In the last two decades microRNAs have received great attention in research because of their ability to regulate gene expression. Many studies have shown that defects in different microRNA molecules are linked to many diseases; however, their contribution towards thyroid disease has not been fully explored. Herein, we present a short review of the present state of knowledge on microRNAs, such as their origin, their biogenesis and biological function, as well as their differential expression in papillary thyroid carcinoma. Dysregulated microRNA has been closely linked to thyroid dysfunction and oncogenicity leading to this type of thyroid cancer. The effects of Single Nucleotide Polymorphisms in microRNA are also discussed with respect to papillary thyroid carcinoma.MicroRNAs (miRNA, miR) are a class of endogenous noncoding RNA molecules. Mature miRNAs are short, singlestranded RNA molecules ranging from 18 to 22 nucleotides in length (1). These molecules play a substantial role in the regulation of gene expression, through the induction of translational repression or silencing effects by complementary binding to target mRNAs (2-4). They may also act as tumor suppressor genes and oncogenes (5). Although miRNAs constitute only 3% of the human genome, it is believed that these molecules altogether regulate more than half of the protein-coding genes. Noteworthy, one single miRNA can alter the expression of hundreds of different transcripts (6). MiRNAs are expressed in a tissue-specific fashion (7) and can be found, apart from tissues, also in blood as components of serum, plasma, mononuclear cells and in other body fluids (i.e. urine, semen, saliva, tears, ascitic fluid, amniotic fluid and breast milk) (8, 9). Circulating miRNA molecules are very stable in the blood plasma and serum because they are incorporated in microparticles, such as exosomes and apoptotic bodies (10,11). Biochemical analyses have revealed that miRNA is resistant to RNase activity as well as to extreme acidic and alkaline pH and temperature (12, 13). Biogenesis of microRNAsBriefly, biogenesis of miRNA is initiated by the generation of non-coding primary miRNA (pri-miRNA) transcripts ( 14). MiRNA is first transcribed as pri-miRNA by RNA polymerase II in the nucleus and then, split into precursor microRNA molecules (pre-miRNA) (15). Next, pre-miRNA is transported through exportin 5 (XPO5) to the cytoplasm where it is processed by the Dicer RNase III enzyme, to form mature miRNA (16,17). Mature miRNAs can promote or inhibit mRNA translation and degradation by targeting with precision complementary sequences in 3'UnTranslated Regions (3'UTR) (14,18). In this way, miRNAs modulate different cellular pathways and can be used as therapeutic means to treat pathological conditions, such as cancer (19). Discovery of microRNAsThis novel class of small regulatory RNAs were first described in 1993 by Lee et al. in Caenorhabditis elegans (20). Since their discovery and original description in the 90s, the number of miRNA sequences deposited in the microRNA da...

Acromegaly is a rare and chronic disease, most often caused by a pituitary adenoma. Excessive secretion of the growth hormone (GH) leads to hepatic secretion of insulin-like growth factor-1 (IGF-1), which in turn causes characteristic changes in the patient's appearance, many skeletal deformities and metabolic disorders. In addition to somatic symptoms, acromegalic patients demonstrate psychosocial and personality deficits, as well as common co-occurrence of mental disorders. There are few studies investigating acromegaly in Poland. In recent years, the concept of quality of life has become fundamental to understanding health problems. Studies dealing with acromegaly likewise tend to include assessments of quality of life of patients suffering from this endocrinopathy (Adv Clin Exp Med 2015, 24, 1, 167-172).

Pasireotide, a novel multireceptor-targeted somatostatin receptor ligand (SRL) is characterized by a higher affinity to somatostatin receptor type 5 than type 2, unlike first-generation SRLs. Because of the broader binding profile, pasireotide has been suggested to have a greater clinical efficacy in acromegaly than first-generation SRLs and to be efficacious in Cushing’s disease. The consequence of this binding profile is the increased blood glucose level in some patients. This results from the inhibition of both insulin secretion and the incretin effect and only a modest suppression of glucagon. A monthly intramuscular formulation of long-acting release pasireotide has been approved for both acromegaly and Cushing’s disease treatment. This review presents data on the efficacy and safety of pasireotide treatment mostly in patients with acromegaly and Cushing’s disease. Moreover, other possible therapeutic applications of pasireotide are mentioned.

IntroductionIn acromegaly, chronic exposure to impaired GH and IGF-I levels leads to the development of typical acromegaly symptoms, and multiple systemic complications as cardiovascular, metabolic, respiratory, endocrine, and bone disorders. Acromegaly comorbidities contribute to decreased life quality and premature mortality. The aim of our study was to assess the frequency of acromegaly complications and to evaluate diagnostic methods performed toward recognition of them.Materials and MethodsIt was a retrospective study and we analyzed data of 179 patients hospitalized in the Department of Endocrinology, Diabetes and Isotope Therapy in Wroclaw Medical University (Poland) in 1976 to 2018 to create a database for statistical analysis.ResultsThe study group comprised of 119 women (66%) and 60 men (34%). The median age of acromegaly diagnosis was 50.5 years old for women (age range 20–78) and 46 for men (range 24–76). Metabolic disorders (hyperlipidemia, diabetes, and prediabetes) were the most frequently diagnosed complications in our study, followed by cardiovascular diseases and endocrine disorders (goiter, pituitary insufficiency, osteoporosis). BP measurement, ECG, lipid profile, fasting glucose or OGTT were performed the most often, while colonoscopy and echocardiogram were the least frequent.ConclusionsIn our population we observed female predominance. We revealed a decrease in the number of patients with active acromegaly and an increase in the number of well-controlled patients. More than 50% of patients demonstrated a coexistence of cardiac, metabolic and endocrine disturbances and only 5% of patients did not suffer from any disease from those main groups.

PurposeThis study aimed to assess bone mineral density (BMD) and trabecular bone score (TBS) in 61 patients from the acromegaly group (AG) with regard to the activity of the disease in comparison to 42 patients—control group (CG). We also analyzed selected bone markers and their association with BMD and TBS.Materials and MethodsLumbar spine and femoral neck BMD measurements were performed. TBS values were obtained. Serum concentrations of selected bone markers, including osteoprotegerin (OPG), were measured.ResultsWe revealed a difference in TBS values between the AG and CG as well as between the TCA (treatment-controlled acromegaly) vs. CG and TCA+CA (cured acromegaly) vs. CG. We did not observe any statistically significant difference in BMD. OPG had a lower concentration in the CG compared to the AG. TBS correlated negatively with OPG in the AG (r = −0.31, p = 0.01) and in the TCA+ CA group (r = −0.3, p = 0.01).ConclusionsThe acromegalic patients have altered bone microstructure as indicated by the decreased TBS regardless of the activity of the disease and BMD. OPG could be a marker of the destruction of the bone microstructure, but further studies are needed.