Carcinomas of the thyroid gland are some of the most common malignancies of the endocrine system. The causes of tumor transformation are genetic changes in genes encoding cell signaling pathways that lead to an imbalance between cell proliferation and apoptosis. Some mutations have been associated with increased tumor aggressiveness, metastatic lymph node spread, tendency to dedifferentiate, and/or reduced efficiency of radioiodine therapy. The main known genetic causes of thyroid cancer include point mutations in the BRAF, RAS, TERT, RET, and TP53 genes and the fusion genes RET/PTC, PAX8/PPAR-γ, and NTRK. Molecular genetic testing of the fine needle aspiration cytology of the thyroid tissue in the preoperative period or of the removed thyroid tissue in the postoperative period is becoming more and more common in selected institutions. Positive detection of genetic changes, thus, becomes a diagnostic and prognostic factor and a factor that determines the extent of the surgical and nonsurgical treatment. The findings of genetic research on thyroid cancer are now beginning to be applied to clinical practice. In preoperative molecular diagnostics, the aggressiveness of cancers with the most frequently occurring mutations is correlated with the extent of the planned surgical treatment (radicality of surgery, neck dissection, etc.). However, clear algorithms are not established for the majority of genetic alterations. This review aims to provide a basic overview of the findings of the most commonly occurring gene mutations in thyroid cancer and to discuss the current recommendations on the extent of surgical and biological treatment concerning preoperatively detected genetic changes.

The subjective and demanding nature of olfactory testing means that it is often neglected in clinic despite loss of smell leading to significant limitations in everyday life. The list of diseases associated with loss of olfaction far exceeds the field of otorhinolaryngology and can also be seen in neurodegenerative disorders. Knowledge of possible clinical testing is essential to determine a proper differential diagnosis for the loss of olfactory sense. Causes of olfactory impairment can be divided into either failure in transferring odour to the organ of perception or damage to the olfactory pathway structure itself. Examination should therefore include methods evaluating cross-sectional area and patency of the nasal cavity as well as subjective or objective assessment of olfactory function. In this report we summarize several articles, studies, and our own experiences to provide a comprehensive review of their current clinical usage including their benefits, limitations, and possible outcomes. We also discuss the mechanism of olfaction step by step to provide a full understanding of the possible errors depending on the localization in the pathway and the methods designed for their detection. We discuss the correlation of the microbiome in nasal polyposis and chronic rhinitis with olfactory impairment using objective olfactometry. The topic of objective olfactometry and the examination of olfactory event-related potentials (OERP) is commented upon in detail.

Background: Acute acoustic trauma (AAT) ranks, among others, as one common cause of inner ear function impairment, especially in terms of military personnel, who are at an increased exposure to impulse noises from firearms. Aim of this study: 1. We wanted to demonstrate whether early treatment of AAT means a higher chance for the patient to improve hearing after trauma. 2. We find the answer to the question of whether hyperbaric oxygen therapy (HBO2) has a positive effect in the treatment of AAT. Methods: We retrospectively analyzed data for the period 2004–2019 in patients with AAT. We evaluated the therapeutic success of corticosteroids and HBO2 in a cohort of patients with AAT n = 108 patients/n = 141 affected ears. Results: Hearing improvement after treatment was recorded in a total of 111 ears (79%). In terms of the data analysis we were able to ascertain, utilizing success of treatment versus timing: within 24 h following the onset of therapy in 56 (40%) ears—54 (96%) ears had improved; within seven days following the onset the therapy was used in 55 (39%) ears—41 (74%) ears had improved; after seven days the therapy started in 30 (21%) ears—16 (53%) ears had improved. Parameter latency of the beginning of the treatment of AAT was statistically significant (p = 0.001 and 0.017, respectively). The success of the medical protocols was apparent in both groups—group I (treated without HBO2): n = 61 ears, of which 50 (82%) improved, group II (treated with HBO2): n = 73 ears, of which 56 (77%) improved. Group II shows improvement at most frequencies (500–2000 Hz). The most serious sensorineural hearing loss after AAT was at a frequency of 6000 Hz. Conclusion: Analysis of our data shows that there is a statistically significant higher rate of improvement if AAT treatment was initiated within the first seven days after acoustic trauma. Early treatment of AAT leads to better treatment success. HBO2 is considered a rescue therapy for the treatment of AAT. According to our recommendation, it is desirable to start corticosteroid therapy immediately after acoustic trauma. If hearing does not improve during the first seven days of corticosteroid therapy, then HBO2 treatment should be initiated.