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Follicular carcinoma in ectopic thyroid gland. A case report.

Ectopic thyroid rest can be seen anywhere along the path of descent of the gland. The most ectopic thyroid tissue is a thyroglossal duct cyst associated with normal thyroid gland. Sublingual location is less common than a lingual ectopia. True malignant transformation in ectopic thyroid tissue is extremely rare. Such a malignancy is virtually always diagnosed only after surgical excision of the lesion at pathological examination. This report discusses a case of ectopic thyroid follicular carcinoma in the right submandibular region in the absence of orthotopic thyroid, discovered by chance after the surgical excision performed for a preoperative ultrasonically and cytologically misdiagnosed submandibular gland adenocystic carcinoma. The possible aetiology of such an unusual anatomical relationship is discussed as well as the importance of thyroid scanning, ultrasound and/or CT in neck lumps.

Adenocarcinoma, Follicular↗

Brown bowel syndrome with manifestation in the gastrointestinal tract and thyroid gland.

Brown bowel syndrome (BBS) is a rare disease accompanied by deposits of lipofuscin predominantly in smooth muscle cells of the gastrointestinal tract. To determine whether cells other than smooth muscle cells show pigment deposition we studied biopsies of the stomach, small and large intestine, and thyroid gland of a 52-year-old male with malabsorption syndrome. Light and electron microscopy found lipofuscin pigment in vascular endothelial cells and in smooth muscle cells of the muscularis mucosae, arterioles and venules of the gastrointestinal tract and thyroid gland. All other cells of bowel and thyroid gland, such as epithelial cells, Schwann cells, nerve fibers, fibroblasts, macrophages and leukocytes, showed no such pigment inclusions. Intracellular lipofuscin deposition is thought to be caused by a deficiency of vitamin E. Such a deficiency existed in our patient and was attributed to a six year history of malabsorption syndrome with complete atrophy of the villi of the intestinal mucosa. Lipofuscin pigmentation has been reported in numerous organs of patients with BBS but not, until now, in the thyroid gland or in endothelial cells of lymph vessels. The origin of lipofuscin pigment is not known exactly. The prevailing opinion is that it derives from degenerating mitochondria. Our findings, however, suggest that autophagocytotic processes may also play a role in the formation of lipofuscin.

Digestive System↗

Serum levels of IGF-I, HGF, TGFbeta1, bFGF and VEGF in thyroid gland tumors.

IGF-I, HGF, TGFbeta1, bFGF and VEGF are involved in the pathogenesis of thyroid gland tumors and their growth. We decided to find whether changes in the production of these cytokines by thyroid tumor cells are reflected by changes of their peripheral blood. Using ELISA kits, we measured the concentrations of growth factors in the peripheral blood serum in 28 patients with thyroid gland tumors (14 adenomas, 14 papillary carcinomas) and compared these concentrations with those in healthy people. We found significantly lower serum levels of IGF-I in patients with thyroid adenoma compared to the healthy population. Serum levels of HGF and bFGF were significantly higher in patients with thyroid adenoma and papillary carcinoma compared with those in healthy subjects. Serum concentrations of TGFbeta1 and VEGF were not significantly different in any groups of investigated subjects. Changes in the production of these cytokines by thyroid gland tumor cells are reflected in their peripheral blood levels, but these levels also depend on a number of other physiological and pathological processes in the organism. However, significant differences of HGF and bFGF serum levels can be explained by their very high production by thyroid tumor cells and by their strong effect on the follicular and endothelial cell proliferation.

Adenoma↗

Fine-needle aspiration biopsy of Hurthle cell lesions of the thyroid gland: A cytomorphologic study of 139 cases with statistical analysis.

BACKGROUND: Lesions of the thyroid gland composed of Hurthle cells encompass pathologic entities ranging from hyperplastic nodules with Hurthle cell metaplasia to Hurthle cell carcinomas. The cytologic distinction between these entities can be diagnostically challenging. Many cytologic features of Hurthle cell lesions that distinguish neoplastic Hurthle cell lesions requiring surgery from those that are benign and nonneoplastic have been described, but with variable usefulness. This is due, in part, to the small numbers of cases examined in previous studies and the limited application of statistical analysis. A morphologic study was made of 139 Hurthle cell lesions of the thyroid gland and statistical analysis applied to identify a set of cytomorphologic features that distinguish benign Hurthle cell lesions (BHCL) from Hurthle cell neoplasms (HCN). METHODS: Fine-needle aspiration biopsies (FNABs) of thyroid nodules with a predominant Hurthle cell component and corresponding histologic followup were included in the study. Cases were divided into BHCL and HCN groups on the basis of the histologic diagnosis. All cases were reviewed to assess the following 14 cytologic features: overall cellularity, cytoarchitecture, percentage of Hurthle cells, percentage of single cells, percentage of follicular cells observed as naked Hurthle cell nuclei, background colloid, chronic inflammation, cystic change, transgressing blood vessels (TBV), intracytoplasmic lumina, presence of multinucleated Hurthle cells, nuclear to cytoplasmic ratio, nuclear pleomorphism/atypia, and nucleolar prominence. The results were evaluated by using univariate and stepwise logistic regression (SLR) analysis; statistical significance was achieved at P-values < 0.05. RESULTS: One hundred thirty-nine FNAB specimens, corresponding to 56 HCN and 83 BHCL, fulfilled the study criteria. Six of the 14 cytologic features evaluated were shown by univariate analysis to be statistically significant in predicting HCN: nonmacrofollicular architecture (P < 0.001), absence of background colloid (P < 0.001), absence of chronic inflammation (P < 0.001), presence of TBV (P < 0.001), > 90% Hurthle cells (P < 0.001), and >10% single Hurthle cells (P = 0.014). The first four of these features were also shown to be statistically significant in the SLR analysis (P = 0.005, 0.010, 0.016, and 0.045, respectively), and when all four of these features were present HCN was correctly identified 86% of the time. CONCLUSIONS: In the current study of 139 FNAB specimens of thyroid Hurthle cell nodules, 14 cytologic features were examined and 6 were found to be statistically significant in identifying HCN. The following four features, when found in combination, were found to be highly predictive of HCN: nonmacrofollicular architecture, absence of colloid, absence of inflammation, and presence of TBV.

Adenoma↗

Ultrastructural study on thyroid glands of Bufo arenarum larvae kept in potassium perchlorate solution.

The ultrastructure of thyroid glands in Bufo arenarum tadpoles was studied with inhibited thyroid function. After hatching, larvae were kept in potassium perchlorate solution, a goitrogenic substance known to prevent absorption of iodine from water or food, resulting in impaired thyroid hormone synthesis. Increased thyroid gland volume and follicular cell height were observed in treated larvae. The changes in size and volume of follicular cells in experimental tadpoles appeared to be mainly a function of the overstimulation of proteinpoietic apparatus. The cell shows a conspicuous development of endoplasmic reticulum and Golgi complex, as well as an increase in number of mitochondria and colloid droplets. These observations in follicular thyroid cells from Bufo arenarum, obtained under such experimental conditions, were interpreted in terms of interruption of negative feedback mechanisms involving the decrease in the thyroxine circulatory level, and therefore the increase in hypothalamo-hypophyseal endocrine secretory stimulation.

Animals↗

Penetrating oesophageal foreign bodies in the thyroid gland.

Oesophageal penetration and migration of oesophageal foreign bodies into the thyroid gland is extremely rare with only occasional case reports appearing in the medical literature over the years. This is a retrospective review of four patients who were managed for penetrating oesophageal foreign bodies in the thyroid gland over an 11-year period. The clinical, radiological and intra-operative findings of the four cases are discussed.

Aged↗

Blunt injury to the thyroid gland: proposed classification and treatment algorithm.

BACKGROUND: Traumatic hemorrhage of the thyroid gland is a rare injury with few published case reports. Surgical and nonsurgical management have been advocated but there is no consensus of opinion. METHODS: This study is a retrospective review of published case reports including two own cases. A classification and an algorithm for diagnosis and treatment of thyroid gland injuries is proposed. RESULTS: A literature review reveals 16 case reports. Of these, 11 patients underwent neck exploration for control of hemorrhage and resection of the associated thyroid abnormality while 5 patients were conservatively managed. Of note is the fact that 10 of the 16 patients (63%) had pre-existing thyroid disease. These 10 patients constituted (91%) of the group requiring surgical treatment. CONCLUSION: Our proposed classification and algorithm offers management guidelines for this rather rare injury. Conservative treatment may be successful in selected patients with lower grade injuries and without concomitant thyroid disease.

Algorithms↗

Histological structure of the thyroid gland in the newborn. With special reference to hypotrophy, hydrops fetalis and Cesarean section delivery.

Histological features of the thyroid gland in the newborns have been described under several circumstances; gestational age, length of survival, and under particular clinical status such as hypotrophy (intrauterine growth retardation), Cesarean section delivery and hydrops fetalis. Gestational age does not modify significantly the histological aspect of the thyroid, while birth process and adjustment to extrauterine life induce dramatic changes such as severe depletion of colloid for about 24 h, followed by a massive repletion after the first day of life. A few exceptions to this phenomenon are described. Thyroid glands of hypotrophic infants and of infants delivered by cesarean section exhibit colloid-filled vesicles already within the first day. Thyroid glands of hydrops fetalis have a reverse tendency. This phenomenon might be secondary to multiple exchange transfusions.

Cesarean Section↗

Hamartomatous adiposity of thyroid gland.

A rare case of hamartomatous adiposity of the thyroid gland was found incidentally in a 73 year old white female with adenocarcinoma of the rectum. Pressure symptoms related to the goiter (120 gms) were the only manifestations noted. Extensive laboratory investigations failed to reveal any demonstrable functional abnormality of the thyroid gland.

Aged↗

[Amiodarone and the thyroid gland].

In an estimated 5% of patients, antiarrhythmic therapy with amiodarone (Cordarone) may have side effects involving thyroid function. These unwanted effects on the thyroid gland can be classified into three entirely different categories. In addition, amiodarone invariably interferes in a characteristic way with the peripheral metabolism of thyroid hormones at the cellular level. These effects are reviewed. 1. Amiodarone contains 39% of iodine. Since its metabolism involves deiodination to inorganic iodide, classical iodine-induced thyrotoxicosis may occur in patients with nodular goiters containing autonomous follicles. 2. An entirely different form of thyrotoxicosis, resembling Graves' disease, may be induced by amiodarone in individuals with previously normal thyroid. The pathogenesis of this phenomenon is unknown. 3. In rare patients of the thyroid gland is unable to cope with pharmacological quantities of iodide, possibly due to genetic anomaly of thyroid metabolism. In these individuals amiodarone may induce hypothyroidism. 4. In contrast to the possible side effects of amiodarone involving the thyroid gland, the drug has an obligate impact on the metabolism of thyroid hormones at the level of the peripheral cells. It inhibits the peripheral conversion of thyroxin to triiodothyronine (T3) and favours the generation of reverse T3, which has no T3 activity. This and other arguments favour the assumption that the effects on the heart observed after prolonged amiodarone treatment are in fact due to selective local hypothyroidism.

Adult↗

[Instrumentation for dislocation and fixation of a cutaneous fat flap in operations on the thyroid gland].

The author describes the specific techniques of operation on the thyroid gland, the operative approach to it used in the Mogilev Regional Hospital in "severe" thyrotoxic struma, low supraclavicular (cosmetic) skin incisions. The peculiarities consist in the following: from the zone of the operative field (projection of the thyroid gland) a flap of skin and fatty tissue is removed (dislocated) in the direction of the chin with a special instrument, a dislocator. The flap is not only removed but is held thereby fixation of the dislocator to the operative arch. The construction of the instrument and the principle of its operation are described. Application of the dislocator makes operation on the thyroid easier.

Equipment Design↗

[Thyroid peroxidase in the differential diagnosis of thyroid gland lesions. A marker of biological behavior or differentiation?].

Human thyroid peroxidase (hTPO) is a membrane protein with a key role in the thyroid hormones synthesis. Loss of hTPO was described in malignant tumours of the thyroid gland. hTPO was tested as a marker of malignancy. Immunohistochemical study of hTPO in 321 thyroid lesions (45 malignant tumours, 72 benign tumours, 199 benign non-tumours lesions, and 5 normal thyroid glands) is presented. The sensitivity of hTPO in predicting malignancy in thyroid is 64%, and the specificity is 87%. Thus, hTPO is of limited value in the diagnosis of thyroid malignancy. The authors discuss the role of hTPO as a marker of differentiation.

Adolescent↗

Hormone-induced modifications of free tyrosine in the rat thyroid gland.

The concentrations of free tyrosine in liver, muscle, kidney and thyroid gland were determined in separate groups of rats maintained on a low iodine diet and treated with intraperitoneal injections of thyroxine (T 4), thyrotrophin (TSH) and TSH plus propylthiouracil (PTU). Groups of hypophysectomized rats also were given T 4. Significant changes in tissue tyrosine were generally confined to the thyroid gland. Animals treated with T 4 showed a decrease of mean thyroid tyrosine from 113.3 +/- 17.9 (S.D.) mug/g wet weight of gland to 76.2 +/- 5.7 mug/g (P < 0.01). Although there was little change in content when TSH was given alone, a significant increase in tyrosine levels was observed when TSH plus PTU were administered (P < 0.01). In hypophysectomized rats thyroid tyrosine decreased and was further lowered (to 46.0 +/- 3.1 mug/g; P < 0.05) by T 4 treatment. When tyrosine concentrations were expressed in relation to ribonucleic acid (RNA) or protein content of the assayed gland, all differences in tyrosine content became greater.

Animals↗

Effect of antiepileptic drugs on the thyroid gland in children with epilepsy (preliminary report).

Description of the side effects of antiepileptic drugs is commonly encountered in paediatric practice. In view of this we investigated the structural and functional changes undergone by the thyroid glands of epileptic children during the course of a long-term antiepileptic treatment. The study included 22 children with epilepsy aged 3.5 to 15 years. The thyroid status was assessed using clinical, ultrasound, and radioimmunological examinations. Clinical signs of initial hyperplasia of the thyroid gland were observed in 3 children. Volume abnormalities of the thyroid gland were found in 4 (18.2%) of the children. Abnormalities in the thyroid hormones and thyrotropin serum concentration were found in 5 children. The ultrasound examination revealed slight structural changes, decreased colloid uptake, and strip-like sprouts in 63.6% of the cases. These changes were significantly more common in children undergoing anticonvulsant polytherapy (12 of 22 children). The most general mechanisms of influence of the antiepileptic drugs on the thyroid status are discussed.

Adolescent↗

In vitro effect of insulin on the uptake of glucose and alpha-aminoisobutyric acid in the thyroid gland of the turtle (Chrysemys dorbigni).

The presence of specific insulin binding sites in the thyroid gland of the turtle Chrysemys dorbigni has been previously reported. The purpose of the present work was to investigate the probable action of insulin on the uptake of [14C]deoxy-D-glucose ([14C]DG) and [14C]alpha-aminoisobutyric acid ([14C]AIB) in turtle (C. dorbigni) thyroid glands in vitro. Thyroid fragments (+/- 40 mg) were incubated at 25 degrees in Krebs-Ringer-bicarbonate buffer containing 0.2 microCi of [14C]DG or [14C]AIB without or with bovine insulin at different periods of time. The uptake of [14C]DG and [14C]AIB increased with incubation time. The presence of insulin (7 x 10(-6) M) in the incubation medium during 240 min did not modify the [14C]DG uptake. However if the thyroid fragments were previously incubated with insulin (60 min) and then incubated (240 min) with the same concentration of the hormone, the [14C]DG uptake was markedly increased. This stimulatory effect of insulin was dose-dependent. In similar experimental conditions, insulin also produced a significant increase in the uptake of [14C]AIB. Therefore, these findings strongly support the hypothesis that insulin might exert a direct action on the thyroid function.

Aminoisobutyric Acids↗

The thyroid gland as an intrinsic biologic response-modifier in advanced neoplasia--a novel paradigm.

The thyroid gland is the major endocrine modulator of physiological processes crucial to growth, maturation and metabolism. There is, however, a coherent body of evidence suggesting that the thyroid hormones modulate multiple neoplasia-dependent mechanisms. Recently spontaneous remission of metastatic non-small cell carcinoma of lung was reported in a man following recovery from myxedema coma. This rare biological event following a life-threatening clinical syndrome suggests that thyroid hormone deficiency directly or indirectly may significantly alter the balance between malignant tumor viability and growth on the one hand vs. cell death on the other. Evidence, therefore, is presented from clinical and experimental studies suggesting that decreased thyroid function (hypothyroidism) is associated with both enhanced response rates and unusual longevity. Possible mechanisms of action that may promote or retard neoplasia and are dependent on the functional state of the thyroid will be discussed. A novel paradigm is proposed; the thyroid gland aside from its known physiological activity is also the central modulator of solid neoplasia and therefore functions as an intrinsic biologic response-modifier of neoplasia. Induction of a clinically tolerable hypothyroid state in patients could become an integral part of the medical care of advanced cancer in conjunction with standard conventional modalities.

Animals↗

Expression of adhesion molecules on infiltrating T cells in thyroid glands from patients with Graves' disease.

The present study was performed to elucidate the role of adhesion molecules in the pathogenesis of Graves' disease. Peripheral blood and intrathyroidal mononuclear cells were obtained from 14 patients with Graves' disease. The expression of adhesion molecules and HLA-DR antigen on CD4+ cells and CD4+ cell subpopulations was analysed by the two- or three-colour immunofluorescence method. The expression of adhesion molecules including LFA-1 alpha, LFA-1 beta, CD2, VLA-4 alpha and VLA-5 alpha on CD4+ cells in the thyroid gland was markedly higher than that in peripheral blood. In peripheral blood CD4+ cell subsets, the CD4+ CD45RO+ cell population had an enhanced expression of the adhesion molecules compared with the CD4+ CD45RA+ cell population. However, there was no significant difference in the expression of adhesion molecules by CD4+ cell populations and subsets between Graves' disease and healthy subjects. The thyroid gland from Graves' disease contained a higher percentage of CD4+ CD45RO+ cells and a lower percentage of CD4+ CD45RA+ cells. In intrathyroidal CD4+ cell subsets, the CD4+ CD45RO+ cell population had an increased expression of LFA-1 and CD2 compared with the CD4+ CD45RA+ cell population, but there was no significant difference in VLA-4 and VLA-5 expression between the two cell subsets. Furthermore, the expression of LFA-1 and CD2 on the CD4+ CD45RO+ cell population in the thyroid was significantly higher than that in matched peripheral blood. A similar finding was also observed for the CD4+ CD45RA+ cell population. The thyroid gland had an increased percentage of CD4+ HLA-DR+ cells compared with matched or healthy peripheral blood. However, there was no significant difference in the percentage of HLA-DR+ cells in the thyroid gland between CD4+ CD45RO+ cell and CD4+ CD45RA+ cell populations. These results suggest that increased expression of adhesion molecules on CD4+ cells may be responsible for the migration of these cells into thyroid glands and cellular interactions between these cells and thyroid epithelial cells.

Adult↗

Mechanisms of nonneoplastic endocrine hyperplasia--a changing concept: a review focused on the thyroid gland.

An important part of clinical endocrinology deals with diseases caused by benign and malignant nodules growing within originally homogeneous endocrine glands. In the search for the pathogenesis of these nodules, two concepts have been advanced: either the hyperplastic tissue is considered to result from chronic intense stimulation by a trophic hormone, eventually causing the growth of polyclonal nodules (a concept known as NNEH) or else, the nodules are thought to represent true clonal tumors. It has been realized rather recently that NNEH accounts only for a small minority of rare endocrine diseases, with the exception of highly prevalent iodine deficiency goiters and, in a broader sense, for Graves' disease. Indeed, secondary hyperplasia of endocrine glands resulting from long-lasting chronic hormonal overstimulation cannot explain a large number of essential features of the diseased glands. As best documented for the thyroid gland, outstanding among the characteristics of hyperplastic glands that do not fit into the simple concept of NNEH are the inevitable nodular transformation, the frequent autonomy and irreversibility of nodular growth, the loss of function in many cells and nodules, and the tremendous regional heterogeneity of growth and function including loss of coordination between these two main features of any living cell. Hyperplasia resulting from long-lasting stimulation by a trophic hormone is not a fully reversible process, as is often thought, but definitely increases the total cell mass and leaves behind, after cessation of the stimulus, a population of newly generated cells. This process is common to NNEH and true neoplastic growth. A review of common and disparate traits between endocrine hyperplasia and neoplasia must be based on the following generally accepted facts (excluding in-depth consideration of malignancy). 1. Many endocrine tumors are clonal while others are polyclonal. For example, pituitary and sporadic parathyroid adenomas are nearly always clonal while in the thyroid, multiple clonal nodules of different origin may coexist with polyclonal nodules. 2. Clonal growth does not necessarily indicate that the autonomous expansion of a tumor is driven by presently known genetic gain-of-function or loss-of-inhibition mutations or by cytogenetic aberrations. 3. Genetic mutations and chromosomal aberration in endocrine tumors are not necessarily primary events in the tumorigenesis but may as well be a late secondary phenomenon in growing tissue. 4. Clonal nodules may overgrow from primarily polyclonal ones. The best evidence to date comes from the rare clonal parathyroid adenomas with allelic loss of chromosome 11 evolving in tertiary hyperparathyroidism.(ABSTRACT TRUNCATED AT 400 WORDS)

Goiter, Nodular↗