The prevalence of subclinical hypothyroidism (SH) is 3-10%. The prevalence of subclinical hyperthyroidism (SHr) is 0.7-9.7%. Thyroid hormones affect cardiac electrophysiology, contractility, and vasculature. SH is associated with an increased risk of coronary heart disease (CHD), especially in subjects under 65. SHr seems to be associated with a slightly increased risk of CHD and an increase in CHD-related mortality. Both SH and SHr carry an increased risk of developing heart failure (HF), especially in those under 65. Both SH and SHr are associated with worse prognoses in patients with existing HF. SH is probably not associated with atrial fibrillation (AF). SHr, low normal thyroid-stimulating hormone (TSH) and high normal free thyroxine (FT4) are all associated with the increased risk of AF. An association between endothelial dysfunction and SH seems to exist. Data regarding the influence of SHr on the peripheral vascular system are conflicting. SH is a risk factor for stroke in subjects under 65. SHr does not increase the risk of stroke. Both SH and SHr have an unfavourable effect on cardiovascular disease (CVD) and all-cause mortality. There is a U-shaped curve of mortality in relation to TSH concentrations. A major factor that modifies the relation between subclinical thyroid disease (SCTD) and mortality is age. SH increases blood pressure (BP). SHr has no significant effect on BP. Lipids are increased in patients with SH. In SHr, high-density lipoprotein cholesterol and lipoprotein( a) are increased. SCTD should be treated when TSH is over 10 mU/l or under 0.1 mU/l. Treatment indications are less clear when TSH is between normal limits and 0.1 or 10 mU/L. The current state of knowledge supports the understanding of SCTD’s role as a risk factor for CVD development. Age is a significant confounding factor, probably due to age-associated changes in the TSH reference levels.

Thyroid function disorders are the most common endocrine disorders in humans. They are frequently diagnosed, with prevalence varying between 2 and 6%, and a female to male ratio of up to 10:1. Disorders of thyroid function in the narrower sense are presented by its hyperactivity or underactivity, although there are conditions that lead to an increased concentration of thyroid hormones, without its increased activity. In iodine-sufficient regions, the most common cause of hyperthyroidism, as well as hypothyroidism, is an autoimmune disease of the thyroid. For hyperthyroidism, it is Graves' disease, with typical symptoms and signs of hypermetabolism. The diagnosis of hyperthyroidism is based on suppressed TSH and elevated fT4 (free, and in the differential diagnosis, elevated TSH-receptor-antibodies are crucial for Graves' disease. Management of Graves' disease relies on three equally potent approaches: medical therapy, ablative treatments with 131I-radiotherapy-RAI, and thyroidectomy. Hashimoto's thyroiditis is the most common cause of hypothyroidism in iodine-sufficient regions. Symptoms and signs of hypothyroidism are non-specific and correspond to the symptoms and signs of hypometabolism. The diagnosis is made based on elevated TSH with decreased fT4. Thyroxine-peroxidaseantibodies and thyroglobuline-antibodies are important in differential diagnosis. Sometimes elevated TRAb is found in Hashimoto's thyroiditis. The treatment of hypothyroidism is levothyroxine replacement therapy.

Background: Although thyroid hormones have significant effect on cardiovascular system, the impact of subtle thyroid dysfunction such as subclinical hypothyroidism (SCH) remains to be determined. We investigated coronary flow reserve (CFR) in patients with subclinical hypothyroidism. Methods: Thirty two subjects with SCH and eighteen control subjects with normal serum thyroid hormones and thyroid-stimulating hormone (TSH) levels were included in the study. TSH, free thyroxine, free triiodothyronine, glucose, insulin, HbA1c, cholesterol, triglyceride and plasma levels of C-reactive protein were measured. Coronary diastolic peak flow velocities in left anterior descending coronary artery were measured at baseline and after adenosine infusion. CFR was calculated as the ratio of hyperemic to baseline diastolic peak velocity. Results: CFR values were not significantly different between the two groups (SCH 2.76±0.35 vs controls 2.76±0.42). There was a significant correlation of CFR with waist to hip ratio, hypertension, smoking habits, markers of glucose status (glucose level, HbA1c, insulin level, HOMA IR), cholesterol, LDL-cholesterol and triglyceride levels in SCH group, whereas only cholesterol level showed significant correlation with CFR in controls. There was no correlation between CFR and thyroid hormones. Conclusions: We concluded that there is a different impact of cardiovascular risk factors on CFR in SCH patients compared to healthy control and that these two groups behave differently in the same circumstances under the same risk factors. The basis for this difference could be that the altered thyroid axis "set point" changes the sensitivity of the microvasculature in patients with SCH to known risk factors.

Medullary thyroid carcinoma is a form of neuroendocrine tumor that arises from parafollicular C cells which produce calcitonin. In addition to calcitonin, these cells produce smaller amounts of other peptides, including carcinoembryonic antigen (CEA), which is used as a nonspecific tumor marker in the follow-up of patients with this tumor. MTC is a rare thyroid tumor and occurs three times more often in women than in men. It can occur in two forms, sporadic (80%) and familial form (20%). The familial form can occur alone or in association with other endocrine tumors within MEN 2A and MEN 2B syndromes. The sporadic form most often occurs in the fifth and sixth decades of life. The familial form is inherited autosomally dominantly, most often based on a mutation in the RET protooncogene located on chromosome 10. C-cell hyperplasia is considered to be a premalignant lesion, which precedes medullary carcinoma. Medullary carcinoma metastasizes very early. We presented a patient with a sporadic form of MTC which appeared at a typical age. Initial values of both baseline and stimulated calcitonin were not in the range for suspected MCT, but due to persistent increases in calcitonin, with elevated baseline (63 pg / mL) and higher stimulated calcitonin (96 pg / mL), the patient was referred for surgical treatment. Due to the strong correlation of calcitonin values with tumor size, the initial calcitonin values were expected to be low because the tumor was 3 mm in size. The histopathological diagnosis was C-cell hyperplasia. However, due to the fact that nodular C-cell hyperplasia is histopathologically difficult to distinguish from medullary microcarcinoma, based on the persistent increase in calcitonin levels, the patient was likely to already have metastatic disease at the time of thyroidectomy. Definitive diagnosis was made by liver biopsy. Therapy with tyrosine kinase inhibitors was introduced, and calcitonin levels strarted to decrea, but there is an increase in carcinoembryonic antigen, which is a poor prognostic parameter.

Introduction. In interpreting thyroid hormones results it is preferable to think of interference and changes in concentration of their carrier proteins. Outline of Cases. We present two patients with discrepancy between the results of thyroid function tests and clinical status. The first case presents a 62-year-old patient with a nodular goiter and Hashimoto thyroiditis. Thyroid function test showed low thyroid-stimulating hormone (TSH) and normal to low fT4. By determining thyroid status (ТSH, T4, fT4, T3, fT3) in two laboratories, basal and after dilution, as well as thyroxine-binding globulin (TBG), it was concluded that the thyroid hormone levels were normal. The results were influenced by heterophile antibodies leading to a false lower TSH level and suspected secondary hypothyroidism. The second case, a 40-year-old patient, was examined and followed because of the variable size thyroid nodule and initially borderline elevated TSH, after which thyroid status showed low level of total thyroid hormones and normal TSH. Based on additional analysis it was concluded that low T4 and T3 were a result of low TBG. It is a hereditary genetic disorder with no clinical significance. Conclusion. Erroneous diagnosis of thyroid disorders and potentially harmful treatment could be avoided by proving the interference or TBG deficiency whenever there is a discrepancy between the thyroid function results and the clinical picture.