Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THYROID DISEASES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1991

Interleukin 2-activated killer cells do not mediate autologous thyrocyte lysis in autoimmune thyroid disease in vitro.

Because of interest in IL-2, and IL-2-activated killer cell-induced hypothyroidism in humans, we attempted to study an in vitro system that might prove to illuminate this disorder. We have thus studied interleukin 2 (IL-2--0, 12.5, 25, or 50 U/mL) activated killer cell-mediated autologous thyrocyte lysis, as well as cytotoxic activity in IL-2-stimulated mononuclear cell supernatants in 7 patients with autoimmune thyroid disease (2 Graves' disease and 5 Hashimoto's thyroiditis) using the 51Cr release assay. Controls included 14 patients with nonautoimmune thyroid disease (3 nontoxic goiter, 8 follicular thyroid adenoma, 2 papillary thyroid carcinoma, and 1 medullary carcinoma of the thyroid). Soluble IL-2 receptor (sIL-2R) in supernatants of peripheral mononuclear cells stimulated by IL-2 from these patients also was measured. Whereas in the control preparations, IL-2-activated killer cell activity was increased in a dose-dependent fashion relative to the IL-2 concentration, as well as to the effector cell/target cell ratio, in preparations from patients with autoimmune thyroid disease, this activity was not elevated as the IL-2 concentration was increased. The susceptibility of thyrocytes to the lytic effect of IL-2-activated killer cells was higher in controls than that in autoimmune thyroid disease (at concentrations of IL-2 of 0, 12.5, 25, and 50 U/mL) (p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Increase in peripheral natural killer cell activity in patients with autoimmune thyroid disease.

Changes in the activity and number of natural killer (NK) cells in peripheral blood in patients with autoimmune thyroid disease were examined. NK activity was measured in a 4-hr 51Cr-release assay and the number of NK cells was analyzed with FITC-conjugated monoclonal antibodies by use of an automated flow cytometer. NK activity in patients with untreated Graves' disease (n = 25, 39.7 +/- 13.5%, P less than 0.05) and Hashimoto's thyroiditis (n = 18, 41.0 +/- 14.2%, P less than 0.05) was high compared to the activity in non-pregnant controls (n = 61, 32.6 +/- 15.0%). NK activity in patients with postpartum Graves' thyrotoxicosis (n = 11, 48.6 +/- 18.9%) was markedly increased compared to the activity in non-pregnant controls (P less than 0.01) and in postpartum controls (n = 29, 33.8 +/- 15.2%, P less than 0.05), although the mean ages of each group did not differ significantly. Moreover, NK activities in the thyrotoxic state were significantly higher than those in the euthyroid state in the same patients with postpartum Graves' thyrotoxicosis or with postpartum destructive thyrotoxicosis. The number of CD16 positive cells increased in patients with postpartum Graves' thyrotoxicosis. However the number of CD16 and CD57 positive cells were normal in all other groups of patients. These results indicate that an increase of NK activity is associated with exacerbation of autoimmune thyroid disease both in Hashimoto's thyroiditis and in Graves' disease and suggest that NK cells might have an important role for the control of disease activity in autoimmune thyroid disease.

Adult↗
PubMed2003

Influence of the refinement of surgical technique and surgeon's experience on the rate of complications after total thyroidectomy for benign thyroid disease.

BACKGROUND: In recent years, many surgeons dealing with endocrine surgery have increasingly performed total thyroidectomy for benign thyroid disease. However, total excision of the thyroid in the treatment of benign lesions has been surrounded by even more controversy than its role in cancer treatment. The complication rate appears to be higher when the operation is done by inexperienced surgeons who have no special skills in endocrine surgery using proper techniques. The aim of this study is to determine whether surgeons experience and the refinement of surgical techniques are associated with postoperative recurrent laryngeal nerve (RLN) palsy or hypocalcemia after total thyroidectomy for benign thyroid disease. METHODS: A total of 68 consecutive patients who underwent total thyroidectomy for benign thyroid disease were reviewed. Twenty-six of these were from between January 1998 and June 1999 (first period) and 42 from between June 1999 and September 2000 (second period). Patients were divided into two subgroups according to different periods and different surgical techniques to identify the RLNs and the parathyroid glands. RLNs function was evaluated pre- and postoperatively by an otolaryngologist, and serum calcium levels were measured at the postoperative follow-up. RESULTS: During the first period of the study, transient hypocalcaemia was determined in 8 (31%) patients. Hypocalcaemia was clinically symptomatic in 5 (19%) patients. Transient RLN palsy developed in 4 (15%) patients. Unilateral permanent RLN palsy due to operative injury was observed in 1 (4%) patient. During the second period, we noted transient hypocalcemia in 11 (26%) patients and symptomatic hypocalcemia in 6 (4%) patients. Serum calcium levels returned to normal within 4 weeks after operation in all patients. Neither transient nor permanent RLN palsy was observed during this period. CONCLUSIONS: Complications of total thyroidectomy can be minimized with increasing experience and the refinement of surgical technique.

Adult↗
PubMed2002

The role of apoptosis in thyroid disease.

Increasing evidence suggests that apoptosis plays an important role in the pathogenesis of autoimmune and proliferative thyroid diseases, and that the apoptotic pathways involved are complex and highly regulated. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease have been associated with differential expression of Fas and TRAIL receptor-mediated apoptosis. Thus, the thyroid cell destruction characteristic of autoimmune thyroiditis can be seen as the consequence of inappropriate expression of Fas or TRAIL death pathway molecules and down-regulation of the apoptosis controlling protein Bcl-2, which may be induced by cytokines released locally by infiltrating lymphocytes. In contrast, Graves' thyrocytes are protected from apoptotic death possibly by the anti-apoptotic action of thyrotrophin receptor antibodies or soluble Fas and/or the overexpression of Fas ligand which all create an anti-apoptotic potential for the thyroid cells and favor apoptosis of the infiltrating lymphocytes. On the other hand, an imbalance between thyroid cell proliferation and cell death may be crucial for goiter formation or cancer development and progression. In human thyroid goiter, Fas-mediated apoptosis is suppressed, leading to thyroid cell hyperplasia. Furthermore, malignant thyroid cells may escape immune attack by over expressing Fas ligand and inducing apoptosis in the invading immune cells. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed that may provide new strategies in the prevention and treatment of these diseases.

Apoptosis↗
PubMedDate not supplied

[Use of the Echoophthalmoscope 21 in the diagnosis of thyroid diseases].

The authors utilized a Soviet apparatus Echoophthalmoscope-21 for investigation of the thyroid. Examination of 51 patients and 10 controls showed that the echographic picture and a degree of ultrasound absorption in different thyroid diseases had significant differences permitting a wide use of the above apparatus for the detection of thyroid diseases during mass screening.

Adult↗
PubMed2002

Surgical management of thyroid diseases--a study on 78 cases.

A total of 78 cases with thyroid diseases were treated surgically in the Department of ENTD, Mymensingh Medical College Hospital during the period from 2000-2001. The different types of surgery were done according to the diagnosis being presented here. Out of 78 cases, 60 (76.9%) were female and 18 (23.1%) were male having female to male ratio of 3.3:1. The highest number, 47 cases (60.3%) belongs to 21-40 year age group. The study revealed the incidence of thyroid diseases as follows: 53 (67.9%) Benign cold single nodular goitre. 17(21.8%) Benign cold multinodular goitre and 08 (10.3%) Papillary carcinoma of thyroid. Regarding surgical management 40 (51.3%) patients underwent hemithyroidectomy. Lobectomy were done for 13 (16.7%), subtotal thyroidectomy for 15 (19.2%), total thyroidectomy for 5 (6.4%) patients and total thyroidectomy with functional neck dissection were performed for 5 (6.4%) patients. The study showed that females were the mostly affected group having benign single cold nodular goitre who were treated surgically by hemithyroidectomy.

Adult↗
PubMed1986

The interaction of MHC and Gm in liability to autoimmune thyroid disease.

In studies on immunogenetic factors in autoimmune thyroid disease, the association among Graves' disease, Hashimoto's disease, HLA and Gm haplotypes was investigated in 37 families in which two or more first degree relatives had Graves' disease. The results showed that two genes linked to HLA and Gm appeared to control susceptibility to Graves' and Hashimoto's disease, respectively, and that the individuals who did not have immunogenetic factors were very unlikely to develop Graves' or Hashimoto's disease. In the second study, the role of HLA-DR antigen expression on thyrocytes was investigated in 18 patients with Graves' disease. It was found that DR-positive thyrocytes increased. DR-positive T-cells (from thyroids and peripheral blood) increased in Graves' disease. Interferon gamma increased DR expression on thyrocytes. The results indicated that these changes may cause a vicious circle to produce and perpetuate autoimmune processes in Graves' disease. Finally, the correlation between thyroids and immunoglobulins was investigated in 11 untreated patients with Graves' disease. Thyroid tissues obtained from untreated patients were incubated in organ culture systems with autologous as well as allogeneic immunoglobulins to observe the release of hormones. The release of hormone was stimulated only by autologous immunoglobulins and it is, therefore, postulated that the role of self-recognition, such as anti-idiotype antibody or anti-MHC antibody is crucial in the pathogenesis of Graves' disease.

Cyclic AMP↗
PubMed1983

Thyroid disease in hemochromatosis. Increased incidence in homozygous men.

The thyroid function of 49 patients homozygous for the hemochromatosis allele was studied by measurement of serum thyroxine and thyrotropin concentrations. Of 34 homozygous men, three were found to be hypothyroid (thyroxine, less than 3.0 micrograms/dL and thyrotropin, greater than 40 ImU/mL) and one was hyperthyroid (thyroxine, 24 micrograms/dL). All 15 homozygous women had normal thyroid function. The hypothyroid patients had elevated titers of antithyroid antibodies. Histologic examination of the thyroid at autopsy of one hypothyroid patient showed notable iron accumulation and fibrosis with modest lymphocytic infiltration. The causative importance of iron deposition in thyroid diseases associated with hemochromatosis was suggested by the reversal of the usual sex ratio of thyroid dysfunction. Men with hemochromatosis had a much greater iron load than women, and they also had a surprisingly higher incidence of thyroid disease. Iron may have caused injury to the thyroid, followed by the development of antithyroid antibodies and hypothyroidism. The frequency of thyroid disorders in men with hemochromatosis is about 80 times that of men in the general population.

Adult↗
PubMed2005

[Autoimmune thyroid disease and associated rheumatic disorders].

Musculosceletal manifestations were found in patients with hyperthyroidism as well as hypothyroidism. This article will review the available evidence that autoimmune thyroid disease is associated with: Sjögren's sydrome (SS), systemic lupus erythematosus (SLE), systemic sclerosis, rheumatoid arthritis (RA) and spondyloarthropathies. Possible pathogenesis of these manifestations has not been completely established. Sjögren's syndrome occurs in about 1/10 of patients with autoimmune thyroid disease; patients with SLE and antithyroid antibodies were significantly older than those pattiens without antibodies. Patients with systemic sclerosis and thyroid disease were significantly younger than those without antibodies. Thyroid disfunction was found three times more often in women with RA than in women with noninflammatory rheumatic diseases, and those with thyroid disease tended to have a shorter duration of arthritis.

Arthritis, Rheumatoid↗
PubMed1996

[Role of total thyroidectomy in the treatment of benign thyroid diseases].

In 1990, total thyroidectomy (T.T.) was performed in 4% of all benign thyroid diseases and in 7% in case of diffuse benign thyroid diseases, operated on in our surgical unit. In 1995, this incidence of T.T. increased to 20% and 37% respectively. Several considerations can explain this rise in T.T. indications. Currently, the incidence of reoperations on benign goiters represents 4.5% of all our thyroid surgery. It can be considered as a failure of a first incomplete operation. Furthermore, most of goiter recurrences are medically treated and the recurrence rate is higher than the reoperation rate. In Grave's disease, surgery is indicated after medical treatment failure or for acute complications. In this case, the aim of surgery is radical cure of hyperthyroidism. Because evaluation of the weight of thyroid remnant for prevention of postoperative hypothyroidism is difficult, indication of T.T. with thyroxin replacement therapy can be proposed. Surgical excision of a multinodular goiter is indicated for large size lesions, tracheal compression or thyrotoxic evolution. Over the years subtotal thyroidectomy was performed for these benign lesions. Subtotal thyroidectomy leaves a diseased remnant gland. Attempts to suppress nodular recurrence by thyroxin treatment do not guarantee success. Then T.T. can be advocated since postoperative thyroxin therapy is often given after subtotal thyroidectomy to prevent hypothyroidism. Total thyroidectomy is an appropriate operation for the management of a benign thyroid disease because it precludes patients from requiring further surgery for recurrent diseases. However, it requires two conditions. In first, the patient must have the psychologic and economic capacity for a permanent medical therapy. The other is that the procedure be performed with low risks of complications in comparison with subtotal thyroidectomies. Currently recurrential palsy and hypoparathyroidism rates are evaluated in the literature between 0 and 3%.

Goiter↗
PubMed1999

Autoimmune thyroid disease in childhood: a study of children and their families.

OBJECTIVE: To study the clinical and laboratory profile of children with autoimmune thyroid disease (AITD) and its familial prevalence. DESIGN: Clinical and investigative evaluation of 96 children and adolescents 5 to 16 years old suspected of having AITD based on clinical and family data and similar assessment of parents and siblings of 30 confirmed cases of AITD. SETTING AND SUBJECTS: Of these 96 cases, 66 were from a private clinic and 30 were institution based thyroid antibody positive with confirmed AITD. On initial testing 36 (55%) of 66 clinic cases were thyroid antibodies (ab) positive and 30 were (ab) negative. In 12 of 30 ab -ve cases retesting for antibodies by newer technique or FNAC confirmed AITD. Clinical and laboratory evaluation of 90 of a total of 106 parents and siblings of the 30 institution based cases. METHODS: Clinical evaluation with goiter grading by WHO criteria was done in all. Family history of thyroid disease was inquired for in all. Clinical examination and thyroid antibody status was assessed in 90 family members as stated above. Thyroid antimicrosomal (AMA) and antithyroglobulin (ATG) antibodies were tested by standard hemogglutination kits. Titers of > 1:100 considered +ve for children and >1:400 for adults. Thyroid (ab) could be tested in ten of the ab-ve cases by ECI technique on follow up. Bone age was assessed. Ultrasonographic or TCM 99 scanning of thyroid gland and FNAC were done as indicated. RESULTS: Of the 96 children suspected to have AITD, thyroid antibodies were positive in high titers in 66 (36+30) cases (69%) on initial testing but with more sensitive ECI technique significant antibody titres were detected in 10 more cases (79%) and FNAC confirmed AITD in 2 more subjects (total 78 - initial 66 + 12). F:M ratio was 2.9:1. Sixty one per cent of children were between 6 to 12 years of age; mean age 10.12+/-2.9 years. Seventy seven per cent had hypothyroidism, 10% had thyrotoxicosis and only 13% were euthyroid. Family history of thyroid disease was elicited in 33% of the series. Survey of 90 parents and siblings of the institution based group revealed, euthyroid goiters in 17%, subclinical hypothyroidism in 10% and significant AMA titers in 43% (65% of mothers, 30% siblings and 43% fathers). CONCLUSION: Juvenile AITD is a common cause of acquired thyroid disease in children above 5 years of age with a 3-fold higher prevalence in girls. The manifestations are heterogeneous. Hypothyroidism was most common (77%), euthyroid goiters (13%) and thyrotoxicosis (10%) were less frequent. Familial aggregation was noted in adult family members (33%) with positive thyroid antibodies in 65% of mothers. Sibling affection was less frequent. The familial and genetic implications of AITD are important; diagnosis of AITD in children may also help detect subclinical disease in adult family members.

Adult↗
PubMed2002

Cardiovascular hemodynamics and exercise tolerance in thyroid disease.

The heart is an organ sensitive to the action of thyroid hormone, and measurable changes in cardiovascular performance are detected with small variations in thyroid hormone serum concentrations. Most patients with thyroid disease experience cardiovascular manifestations, and the most serious complications of thyroid dysfunction occur as a result of cardiac involvement. The increased metabolic state and oxygen consumption that occur in hyperthyroid patients require an increased supply of oxygen and removal of metabolic products from the periphery. This is accomplished by increasing the cardiac output to meet the needs of the periphery. Circulation time is decreased in hyperthyroid patients, and a lowered arterial resistance and increased venous resistance promote the return of blood to the heart. Thyroid hormones may significantly decrease the strength of respiratory and skeletal muscles and affect regulatory mechanisms of adaptation to incremental effort. In hyperthyroidism, cardiovascular exercise testing and analysis of respiratory gas exchange demonstrate low efficiency of cardiopulmonary function as well as impaired chronotropic, contractile, and vasodilatatory reserves, which are reversible when euthyroidism is restored. During exercise, the increment (delta) of minute ventilation (respiratory rate x tidal volume), and oxygen pulse (oxygen uptake per heart beat) are significantly lower in dysthyroidism versus euthyroidism. Especially in older patients with thyroid dysfunction, markedly reduced workload, delta ejection fraction, and delta heart rate, both at the anaerobic threshold as well as at maximal exercise, are observed. In thyrotoxicosis, mitochondria oxidative dysfunction during exercise mostly causes intracellular acidosis, whereas in hypothyroidism, inadequate cardiovascular support appears to be one of the principal factors involved. These abnormalities partly explain why subjects with dysthyroidism are intolerant to exertion. Thus, in thyroid disease, both cardiac structures and function may remain normal at rest, however impaired cardiovascular and respiratory adaptation to effort becomes unmasked during exercise.

Age Factors↗
PubMed1993

[Autoimmune thyroid disease diagnosed during puerperium: evaluation 2 years later].

This is a 2 years follow-up study of seventeen women who were found to have mild goiter and post-partum thyroid disease two years earlier in order to establish if post-partum thyroid disease is a self-limited entity or the relapse of a chronic pre-existing disease. When first studied, the 17 women had thyroid dysfunction (15 with hyperthyroidism and 2 with hypothyroidism). Eight women had also elevated antimicrosomal antibodies (AMA) titers and 9 were negative for AMA. In the present study, all women were reexamined for the presence of goiter, and free thyroxine index (FT4I), TSH and AMA were determined. Mild (grade I-II, less than 30 g) goiter was found in 11 women. Six out seventeen women, still had altered functional tests (3 with hypothyroidism and 3 with hyperthyroidism). The elevated AMA titers seen in 8 patients in the first study, remained high in 6 (1:100-1:25600). None of the 9 patients who in the first study had negative AMA changed to positive titers. Results indicate that post-partum thyroid disease is not always a self-limited entity. The presence of elevated AMA titers in the initial post-partum period can express a chronic thyroid disease compromise. In these patients a longterm clinical and biochemical follow-up is recommended.

Autoantibodies↗
PubMedDate not supplied

Clinical evaluation of a hemagglutination method for microsomal and thyroglobulin antibodies in autoimmune thyroid disease.

A simple and reproducible hemagglutination technique for detecting microsomal and thyroglobulin antibodies has been evaluated in normal subjects and in patients with thyroid disease. Microsomal antibodies were detected in 89 percent of all patients with autoimmune thyroid disease and in 97 percent of patients with biopsy proven Hashimoto's thyroiditis. In contrast, thyroglobulin antibodies were present in only 55 percent of patients with biopsy proven Hashimoto's thyroiditis and in 44 percent of all patients with suspected autoimmune thyroid disease. It is suggested, therefore, that measurement of microsomal antibodies by a simple hemagglutination techniques be carried out in all patients with suspected thyroid disorders.

Antibodies↗
PubMedDate not supplied

Medical therapy of benign thyroid diseases.

Main guide-lines of medical therapy of benign thyroid diseases are reviewed. The most common drug therapy of the various forms of hyperthyroidism is represented by thionamide drugs (methimazole and propylthiouracil). Therapeutic protocols are diversified according to the disease. In Graves'disease medical therapy may present the definitive treatment, leading to remission in little less than 50% of cases while in hyperfunctioning nodular thyroid diseases, medical therapy is merely in preparation for ablation therapy. Other drugs used in hyperthyroidism are also mentioned (inorganic iodine, potassium perchlorate, beta-blockers). Thyroxine replacement therapy in the various forms of hypothyroidism is then analyzed, discussing in particular the therapeutic protocols and follow-up of the various forms of hypothyroidism. Finally, the controversy about the indications and efficacy of TSH-suppressive thyroxine therapy is considered.

Adrenergic beta-Antagonists↗
PubMed1995

Fine-needle aspiration cytology of benign nodular thyroid disease. Value of re-aspiration.

Fine-needle aspiration cytology (FNAC) has become a widespread procedure for the study of thyroid nodules (TN). Some authors recommend the practice of repeated punctures for their follow-up. This study was done to determine the usefulness of repeated FNAC in patients with benign nodular thyroid disease. We have studied 251 fine-needle re-aspirations performed on 116 females aged 45.6 +/- 14 years with benign nodular thyroid disease. The time elapsed between each consecutive FNAC was 1 year. No patients presented any changes in the size or consistency of their nodular goiters during this period; all FNACs were carried out by the same physician in the same thyroid area according to the Löwhagen technique, with a minimum of two or three aspirations of each nodule, and processed in the same way and valued by the same cytologist without any knowledge of previous cytological diagnoses. These were done using strictly classical criteria (Löwhagen). One hundred and five out of 116 patients (90.51%) with two consecutive FNACs (210) showed identical cytological diagnoses in the two specimens studied. The remaining 11 patients (9.48%) with two FNACs were diagnosed with colloid goiter and cyst alternately. Fifteen out of 19 patients (78.94%) with three FNACs showed identical cytological diagnoses in the three samples and the rest (21%) also demonstrated alternate diagnoses of colloid goiter and cyst. Our results show that the routine performance of repeated FNAC in the follow-up of females with benign nodular thyroid disease, without any clinical changes, is of limited usefulness.

Adult↗
PubMed1990

Thyroid peroxidase and the induction of autoimmune thyroid disease.

Animal models of autoimmune thyroid disease are associated with thyroglobulin (Tg) as autoantigen whereas in man the autoimmune response to microsomal antigen/thyroid peroxidase (TPO) appears to play a major role in thyroiditis. Consequently, we have compared the ability of TPO and Tg to induce thyroid autoantibodies and thyroid damage in mice known to be susceptible (CBA/J) or resistant (BALB/c) to thyroiditis induced using murine Tg. Groups of three to five mice were immunized twice using Freund's complete adjuvant with 80-100 micrograms highly purified porcine (p) TPO, pTg, rat (r) Tg, human Tg, bovine serum albumin (BSA) or BSA + 0.2 micrograms pTg (the level of Tg contamination of TPO). Four weeks after immunization with TPO, plasma from CBA/J (but not BALB/c) mice contained IgG class antibodies which bound to TPO-coated tubes in the presence or absence of excess Tg (and could therefore be clearly distinguished from Tg antibodies) but there was no evidence of thyroiditis in either strain of mice. In contrast, in CBA/J mice immunized with rTg and, to a lesser extent in mice that had received pTg, thyroid tissue was infiltrated with lymphoid cells and/or neutrophils and antibodies to pTg (but not pTPO) were present. Our observations demonstrate that induction of TPO antibody alone is insufficient to lead to thyroiditis in CBA/J mice. Further, these studies emphasize the complex interactions between MHC and different thyroid antigens in the processes leading to thyroid destruction.

Animals↗