COVID‑19‑related thyroid conditions (Review)

  • Authors:
    • Florica Șandru
    • Mara Carsote
    • Răzvan Cosmin Petca
    • Ancuta Augustina Gheorghisan-Galateanu
    • Aida Petca
    • Ana Valea
    • Mihai Cristian Dumitrașcu
  • View Affiliations

  • Published online on: May 13, 2021     https://doi.org/10.3892/etm.2021.10188
  • Article Number: 756
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

In patients who were not previously diagnosed with any thyroid conditions, the scenario of COVID‑19‑related anomalies of the hypothalamus‑pituitary‑thyroid axes may include either: A process of central thyroid stimulating hormone (TSH) disturbances via virus‑related hypophysitis; an atypical type of subacute thyroiditis which is connected to the virus spread or to excessive cytokine production including a destructive process with irreversible damage of the gland or low T3 (triiodothyronine) syndrome (so called non‑thyroid illness syndrome) which is not specifically related to the COVID‑19 infection, but which is associated with a very severe illness status. Our objective here was to briefly review thyroid changes due to the COVID‑19 infection. Ongoing assessment of the effects of the COVID‑19 pandemic will reveal more information on coronavirus‑induced thyroid conditions. Routine thyroid assays performed in patients with severe infection/at acute phase of COVID‑19 are encouraged in order to detect thyrotoxicosis. After recovery, thyroid function should be assessed to identify potential hypothyroidism. There remain unanswered questions related to the prognostic value of interleukin‑6 in infected patients, especially in cases with cytokine storm, and the necessity of thyroid hormone replacement in subjects with hypophysitis‑related central hypothyroidism.

1. Introduction

Human coronaviruses such as COVID-19 (Coronavirus Disease 2019) are part of a large virus family, specifically causing respiratory tract infections that underlie a heterogeneous area of severity from mild to fatal diseases, including severe acute respiratory syndrome coronavirus (SARS-CoV) (1,2). Angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV-2, plays a crucial role in the pathogenesis of COVID-19, as it provides viral entry into human cells. Because the virus follows ACE2 expression as a key player of viral transmission into the human body, every organ may be potentially affected and shut down (2,3). Severe dysfunction is particularly found in previously damaged organs and in cases when the human-virus communication goes through a cytokine storm (1-4). However, despite the massive amount of data gathered to date concerning this virus, we cannot rely on predictive models as multiple factors are actually involved in the disease evolution and prognosis as well as in patient recovery (5). Endocrine-related conditions that are likely to be correlated with a more severe prognosis are diabetes mellitus, obesity and high blood pressure, including secondary endocrine causes (6-8). In addition, a specific impact on virtually each endocrine gland might be expected due to particular virus tropism (1,9).

2. Research aim and methods

Aim

Our objective of this review is a brief update of changes in thyroid conditions due to COVID-19 infection including immune-mediated changes.

Methods

This is a narrative review. Most papers were accessed through the PubMed database. Up until the preparation of the paper, 108 PubMed articles were selected by searching the key words ‘COVID-19 and thyroid’. A total number of 61 studies were referenced (52 of them were published in 2020 and many were published ahead of print). The level of statistical evidence varies from original studies to reviews, opinions, case reports or position statements.

3. Endocrine focus during the pandemic

Autopsy studies have shown that the virus can enter almost every endocrine gland including the endocrine pancreas, pituitary gland, thyroid, parathyroids, adrenals and testis (9). The dysfunction may be transitory or definitive (9,10). The mechanisms underlying COVID-19-related endocrine anomalies consist of inflammation, vessel damage, necrosis, degeneration, respective immune and autoimmune processes (9-12).

To date it is known that, in patients who were not previously diagnosed with any thyroid conditions, the scenario of COVID-199-related hypothalamus-pituitary-thyroid axis anomalies may include either: i) A process of central thyroid stimulating hormone (TSH) disturbances via virus-related hypophysitis; or ii) an atypical type of subacute thyroiditis which is connected to the virus spread or to excessive cytokine production including a destructive process with irreversible damage of the gland (9,13). A third category, namely euthyroid sick syndrome or low T3 (triiodothyronine) syndrome or non-thyroid illness syndrome, is not specifically related to the COVID-19 infection, but is also diagnosed in other severe conditions such as sepsis, trauma, severe kidney and liver failure or acute myocardial infarction (14,15). It is an adjustment of the body to the new conditions and it does not require thyroid hormone replacement (14,15). However, molecular studies have revealed the benefits of T3 action on p38 MAPK signal transduction pathways on sepsis-related conditions thus there are ongoing trials to assess the potential benefits for critically ill COVID-19 patients to receive T3 (16,17).

4. Thyroiditis

Early reports in 2020 showed an atypical subtype of thyroiditis in COVID-19 patients. Many patients with COVID-19 infection, especially those with severe forms or admitted to intensive care units, displayed anomalies of thyroid hormones and TSH (13,14). Thus, a novel etiology of subacute thyroiditis was identified (18,19). This condition presents with thyroid hormone flare-up and usually the thyrotoxicosis is self-limited and does not require specific anti-thyroid drugs (18,19). A study on COVID-19-positive patients admitted to intensive care units in Milan, Italy showed a 10% prevalence of thyrotoxicosis; statistically significant higher than the 0.5% prevalence in COVID-19 negative patients who were admitted one year prior to the same units (18).

The overlap of a typical episode of non-COVID subacute De Quervain thyroiditis (such as coxsackie virus, mumps virus, cytomegalovirus, enterovirus and adenovirus-induced) to COVID-19 infection has been reported (19). The clinical picture also includes thyrotoxicosis, and glucocorticoid therapy may improve the severe evolution (19). Some authors suggest that COVID-19-related subacute thyroiditis might be actually underestimated in many cases (20). In addition, there are reports of COVID-19-related subacute thyroiditis in patients who were not critically ill (21,22). Subacute thyroiditis associated with thyrotoxicosis overlaps with destructive thyroiditis as autopsy studies have shown (as well as some cytology reports) but thyroid inflammation can be immune-mediated (9,23,24).

Immune-related thyroiditis is described in critically ill COVID-19-positive patients, especially at the moment of cytokine storm in addition to multiple organ failure (4,25). The THYRCOV study provides early evidence that patients with acute coronavirus infection presenting with thyrotoxicosis have statistically significant higher levels of interleukin-6 (IL-6) (26). This was a single center, retrospective study on 287 adult subjects with an average age of 66 years who were admitted to non-intensive care units (26). Thyrotoxicosis was confirmed in 20.2% of cases while 5% of them experienced hypothyroidism (26). IL-6 represents a major player of the pro-inflammatory status in addition to IL-1 and tumor necrosis factor (TNF)α which may also act at the thyroid level (9,27). Based on another retrospective study on 728 adult COVID-19-positive patients, IL-6 was found to be independently associated with the severity of the disease and also to mortality during hospitalization (27). It may become a new standard in disease assessment as a predictive factor including during follow-up (27).

5. Thyroid assessments during the pandemic period

The coronavirus may also damage the pituitary gland, and mostly transient hypophysitis has been reported developing central hypocortisolism and central hypothyroidism (less frequently) by decreasing the synthesis of adrenocorticotropic hormone (ACTH) and TSH (9,28). The condition is difficult to diagnose, and there is current debate whether levothyroxine replacement has a major impact on improvement of the clinical outcome (28).

Another issue relates to the primary hyperthyroidism developed during the pandemic period (9). When a patient is COVID-19-positive, then there is a higher risk of developing arrhythmia and thrombo-embolic events while specific anti-thyroid drugs may be associated with agranulocytosis, thus worsening the overall prognosis (9,29,30).

Regarding the patients with previously known thyroid conditions, the majority are not at a higher risk of contracting the coronavirus, or at risk of being admitted for more severe infections unless the subject is currently being treated with glucocorticoid medication against Graves' orbitopathy (31,32). Massive information has been published to date on the risk of using pharmacological doses of glucocorticoids, especially during COVID-19-related cytokine storm (33,34).

Changes during the pandemic period are reflected in the telemedicine concept which is largely applicable to subjects who have a prior history of different endocrine pathologies (35). Other issues associated with the lockdown, the altered access to usual medical care services and new daily habits such as wearing facial mask, social distancing, and isolation, are reflected in the approach of individuals with a pre-pandemic diagnosis of thyroid diseases (36,37). Apart from the COVID-19 infection itself, we need to take into consideration the pandemic-related stress which may act as a trigger for various autoimmune conditions (38). Some data suggest a higher risk of autoimmune disorders (including autoimmune thyroiditis and Graves' disease) after recovery from the cytokine storm (9). This remains a topic of debate but actually we do not have enough longitudinal data to sustain this observation. The current increasing prevalence of coronavirus worldwide will unfortunately provide the necessary data on the follow-up of endocrine autoimmune conditions. Generally, patients with autoimmune thyroiditis have a higher risk of developing other antibody-related conditions such as vitiligo, alopecia areata, dermatitis herpatiformis, hypophysitis, autoimmune hepatitis, Sjogren's syndrome, Raynaud's syndrome, premature ovarian failure, primary adrenal insufficiency, type 1 diabetes mellitus, rheumatoid arthritis, atrophic gastritis, lupus, sclerodermia, vasculitis, and celiac disease (39,40).

A severe situation is observed in the particular situation of COVID-19-positive diabetic patients of either type (including type 1 as seen in polyglandular autoimmune syndrome also associating autoimmune thyroiditis or antibody-related chronic primary adrenal insufficiency) (41,42). In COVID-19 patients the prognostic is more severe and the glycemia profile may be worse due to the virus attack against the pancreas at the level of β-cells (43,44). The term ‘covidiabetology’ has been suggested for covering the immense area of overlap of diabetes mellitus and COVID-19(45). Moreover, we need to take into consideration the association of thyroiditis with autoimmune primary adrenal insufficiency which is a condition with a higher risk of COVID-19 infection or other infections of different etiologies (46). Higher doses of glucocorticoid replacement are needed (46). Pre-pandemic studies have shown that conditions associated with thyroid autoimmune disorders such as celiac disease and rheumatoid arthritis are associated with vitamin D deficiency, a part from bone status anomalies (47-49). Pandemic data have shown an increased risk of developing hypovitaminosis D due to low sun exposure or the use of facial masks. Thus, under these circumstances it becomes necessary to supplement vitamin D (regardless of the real immune role of vitamin D when cross talk to the virus molecule) (50).

Another domain of thyroid conditions is related to thyroid cancer and the COVID-19 era. Consequently, physicians must rethink the strategies of approach (51). Most of these patients do not seem at a higher risk of COVID-19 infection but we still need convincing data (52). Risk-benefit analysis in each case will indicate the adequate approach considering the reality of the pandemic period (53). New models of telemedicine allow medical access based on a stratified risk strategy including criteria for deciding thyroid surgery (54). A study on the expression of 5 genes which may interact with the virus such as ACE2, TMPRSS11D, respective TMPRSS2, CLEC4M and DPP4 showed significant alterations in thyroid cancer for the last mentioned three genes (55). However routine genetic testing in non-medullar thyroid cancer is hardly encouraged (56).

Overall, the viral and immune-mediated thyroid status due to coronavirus infection represents a small part of an otherwise complex, large and dynamic picture of the disease (57-59). Due to the fact that the virus challenges the native immunity of the host organism, thyroid interaction is expected (59).

6. Conclusions

Ongoing reality of the COVID-19 pandemic will reveal more information on virus-related thyroid conditions. Routine thyroid assays in patients with severe infection/acute phase of COVID-19 are encouraged in order to detect thyrotoxicosis. After recovery, thyroid function should be assessed to identify potential hypothyroidism. Still unanswered questions are related to the prognostic value of IL-6 assays or thyroid hormone replacement therapy necessary due to virus-related hypophysitis underlying central hypothyroidism.

Acknowledgements

Not applicable.

Availability of data and materials

Not applicable.

Authors' contributions

FS performed the critical review of the manuscript for its content. MC reviewed the findings and wrote the manuscript. AV checked and revised the manuscript and is the corresponding author. RCP revised the literature data. AAGG and AP researched the studies that were included as references. MCD critically revised the manuscript and approved the current form of the article in order to be submitted to the journal for publishing. All authors read and approved the final manuscript.

Ethics approval and consent to participate

Not applicable.

Patient consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

References

1 

Parolin M, Parisotto M, Zanchetta F, Sartorato P and De Menis E: Coronaviruses and endocrine system: A systematic review on evidences and shadows. Endocr Metab Immune Disord Drug Targets: Sep 5, 2020 (Epub ahead of print).

2 

Sarkesh A, Daei Sorkhabi A, Sheykhsaran E, Alinezhad F, Mohammadzadeh N, Hemmat N and Bannazadeh Baghi H: Extrapulmonary clinical manifestations in COVID-19 patients. Am J Trop Med Hyg. 103:1783–1796. 2020.PubMed/NCBI View Article : Google Scholar

3 

Young MJ, Clyne CD and Chapman KE: Endocrine aspects of ACE2 regulation: RAAS, steroid hormones and SARS-CoV-2. J Endocrinol. 247:R45–R62. 2020.PubMed/NCBI View Article : Google Scholar

4 

Caricchio R, Gallucci M, Dass C, Zhang X, Gallucci S, Fleece D, Bromberg M and Criner GJ: Temple University COVID-19 Research Group. Preliminary predictive criteria for COVID-19 cytokine storm. Ann Rheum Dis. 80:88–95. 2021.PubMed/NCBI View Article : Google Scholar

5 

Shamsoddin E: Can medical practitioners rely on prediction models for COVID-19? A systematic review. Evid Based Dent. 21:84–86. 2020.PubMed/NCBI View Article : Google Scholar

6 

Kruglikov IL, Shah M and Scherer PE: Obesity and diabetes as comorbidities for COVID-19: Underlying mechanisms and the role of viral-bacterial interactions. Elife. 9(e61330)2020.PubMed/NCBI View Article : Google Scholar

7 

John JE and John NA: Imminent risk of COVID-19 in diabetes mellitus and undiagnosed diabetes mellitus patients. Pan Afr Med J. 36(158)2020.PubMed/NCBI View Article : Google Scholar

8 

Kwok S, Adam S, Ho JH, Iqbal Z, Turkington P, Razvi S, Le Roux CW, Soran H and Syed AA: Obesity: A critical risk factor in the COVID-19 pandemic. Clin Obes. 10(e12403)2020.PubMed/NCBI View Article : Google Scholar

9 

Caron P: Thyroid disorders and SARS-CoV-2 infection: From pathophysiological mechanism to patient management. Ann Endocrinol (Paris). 81:507–510. 2020.PubMed/NCBI View Article : Google Scholar

10 

Gorini F, Bianchi F and Iervasi G: COVID-19 and thyroid: Progress and prospects. Int J Environ Res Public Health. 17(6630)2020.PubMed/NCBI View Article : Google Scholar

11 

Gavriatopoulou M, Korompoki E, Fotiou D, Ntanasis-Stathopoulos I, Psaltopoulou T, Kastritis E, Terpos E and Dimopoulos MA: Organ-specific manifestations of COVID-19 infection. Clin Exp Med. 20:493–506. 2020.PubMed/NCBI View Article : Google Scholar

12 

Lazartigues E, Qadir MMF and Mauvais-Jarvis F: Endocrine significance of SARS-CoV-2's reliance on ACE2. Endocrinology. 161(bqaa108)2020.PubMed/NCBI View Article : Google Scholar

13 

Marazuela M, Giustina A and Puig-Domingo M: Endocrine and metabolic aspects of the COVID-19 pandemic. Rev Endocr Metab Disord. 21:495–507. 2020.PubMed/NCBI View Article : Google Scholar

14 

Chen M, Zhou W and Xu W: Thyroid function analysis in 50 patients with COVID-19: A retrospective study. Thyroid. 31:8–11. 2021.PubMed/NCBI View Article : Google Scholar

15 

Cocolos AM, Dumitru N, Petrova EN, Cocolos I, Tiglis M, Dragomirescu RFI, Olaru M, Dumitru A and Ghemigian AM: Endocrine disrupting chemicals-the X factor in different pathologies. Rev Chim (Bucharest). 69:136–139. 2018.

16 

Davis PJ, Lin HY, Hercbergs A, Keating KA and Mousa SA: Coronaviruses and integrin αvβ3: Does thyroid hormone modify the relationship? Endocr Res. 45:210–215. 2020.PubMed/NCBI View Article : Google Scholar

17 

Pantos C, Kostopanagiotou G, Armaganidis A, Trikas A, Tseti I and Mourouzis I: Triiodothyronine for the treatment of critically ill patients with COVID-19 infection: A structured summary of a study protocol for a randomised controlled trial. Trials. 21(573)2020.PubMed/NCBI View Article : Google Scholar

18 

Muller I, Cannavaro D, Dazzi D, Covelli D, Mantovani G, Muscatello A, Ferrante E, Orsi E, Resi V, Longari V, et al: SARS-CoV-2-related atypical thyroiditis. Lancet Diabetes Endocrinol. 8:739–741. 2020.PubMed/NCBI View Article : Google Scholar

19 

Mattar SAM, Koh SJQ, Rama Chandran S and Cherng BPZ: Subacute thyroiditis associated with COVID-19. BMJ Case Rep. 13(e237336)2020.PubMed/NCBI View Article : Google Scholar

20 

Brancatella A, Ricci D, Cappellani D, Viola N, Sgrò D, Santini F and Latrofa F: Is subacute thyroiditis an underestimated manifestation of SARS-CoV-2 infection? Insights from a case series. J Clin Endocrinol Metab. 105(dgaa537)2020.PubMed/NCBI View Article : Google Scholar

21 

Asfuroglu Kalkan E and Ates I: A case of subacute thyroiditis associated with Covid-19 infection. J Endocrinol Invest. 43:1173–1174. 2020.PubMed/NCBI View Article : Google Scholar

22 

Ippolito S, Dentali F and Tanda ML: SARS-CoV-2: A potential trigger for subacute thyroiditis? Insights from a case report. J Endocrinol Invest. 43:1171–1172. 2020.PubMed/NCBI View Article : Google Scholar

23 

Brancatella A, Ricci D, Viola N, Sgrò D, Santini F and Latrofa F: Subacute thyroiditis after Sars-COV-2 infection. J Clin Endocr Metab. 105(dgaa276)2020.PubMed/NCBI View Article : Google Scholar

24 

Bellastella G, Maiorino MI and Esposito K: Endocrine complications of COVID-19: What happens to the thyroid and adrenal glands? J Endocrinol Invest. 43:1169–1170. 2020.PubMed/NCBI View Article : Google Scholar

25 

Bordallo B, Bellas M, Cortez AF, Vieira M and Pinheiro M: Severe COVID-19: What have we learned with the immunopathogenesis? Adv Rheumatol. 60(50)2020.PubMed/NCBI View Article : Google Scholar

26 

Lania A, Sandri MT, Cellini M, Mirani M, Lavezzi E and Mazziotti G: Thyrotoxicosis in patients with COVID-19: The THYRCOV study. Eur J Endocrinol. 183:381–387. 2020.PubMed/NCBI View Article : Google Scholar

27 

Liu Z, Li J, Chen D, Gao R, Zeng W, Chen S, Huang Y, Huang J, Long W, Li M, et al: Dynamic interleukin-6 level changes as a prognostic indicator in patients with COVID-19. Front Pharmacol. 11(1093)2020.PubMed/NCBI View Article : Google Scholar

28 

Pal R: COVID-19, hypothalamo-pituitary-adrenal axis and clinical implications. Endocrine. 68:251–252. 2020.PubMed/NCBI View Article : Google Scholar

29 

Gaman MA, Dobrica EC, Pascu EG, Cozma MA, Epingeac ME, Gaman AM, Pantea Stoian A, Bratu OG and Diaconu CC: Cardio metabolic risk factors for atrial fibrillation intype 2 diabetes mellitus: Focus on hypertension,metabolic syndrome and obesity. J Mind Med Sci. 6:157–161. 2019.

30 

Djakpo DK, Wang Z, Zhang R, Chen X, Chen P and Antoine MM: Blood routine test in mild and common 2019 coronavirus (COVID-19) patients. Biosci Rep. 40(BSR20200817)2020.PubMed/NCBI View Article : Google Scholar

31 

Kahaly GJ: Management of graves thyroidal and extrathyroidal disease: An update. J Clin Endocrinol Metab. 105:3704–3720. 2020.PubMed/NCBI View Article : Google Scholar

32 

Shams PN: High-dose oral methylprednisolone for the management of severe active thyroid eye disease during the coronavirus disease 2019 pandemic. Ophthalmic Plast Reconstr Surg. 36:418–419. 2020.PubMed/NCBI View Article : Google Scholar

33 

Kaiser UB, Mirmira RG and Stewart PM: Our response to COVID-19 as endocrinologists and diabetologists. J Clin Endocrinol Metab. 105(dgaa148)2020.PubMed/NCBI View Article : Google Scholar

34 

Isidori AM, Pofi R, Hasenmajer V, Lenzi A and Pivonello R: Use of glucocorticoids in patients with adrenal insufficiency and COVID-19 infection. Lancet Diabetes Endocrinol. 8:472–473. 2020.PubMed/NCBI View Article : Google Scholar

35 

Blevins T and Ozer K: Telemedicine during the COVID-19 crisis and beyond. Tex Med. 116:4–5. 2020.PubMed/NCBI

36 

Pal R and Banerjee M: COVID-19 and the endocrine system: Exploring the unexplored. J Endocrinol Invest. 43:1027–1031. 2020.PubMed/NCBI View Article : Google Scholar

37 

Boelaert K, Visser WE, Taylor PN, Moran C, Léger J and Persani L: Endocrinology in the time of COVID-19: Management of hyperthyroidism and hypothyroidism. Eur J Endocrinol. 183:G33–G39. 2020.PubMed/NCBI View Article : Google Scholar

38 

Velayoudom FL, Alwis Wijewickrama PS, Ranathunga HI and Somasundaram N: Endocrine vigilance in COVID-19. J Pak Med Assoc. 70 (Suppl 3):S83–S86. 2020.PubMed/NCBI View Article : Google Scholar

39 

Poiana C, Chirita C, Carsote M, Hortopan D and Goldstein A: Galactocele and prolactinoma-a pathogenic association? Maturitas. 62:98–102. 2009.PubMed/NCBI View Article : Google Scholar

40 

Sandru F, Carsote M, Albu SE, Valea A, Petca A and Dumitrascu MC: Glucagonoma: From skin lesions to the neuroendocrine component (Review). Exp Ther Med. 20:3389–3393. 2020.PubMed/NCBI View Article : Google Scholar

41 

Kumar A, Arora A, Sharma P, Anikhindi SA, Bansal N, Singla V, Khare S and Srivastava A: Clinical features of COVID-19 and factors associated with severe clinical course: A systematic review and meta-analysis. SSRN: 3566166, 2020.

42 

Diaconu C: Treatment of diabetes in patients with heart failure. In: The 3rd International Conference on Interdisciplinary Management of Diabetes Mellitus and its Complications-Diabetes Mellitus in Internal Medicine, INTERDIAB 2017 Proceedings. Serafinceanu C, Negoita O and Elian V (eds). Niculescu, Bucharest, pp170-177, 2017.

43 

Al Hayek AA, Robert AA, Alotaibi ZK and Al Dawish M: Clinical characteristics of hospitalized and home isolated COVID-19 patients with type 1 diabetes. Diabetes Metab Syndr. 14:1841–1845. 2020.PubMed/NCBI View Article : Google Scholar

44 

Iughetti L, Trevisani V, Cattini U, Bruzzi P, Lucaccioni L, Madeo S and Predieri B: COVID-19 and type 1 diabetes: Concerns and challenges. Acta Biomed. 91(e2020033)2020.PubMed/NCBI View Article : Google Scholar

45 

Kalra S and Mittal S: COVID-19 and diabetes: Covidiabetology. J Pak Med Assoc. 70:954–955. 2020.PubMed/NCBI

46 

Isidori AM, Arnaldi G, Boscaro M, Falorni A, Giordano C, Giordano R, Pivonello R, Pofi R, Hasenmajer V, Venneri MA, et al: COVID-19 infection and glucocorticoids: Update from the Italian society of endocrinology expert opinion on steroid replacement in adrenal insufficiency. J Endocrinol Invest. 43:1141–1147. 2020.PubMed/NCBI View Article : Google Scholar

47 

Radu L, Carsote M, Gheorghisan-Galateanu AA, Preda SA, Calborean V, Stanescu R, Gheorman V and Albulescu DM: Blood parathyrin and mineral metabolism dynamics. A clinical analyze. Rev Chim (Bucharest). 69:2754–2758. 2018.

48 

Albulescu DM, Carsote M, Ghemigian A, Popescu M, Predescu AM, Tuculina MJ, Bugala AS, Bataiosu M, Marinescu RI, Dascalu IT, et al: Circulating 25-hydroxycholecalciferool in relationship to central dual-energy X-Ray absorptiometry assesses. A clinical study. Rev Chim (Bucharest). 69:3683–3687. 2018.

49 

Carsote M, Preda SA, Mitroi M, Camen A and Radu L: Serum osteocalcin, P1NP, alkaline phosphase, and crosslaps in humans: The relationship with body mass index. Rev Chim (Bucharest). 70:1615–1618. 2019.

50 

Teymoori-Rad M and Marashi SM: Vitamin D and Covid-19: From potential therapeutic effects to unanswered questions. Rev Med Virol. 31(e2159)2021.PubMed/NCBI View Article : Google Scholar

51 

Smulever A, Abelleira E, Bueno F and Pitoia F: Thyroid cancer in the era of COVID-19. Endocrine. 70:1–5. 2020.PubMed/NCBI View Article : Google Scholar

52 

Klain M, Nappi C, Maurea S, De Risi M, Volpe F, Caiazzo E, Piscopo L, Manganelli M, Schlumberger M and Cuocolo A: Management of differentiated thyroid cancer through nuclear medicine facilities during Covid-19 emergency: The telemedicine challenge. Eur J Nucl Med Mol Imaging: Sep 23, 2020 (Epub ahead of print).

53 

Vrachimis A, Iakovou I, Giannoula E and Giovanella L: Endocrinology in the time of COVID-19: Management of thyroid nodules and cancer. Eur J Endocrinol. 183:G41–G48. 2020.PubMed/NCBI View Article : Google Scholar

54 

Zhang D, Fu Y, Zhou L, Liang N, Wang T, Del Rio P, Rausei S, Boni L, Park D, Jafari J, et al: Thyroid surgery during coronavirus-19 pandemic phases I, II and III: Lessons learned in China, South Korea, Iran and Italy. J Endocrinol Invest: Sep 2, 2020 (Epub ahead of print).

55 

Facchiano A, Facchiano F and Facchiano A: An investigation into the molecular basis of cancer comorbidities in coronavirus infection. FEBS Open Bio. 10:2363–2374. 2020.PubMed/NCBI View Article : Google Scholar

56 

Buruiana A, Dumitru N, Ghemigian A and Petrova EN: Genetic testing in differentiated thyroid carcinoma-important or not? Rev Chim (Bucharest). 68:1557–1559. 2017.

57 

Docea AO, Tsatsakis A, Albulescu D, Cristea O, Zlatian O, Vinceti M, Moschos SA, Tsoukalas D, Goumenou M, Drakoulis N, et al: A new threat from an old enemy: Re-emergence of coronavirus (Review). Int J Mol Med. 45:1631–1643. 2020.PubMed/NCBI View Article : Google Scholar

58 

Calina D, Docea AO, Petrakis D, Egorov AM, Ishmukhametov AA, Gabibov AG, Shtilman MI, Kostoff R, Carvalho F, Vinceti M, et al: Towards effective COVID-19 vaccines: Updates, perspectives and challenges (Review). Int J Mol Med. 46:3–16. 2020.PubMed/NCBI View Article : Google Scholar

59 

Montesinos MDM and Pellizas CG: Thyroid hormone action on innate immunity. Front Endocrinol (Lausanne). 10(350)2019.PubMed/NCBI View Article : Google Scholar

Related Articles

Journal Cover

July-2021
Volume 22 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Șandru F, Carsote M, Petca RC, Gheorghisan-Galateanu AA, Petca A, Valea A and Dumitrașcu MC: COVID‑19‑related thyroid conditions (Review). Exp Ther Med 22: 756, 2021
APA
Șandru, F., Carsote, M., Petca, R.C., Gheorghisan-Galateanu, A.A., Petca, A., Valea, A., & Dumitrașcu, M.C. (2021). COVID‑19‑related thyroid conditions (Review). Experimental and Therapeutic Medicine, 22, 756. https://doi.org/10.3892/etm.2021.10188
MLA
Șandru, F., Carsote, M., Petca, R. C., Gheorghisan-Galateanu, A. A., Petca, A., Valea, A., Dumitrașcu, M. C."COVID‑19‑related thyroid conditions (Review)". Experimental and Therapeutic Medicine 22.1 (2021): 756.
Chicago
Șandru, F., Carsote, M., Petca, R. C., Gheorghisan-Galateanu, A. A., Petca, A., Valea, A., Dumitrașcu, M. C."COVID‑19‑related thyroid conditions (Review)". Experimental and Therapeutic Medicine 22, no. 1 (2021): 756. https://doi.org/10.3892/etm.2021.10188