Thiocyanate in excess develops goiter followed by auto immune thyroid diseases even after effective salt iodization in a rural community of north east India.

PURPOSE: Salt iodization in Manipur of north-east India failed to prevent endemic goiter, therefore an in depth study carried out to evaluate thyroid functions of goitrous subjects in a randomly selected region. METHODS: Goiter survey conducted in children and women of reproductive ages by palpation followed by measurement of urinary iodine, thiocyanate and house-hold salt iodine to evaluate iodine nutritional status and consumption pattern of bamboo-shoots (BS). In all grade-2 goitrous subjects, free thyroxine, triiodothyronine, TSH, TPO and Tg antibodies, thyroid volume and echogenecity by ultrasonography and cytomorphology of thyroid by FNAC studied. RESULTS: Study population was 2486 children and 1506 women, goiter prevalence was 12.59% and 16.27% respectively; median urinary iodine and mean thiocyanate were 166 µg/l and 0.729 ± 0.408 mg/dl while salt iodine was ≥30 ppm. Serum thyroid hormones and TSH profiles of all grade-2 goitrous subjects showed 16.21% were subclinically hypothyroid, 2.16% overt hypothyroid, 4.86% subclinically hyperthyroid and 6.48% overt hyperthyroid, serum TPO- and Tg-antibodies found positive in 41.62%. Ultrasonographic results showed 24% had enlarged thyroid and 86.4% hypoechoic. Cytomorphological studies showed prevalence of colloid goiter (41.08%), lymphocytic thyroiditis (37.83%), Hashimoto's thyroiditis (8.10%), autoimmune thyroiditis (4.32%), sub-acute thyroiditis (2.16%) and 1.62% each papillary, medullary carcinoma, simple diffused hyperplasia and adenomoid nodular goiter. CONCLUSIONS: Grade-2 goitrous individuals in this mild goiter endemic region were affected by hypo- and hyperthyroidism with hypoechoic thyroid and thyroiditis. Thiocyanate that originates from BS even in presence of adequate iodine developed goiter and led goitrous population towards such diseases.

Involvement of inducible costimulator ligand (ICOSL) expression in thyroid tissue in hyperthyroidism of Graves' disease patients.

BACKGROUND: The role of costimulatory molecules expressed on lymphocytes and thyrocytes in hyperthyroidism has attracted increasing attention and research has shown a close correlation between variant expression of these molecules on lymphocytes and thyrocytes and the development of GD. MATERIALS AND METHODS: [corrected] Thyroid tissues were collected from GD patients during surgery and from Hashimoto disease (HT) and non-toxic goiter (NTG) patients as controls. ICOSL expression on infiltrated B cells and TFC was detected by flow cytometry (FCM), reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC). Variation in ICOSL expression on TFC in primary cultures was analyzed in the absence or presence of cytokines using FCM assays. The role of ICOS-ICOSL signaling in proliferation, thyroid hormone production and thyroglobulin (Tg) release was investigated in primary TFC cultures using ICOS gene transfected L929 cells (ICOS-L929 cells) and the blocking ICOSL antibody (11 C4) in MTT assays and radioimmunoassays. RESULTS AND DISCUSSION: ICOSL expression on infiltrated B cells and TFC was detected in GD patient tissue. However, ICOSL expression was only detected on infiltrated B cells in control HT and NTG patient tissue. ICOSL expression on TFC was induced in vitro by the proinflammatory cytokines IFN-γ, IL-6 and TNF-α. Compared with mock transfected L929 (mock-L929) control cells, ICOS-L929 cells promoted significant proliferation of primary cultured TFC, with increased thyroid hormone and Tg production (all P < 0.01). TFC proliferation and production of thyroid hormones and Tg were inhibited significantly in the presence of ICOSL blocking antibody (11 C4) (all P < 0.05). Our observations suggest that ICOS-ICOSL signal plays a direct role in proliferation and differentiation of TFC and may exert important effects in the initiation, maintenance and exaggeration of autoimmune responses in local tissue.

[Interleukin-6 in endemic goiter patients in the south Ural region].

The cytokine and thyroid status was studied in patients with endemic goiter (EG) depending on thyroid function. IL-6 correlated with free T3 levels (a negative relationship) in hyperthyroidism, with IL-2 and IFN-gamma levels in EG patients with euthyroidism, and with IL-1beta, IL-2, IL-8, IL-10, and IFN-gamma in hypothyroidism. The EG patients with high IL-6 levels showed positive relationships to IL-2 and thyroid peroxidase antibodies and a negative relationship to free T3. In these patients, IL-6 acted to stimulate the secretion of antithyroid antibodies, which is a risk of autoimmune thyroiditis.

The role of thyroid autoantibodies in the etiology of endemic goiter in schoolchildren of Isfahan, Iran.

BACKGROUND: Eleven years after the initiation of universal salt iodization program in Iran, the prevalence of goiter is still high in some areas. AIM: To investigate the role of thyroid autoimmunity in the etiology of residual goiter in schoolchildren of Isfahan, Iran. MATERIAL AND METHODS: In a cross-sectional study, 2331 schoolchildren were selected by multi-stage random cluster sampling. Thyroid size was estimated in each child by inspection and palpation. Urinary iodine concentration (UIC), serum anti-thyroperoxidase antibody (anti-TPO Ab), and anti-thyroglobulin antibody (Anti-Tg Ab) were measured. RESULTS: Overall, 32.9% of children had goiter. The median UIC was 1955.5 microg/dl. There was significant difference in prevalence of positive anti-TPO Ab in goitrous (grade 2) and non-goitrous children (9.7 vs 3.7%, p= 0.02). Goitrous children had higher prevalence of positive anti-Tg Ab than non-goitrous ones (15.1 vs 3.1%, p<0.001). CONCLUSIONS: According to the present study, goiter is still a public health problem in this region. This study suggests that thyroid autoimmunity is among the contributors of goiter persistence after elimination of iodine deficiency in Isfahan.

Thyroid autoantibodies in women with and without thyroid disorders in an iodine-replete area.

To compare the prevalence of positive autoantibodies in patients with thyroid disorders and healthy subjects in an iodine-replete area of the Islamic Republic of Iran, we studied 930 women in a clinic-based study: 698 patients (286 hypothyroid, 140 hyperthyroid, 272 with simple goitre) and 232 healthy women. Serum thyroxine (T4), triiodothyronine (T3), thyroid stimulating hormone, and anti-thyroid antibodies were measured. Positive autoantibodies were detected in 75.5% of patients with hypothyroidism, 73.6% of those with hyperthyroidism, 48.9% of those with simple goitre and 35.8% of the control group (P < 0.001). Autoimmunity may have a role in the genesis of common thyroid disorders.

Goiter rate, serum thyrotropin, thyroid autoantibodies and urinary iodine concentration in Tehranian adults before and after national salt iodization.

Goiter rate, serum TSH, antithyroperoxidase (TPOAb), antithyroglobulin (TgAb) antibodies, and urinary iodine concentration (UIC) were evaluated 10-11 yr prior (1983-1984) and 5-6 yr after (1999-2000) national salt iodization in Iran. Pre- and post-iodization groups consisted of 465 and 1426 adults aged > or =20 yr, respectively, selected by random cluster sampling in Tehran province. Total, grade 1 and grade 2 goiter rates were 65.2, 53.1, and 12.1% in 1983-1984 vs 25.2, 15.5, and 9.7% in 1999-2000 (p<0.0001). Median serum TSH was 1.5 mIU/l in 1983-1984 vs 0.8 mIU/l in 1999-2000 (p<0.0001). Median TSH also decreased in 20-29, 30-39, 40-49, 50-59, and > or =60- yr-adults in 1983-1984 vs 1999-2000 (p<0.0001). In 1983-1984, positive TPOAb and positive TgAb were detected in 3.2 and 4%, respectively, using agglutination test. Corresponding values were 12.5 and 16.8% using immunoenzymometric assay in 1999-2000. Overt and subclinical hypothyroidism was present in 0 and 32.8/1000 in 1983-1984 vs 3.5 and 21.7/1000 in 1999-2000, respectively. Overt and subclinical hyperthyroidism was detected in 4.4 and 4.4/1000 in 1983-1984 vs 0.7 and 5.6/1000 in 1999-2000, respectively. Subclinical hypothyroidism in males was significantly more frequent in 1983-1984 vs 1999-2000 (odds ratio 5.02, 95% confidence interval 1.72-14.68; p=0.004). Salt iodization resulted in adequate UIC, decrease in serum TSH and subclinical hypothyroidism in males, and an increase in thyroid autoantibodies without significant change in thyroid abnormalities. Benefits of iodine supplementation far outweigh its hazards in Tehranian adults.

The role of iodine in the evolution of thyroid disease in Greece: from endemic goiter to thyroid autoimmunity.

The thyroid gland is dependent on dietary iodine for the production of thyroid hormones, normal iodine requirement being about 150-200 microg/day. Long-term deficiency in iodine intake is associated with the development of goiter. When the prevalence of goiter in a population rises above 5-10%, the problem is considered endemic. Greece is a country with a recent history of moderate iodine deficiency, endemic goiter being prevalent in the 1960s in inhabitants of mountainous regions. Despite recognition of the problem, an iodine prophylaxis program was never officially implemented. Instead, "silent iodine prophylaxis" took place during the 1980s and 1990s with Greece's improvement in socioeconomic conditions. This resulted in the elimination of iodine deficiency and a parallel decrease in the prevalence of goiter among schoolchildren in formerly iodine deficient areas. However, the transition from iodine deficiency to iodine sufficiency or excess was followed by the emergence of autoimmune thyroiditis, especially among young girls, indicating that exposure to excess iodine may trigger thyroid autoimmunity. Thus, the modification of an environmental factor, ie dietary iodine, over the last 40 years in Greece has been associated with changes in the phenotypic expression of thyroid disease from endemic goiter to goiter associated with autoimmune thyroiditis.

Failure to detect thyroid growth-promoting activity in immunoglobulin G of patients with endemic goiter.

The [3H]thymidine incorporation assay in FRTL-5 cells was used to measure thyroid growth-stimulating antibody in the purified immunoglobulin G (IgG) fraction of patients with endemic nontoxic goiter (grade I-III) living in Italy (n = 34) or Peru (n = 37). IgG of euthyroid nongoitrous subjects living in the same endemic area (n = 25) and from an area of sufficient iodine intake were used as controls. Bovine TSH (10 mU/L) and thyroid-stimulating antibody of Graves' disease produced a significant increase in [3H]thymidine incorporation and DNA content in FRTL-5 cells. IgG from Italian or Peruvian patients with endemic goiter produced a small increase in [3H]thymidine incorporation in FRTL-5 cells (131 +/- 54% and 165 +/- 57%, respectively), which was indistinguishable from that obtained with IgG from normal nongoitrous subjects residing in endemic or nonendemic areas (167 +/- 80% and 161 +/- 36%, respectively). For comparison 18 of 25 (72%) IgG of hyperthyroid patients with Graves' disease produced clear-cut increases in [3H]thymidine incorporation (1142 +/- 1065%) and DNA content (219%) in FRTL-5 cells. IgG from patients with endemic goiter, at variance with Graves' IgG, did not cause an increase in DNA in FRTL-5 cells. All Graves' IgG that stimulated [3H]thymidine incorporation in FRTL-5 cells also stimulated cAMP production in this culture system, whereas no adenylate cyclase stimulation was produced by IgG from patients with endemic goiter. The prevalence of thyroglobulin antibody and thyroperoxidase antibody in endemic goiter patients did not differ from that in control subjects residing in the same iodine-deficient area. Our data show that sera of endemic goiter patients are devoid of thyroid growth-stimulating antibody and thyroid-stimulating antibody activities. These observations argue against a direct role of thyroid autoimmunity in the development of goiter in iodine-deficient areas.

Thyroid hormone and immunological studies in endemic goiter.

Iodized oil (1 ml im) was given to 58 goitrous patients from a mildly iodine-deficient area in Greece. Goiter size, urinary iodine, and serum T4, T3RU, T3, rT3, TSH, thyroxine-binding globulin (TBG), and thyroid autoantibodies were measured before and 1, 3, and 6 months after the injection. Goiter size decreased. Serum T4 remained relatively constant, but TBG decreased and therefore T3RU and FTI increased. Serum T3 and rT3 initially decreased (P less than 0.001) and then increased at the sixth month (P less than 0.001), both showing roughly parallel changes. Serum TSH, initially normal (1.42 +/- 0.11 (SEM) mU/liter), decreased to 0.65 +/- 0.01 and 0.76 +/- 0.05 mU/liter at the third and sixth month (difference from baseline P less than 0.001). Thyroid autoantibodies, both against thyroglobulin and the microsomal antigen, were undetectable before treatment, but became positive in 42.8% of the patients 3 and 6 months later. Three patients developed transient hyperthyroidism. This occurred 3 or 6 months after treatment, and was associated with high titers of thyroid autoantibodies. These results indicate that: 1) transient hyperthyroidism may occur after the administration of iodized oil, possibly because of thyroid tissue necrosis and leakage of hormones, and 2) serum TBG decreases after iodized oil, a finding not previously reported and one whose cause is not known.

Similar serum IgM concentrations in Greek endemic goiter and control populations: failure to confirm previous experience.

Circulating immunoglobulin M (IgM) concentrations were determined in 47 nontoxic goiter patients from four Greek endemic goiter areas, and in 13 patients from Athens, a non-goitrous area; and compared with 38 control non-goitrous subjects from the same goiter regions, and 23 more controls from Athens. The values in both goitrous and non-goitrous groups were indistinguishable. Current techniques for single radial immunodiffusion were employed. The results are expressed in standardized international units/ml serum, instead of the formerly used mg/dl. The present findings are in disagreement with the earlier observation from this laboratory that 40 per cent of goitrous patients had elevated IgM values compared with 10 per cent of control subjects.

Thyroid growth immunoglobulins in large multinodular endemic goiters: effect of iodized oil.

Iodized oil (IO) was administered to 10 goitrous patients recently emigrated to São Paulo (SP) from iodine deficiency areas and to 42 goitrous patients from 2 Brazilian chronic iodine deficiency regions, Loreto and Luziania (L). Thyroid growth-promoting immunoglobulin G (IgG) thyroid-stimulating antibody, serum thyroglobulin (Tg), TSH, and thyroid hormones were measured before and 1 yr after IO administration. In all patients there was a remarkable reduction of gland mass associated with a significant decrease (P less than 0.01) in both basal serum Tg and peak Tg levels after bovine TSH administration. The mean percent Tg increase after bovine TSH treatment was reduced to 82% above basal levels compared with 224% before IO. Mean serum TSH levels, elevated only in the L group [7.3 +/- 11 (+/- SD) microU/ml] decreased to the normal range after IO (2.5 +/- 2.1 microU/ml). Serum T3 and T4 concentrations did not change greatly. Tests for microsomal antibodies were negative before and after IO. IgG concentrates of serum obtained before and after IO were tested for their ability to stimulate incorporation of [3H]thymidine into DNA or to increase intracellular generation of cAMP in FRTL-5 cells. Thymidine incorporation activity was found in 8 of 10 patients from SP [316 +/- 37% (+/- SEM); range, 140-480%] and 25 of 42 patients in the L group (mean, 206 +/- 14; range, 120-500%) before IO. Stimulation of thymidine incorporation reflected true growth-promoting activity, as confirmed by experiments measuring cell number, was not accounted for by TSH in the preparation, and reflected IgG action because it was abolished by absorption with antihuman IgG. IgG from only 1 patient in group SP and 4 patients in group L stimulated intracellular production of cAMP in FRTL-5 cells. All patients except 1 in both groups had no IgG stimulation (less than 120%) of growth-promoting activity 1 yr after IO treatment. There was a significant positive correlation between thyroid growth-promoting activity and serum Tg concentrations (r = 0.58; P less than 0.001), but no significant correlation was found with other parameters (TSH, T4, and T3). We conclude that growth-promoting IgGs lacking ability to stimulate cAMP production may play a role in the large multinodular goiters due to chronic iodine deficiency.

Chromatographically purified immunoglobulin G of endemic and sporadic goiter patients stimulates FRTL5 cell growth in a mitotic arrest assay.

A strain of differentiated rat thyroid cells (FRTL5) in continuous culture was used to study the presence of thyroid growth-promoting immunoglobulins (TGI) in the serum of patients with endemic and sporadic euthyroid goiters. To identify true in vitro cell proliferation a microscopic mitotic arrest assay was used. Immunoglobulins G (IgGs) were prepared with QAE-Sephadex A-50 or protein-A-Sepharose. A positive growth stimulation index was found in IgG preparations of 65 of 71 patients with endemic goiter and in 9 of 14 IgG preparations of patients with sporadic goiter. IgG preparations of 15 control subjects from an area where endemic goiter due to iodine deficiency does not occur and of 18 subjects without iodine deficiency and without thyroid enlargement living in the endemic area did not stimulate FRTL5 cell growth. FRTL5 cell growth stimulation with IgGs of these euthyroid goiter patients could only be detected when IgG was tested in combination with a small dose of TSH. Immunoprecipitation with polyclonal and monoclonal antihuman IgG was able to abolish the growth-promoting effects. In 32 blinded samples the Feulgen cytobiochemical assay, formerly used to detect TGI, was compared with the FRTL5 mitotic arrest assay. The two methods showed similar results. Our observations of chromatographically purified IgG promoting thyroid cell proliferation in vitro provide good evidence that IgG was responsible for thyroid cell growth in vitro and suggest that autoimmune growth mechanisms may be involved in the pathogenesis of both endemic and sporadic goiters.

Elevated anti-galactosyl antibody titers in endemic goiter.

Anti-Gal is a human polyclonal antibody that constitutes approximately 1% of the circulating immunoglobulin G (IgG), interacts specifically with the mammalian carbohydrate alpha-galactosyl epitope. Furthermore, it was found to mimic in vitro thyrotropin (TSH) effects regarding stimulation for cyclic adenosine monophosphate (cAMP) synthesis, 125I uptake, and cellular proliferation on cultured porcine thyrocytes and on Graves' disease thyrocytes, but not on normal human thyrocytes. As immune activation in sporadic and endemic goiters might play a secondary role in regulating thyrocyte proliferation and function, we evaluated anti-Gal titers in endemic goiter. Serum was obtained from 109 Chagas'-negative patients living in an endemic goiter area of Brazil (Grao Mogol, MG) and 160 controls. The patients were divided into 3 groups, according to their goiter size (World Health Organization [WHO] classification): grade 0 (group 1, n = 24), grade I-II (group 2, n = 41), and grade III-IV (group 3, n = 44). Anti-Gal was assessed by a radioimmunological procedure (results expressed as the percentage of bound radioactivity/total activity [%B/T]). The antibody titer was significantly more elevated in group 1 (mean +/- SEM: 9.27%+/-0.80%), in group 2 (mean +/- SEM: 16.17%+/-0.97%), and in group 3 (20.97%+/-1.30%) than in normal controls (6.46%+/-0.33%). Analysis of the male and female data separately for anti-Gal titer did not substantially alter these results. We concluded that the anti-Gal titer is higher in patients with endemic goiter and presented a possible relationship with the size of goiter. Whether these antibodies contribute to the pathogenesis of the disease needs further clarification.

[Iodine and delayed immunity]. / Iodio e immunità ritardata.

Iodine was and is sometimes used therapeutically in various pathologies where the immune mechanism is known to play a dominant role. It has in fact been administered to patients with tubercular granulomatous, lepromatous, syphilitic and mycotic lesions where it facilitates cure. This effect does not depend on iodine's action on the micro-organism responsible. Iodine may also be used in Villanova-Panol Panniculitis, in erythema nodosum, in nodular vasculitis, erythema multiforme and Sweet's syndrome. Oral iodine is also very effective in the lymphatic-cutaneous form of sporotrichosis. In order to establish a relationship between dietary iodine and immune response, 607 infants residing in an area of endemic goitre were studied: 215 were given Lugol solution (2 drops a week for about 8 months) and 392 not. The immune response was assessed by the skin test method using tetanic toxoid and a clear correlation was shown between this and lymphocyte stimulation and monocytic chemotaxis tests. The test was considered positive when an infiltration of at least 5 mm in diameter was shown after 48 hours (in the U.S. 80% of paediatric cases aged 2-10 years old were positive). A significant difference was noted in the average diameter of the infiltrations after the tetanic toxoid skin test in the two groups considered (P less than 0.001). The results appear to indicate that an adequate iodine intake is necessary for normal retarded immune response. The molecular mechanism by which iodine increases immune response is still to be decided.

[Endemic goiter in Latium: environmental and genetic factors]. / Gozzo endemico nel Lazio: fattori ambientali e fattori genetici.

Most studies on the pathogenesis of endemic goiter focus above all on iodine deficiency. In some endemic goiter areas (i.e. Nigeria) there is no evidence of iodine deficiency; therefore, we suggest the taking into account of various factors, both environmental and non-environmental. We report the results of two studies carried out in three different areas in Latium: one of them (Cerveteri, RM) could be classified as high prevalence of goiter area, while the two others (Roccasecca dei Volsci, LT and Castel San Pietro Romano, RM) are true endemic goiter areas. The role of environmental factors, radioactivity and electromagnetism, foodstuff, the hydrogeological and chemical composition of natural water and the importance of genetics are here discussed, assuming that the endemic goiter could have a multifactorial pathogenesis.

[Iodine therapy for iodine deficiency goiter and autoimmune thyroiditis. A prospective study]. / Jodtherapie der Jodmangelstruma und Autoimmunthyreoiditis. Eine prospektive Studie.

PROBLEM: There is epidemiological and clinical evidence that iodine may induce or promote the manifestation of autoimmune thyroiditis. For this reason it is important to know if substitution of alimentary iodine deficiency or iodine treatment of endemic goitre can cause formation of thyroid antibodies. On the other hand the practical importance of this phenomenon should be evaluated. PATIENTS AND METHODS: During a prospective study we examined 209 patients with endemic non-toxic goitre and 53 healthy people. For treatment were used 200 micrograms iodine/d (n = 119), 500 micrograms iodine/d (n = 27), 1.5 mg iodine/week (n = 41), 150 micrograms iodine/d plus 75 to 100 micrograms T4/d (n = 26), 100 micrograms iodine plus 100 micrograms T4/d (n = 24). The observation took 1 year with a 3-month interval for check ups including clinical examination, ultrasound, TSH, T3, fT4, TPO- and thyreoglobuline antibodies and urinary iodine. RESULTS: After 12 months 7.5% of iodine treated persons had produced antibodies, most of them at low levels. In healthy people we found increased antibody-levels in 3.8%, in patients with goitre in 9.0%, in patients with nodular goitres in 11.1%. 500 micrograms iodine caused the most antibody reaction in 14.8%. People treated with 200 micrograms iodine/d showed positive antibody levels in 5%. T4 seems to reduce antibody-reactions. Pathological antibody-levels were not found in patients with combined iodine/T4- and single-T4 therapy. Among the 22 primary pathological antibody levels only 4 increased further (18.2%). Three of them belonged to the group of 5 persons treated with 500 micrograms iodine/d. Primary high antibody values were normalized in 5 patients (22.7%). Hypothyroid disturbances were not found. Ultrasound did not show any alterations, and the reduction of thyroid volumes in antibody-positive patients was not affected. Median urinary iodine excretion during the observation-interval was 5.2 to 7.2 micrograms/dl. CONCLUSIONS: Possible antibody reactions have no clinical importance at all. Individual cases must be observed. Low iodine doses should be preferred. Combined iodine/T4 treatment seems to have an advantage regarding immunological thyroidal reactions.

Prevalence of antithyroid microsomal antibody in thyroid patients of endemic goitre area.

The region of greater Mymensingh known for iodine endemicity, recently came under iodine supplementation as a result of mandatory universal iodination of salt program. Autoimmune thyroid diseases (AITD) are among the most common human autoimmune disorders & presence of autoantibodies to the microsomal antigen (AntiMCAb) is a hallmark of disease activity. Both iodine deficiency & iodine supplementation precipitate increase rate of autoimmunity to the thyroid gland. Study was undertaken to determine prevalence of AntiMCAb positive cases among patients with various thyroid diseases. High resolution ultrasound (HRUS), serum thyroid hormone assays & scintiscan were used to classify the thyroid patients into 8 categories. 221 patients were studied during the stipulated period of 3 months. Male patients were 60 & female patients were 161. Age ranged from 11 to 65 years with median age 29.4 years. AntiMCAb test were done with radioimmunoassay (RIA). 126 patients had antimicrosomal antibody (57.01%). All form of hypothyroid (atrophic, goitrous, Hashimoto's) have very high rate of AntiMCAb positive cases. Highest 89.28% were seen in patients showing feature of Hashimoto's thyroiditis or generalized feature of AITD in HRUS with hypothyroidism, followed had 61.29% positive cases, However, antithyroid antibody was found in all form of thyroid disorders. Nodular goiter had 21.73% antiMCAb positive cases. AntiMCAb found positive at the rate of 33.33% in euthyroid patients with HRUS feature of AITD & diffuse euthyroid goiter, 40% in subclinical hypothyroid, 40% in subclinical hyperthyroid. Female rated higher in range of antimicrosomal antibody positivism. 59% of all thyroid patients among female subjects were AntMCAb positive, where as 51.67% male thyroid patients were positive. Highest number of positive cases found in the 30-35 age group. No definite pattern, however, was observed among age distribution. 20 age matched sample from patients unsuspected of thyroid disease shows 10% AntiMCAb positive compared to 73.33% of the same among same age group of thyroid patients. Frank Hashimoto's thyroiditis with positive antiMCAb and hypothyroidism were all detected by HRUS.

[General pathology of trace element deficiency]. / Obshchaia patologiia gipomikroélementozov.

According to the authors' concept, different forms of trace element deficiency show some general rules of development. All of them are followed by a decrease of immune resistance. Trace element deficiency is never isolated, it is always characterized by trace element unbalance and is followed by a considerable disturbance of metabolism (mineral, lipid, carbohydrate and protein) with relevant manifestations. Reduced immune resistance and pluriglandular endocrinopathy create the conditions for various malignancies.

[Behavior of thyroid autoantibodies in persons inhabiting an endemic goiter area]. / Zachowanie sie przeciwcial przeciwtarczycowych u osób z terenu endemii wola.

The study was aimed at investigating the occurrence of thyroid autoantibodies (ATMA and TGA) in persons inhabiting the area of goiter endemy of mild degree. The survey comprised 1508 persons of age ranging from 3 to 68 years. The subjects studied have been divided into the groups taking into account age, sex, degree of thyroid enlargement (according to WHO, 1974), and the characteristics of the goiter. The occurrence of ATMA or TGA antibodies was demonstrated in 17% of the subjects. An increase in the incidence and titer of thyroid autoantibodies with age was observed. The occurrence of thyroid autoantibodies was observed more frequently in the subjects with parenchymatous goiter. No correlation was found between the incidence of the antibodies and goiter size. Thyroid autoantibodies have also been found in 10% of subjects without goiter. The results obtained do not indicate convincingly the role of the thyroid autoantibodies in the pathogenesis of endemic goiter.

[Role of some environmental factors in the development of endemic goiter (a review)]. / Rol' nekotorykh faktorov okruzhaiushchei sredy i razvitii éndemicheskogo zoba (obzor).

The review presents possible causes of endemic goiter since only iodine deficiency fails to explain such a great spread of this disease. Etiological factors of endemic goiter, such as the imbalance of trace elements, the use of contaminated drinking water, the toxic action of chemicals, exposure to ionizing radiation, genetic factors, are discussed. Prevalence rates of endemic goiter in Russia and other countries of the world are presented. The causes of a significant increase in the incidence of this disease are discussed.