During COVID-19 era, a special attention was considered for autoimmune disorders (AD), including at thyroid, which are regarded at higher risk knowing that stress and infections might aggravate the pattern of anti-thyroid antibodies as well as thyroid dysfunction. In this study, we aim to analyse how COVID-19 infection influenced the evolution of HT parameters versus patients with HT who did not go through infection. Study design: an observational, bi-centric study in Romania during first 14 months of pandemic. By the end of April 2022, Romania registered 1,047,520 total cases of COVID- 19 infection (a morbidity rate calculated for entire Romanian population of 5.23%) with 27,267 total deaths (a lethality rate of 2.6%) and around 2000 new patients a day. From our database of 2210 HT patients, a number of 386 HT subjects were assessed (14 months). Among them, 33/386 patients had a different form of COVID-19 infection. The prevalence of COVID- 19 infection among HT patients was 9.35% which is statistically significant higher when compare with official ratio for entire Romanian population (a morbidity rate of 5.23%, z = 3.162, p = 0.00033). A feminine prevalence was identified (89.37%, N=31/33), while age was not different between subgroups (average age over 50 y). At the moment of diagnostic, thyroid levels at the diagnostic time was 650 UI/mL in group 1 versus 840 UI/mL in group 2 (both groups had very high ATPO values, normal cut-offs below 34 UI/mL) with not statistical significance difference - of ATPO evolution was undulatory in 74.07% of patients, decreasing - 3.7%, increasing - 11.11%, unmodified (stationary) - 11.11%, similarly with group 2, meaning that ATPOs had the same profile, regardless the fact that some subjects went through COVID-19 infection. The rate of associated AD was 28.24% (N=2210), COVID-group of 42.42%, non-COVID group of 38.53% (z = 0.44, p = 0.66). In our COVID cohort of 33 patients with HT, we registered the following clinical stages of coronavirus infection: 4/33 patients who were asymptomatic; all women, average age: 65.65 years; 2/33 patients with lack of smell and taste; women, over 65 years old; 14/33 patients with mild form; from 31 years old to 70.5 years old (only one man); 10 patients with a moderate form; all women, from 34 to 71 years old; one 87-year-old male with a severe form; one 50-year old female with a very severe form in addition to a hematologic disease and a history of severe allergic reactions; and a single patient (a 68-year-old, obese female with a severe allergic background) died of COVID-19 infection (thus generating a lethality rate of 3.03%). Conclusion. Our study showed a higher prevalence of COVID-19 infection among HT patients. These individuals do not associate increased levels of ATPO or a elevated prevalence of AD when compare with non- COVID – HT group, and have similar age and sex ratio. Whether HT exposes the subjects to coronavirus infection is an open issue.
Melanoma outcome seems different between females and males, with a potential protective role of estrogen (E) through estrogen receptors (ER) expression into the tumor. In the study of ERs, both alfa (ERα) and beta (ERβ) is a well-known endocrine elements in non-melanoma tumors, like mammary and endometrial cancer. Immunohistochemistry (IHC) assessment of melanoma concerning ERs represents a path to explore the tumor profile to provide useful information concerning the prognostic and potential adjuvant treatment. Currently, this is not a routine practice, nor a mandatory step for deciding the medical therapy. Typically, IHCs are based on usual kits for mammary tumors regarding ERs configuration. Prior/concomitant use of oral contraceptives and hormonal replacement therapy is not correlated with a better prognostic in melanoma; neither have they represented a contraindication for survivors of melanoma; a subset of tumors might present a higher ER expression which is potentially targeted by the hormone-based treatment as SERMs (Selective Estrogen Receptors Modulator), for instance, tamoxifen. Experimental studies on melanoma cell lines confirmed the anti-tumor activity of ERβ which might function as a prognostic marker. G-protein-coupled estrogen receptors in melanocytes and keratinocytes might be involved, too. Additional crosstalk of TGF-β (Transforming Growth Factor β), respective IGF1 (Insulin-like Growth Factor), and ERα expression are involved in tumorigenic pathways. Recent preclinical studies showed the potential benefits of diarylpropionitrile, a selective agonist of ERβ; pyrazole derivates 21-23 can block ERs. Murine melanoma models showed the interference of anti-estrogenic medication (like molecule fulvestrant) to enhance immune checkpoint blockade, a modern approach to solid cancers. The proliferation of melanoma might be partially explained by ERs; whether this is generally applicable or there is a subgroup of tumors particularly related to E status is still debatable. The subject of E status in melanoma is far from clear at this point and further studies are necessary concerning this particular issue to implement it as a practical approach in the daily management of a disease that still has a very severe prognostic nowadays.
