) and direct lymphocyte cytotoxicity was developed using human, thyroid epithelial cells as targets. Thyroid tissue was obtained from patient with Graves' disease and was treated with collagenase and then trypsin. The red blood cells, interfollicular fibroblasts and infiltrating lymphoid cells in thyroid tissue from patients with Graves' disease could be removed by this procedure. To obtain entirely single cells as target cells, the suspension of dispersed thyroid epithelial cells was allowed to stand for 1 h at 4 degree C in culture medium to allow cell clumps to settle. For assay of cytotoxic antibody, a mixture of the single target cells, patient's serum and human complement was incubated in microwells for 18 h. After removing the detached cells, remaining target cells in the wells were fixed, stained and counted to assess cytotoxicity. For assay of ADCC and of direct lymphocyte cytotoxicity, target thyroid cells were precultured in the microwells for 18 h. Then effector cells with or without patient's serum were added and cultured further for 24-72 h. Cytotoxicity was assessed as described above. Adherence of effector cells to target thyroid cells sometimes disturbed the enumeration of target cells when the effector/target cell ratio was high. With this microassay system 3 different cytotoxic immune reactions against human thyroid cells could be measured quantitatively at the same time on 2-3 ml blood samples.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1991

Previous thyroid disease and risk of thyroid cancer in Switzerland.

A hospital-based case-control study of 86 cases of thyroid cancer and 317 controls was done in the Swiss Canton of Vaud. Patients with thyroid cancer tended to be better educated (odds ratio [OR] 2.1 for greater than or equal to 14 vs. less than or equal to 8 years of education 95% CI 1.1-4.1) and of higher social class than controls. Cases more often had a history of benign thyroid nodules (OR 25.2, 95% CI 7.6-83.6) and non-toxic goitre (OR 5.3, 95% CI 2.5-11.2). Furthermore, patients with thyroid cancer were more likely to have resided in endemic goitre areas (OR 1.7, 95% CI 1.0-3.0) and to have had first-degree relatives affected by benign thyroid disease (OR 3.9, 95% CI 2.1-7.1). Therefore, this study offers quantitative evidence of the association between various thyroid diseases and the risk of thyroid cancer which, despite difficulties in the classification of benign and malignant thyroid diseases, is remarkably consistent in studies from different countries.

Adolescent↗
PubMedDate not supplied

A study of thyroid function and prevalence of thyroid autoantibodies in an African diabetic population.

It is generally believed that autoimmune disorders are uncommon in Africans. Some workers have argued that insulin-dependent diabetes mellitus (IDDM) is rare in Africa on account of this reduced proneness to autoimmunity. However, it is undetermined whether or not Africans with IDDM have increased prevalence of thyroid dysfunction and autoimmunity, two phenomena strongly associated with Caucasian IDDM. We determined thyroid function and the prevalence of thyroid autoimmunity in IDDM Africans. The results are compared with those of a nondiabetic group and a group with non-insulin-dependent diabetes mellitus (NIDDM). Thyroid hormone levels were significantly lower in IDDM patients than in the control population and the NIDDM population. Subclinical hypothyroidism was present in 21% of the 28 IDDM patients. One patient was hypothyroid and another hyperthyroid. Of the 60 NIDDM patients, 5 (8.3%) had subclinical hypothyroidism. Forty-six percent of the IDDM patients had significant levels of serum thyroid autoantibodies (TAAB). This was significantly higher than the 1.4% and 1.7%, respectively, in the controls and NIDDMs. Presence of TAAB in the patients was strongly associated with thyroid dysfunction, female preponderance, and duration of diabetes mellitus. Thyroid dysfunction and autoimmunity are common in Nigerians clinically diagnosed as IDDM, and have prevalence rates comparable to other populations but higher than rates previously reported from some other African groups. The increased prevalence of thyroid autoimmunity in the IDDM supports the view that these patients are true IDDMs rather than variants of NIDDM or malnutrition-related diabetes mellitus (MRDM) as has been suggested by some workers.

Adult↗
PubMed2004

Ultrastructural localization of thyroid peroxidase, hydrogen peroxide-generating sites, and monoamine oxidase in benign and malignant thyroid diseases.

Despite thyroid tissue heterogeneity, biochemical and morphological features have been associated with certain thyroid diseases. We analyzed the ultracytochemical localization of thyroperoxidase (TPO), TPO-associated hydrogen peroxide-generating sites (H(2)O(2) sites), and monoamine oxidase (MAO) in terms of morphology and biochemical TPO activity in abnormal thyroids. We examined 11 cases of nontoxic multinodular goiter, 5 cases of Hashimoto's thyroiditis, 1 case of oncocytic (Hürthle or oxyphilic cell) adenoma, 5 cases of Graves' disease, 4 cases of papillary carcinoma, and 4 cases of perinodular normal tissue. In the perinodular tissue, TPO was detected mainly in the nuclear envelope, rough endoplasmic reticulum (RER), and subapical vesicles, but not in the apical surface. In multinodular goiter, heterogeneous TPO reactivity ranging from almost null to strongly positive was detected in similar locations as in the perinodular tissue, and was absent in the microvilli. Follicular cells from Hashimoto's thyroiditis displayed TPO in the nuclear envelope and the scarce RER. Remarkably, oncocytic cells from both Hashimoto's thyroiditis and oncocytic adenoma, typically packed with mitochondria, displayed evident TPO reaction exclusively in mitochondrial cristae. In Graves' disease, the nuclear envelope, enlarged RER, and apical vesicles were strongly TPO positive, and microvilli also exhibited TPO activity. Papillary carcinoma cells were negative for TPO. The localization and characteristics of TPO activity in the H(2)O(2) sites were similar to that of TPO in all tissues. MAO was positive in mitochondria of perinodular tissues, multinodular goiter, and oncocytes and negative in Hashimoto's thyroiditis and Graves' disease. Interestingly, MAO was intensely positive in the nuclear envelope of papillary carcinoma but unreactive in mitochondria. Biochemical TPO activity was increased in multinodular goiter and Graves' disease. In conclusion, several changes in ultracytochemical characteristics of TPO, H(2)O(2) sites, and MAO were associated with thyroid disease. Nonmalignant oncocytic cells exhibited an unusual mitochondrial location of TPO and H(2)O(2) sites. The distribution of MAO in nuclear envelope of papillary carcinoma cells could be a further feature of malignancy.

Humans↗
PubMed2002

Differentiation between healthy thyroid remnants and tumor tissue after radioiodine therapy in patients with differentiated thyroid carcinoma using in vitro phosphorus-31 magnetic resonance spectroscopy.

BACKGROUND: The growth and spread of many tumors are triggered by changes in cell membrane metabolism, which can lead to systemic alterations in levels of phospholipids. We sought to determine whether plasma levels of several phospholipids could differentiate between healthy remnants of thyroid tissue and residual tumor tissue or metastases in patients with thyroid carcinoma. METHODS: We measured plasma phospholipid levels by phosphorus-31 magnetic resonance spectroscopy (31P-MRS) in blood samples from 30 patients with thyroid cancer who had been rendered hypothyroid in preparation for diagnostic or therapeutic administration of iodine-131. All patients had undergone total thyroidectomy. Iodine-131 whole-body scintigraphy and measurements of thyroglobulin values during up to 3 years of follow-up were used to distinguish patients in remission from those with only healthy thyroid remnants and those with tumor tissue or metastases. RESULTS: Mean (+/- SD) levels of sphingomyelin (0.33 +/- 0.06 mmol/L vs. 0.46 +/- 0.03 mmol/L, P <0.0001) and phosphatidylcholine (1.34 +/- 0.19 mmol/L vs. 2.15 +/- 0.33 mmol/L, P <0.0001) were significantly lower in patients with metastatic thyroid cancer (n = 8) than in patients (n = 12) who were in remission. Patients with only remnants of thyroid tissue (n = 10) also had significantly lower phospholipid levels than did patients in remission, but significantly greater levels that did patients with tumor tissue or metastases. CONCLUSION: These preliminary results suggest that 31P-MRS may be useful in helping to differentiate the presence of tumor tissue, remnants of thyroid tissue not requiring further treatment, and remission in patients with thyroid cancer.

Adult↗
PubMed2001

[Immunodetection of thyroid peroxidase in the diagnosis of follicular variants of thyroid papillary cancer].

STUDY AIM: The aim of this retrospective study was to assess the role of thyroid peroxidase immunodetection in the cytological diagnosis of follicular variants of thyroid papillary cancer (FVTPC) which are difficult to identify by standard cytology. PATIENTS AND METHODS: Between 1991 and 1998, 3,505 thyroid fine needle aspiration biopsies were performed by thyroid peroxidase immunocytochemistry and 1,576 patients were operated on. Out of a total of 227 thyroid papillary cancers (TPC), 42 (18.5%) were diagnosed as FVTPC. The results of standard cytology and thyroid peroxidase immunodetection were compared with the histological findings. RESULTS: The rate of false negatives for TPC in standard cytology was 11% (25/227 cases), with 40% of these false negatives being FVTPC; ten out of 42 (23.8%) cases of FVTPC were not identified by standard cytology. However, cytology with thyroid peroxidase immunodetection diagnosed 224 out of the 227 TPC (99%), and all the FVTPC were correctly identified (100%). CONCLUSION: FVTCP are the most frequent source of false negatives in standard cytology. Thyroid peroxidase immunodetection allows most of these errors to be avoided, and correctly identifies 99% of TPC including FVTPC.

Biopsy, Needle↗
PubMed1988

Primary B cell lymphoma of the thyroid and its relationship to Hashimoto's thyroiditis.

Twenty-one cases were selected from 236 thyroidectomies with a diagnosis of Hashimoto's disease for detailed clinicopathologic study on the basis of "early" changes in three cases and an unusually heavy lymphoplasmacytic infiltrate in 18 cases. These cases were studied in conjunction with ten cases of high-grade non-Hodgkin's lymphoma of the thyroid. Immunoglobulin light chain restriction was demonstrated in five cases of Hashimoto's thyroiditis and the diagnosis was accordingly changed to low-grade lymphoma. All ten high-grade lymphoma cases were of B phenotype and light chain restriction could be demonstrated in eight of them. The study revealed close homology between the lymphoplasmacytic infiltrate in Hashimoto's thyroiditis and normal mucosa-associated lymphoid tissue (MALT). Like lymphomas of mucosal sites, thyroid lymphoma appears to be derived from the parafollicular ("centrocyte-like") B cells. The high-grade thyroid lymphomas appear to be derived from low-grade tumors. There were close histologic, immunohistologic, and clinical similarities between low- and high-grade non-Hodgkin's lymphomas of the thyroid and those appearing in mucosal sites. This study confirms the close association between Hashimoto's thyroiditis and B cell lymphoma of the thyroid gland and suggests that this tumor belongs to the group of non-Hodgkin's lymphomas derived from MALT.

Adult↗