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PubMed1984

Influence of cigarette smoking on goiter formation, thyroglobulin, and thyroid hormone levels in women.

The possible influence of cigarette smoking on goiter formation, thyroglobulin (Tg) secretion, and thyroid hormone production was assessed by estimations of the presence of palpable goiter and by RIAs of Tg, T3, rT3, T4, and TSH in sera from 441 women (48-53 yr old), representing a normal population included in a study on the prevalence of thyroid disease. Smoking habits were evaluated by a questionnaire, and the women were then classified as never smokers (n = 192), smokers (n = 169), and exsmokers (n = 80). Smokers were subdivided as moderate (1-19 cigarettes/day) and heavy (greater than or equal to 20 cigarettes/day). Palpable goiter was found in 15% of the smokers, in contrast to only 4% of the exsmokers and 9% of the never smokers. Among smokers, 37% had serum Tg values over 30 micrograms/liter (third quartile), while such values were found in only 16% of the exsmokers and 18% of the never smokers. In addition, smokers were found to have higher serum T3 and lower rT3 concentrations than never smokers; this difference was most pronounced in heavy smokers. Serum T4 was not different, while TSH was insignificantly lower in smokers than in nonsmokers. Exsmokers did not differ significantly from never smokers in any of these parameters. It seems possible that cigarette smoking may have two, calorigenically opposed, effects on thyroid hormone production; it may be goitrogenic (possibly due to inhaled thiocyanate), but it may also enhance the formation of T3 at the expense of rT3 formation.

Body Weight↗
PubMed1985

The effectiveness of oral iodized oil in the treatment and prophylaxis of endemic goiter.

In a longitudinal study carried out for 2 yr in the Darfur region, western Sudan, 2316 school children received a single dose of 2 capsules of iodized oil (400 mg iodine) orally, and 1161 school children received 1 ml of the same preparation im (475 mg iodine); 2393 school children served as controls. One year after treatment, goiter prevalence was reduced from 67.0% to 36.0% among the children who had received oral iodized oil and from 71.0% to 42.0% in those who received it im. The prevalence in the control group did not change. The prevalences in each group were approximately the same 2 yr after treatment. Urinary iodine excretion increased after treatment and remained significantly higher than the initial value during the trial. In subjects from rural Darfur, serum T4 levels were increased 1 yr after treatment with oral iodized oil (P less than 0.001) and im iodized oil (P less than 0.01), and remained high in the former (P less than 0.05) but not in the latter. This increase was accompanied by reduction of serum T3 and TSH levels. Sialadenitis occurred in 3.7% of the children who received oral iodized oil. Thyroid antibodies were not detected before treatment, but microsomal antibodies were detected in 2 of the 128 subjects studied who received iodized oil orally. Comparable results occurred when oral and im iodized oil were given to 841 individuals covering a wider age range. It is concluded that a single oral dose of iodized oil is effective in the correction of iodine deficiency, reducing the goiter size and preventing the recurrence of goiter for at least 2 yr.

Administration, Oral↗
PubMed1990

Defective neuromotor and cognitive ability in iodine-deficient schoolchildren of an endemic goiter region in Sicily.

Visual perceptual integrative motor ability was investigated in 719 6- to 12-yr-old, presumably normal, primary schoolchildren living in 2 iodine-deficient endemic goiter areas in Sicily, identified on the basis of the presence (area A) or absence (area B) of endemic cretinism, by administrating the Bender Gestalt test. All of these clinically euthyroid schoolchildren were also examined neurologically by an investigator unaware of the result of the Bender test. Ninety-nine (13.76%) schoolchildren were found to be defective by the Bender test; this prevalence was significantly higher than that (3.0%) found in an iodine-sufficient goiter-free control area (area C) lying at sea level (chi 2 = 36.25; P less than 0.000001). No difference in the prevalence of Bender abnormalities was apparent if the children were divided according to the area of provenience (area A, 14.4%; area B, 13.1%). A high percentage of children falling in the lower range of normality was found in both area A (15.5%) and area B (19.0%); this was significantly higher than that in area C (3.8%; chi 2 = 77.55; P less than 0.000001). Neuromuscular and neurosensorial abnormalities, including increased tendon reflexes, clonus of the foot, Babinski sign, minor disturbances in balance, and gait, and minor defects in hearing and speech, were apparent in 19.3% (area A) and 18.5% (area B) of the children. These disorders were significantly more frequent in defective children identified by the Bender test (33.3%) than in normal children (15.3%; (chi 2 = 17.29; P less than 0.00005). The general intellectual aptitude in Bender deficient subjects was evaluated by the Terman Merrill test and was found to be impaired in 95%, thus confirming the existence of an endemic cognitive deficiency (ECD), distinct from the endemic mental deficiency previously found in other endemic goiter, iodine-deficient areas. ECD seems to be epidemiologically independent of the existence of endemic cretinism. Further clinical auxological and biochemical studies in a selected group of ECD children suggested the epidemiological and, possibly, pathogenic association of cognitive impairment with iodine deficiency.

Bender-Gestalt Test↗
PubMed1990

Cold follicles in a multinodular human goiter arise partly from a failing iodide pump and partly from deficient iodine organification.

To investigate whether the common cold follicles in human multinodular goiters are the consequence of a functional defect of the apical membrane peroxidase, a failure of the iodide transport system, or both deficiencies, we studied iodide accumulation and iodine organification in 30 fragments of a large multinodular goiter transplanted to nude mice and labeled with 125I. Transplants were frozen to -80 C immediately after removal to avoid diffusion of inorganic iodide. Autoradiographic assessment of over 1000 cryosections (exposed either at -20 C or after thawing and washing out unbound iodide) showed two types of cold follicles, namely those that failed to accumulate iodide and, therefore, did not organify iodine, and those that readily accumulated iodide but failed to bind it, suggesting a failure of apical membrane peroxidase. The two types of pathogenetically different cold follicles coexisted in an apparently randomly intermingled fashion throughout the whole goiter.

Aged↗
PubMed1993

Integrin expression in thyroid cells from normal glands and nodular goiters.

To assess the expression of the very late antigens family of the integrin superfamily in normal and diseased thyroid glands, tissue specimens were digested to a single cell suspension and analyzed by flow cytometry with antibodies against the common beta 1 chain and the six alpha chains known to be associated to beta 1. In multinodular goiters, two cell populations were recognized. The thyroglobulin containing follicular cell population, represented the majority of cells; a minor population was composed of leukocytes. In normal glands, more than 97% of follicular cells expressed the beta 1 chain, associated with high levels of alpha 3 and very low levels of alpha 1, alpha 5, and alpha 6. The remaining cells (< 3%) expressed the beta 1 chain with a 10-fold higher intensity, associated with relatively high levels of alpha 1, alpha 5, and alpha 6, in addition to alpha 3. This small subset was much more represented in multinodular goiters, where it ranged from 10-60% of the total follicular cell population. Immunofluorescence on tissue sections showed that very late antigens were mostly located on the basal cell membrane and that in multinodular goiters cells expressing the alpha 1, alpha 5, and alpha 6 chains occurred in clusters.

Flow Cytometry↗
PubMed1999

Is routine thyroxine treatment to hinder postoperative recurrence of nontoxic goiter justified?

Previous reports regarding the efficacy of levo-T4 (L-T4) in preventing postoperative recurrence of nontoxic goiter have been controversial. This study was designed to evaluate the influence of long-term L-T4 treatment on thyroid volume after thyroidectomy for nontoxic goiter. We studied 202 consecutive patients operated on for benign nontoxic goiter and followed them for a minimum of 12 months (median, 10 yr; range, 1-14 yr). Three months after thyroidectomy, patients were randomized to L-T4 treatment (group A, n = 100) with an initial dose of 150 microg daily and to no treatment (group B, n = 102). All were clinically and biochemically euthyroid, and preoperatively none were taking any thyroid and/or antithyroid medication. Standard thyroid function variables and ultrasonically determined thyroid volume (normal range, 9-28 mL) were determined before and 3 and 12 months after randomization and yearly thereafter. Recurrence was defined as an ultrasonically enlarged thyroid gland. Clinical data were similar between the two groups. Incidence of recurrence in group A was 19/100 (21%; 95% CL 0-42%; life-table analysis) and in group B 27/102 (35%; CL 7-64%) (P = 0.16) and was related to removed amount, remnant size, and pathoanatomical diagnosis but not type of operation or postoperative level of serum TSH and T4. L-T4 dose had to be reduced in 36 of 100 patients because of side effects of the treatment. In conclusion, the possible benefits of L-T4 treatment should be weighed against the possible side effects. Our study does not support the routine postoperative use of L-T4.

Adult↗
PubMed1999

Concurrence of Pendred syndrome, autoimmune thyroiditis, and simple goiter in one family.

Pendred syndrome is the autosomal recessively transmitted association of familial goiter and congenital deafness. There is no specific biochemical marker of this disease, and the diagnosis depends upon the demonstration of the triad of congenital sensorineural hearing loss, goiter, and abnormal perchlorate discharge test. Pendred syndrome is caused by mutations within the putative ion transporter gene (PDS gene), located on chromosome 7q. A wide variation in the clinical presentation of this condition, and its well documented phenotypic overlap with other thyroid disorders (such as Hashimoto's thyroiditis), can lead to diagnostic difficulties. The potential for misdiagnosis increases when these disorders occur coincidentally in the same family. We describe a kindred in which Pendred syndrome, autoimmune thyroiditis, and simple goiter coexisted, to highlight these diagnostic pitfalls and to illustrate the use of mutational analysis in resolving diagnostic confusion.

Adult↗
PubMed2000

Activating thyrotropin receptor mutations are present in nonadenomatous hyperfunctioning nodules of toxic or autonomous multinodular goiter.

Toxic multinodular goiter, a heterogeneous disease producing hyperthyroidism, is frequently found in iodine-deficient areas. The pathogenesis of this common clinical entity is still unclear. The aim of the present study was to search for activating TSH receptor (TSHr) or Gs alpha mutations in areas of toxic or functionally autonomous multinodular goiters that appeared hyperfunctioning at thyroid scintiscan but did not clearly correspond to definite nodules at physical or ultrasonographic examination. Surgical tissue specimens from nine patients were carefully dissected, matching thyroid scintiscan and thyroid ultrasonography, to isolate hyperfunctioning and nonfunctioning areas even if they did not correspond to well-defined nodules. TSHr and Gs alpha mutations were searched for by direct sequencing after PCR amplification of genomic DNA. Only 2 adenomas were identified at microscopic examination, whereas the remaining 18 hyperfunctioning areas corresponded to hyperplastic nodules containing multiple aggregates of micromacrofollicules not surrounded by a capsule. Activating TSHr mutations were detected in 14 of these 20 hyperfunctioning areas, whereas no mutation was identified in nonfunctioning nodules or areas contained in the same gland. No Gs alpha mutation was found. In conclusion, activating TSHr mutations are present in the majority of nonadenomatous hyperfunctioning nodules scattered throughout the gland in patients with toxic or functionally autonomous multinodular goiter.

Adenoma↗
PubMed2001

Tie-2 is expressed on thyroid follicular cells, is increased in goiter, and is regulated by thyrotropin through cyclic adenosine 3',5'-monophosphate.

Angiogenesis is coordinated with follicular cell growth in goitrogenesis. The angiopoietins, Ang-1 and Ang-2, are angiogenic growth factors acting through Tie-2, a tyrosine kinase receptor. We have examined the expression and regulation of the angiopoietins and Tie-2 in human and rat thyroids. In human goiters there was increased Tie-2 immunostaining, compared with that in normal thyroids, on both follicular and endothelial cells. In an induced goiter in rats, in situ hybridization showed increased expression of messenger ribonucleic acids (mRNAs) for Tie-2 and Ang-1 in follicular cells. As Tie-2 has previously been believed to be restricted to cells of endothelial lineage in adults, we examined its expression further in isolated follicular cells. Tie-2 and Ang-1 mRNA expression in human thyrocytes was confirmed by ribonuclease protection assay. Ang-2 mRNA was not detected in human cultures or rat thyroids. In both human follicular cell cultures and FRTL-5 cells, immunoblotting showed that Tie-2 expression was increased by TSH and agents that increased intracellular cAMP. In conclusion, we have demonstrated the expression of Tie-2 and Ang-1 in thyroid epithelial and endothelial cells, and have shown the regulation of Tie-2 by TSH and cAMP in follicular cells. Tie-2 expression is increased in goiter in both humans and rats, consistent with a role in goitrogenesis.

Angiopoietin-1↗
PubMed2002

Management of the nontoxic multinodular goiter: a North American survey.

To assess approaches to the diagnosis and therapy of patients with nontoxic multinodular goiter, a questionnaire was circulated to all members of the American Thyroid Association (ATA). An index case report was presented (42-yr-old woman with an irregular, nontender, bilaterally enlarged thyroid of 50-80 g and no clinical suspicion of malignancy or thyroid dysfunction), and 11 variations were proposed to evaluate how each alteration would affect management. One hundred and forty responses were retained (approximately 50% of clinically active ATA members). For the index case, a TSH determination was the routine choice of 100%, and serum thyroid autoantibodies were measured by 74%. Simultaneous use of serum TSH, a thyroid hormone assay, and antithyroid peroxidase was employed by 49%. Only 4% included a calcitonin assay. The median number of blood tests ordered was 3 (range, 1-7). Ultrasound was used by 59%, thyroid scintigraphy by 24%, and both imaging modalities by 11%. Fine needle aspiration biopsy (FNAB) was performed by 74%. If scintigraphy showed inhomogeneous tracer distribution or a dominant hypofunctioning region, FNAB was performed by 15% and 97%, respectively. L-T4 treatment was preferred by 56%, radioiodine by 1%, surgery by 6%, and 36% would recommend no treatment. A large goiter, a history of external radiation, or rapid growth increased the preference for surgery. In case of a suppressed serum TSH level, radioiodine was used by 56%. In conclusion, in the work-up of patients with nontoxic multinodular goiter, ATA clinicians employ determinations of TSH often combined with a T4 and/or T3 assay and antithyroid peroxidase antibodies. Thyroid imaging, primarily ultrasound, is performed by more than two thirds, and FNAB by three fourths. This diagnostic evaluation is significantly less extensive than that of the European Thyroid Association members, but the distribution of treatment choices is quite similar. In accordance with their European colleagues, the majority of ATA members prefer the use of L-T4 therapy. There is, however, still a wide variation in the perceived optimal management of this condition among members of both organizations.

Autoantibodies↗
PubMed1991

Epidemiological and pathological studies on congenital diffuse hyperplastic goiter in calves.

Perinatal diseases such as weak calf, stillbirth, or abortion were found in 86 calves from about 600 cows in a farm (A Farm) in 1987 and 1988. Such perinatal diseases were decreased to 36 calves in 1989 and 1990 after an additional supply of seaweed was made to the maternal feeds. From these cases, 23 stillborn and weak calves were pathologically examined. The mean weight with standard deviation of the 18 thyroid glands was 36.3 +/- 28.6 g before feeding of the seaweed supplement, and 12 (67%) of the glands showed moderate to marked degree of diffuse hyperplastic goiter in histological criteria. On the other hand, 5 glands weighed 12.0 +/- 3.4 g and revealed no such histological lesions after the additional supply. These results suggest that the goiter had been associated with birth of weak calves. Further study was performed on 37 newborn calves affected with Akabane disease in 1986 in A Farm and the neighbouring B Farm located. Seven (54%) of 13 thyroid glands from A Farm and 1 (4%) of 24 glands from B Farm showed histologically moderate to marked goitrous lesions. There were dotted "Inugarashi", Rorippa indica, family Cruciferae in both pastures. The mean iodine contents of the orchard grasses were 87 and 121 micrograms/kg on dry basis in A and B Farms. Marginal deficiency or lower limit of iodine and possible thiocyanate content of "Inugarashi" may have been responsible for the goiter in the farms.

Abortion, Veterinary↗
PubMed1983

[2 cases of Hashitoxicosis with histological features of adenomatous goiter].

Two male patients with 'Hashitoxicosis', who revealed histologic pictures of adenomatous goiter in addition to findings of chronic thyroiditis, are described. Case 1. A 55-year-old man was admitted on May 7, 1981, for evaluation of hyperthyroidism. He had exophthalmos with positive Moebius and von Graefe's signs, and a firm, asymmetrically enlarged non tender thyroid gland with multiple cysts. The BMR was +60%, T4 26.4 micrograms/dl, free T4 7.2 ng/dl, T3 5.62 ng/ml and 24 hr radioiodine uptake 49.5%. TSH was undetectable and did not respond to TRH. 123I scan showed multiple defects in the bilateral upper poles of the thyroid gland. Antithyroglobulin and antimicrosomal antibodies were positive. He then underwent a total thyroidectomy with removal of multinodular goiter. The mutinodular goiter was associated with cystic degeneration which contained the thyroid hormone-rich fluid. Histologic examination revealed multiple adenomatous nodules and lymphocytic infiltration and degeneration in the surrounding tissues of the nodules. Case 2. A 43-year-old man was admitted on May 14, 1975, because of an 8 month history of hand tremor, weight loss (5 kg), facial and upper palpebral edema and an enlarged thyroid. He had mild exophthalmos and a firm, asymmetrically enlarged thyroid gland with multiple nodules. The BMR was +35%, T4 20.0 micrograms/dl, T3(Resomat) 0.78 ng/ml and PBI 20.0 micrograms/dl. TSH was 1.0 muU/ml and responded slightly to TRH. 24 hr radioiodine uptake was 84.4% and did not respond to T3 administration. Antithyroglobulin and antimicrosomal antibodies were positive. 123I scan showed diffusely increased uptake and no defects. Histologic examination of the biopsy specimen of the thyroid gland showed multiple adenomatous nodules in addition to typical findings of chronic thyroiditis in the surrounding tissues of the nodules. From the above observations, it is suggested that multiple adenomatous nodules accompanying chronic thyroiditis show clinical features resembling Basedow's disease rather than Plummer's disease.

Adenoma↗
PubMed1998

Missense mutation (C1263R) in the thyroglobulin gene causes congenital goiter with mild hypothyroidism by impaired intracellular transport.

Metabolic abnormalities in thyroid hormonogenesis cause congenital goiter. Here we studied a case of mild hypothyroidism caused by a novel missense mutation in the thyroglobulin (TG) gene. A female patient underwent thyroidectomy twice at the age of 27 and 43 years because of gradual enlargement of the thyroid. By RNase cleavage assay and PCR direct sequencing we identified a thymine to cytosine transition at nucleotide 3828 (from the transcription start site) which causes amino acid change from cysteine to arginine at codon 1263. A pedigree study suggested autosomal recessive inheritance due to consanguineous marriage of her parents. Immunohistochemical study suggested impaired intracellular transport of the mutant TG. Sensitivity to endoglycosidase H confirmed that the mutant TG failed to reach the Golgi compartment. Native polyacrylamide gel electrophoresis and Western blot analyses showed that formation of monomers and homodimers was defective with abundant high molecular-weight aggregates which are normally formed transiently after translation. To examine if the mutant TG is functionally defective, we separated thyroid tissue extract on a Biogel A5m column and measured T4 and T3 released from proteins in each fraction by treatment with proteinase K. Although thyroid hormones released per mole of the mutant TG protein did not decrease, those released per mg of total protein decreased. In conclusion, the missense mutation in the TG gene caused congenital goiter with mild hypothyroidism due to an altered protein structure which resulted in defective intracellular processing and premature degradation by "quality control" mechanisms. Although the tissue TG content was greatly reduced, the hypothyroidism was mild with slow progression of the goiter, because the mutant TG was a relatively good substrate for the synthesis of the thyroid hormones.

Adult↗
PubMed2005

Mutations in the thyrotropin receptor signal transduction pathway in the hyperfunctioning thyroid nodules from multinodular goiters: a study in the Turkish population.

Many studies have been carried out to determine G(s) alpha and TSHR mutations in autonomously functioning thyroid nodules. Variable prevalences for somatic constitutively activating TSHR mutations in hot nodules have been reported. Moreover, the increased prevalence of toxic multinodular goiters in iodine-deficient regions is well known. In Turkey, a country with high incidence rates of goiter due to iodine deficiency, the frequency of mutations in the thyrotropin receptor signal transduction pathway has not been evaluated up to now. In the present study, a part of the genes of the TSHR, G(s)alpha and the catalytic subunit of the PKA were checked for activating mutations. Thirty-five patients who underwent thyroidectomy for multinodular goiters were examined. Genomic DNAs were extracted from 58 hyperactive nodular specimens and surrounding normal thyroid tissues. Mutation screening was done by single-strand conformational polymorphism (SSCP) analysis. In those cases where a mutation was detected, the localization of the mutation was determined by automatic DNA sequencing. No G(s)alpha or PKA mutations were detected, whereas ten mutations (17%) were identified in the TSHR gene. All mutations were somatic and heterozygotic. In conclusion, the frequency of mutations in the cAMP signal transduction pathway was found to be lower than expected in the Turkish population most likely because of the use of SSCP as a screening method and sequencing only a part of TSHR exon 10.

Adolescent↗
PubMedDate not supplied

Huge adenomatous goiter reaching the aortic arch with elevated thyroglobulin.

We report a 14 year-old girl with a huge adenomatous goiter in the left lobe in the thyroid gland reaching the aortic arch with elevated thyroglobulin. The tumor grew rapidly for two years since the initial diagnosis as an euthyroid hemilateral goiter. Ultrasonography revealed multinodular tumors and magnetic resonance imaging made clear the lower expanding site of the tumor. We recommend careful follow up of hemilateral diffuse goiters by ultrasonography for earlier detection of nodular changes as seen in our case.

Adenoma↗
PubMed2001

Fas and Bcl-2 protein expression in thyrocytes of patients with nodular goiter.

OBJECTIVE: The relative expression of the apoptotic protein Fas and the anti-apoptotic protein Bcl-2 were investigated in thyrocytes from patients with non-toxic nodular goiter (NTG, n=20) and Hashimoto's thyroiditis (HT, n=5), who underwent fine-needle aspiration biopsy for diagnostic reasons. On the basis of the clinical and cytological findings, the patients with NTG were sub-classified into the group of those with colloid nodules (n=9), degenerative nodules (n=6) and adenomatous nodules (n=5). METHODS: Fine-needle biopsy aspirates were examined by immunocytochemistry for Fas and Bcl-2 expression, using specific monoclonal antibodies. For the evaluation of Fas and Bcl-2 immuno-reactivity, an expression index, based on the number of cells with positive staining, was used: grade 1 included samples with positive staining in <20% of cells; grade 2 included samples with 20-50% positive cells; and grade 3 included samples with >50% positive cells. RESULTS: Fas protein expression was generally low (grade 1) in patients with nodular goiter, in contrast to patients with HT, in whom high expression was detected (grade 3). Only in aspirates from degenerative nodules (four out of six), and in which lymphocytes were also present, was Fas expressed at an intermediate level (grade 2). On the other hand, Bcl-2 protein was differentially expressed among the nodule subtypes. It was low in colloid and degenerative nodules (grade 1) but high in adenomatous ones (grades 2 and 3). Bcl-2 expression was also low in patients with HT (grade 1). CONCLUSION: It is concluded that in comparison to HT, where there is up-regulation of Fas and down-regulation of Bcl-2 protein, Fas expression is low in human goiter, indicating low apoptotic activity. The regulation of Bcl-2 protein differs between adenomatous and colloid nodules, suggesting that this protein may play a role in the differentiation of thyroid nodules.

Adult↗
PubMed2003

[Papillary carcinoma of the thyroid in intrathoracic goiter].

Intrathoracic goiter (more than 80% of tissue in the thoracic cavity) represents very rare clinical entity (less than 1% of total number of thyroid gland surgical procedures). Cancer incidence in these goiter is 0-5%. The aim of this article is to present a case report of intrathoracic thyroid papillary carcinoma with multiple compressive syndrome and review of compressive intrathoracic syndrome of thyroid etiology. In our patient we have found: tracheal and oesophageal deviation and compression, superior vena cava syndrome, downhill varices, chylothorax, pericardial effusion, compress of the left a. subclavia, unilateral lesion of recurrent and phrenic nerve, and brachial plexopathy. This was a unique case with multiple compressive syndrome between 3000 patients surgically treated for all kinds of thyroid diseases. Intrathoracic goiter can cause all the known symptoms and syndromes of intrathoracic compression with possibility of rapid deterioration and fatal end.

Carcinoma, Papillary↗
PubMed2003

[Characteristics of thyroid carcinoma in Grave's disease Hashimoto's thyroiditis and nodular goiter].

The biology of thyroid cancer represents a spectrum of behavior ranging from well-differentiated lesions with an excellent prognosis to anaplastic carcinoma, which is almost fatal. For this reason, it is important that clinicians have methods at their disposal to asses the characteristics of patient's thyroid malignancy. In this work we discuss the behavior of differentiated thyroid cancer in associated diseases of thyroid as: Graves' disease, chronic lymphocytic thyroiditis--Hashimoto and nodular goiter. This is retrospectively reviewing of 50 patients treated for differentiated thyroid carcinoma at Department of surgery, Clinical Centre of Montenegro in Podgorica from 1998 until 2003. We evaluated occurrence, as well as the role of this diseases in patients with thyroid cancer. We found a more favorable course of thyroid cancer in the presence of chronic lymphocytic thyroiditis and nodular goiter, a contrary Graves' disease. In associated diseases of thyroid, a significantly greater proportion of patients with thyroid cancer, have modular goiter.

Carcinoma↗