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OBJECTIVES: Upper respiratory tract infections, including COVID-19, are associated with olfactory dysfunction and there is a need for novel therapeutic approaches. The aim of study was evaluating the effectiveness of adding melatonin, multivitamin and sodium citrate to olfactory training for the treatment of olfactory loss caused by COVID-19. METHODS: We evaluated olfactory function using University of Pennsylvania Smell Identification Test (UPSIT ®) scores and self-reported patient outcomes in post-infectious smell loss cases. We investigated the effectiveness involved olfactory training combined with sodium citrate, melatonin, and multivitamin supplements with zinc over a three-month period compared to an olfactory training alone. RESULTS: A total of 66 patients were included, with 33 in each group. There was no significant difference in the proportion of participants who showed improvement in UPSIT scores between the groups (OR = 1.43, 95% CI 0.43-4.8, p =  0.56). Both groups showed improvement in average test scores, but there were no significant differences in self-reported olfactory ability or discomfort with olfactory loss. Qualitative symptoms, such as parosmia and phantosmia, were reported by a similar proportion in both groups before and after the treatment (p =  0.11, p =  1, respectively). CONCLUSIONS: Olfactory training alone and olfactory training with associated with melatonin, multivitamins and topical sodium citrate did not show significant differences in improving olfactory function in post-COVID-19 patients.

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OBJECTIVES: The aim of this observational cross-sectional study was to determine the endotypic inflammatory pattern of a sample of patients with CRS in Brazil, correlate it with olfactory function, and evaluate the clinical severity of the disease. METHODS: In this cross-sectional study, 73 CRS patients were recruited. Patients were classified into type 2 and non-type 2 endotypic patterns based on IgE and eosinophilia levels. All subjects performed the University of Pennsylvania Smell Identification Test (UPSIT®) and responded to the Sino-Nasal Outcome Test (SNOT-22). RESULTS: The majority of patients had type 2 CRS (n=57, 78.1%). Patients with type 2 CRS compared to non-type 2 CRS had a higher prevalence of nasal polyps (93% vs. 12.5%), asthma (40.3% vs. 12.5%), and non-steroidal anti-inflammatory drug exacerbated respiratory disease (NERD, 17.5% vs. 0%). Type 2 patients also had significantly lower UPSIT® and higher SNOT-22, Lund-Kennedy, and Lund-Mackay scores. CONCLUSION: Our study provides evidence that type 2 CRS is associated with a higher prevalence of nasal polyps, asthma, and NERD, as well as decreased olfactory function and worse quality of life scores. These data will contribute to the body of knowledge on CRS and the development of treatments for this disease in Brazil.

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Abstract Objectives The aim of this observational cross-sectional study was to determine the endotypic inflammatory pattern of a sample of patients with CRS in Brazil, correlate it with olfactory function, and evaluate the clinical severity of the disease. Methods In this cross-sectional study, 73 CRS patients were recruited. Patients were classified into type 2 and non-type 2 endotypic patterns based on IgE and eosinophilia levels. All subjects performed the University of Pennsylvania Smell Identification Test (UPSIT®) and responded to the Sino-Nasal Outcome Test (SNOT-22). Results The majority of patients had type 2 CRS (n = 57, 78.1%). Patients with type 2 CRS compared to non-type 2 CRS had a higher prevalence of nasal polyps (93% vs. 12.5%), asthma (40.3% vs. 12.5%), and non-steroidal anti-inflammatory drug exacerbated respiratory disease (NERD, 17.5% vs. 0%). Type 2 patients also had significantly lower UPSIT® and higher SNOT-22, Lund-Kennedy, and Lund-Mackay scores. Conclusion Our study provides evidence that type 2 CRS is associated with a higher prevalence of nasal polyps, asthma, and NERD, as well as decreased olfactory function and worse quality of life scores. These data will contribute to the body of knowledge on CRS and the development of treatments for this disease in Brazil. Level of evidence: 3.

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PURPOSE: Papillary thyroid carcinoma (PTC) is the most frequent subtype of thyroid cancer; Hashimoto's thyroiditis (HT), autoimmune disease, commonly affects the thyroid gland; there is possibly a correlation between both, but the exact mechanisms that involve this relationship are still under debate. Since oxidative stress (OS) and the inflammatory environment participate in the development of several types of cancer, the objective of the present study was to establish the microenvironment and systemic participation of OS and inflammatory markers in patients with PTC and HT. METHODS: Blood and tissue samples were collected from 115 patients: BENIGN (n = 63); PTC (n = 27); HT (n = 15) and PTC + HT (n = 10), and sixty-three were samples from healthy individuals (control group). RESULTS: Superoxide dismutase, Catalase, reduced Glutathione, markers of lipid peroxidation and inflammation were evaluated in blood. Immunohistochemistry was performed on 3-nitrotyrosine, 4-hydroxynonenal, Ki-67 and VEGF. The results indicate that antioxidant enzymes were more active in groups with thyroid disorders compared to control, while the concentration of Reduced glutathione was reduced in BENIGN and PTC groups. When PTC and PTC + HT groups were analyzed, no significant differences were found in relation to the antioxidant defense and inflammatory markers. The ability to contain the induced lipid peroxidation was lower and a high level of malondialdehyde was observed in the PTC group. All immunohistochemical markers had higher scores in the PTC group compared to PTC + HT. CONCLUSION: There was a more pronounced presence of OS and a greater activity of cell proliferation and angiogenesis markers in PTC than in PTC + HT group.

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Metformin was shown to sensitize multidrug resistant breast cancer cells; however, the mechanisms involved in this capacity need to be clarified. We investigated oxidative stress and inflammatory-related pathways during the induction of doxorubicin resistance in MCF-7 and MDA-MB-231 human breast cancer cells (DOX-res group), and evaluated metformin-induced cellular responses that resulted in the prevention of doxorubicin resistance (Met-DOX group). Microarray analysis demonstrated that DOX-res changed the expression of genes involved in oxidative stress (OS) and the TGF- ß1 pathway. The DOX-res group presented increased thiols and reduced lipoperoxidation, increased levels of nitric oxide, nuclear NF-kB and Nrf2, and reduced nuclear p53 labelling. Analysis of the TGF-ß1 signaling pathway by RT-PCR array showed that DOX-res developed adaptive responses, such as resistance against apoptosis and OS. Metformin treatment modified gene expression related to OS and the IFN-α signaling pathway. The Met-DOX group was more sensitive to DOX-induced OS, presented lower levels of nitric oxide, nuclear NF-kB and Nrf2, and increased nuclear p53. Analysis of the IFN-α signaling pathway showed that Met-DOX presented more sensitivity to apoptosis and OS. Our findings indicate that metformin is a promising tool in the prevention of chemoresistance in patients with breast cancer submitted to doxorubicin-based treatments.

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