Thyroglobulin (TG) is a dimeric glycoprotein produced exclusively by mature thyroid tissue and stored within the follicular lumen. It is essential for the organification of iodine and the production of thyroid hormones. The concentration of TG in the bloodstream varies between individuals and depends on factors such as thyroid mass, stimulation of the gland by thyrotropin or autoantibodies, and tissue destruction. TG is essential to monitor patients with differentiated thyroid cancer; however, its use is not limited only to this clinical entity. Measurement of circulating TG can provide better insight into numerous clinical scenarios, such as destructive thyroiditis, presence of ectopic thyroid tissue, thyroid trauma, factitious thyrotoxicosis, or iodine nutrition. Lately, TG has found its new clinical use in immune checkpoint-related thyroid dysfunction. TG measurement should be performed carefully in patients with antithyroglobulin antibodies due to possible laboratory interferences. In this review, we offer a summary of current knowledge about the clinical use of TG and the implications it brings to daily practice.

Dexamethasone suppression tests are basic tools in diagnostics of hypercortisolemia. Low-dose tests play major role in screening and initial assessment. High-dose tests are aimed at more elaborate diagnostics, however their clinical value is questionable. Dexamethasone is a highly potent, synthetic steroid. It is metabolized by cytochrome P450 3A4 (CYP3A4), and so are various other xenobiotics. Due to wide spectrum of substances processed by CYP3A4, interferences and interactions are not uncommon. Physicians should be familiar with drugs modifying dexamethasone metabolism, and therefore the results of dynamic tests. Other important concerns are: drugs enhancing cortisol-binding globulin production, organ dysfunction, pseudo-Cushing states, pregnancy and other physiological conditions leading to elevated blood cortisol, cyclic Cushing disease. To properly assess and assist patients, it is crucial for health professionals to understand and be able to overcome such clinical dilemmas.

COVID-19 often results in generalized inflammation and affects various organs and systems. Endocrine research focused on the possible sequelae of COVID-19, with special interest given to the thyroid gland. Clinical problems such as thyroid function in non-thyroidal illness (NTI), autoimmune thyroiditis, and COVID-19-related subacute thyroiditis (SAT) quickly gained wide coverage. Thyrotoxicosis of various origins leads to the release of peripheral thyroid hormones and thyroglobulin (TG), the main glycoprotein contained within the thyroid follicular lumen. In our study, we evaluated TG levels in COVID-19-positive patients and investigated the possible relationships between TG, thyroid function tests (TFTs), and inflammatory markers. Our approach included separate subanalyses of patients who received and those who did not receive glucocorticoids (GCs). In the entire population studied, the concentration of TG tended to decrease with time (p<0.001; p1,2 = 0.025, p1,3 = 0.001, p2,3 = 0.003), and this pattern was especially clear among patients treated with GCs (p<0.001; p1,2=<0.001; p1,3=<0.001; p 2,3=<0.001). The concentration of TG differed significantly between patients treated and those not treated with GC at the second and third time points of observation (p=0.033 and p=0.001, consecutively). TG concentration did not differ between the patients with normal and abnormal TFTs. The correlations between TG, TFTs, and inflammatory markers were very limited. 19 patients had elevated TG levels, but a TFT pattern suggestive of thyrotoxicosis was not common in this group. There were no statistically significant differences between patients who met and those who did not meet the predefined combined primary endpoint.

The ongoing coronavirus disease 2019 (COVID-19) pandemic forced a change in the way we provide medical treatment. Endocrinology in the era of COVID-19 had to transform and reduce its vast potential to the absolute necessities. Medical professionals needed to update their clinical practice to provide their patients as much support and as little harm as possible in these increasingly difficult times. International expert statements were published to offer guidance regarding proper care. It was suggested to simplify the diagnostic scheme of hypercortisolemia and to modify the approach to treatment. Hypercortisolemic patients with COVID-19 and iatrogenic hypercortisolemia due to glucocorticoid use are important clinical scenarios – we aimed to provide a cohesive summary of issues to consider.

Most cases of COVID-19 are non-severe, but some patients require urgent hospital care. In the past, it has been established that adrenal hyperactivity predicts poorer prognosis in severely ill patients. We wanted to verify if cortisol levels can be tied to clinical outcomes and the degree of inflammation in hospitalized COVID-19 patients. We recruited 180 adult patients with PCR-confirmed COVID-19. The group was divided into smaller subgroups based on the glucocorticoid treatment status; the subgroups were evaluated in three separate time points. The assessment involved hormonal function (cortisol, ACTH), inflammatory markers, and occurrence of the pre-selected endpoints (death, hospitalization ≥10 days, non-invasive ventilation or high-flow oxygenation, mechanical ventilation, vasopressors). In the evaluated group, 121 patients showed signs of abnormal adrenal function. There was a clear correlation between cortisol and IL-6 concentrations in all three time points regardless of glucocorticoid treatment. A total of 71.1% of patients displaying abnormal cortisol production met the preselected endpoints. Our analysis showed that a cutoff cortisol concentration prognosing endpoint occurrence could be set at 15.45 μg/dL for patients not treated with glucocorticoids. Cortisol concentration can be seen as an independent prognostic factor for unfavorable outcomes in selected adults hospitalized with COVID-19.

The ongoing COVID-19 pandemic calls for extensive research on various medical topics. Since the beginning of the pandemic, multiple studies investigated the impact of SARS CoV-2 on thyroid function. However, crucial data, such as trend progression over time or influence of commonly used drugs, might still be missing. We checked the thyroid function in 174 patients with PCR-confirmed COVID-19. Our research covered three separate time points of hospitalization (days 1, 4, and 10). We did not exclude patients treated with glucocorticoids but, instead, compared them with patients not treated with steroids. We correlated the results of thyroid function tests with markers of systemic inflammation. We checked if abnormal thyroid function can predict unfavorable outcomes defined as combined primary endpoint and/or secondary endpoints; the combined primary endpoint was the occurrence of death, mechanical ventilation, non-invasive ventilation, vasopressor infusion, or prolonged hospital stay, and the secondary endpoint was any of the listed events. In general, 80.46% of evaluated patients displayed abnormalities in thyroid function tests over at least one time point throughout the observation. We noticed a high prevalence of features typical for thyroid dysfunction in non-thyroidal illness (NTI). Free triiodothyronine (fT3) concentration was significantly lower in the group requiring glucocorticoids. Patients displaying abnormal thyroid function were statistically more likely to meet the predefined combined primary endpoint. We found that fT3 measured at admission could be perceived as an independent predictor of endpoint completion for all analyzed groups. Thyroid involvement is common in COVID-19. Our study supports the idea of thyroid function abnormalities being important clinical tools and allowing early recognition of possible detrimental outcomes of the disease.