Autoimmune thyroid disease (AITD) is the most common organ specific autoimmune disorder usually resulting in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland. The syndromes comprising autoimmune thyroid disease are many intimately related illnesses: Graves' disease with goitre, hyperthyroidism and, in many patients, associated ophthalmopathy, Hashimoto's thyroiditis with goitre and euthyroidism or hypothyroidism but also thyroid dysfunction occurring independently of pregnancy and in 5-6% of postpartum women and thyroiditides induced by different drugs and other environmental influences. The immunological mechanisms involved in these diseases are closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. The syndromes are connected together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to another within the same individual over time. In some patients, other organ specific and nonorgan specific autoimmune syndromes are associated with autoimmune thyroid disease, including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, celiac disease, rheumatoid arthritis or lupus. Thyroid peroxydase, TPO, the primary enzyme involved in thyroid hormonogenesis, was initially identified in 1959 as the 'thyroid microsomal antigenn. It is uncertain whether TPO autoantibodies or TPO-specific T cells are the primary cause of thyroid inflammation, which can lead, in some individuals, to thyroid failure and hypothyroidism. TPOAbs are the hallmark of AITB and are present in almost all patients with Hashimoto's thyroiditis, in two-thirds of patients with postpartum thyroiditis and also in 75% of patients with Graves' hyperthyroidism. The antibodies are mainly produced by lymphocytic infiltrate in the thyroid gland and only to a small extent by regional lymph nodes or the bone marrow. Unlike antibodies against thyroglobulin (Tg), TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity. Antibodies to TSH-R mimic the function of TSH, and cause disease by binding to the TSH-R and stimulating (or inhibiting) thyroid cells. The TSHR, a member of the G protein-coupled receptor family with seven membrane-spanning segments. Patients with autoimmune thyroid disease may have both stimulating and blocking antibodies in their sera, the clinical picture being the result of the relative potency of each species; blocking antibodies seem more common in Graves' patients with ophthalmopathy compared to those without this complication. The major T cell epitopes are heterogeneous and T cell reactivity against certain TSH-R epitopes has been present in high proportion in normal subjects. More diversified response to TSH-R, with heterogeneity of epitope recognition by TSAb, is predictive of likely remission after antithyroid drug treatment for Graves' disease.

Background: Ample evidence has proven that the functional property of cells decreases over the years. Nevertheless, although it has taken decades to convince ourselves that elderly people belong to a specific age group both biologically and medicinally, and in whom special criteria have to be taken into consideration, it seems that even they themselves do not present an homogenous group. Objective: Today we often hear of authors of studies speaking of two subpopulation groups – one group that ages by all the laws of aging that we have encountered and accepted thus far, and the other group that seems to postpone aging due to ‘programmed death’, or more specifically due to low mastery/low emotional support or because of additional reasons; however, the existence of the two groups seems eminent. Methods: The identification of these two groups would allow us to find more realistic results in studies, and therefore a more efficient therapy for certain diseases. Results: This hypothesis does not contradict the theories of aging that we have accepted (at least not the majority) and also does not contradict the fact that there is a large interindividual variability. This hypothesis doubts and claims there are exceptions to the initial assumption of geriatrists and gerontologists that ‘parallel to the aging process, the functions of all organs and organ systems lessen.’ Conclusion: The identification of these two groups would allow us to find more realistic results in studies, and therefore more efficient therapy for certain diseases.

Magnesium, beyond any doubt, plays an important role in metabolism. Alterations of magnesium levels have an impact on many organs and systems, especially during aging. We had 156 participants aged 60–93 years (average 74.7 years) in our survey. Of them, 49 were men and 107 were women. Treatment with loop diuretics (Furosemid and Bumetanide) and magnesium levels was correlated, as well as the influence of magnesium levels on life span. Serum magnesium levels were measured in patients receiving diuretics and in the control group. Also, magnesium levels were measured in patients who passed away in the course of their disease and were compared with the control group. Magnesium levels in the diuretic group (100 patients) were 0.93 ± 0.094 mmol/l, while the average levels in the control group of 56 patients were 0.89 ± 0.075 mmol/l. In 29 patients who passed away, average magnesium levels were 0.92 ± 0.078 mmol/l, while in the control group (127 patients), magnesium levels were 0.93 ± 0.083 mmol/l. The differences were not statistically significant. There were no differences in serum magnesium of the elderly persons investigated regarding age group, gender, or type of diuretics. If methods of determining ionizing magnesium in serum or intracellular magnesium are not available, normal magnesium values in the serum are to be taken with a qualified acceptance.

Increased thyroglobulin (Tg) serum level in females (n = 49) suffering from scintigraphically "cold" thyroid nodule (395 +/- 168, micrograms/l, mean +/- SD) is significantly higher (p less than 0.001) in comparison with the data obtained from euthyroid healthy persons (28 +/- 10, n = 15) or those diagnosed with scintigraphically functional thyroid nodule (72 +/- 14, n = 15). No correlation between Tg and TSH serum levels has been seen before surgical removal of "cold" nodule (rxy = +0.34). In 49 out of 75 cases (65.3%) struma colloids were confirmed pathohistologically. After surgery, "cold" thyroid nodule was removed, serum Tg level decreased progressively within several days and three months afterwards, Tg level in most patients was mainly within the normal range for a healthy subject. The positive correlation between Tg and TSH was established three months after surgical removal of the nodule (rxy = +0.90). An elevation of serum Tg level was found in 16 out of the 49 patients during different postoperative periods (from 2 to 9 years). Under thyroxine treatment, in most of these patients a significant decrease of serum Tg level was observed. However, in a few treated patients, no change in Tg level was seen. Further clinical control in thyroxine-nonsuppressive patients discovered a compensatory hypertrophy of thyroid tissue and the appearance of a new thyroid nodule later. Present data and clinical experience suggest that long-term follow-up of serum Tg level in patients after surgical removal of "cold" thyroid nodule, brings about to early diagnosis of thyroid tissue postoperative hypertrophy before the appearance of thyroid gland nodule relapse.

Autoimmune diseases are manifested in a broad spectrum. Classic examples of organ-specific autoimmune disease include Addison's disease, insulin-dependent type-1 Diabetes mellitus, Grave's disease (MGB), and Hashimoto thyroiditis (HT). The initial report of this autoimmune thyroid disease (AITD) dates back to Hakira Hashimoto (1912). In HT, as an organ-specific autoimmune disease, massive infiltration of lymphoid cells and parenchyma destruction are a consistent feature. The infiltration appears to be immune-mediated, primarily lymphocytic (T helper, T suppressor cells), NK cells and B cells. The pathological characteristics of AITD include development of the goitre (atrophic form is not so frequent), impaired thyroid gland function (from hyperthyroidism to subclinical and manifested hypothyroidism) and the formation of antithyroidal antibodies against thyroglobulin (AbTg) and the microsomal antigen (Ab TPO). There is a very good correlation between the antibodies against TPO and the histological findings. Morbus Graves Basedow is characterized by autoimmune hyperthyroidism with goitre, and infiltrative orbitopathy. Autoantibodies against the TSH-receptor molecule on the plasma membrane of the thyroid gland follicles cause a nonphysiological activation and an increase of the cellular function. Besides this hyperthyroidal condition, an autoimmune attack against the retrobulbar tissue leading to endocrine orbitopathy, can be noted in about 40% of patients suffering from MGB.

Out of 362 patients with diagnosis of autoimmune haemopathy treated in eight-year period at the Hematology centre, concomitant autoimmune thyreoideopathy was confirmed in 22 (5.52%). The most frequent was simultaneous manifestation of pernicious anemia and autoimmune thyreoiditis-Phenomenon was less frequently observed in patients with immune thrombocytopenic purpura and Graves disease. In the subgroup of patients with autoimmune hemolytic anemia, there was no evidence of simultaneous autoimmune thyreoideopathy. General opinion is that etiopathogenesis of these immunological disorders does not include unique mechanism of humoral and cellular immune response; more probable, it is the question of normal immune response regulation impairment, based on the paerticular genetic predisposition.

This study analysed the concentrations of thyroid binding globulin (TBG) in the serum as well as the level of triiodothyronine (T3), thyroxine (T4), thyreostimulating hormone (TSH), thyroglobulin (Tg) and T4/TBG coefficient, before therapy and on the fifth day of therapy in 27 patients of both sexes suffering from neoplasia. The patients were treated with cytostatic antibiotics, alkylating agents and podophyllines derivates, by protocol. Serum T3 gains in concentration already after 5 days since the beginning of treatment (from 1.65 +/- 0.20 to 1.73 +/- 0.18 nmol/l), but it is retained within physiological ranges as well as TSH, rT3 and Tg. Thyroxine remains within the permitted ranges, but slightly decreased after therapy (64.00 +/- 11.00 nmol/l, mean +/- SEM) in comparison to the value before (71.00 +/- 19.00), p(F) less than 0.1. A reduction of concentrations in total serum proteins at an average 7.88% was found. The level of inter-alpha globulin, TBG, in patients with proved malignancy is low before therapy (14.97 +/- 4.73 micrograms/l, mean +/- SEM, in males and 14.83 +/- 3.70 in females) but, with application of cytostatics it decreases considerably to the level of 11.68 +/- 4.46 (p less than 0.05) in males and to 13.68 +/- 3.89 in females (NS). In view of these facts, T4/TBG coefficient remains normal and contributes to the maintenance of euthyroid gland function.

Chronic thyroiditis (Hashimoto's disease) is a slowly developing persistent inflamation of the thyroid gland, which frequently leads to hypothyroidism. Some of the up-to-date knowledge about hypothyroidism, both subclinical and manifested, caused by autoimmune disease, was presented. Autoimmune thyroid gland disease can occur at any age, but predominantly affects women after periods of high emotional and physical stress or accidents, as well as during periods of hormonal changes. It can also develop in families, and having an autoimmune disease slightly increases the risk of developing another. This paper showed an increasing incidence of subclinical hypothyroidism (4.17%) in elderly, and, at the same time, the incidence of primary hypothyroidism accounting for 1%. It is very usefull to estimate the stimulated thyrotropin (TSH) response, as well as the value of fast, short time thyroid gland reserves, analyzed by T3 and T4 serum level at 60th minute after TRH stimulation. Treatment of choice for HT (hypothyroidism of any cause) is thyroid hormone replacement. Drug of choice is orally administered levothyroxine sodium, usually for life-time. The standard dose is 1.6-1.8 mcg/kg body weight per day, but is in most cases patient dependent. Elderly patients usually require smaller replacement dose of levothyroxine, sometimes less than 1 mcg/kg body weight per day with coronary dilatator at the same time.