Objective: Abnormalities in haematological parameters have been noted in patients with thyroid diseases. Nevertheless, the exact mechanism of thyroid hormones' (THs) action on human haematopoiesis is still not entirely clear. Design: The influence of THs through TH receptors (TRa-1 and TRb-1) on haematopoiesis in patients with hypo-and hyperthyroidism was analysed. Methods: TR gene expression at the mRNA and protein levels in human CD34C -enriched haematopoietic progenitor cells (HPCs) obtained from the peripheral blood of patients with thyroid disorders and healthy volunteers was analysed. The cell populations were also investigated for clonogenic growth of granulocyte macrophage-colony forming units and erythrocyte-burst forming units (BFU-E). The level of apoptosis was determined by annexin V/propidium iodide staining and quantitative RT-PCR. Results: The studies revealed that hypo-and hyperthyroidism modify TR gene expression in HPCs in vivo. TH deficiency resulted in a decrease in total blood counts and clonogenic potential of BFU-E. In contrast, hyperthyroid patients presented increased clonogenic growth and BFU-E number and significantly higher expressions of cell cycle-regulating genes such as those for PCNA and cyclin D1. Finally, an increase in the frequency of apoptotic CD34C -enriched HPCs in hypo-and hyperthyroidism with a modulation of apoptosis-related genes was detected. Conclusions: The following conclusions were derived: i) TR expression in human haematopoietic cells depends on TH status, ii) both hypo-and hyperthyroidism significantly influence clonogenicity and induce apoptosis in CD34 C -enriched HPCs and iii) the molecular mechanism by which THs influence haematopoiesis might provide a basis for designing novel therapeutic interventions in thyroid diseases.

It has been widely accepted that obesity is associated with chronic, low-grade inflammation that affects the adipose tissue as well as the entire system. The aim of this study was to assess whether past Chlamydia pneumoniae infection influences obesity phenotypes and serum levels of low-grade inflammation markers in obese, healthy premenopausal women. The study was performed on 48 obese and 42 normal-weight women, aged 31.2 +/- 7.2 years. Serum levels of C-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha) and its soluble receptor R2 (sTNF-R2), and interleukin 6 (IL-6) were measured. Body composition was assessed by bioimpendance. Insulin sensitivity was assessed by quantitative insulin sensitivity check index (QUICKI). The seroprevalence of C. pneumoniae infection was 69.1% and was similar in obese and normal-weight women (75.2% and 61.9%, respectively; P = 0.18). Obese women had higher CRP than healthy controls (P < 0.05). IL-6, TNFalpha, and sTNF-R2 showed no significant differences when comparing obese and normal-weight or C. pneumoniae infected and uninfected women. In multivariate regression analysis, fat mass (P < 0.001) and QUICKI (P < 0.01), accounting for 35% of the variance of CRP and C. pneumoniae infection, did not significantly contribute to this model (P = 0.51). In conclusion, past C. pneumoniae infection was not associated with changes in chronic inflammation markers in premenopausal obese women.

Preoperative diagnostic investigations of nodular goiter are based on two main examinations: ultrasonography of the thyroid gland and ultrasound-guided fine-needle aspiration biopsy. So far, FNAB has been the best method for the differentiation of nodules, but in some cases it fails to produce a conclusive diagnosis. Some of the biopsies do not provide enough material to establish the diagnosis, in some other biopsies cytological picture is inconclusive.Determining the eligibility of thyroid focal lesions for surgery has been more and more often done with molecular methods. The most common genetic changes leading to the development of thyroid cancer include mutations, translocations and amplifications of genes, disturbances in gene methylation and dysregulation of microRNA. The mutations of Ras proto-oncogenes and BRAF gene as well as disturbances of DNA methylation in promoter regions of genes regulating cell cycle (e.g. hypermethylation of RASSF1A gene and TIMP-3 gene) play an important role in the process of neoplastic transformation of thyreocyte. The advances in molecular biology made it possible to investigate these genetic disturbances in DNA and/or RNA from peripheral blood, postoperative thyroid tissue material and cytology specimens obtained through fine-needle aspiration biopsy of focal lesions in the thyroid gland.As it became possible to analyze the mutations and methylation of genes from cell material obtained through fine-needle aspiration biopsy, it would be beneficial to introduce the techniques of molecular biology in the pre-operative diagnosis of nodular goiter as a valuable method, complementary to ultrasonography and FNAB. The knowledge obtained from molecular studies might help to determine the frequency of follow-up investigations in patients with nodular goiter and to select patients potentially at risk of developing thyroid cancer, which would facilitate their qualification for earlier strumectomy.

Thyroid metastases account for approximately 1.4-3% of all malignancies of the thyroid gland. Thyroid metastases are most common in: clarocellular carcinoma of the kidney, lung cancer, breast cancer, malignant melanoma and cancers of gastrointestinal tract. A rare situation is when thyroid metastasis is diagnosed before detecting primary malignant focus and when it is the first manifestation of underlying disease. We present a case of 64-year-old male with thyroid metastasis being the first manifestation of lung adenocarcinoma.The authors emphasize that patients with the history of malignancy should undergo an ultrasound examination of the thyroid gland in order to exclude a focal lesion, and if such lesion is detected, fine-needle aspiration biopsy is recommended. The authors also point out that establishing final diagnosis of thyroid metastasis of cancer in other organs is only possible on the basis of postoperative histopathology and immunohistochemistry.

The changed activity of the somatotropin-somatomedin, gonadal, and corticotrophin axes corresponds to the clinical stage of AN. Plasma IGF-1 seems to be the most sensitive and useful independent hormonal marker of cachexia.