COVID-19 and Hypothalamic–Pituitary Diseases: Comparison
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Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection, is a condition where individuals who have recovered from the acute phase of COVID-19 continue to experience a range of symptoms for weeks or even months afterward. While it was initially thought to primarily affect the respiratory system, it has become clear that Long COVID-19 can involve various organs and systems, including the endocrine system, which includes the pituitary gland. In the context of Long COVID-19, there is a growing understanding of the potential implications for the pituitary gland. The virus can directly affect the pituitary gland, leading to abnormalities in hormone production and regulation.

  • Long COVID-19
  • pituitary

1. Introduction

The most recent pandemic declared to date is the coronavirus disease 2019 (COVID-19). In December 2019, Chinese authorities informed the World Health Organization (WHO) about clusters of viral pneumonias detected in the city of Wuhan [1]. The causative virus is severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a single-stranded positive-sense RNA virus enveloped in the coronavirus subfamily, highly contagious among humans [1]. COVID-19 defines the disease caused by SARS-CoV-2. As of now, over 769 million people worldwide have been infected with COVID-19, and the WHO has recorded more than 6.9 million deaths [2].
SARS-CoV-2, like other coronaviruses, enters cells via the Angiotensin 2 Conversion Enzyme (ACE2) receptor and Transmembrane Serine Protease 2 (TMPRSS2) [3]. The extensive spectrum of SARS-CoV-2-induced lesions is attributed to the presence of the ACE2 receptor in numerous tissues, including the colon, liver, brain, and various endocrine tissues such as the pancreas, thyroid, and gonads [4,5][4][5].
Endocrine disorders associated with COVID-19 have been reported in several studies, exhibiting an endocrine phenotype ranging from clinically paucisymptomatic presentations to potentially life-threatening endocrine emergencies [6,7,8][6][7][8]. The pancreas is the endocrine organ most frequently affected by SARS-CoV-2. COVID-19 is responsible for impairing the glycemic balance in diabetic patients and increasing the incidence and severity of inaugural diabetic ketoacidosis during the pandemic [8,9,10,11][8][9][10][11].
The thyroid is the second most commonly affected endocrine gland in COVID-19. The most common abnormality in patients infected with SARS-CoV-2 is a decrease in thyroid-stimulating hormone (TSH) and free Tri-iodothyronine. An increased prevalence of thyrotoxicosis and primary hypothyroidism secondary to COVID-19 has also been reported [6,12,13,14,15,16][6][12][13][14][15][16]. Involvement of the adrenal glands by SARS-CoV-2 has been less frequently reported, with preserved adrenal function in the vast majority of patients [17,18,19][17][18][19]. However, primary adrenal involvement by SARS-CoV-2 has been primarily reported due to adrenal hemorrhages and infarctions. It has also been suggested that COVID-19 may play a role in the pathogenesis of Addison’s disease [20,21,22][20][21][22].
Gonadal involvement during COVID-19 has been rarely described. In males, it primarily manifests as orchitis-epididymitis and a tendency towards hypergonadotropic hypogonadism. Disturbances in spermatogenesis have also been reported [23,24,25,26,27][23][24][25][26][27]. Regarding ovaries, a few studies have concluded the absence of modification in the ovarian hormonal profile [28,29,30,31][28][29][30][31].
The central nervous system (CNS) is also a frequent target of SARS-CoV-2. A less explored compartment within the CNS in COVID-19 research, relative to other CNS structures, is the pituitary gland. COVID-19 infection has been associated with hypothalamo–hypophyseal (HH) disorders, such as pituitary apoplexy, diabetes insipidus, and hypophysitis [4,32,33,34,35][4][32][33][34][35]. In addition to the ongoing global relevance of the viral infection, the long-term impact of SARS-CoV-2 remains poorly understood. Many patients report the persistence or onset of symptoms, such as fatigue and cognitive impairments, several months after infection. This has led to the definition of a new entity, known as ‘Post COVID-19 Syndrome,’ or more commonly referred to as ‘Long COVID-19’ [36]. The proportion of patients affected by Post COVID-19 Syndrome varies from low percentages to as high as 93% of SARS-CoV-2-infected individuals [37]. Virological and histological hypotheses analyzing these residual symptoms suggest the persistence of certain post-inflammatory lesions, including vascular issues [38]. Other authors have postulated the theory that nano-antioxidants play a role in the pathogenesis of this syndrome [39,40][39][40]. However, when closely examining the remaining symptoms in these patients, some are strikingly similar to those seen in antehypophyseal deficiencies, notably corticotrop and somatotrop. Some studies investigating the HH axis have also identified antehypophyseal deficiencies, particularly corticotrop and somatotrop, during the acute phase of COVID-19 infection and in the late post-infectious phase, several months later [4,41][4][41].
Recently, some authors have suggested the involvement of the pituitary gland in COVID-19 infection and in Post COVID-19 Syndrome [4]. Certain symptoms could be explained by these pituitary deficiencies. The ACE2 receptor, which enables SARS-CoV-2 entry into cells, is expressed in the HH axis [4]. The exact mechanisms of viral action on infected cells remain under discussion, but inflammatory and autoimmune mechanisms are primarily implicated. Pituitary exploration during infection and follow-up in Post COVID-19 patients has not been systematically established due to the insidious nature of these lesions [4,41][4][41].

2. COVID-19 and Hypothalamic–Pituitary Diseases

Severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 belong to the coronavirus family [42]. The principal receptor for SARS-CoV-2, ACE2, manifests a ubiquitous expression across the cellular landscape of endocrine organs, notably prominent in the pancreatic and thyroid tissues [43,44][43][44]. This receptor has also been identified in hypothalamo–hypophysial tissues, albeit with a lesser degree of expression compared to other endocrine tissues [45,46][45][46].
SARS-CoV has been associated with various endocrinopathies, particularly pituitary-related [45,47][45][47]. SARS-CoV-2 has demonstrated a binding affinity to ACE2 10 to 20 times higher than that of SARS-CoV, explaining at least its higher infectious potential [4,48][4][48].
Throughout the evolution of the COVID-19 pandemic, several studies have reported hypothalamo–hypophyseal involvement potentially linked to SARS-CoV-2. These mainly include cases of hypophysitis, hypopituitarism, pituitary apoplexies, inappropriate secretion of antidiuretic hormone (SIADH), and diabetes insipidus. Hypothalamic involvement, on the other hand, has been very rarely described [4,8,35,49,50,51,52,53,54][4][8][35][49][50][51][52][53][54]. All these descriptions are summarized in Table 1.
Table 1. Types of lesions occurring to hypothalamo–hypophyseal gland during COVID-19 infection.
Type of Lesions Authors Year Country Results Study Description
Pituitary apoplexy Hazzi et al. [32] 2023 Canada 14 cases Literature review
Syndrome of Inappropriate ADH secretion Khidir et al. [33] 2022 Sudan 36% of Hyponatremia Meta-analysis
Hypophysitis Capatina et al. [4] 2023 Romania Not precise Several cases reported but widely underestimated according to the authors [44,45,46,47,48][44][45][46][47][48]
Isolated central diabetes insipidus Yavari et al. [34] 2022 Iran 1 case Literature review
Hypothalamitis Facondo et al. [35] 2022 Italy 5 cases Literature review

2.1. Pituitary Apoplexy

Pituitary apoplexy is a medical emergency that occurs when there is bleeding or impaired blood flow to the pituitary gland, often in the context of a pituitary adenoma. It can cause sudden-onset headaches, visual disturbances, and hormonal imbalances. Patients with severe COVID-19 may be at an increased risk of developing blood clotting disorders, which could potentially lead to conditions like stroke or apoplexy. The virus can trigger an inflammatory response and cause abnormalities in blood coagulation, contributing to the formation of blood clots. The evolution of apoplexy in infected patients is not well evaluated. In common apoplexies, for example, in the study of Falhammar et al., 33 patients had a pituitary apoplexy, 55% of them were men, and the mean age was 46 years. Only 9% of the patients required acute pituitary surgery, while eight patients were operated after more than one week. During follow-up [7.6 ± 4.3 years], none of the hormonal deficiencies regressed, and three patients died from non-related causes [55].

2.2. Hypophysitis

Hypophysitis is an inflammation of the pituitary gland and is a rare cause of hypopituitarism. Autoimmune hypophysitis is a known condition in COVID-19, where the body’s immune system attacks the pituitary gland [56]. Determining the actual occurrence rate of hypophysitis following COVID-19 proves to be challenging. Given that a significant number of symptomatic COVID-19 patients undergo glucocorticoid treatment in the early stages of the disease, and in some cases, for extended durations, there exists the potential for a substantial underassessment of hypophysitis diagnoses. In the meta-analysis of Capatina et al., there are only some cases that were reported in the literature, with one case being that of Misgar et al., describing a case of infundibuloneuro hypophysitis, which presented without involvement of the anterior pituitary [4,54][4][54].

2.3. Syndrome of Inappropriate Antidiuretic Hormone Secretion and Arginine Vasopressin Deficiency

Initial observational studies indicated that around half of COVID-19 patients experienced hyponatremia [57]. However, a retrospective examination of an extensive global registry tracking hospitalized COVID-19 cases, known as the Health Outcome Predictive Evaluation for COVID-19, identified substantially lower frequencies: hyponatremia in 20.5% of cases, hypernatremia in 3.7%. Both conditions were found to be associated with increased mortality and incidences of sepsis [33].
The prevalent cause of hyponatremia, particularly in individuals with COVID-19 pneumonia, was reported to be SIADH. However, whether SIADH directly results from the viral infection remains unclear. It is noteworthy that in various cases, there were reports of newly developed AVP deficiency either during or, more commonly, shortly after COVID-19 infection. This observation raises the prospect of a potential causal association [33].

2.4. Central Diabetes Insipidus

Several pathophysiological mechanisms have been proposed to explain CDI secondary to COVID-19. Ong et al. verified the expression of ACE2 in the paraventricular nucleus, making it susceptible to SARS-CoV-2 [58]. Iadecola and colleagues noted the presence of ACE2 and transmembrane protease serine on median eminence capillaries [59]. In a review conducted by Haidar et al. on the involvement of SARS-CoV-2 in central nervous system tissue damage, postmortem examinations have identified the presence of the SARS-CoV-2 genome in the hypothalamus, along with observations of degenerated and edematous neurons [60].
There is a variation in the timeframe between the diagnosis of COVID-19 and the onset of CDI. Yavari A et al. documented a case where central DI manifested six weeks after the initial COVID-19 diagnosis [34].
Similarly, Misgar et al. presented a case in which central DI developed eight weeks after the onset of COVID-19 [54].

2.5. Hypothalamic Lesions

There are intricate anatomical and functional interconnection between the hypothalamus and the olfactory bulb. Consistent with prior findings, recent evidence has revealed magnetic resonance imaging (MRI) alterations in the olfactory cortex among COVID-19 patients, underscoring the participation of the olfactory system in viral neuroinvasion [61]. This observation was further elucidated through the utilization of three- and two-dimensional fluid-attenuated inversion recovery images, which delineated cortical hyperintensity in the right gyrus rectus and hyperintensity in the olfactory bulbs [61].

References

  1. Fernandes, Q.; Inchakalody, V.P.; Merhi, M.; Mestiri, S.; Taib, N.; Moustafa Abo El-Ella, D.; Bedhiafi, T.; Raza, A.; Al-Zaidan, L.; Mohsen, O.M.; et al. Emerging COVID-19 variants and their impact on SARS-CoV-2 diagnosis, therapeutics and vaccines. Ann. Med. 2022, 54, 524–540.
  2. WHO. WHO COVID-19 Dashboard 2023. Available online: https://covid19.who.int/ (accessed on 18 August 2023).
  3. Senapati, S.; Banerjee, P.; Bhagavatula, S.; Kushwaha, P.P.; Kumar, S. Contributions of human ACE2 and TMPRSS2 in determining host-pathogen interaction of COVID-19. J. Genet. 2021, 100, 12.
  4. Capatina, C.; Poiana, C.; Fleseriu, M. Pituitary and SARS CoV-2: An unremitting conundrum. Best Pract. Res. Clin. Endocrinol. Metab. 2023, 37, 101752.
  5. Li, M.Y.; Li, L.; Zhang, Y.; Wang, X.S. Expression of the SARS-CoV-2 cell receptor gene ACE2 in a wide variety of human tissues. Infect. Dis. Poverty 2020, 9, 45.
  6. Puig-Domingo, M.; Marazuela, M.; Yildiz, B.O.; Giustina, A. COVID-19 and endocrine and metabolic diseases. An updated statement from the European Society of Endocrinology. Endocrine 2021, 72, 301–316.
  7. Shen, Q.; Li, J.; Zhang, Z.; Guo, S.; Wang, Q.; An, X.; Chang, H. COVID-19: Systemic pathology and its implications for therapy. Int. J. Biol. Sci. 2022, 18, 386–408.
  8. Frara, S.; Allora, A.; Castellino, L.; di Filippo, L.; Loli, P.; Giustina, A. COVID-19 and the pituitary. Pituitary 2021, 24, 465–481.
  9. Mastromauro, C.; Blasetti, A.; Primavera, M.; Ceglie, L.; Mohn, A.; Chiarelli, F.; Giannini, C. Peculiar characteristics of new-onset Type 1 Diabetes during COVID-19 pandemic. Ital. J. Pediatr. 2022, 48, 26.
  10. Chang, R.; Yen-Ting Chen, T.; Wang, S.I.; Hung, Y.M.; Chen, H.Y.; Wei, C.J. Risk of autoimmune diseases in patients with COVID-19: A retrospective cohort study. EClinicalMedicine 2023, 56, 101783.
  11. Gorchane, A.; Ach, T.; Sahli, J.; Abdelkrim, A.B.; Mallouli, M.; Bellazreg, F.; Hachfi, W.; Chaieb, C.M.; Ach, K. Uncovering the alarming rise of diabetic ketoacidosis during COVID-19 pandemic: A pioneer African study and review of literature. Front. Endocrinol. 2023, 14, 1234256.
  12. Lania, A.; Sandri, M.T.; Cellini, M.; Mirani, M.; Lavezzi, E.; Mazziotti, G. Thyrotoxicosis in patients with COVID-19: The THYRCOV study. Eur. J. Endocrinol. 2020, 183, 381–387.
  13. 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. 2020, 8, 739–741.
  14. Tee, L.Y.; Harjanto, S.; Rosario, B.H. COVID-19 complicated by Hashimoto’s thyroiditis. Singap. Med. J. 2021, 62, 265.
  15. Taieb, A.; Sawsen, N.; Asma, B.A.; Ghada, S.; Hamza, E.; Yosra, H. A rare case of grave’s disease after SARS-CoV-2 vaccine: Is it an adjuvant effect? Eur. Rev. Med. Pharmacol. Aci. 2022, 26, 2627–2630.
  16. Chen, T.; Wu, D.; Chen, H.; Yan, W.; Yang, D.; Chen, G.; Ma, K.; Xu, D.; Yu, H.; Wang, H.; et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: Retrospective study. BMJ 2020, 368, m1091.
  17. Tan, T.; Khoo, B.; Mills, E.G.; Phylactou, M.; Patel, B.; Eng, P.C. Association between high serum total cortisol concentrations and mortality from COVID-19. Lancet Diabetes Endocrinol. 2020, 8, 659–660.
  18. Yavropoulou, M.P.; Filippa, M.G.; Mantzou, A.; Ntziora, F.; Mylona, M.; Tektonidou, M.G.; Vlachogiannis, N.; Paraskevis, D.; Kaltsas, G.A.; Chrousos, G.P.; et al. Alterations in cortisol and interleukin-6 secretion in patients with COVID-19 suggestive of neuroendocrine-immune adaptations. Endocrine 2022, 75, 317–327.
  19. Ahmadi, I.; Estabraghnia Babaki, H.; Maleki, M.; Jarineshin, H.; Kaffashian, M.R.; Hassaniazad, M.; Kenarkoohi, A.; Ghanbarnejad, A.; Falahi, S.; Jahromi, K.M.; et al. Changes in Physiological Levels of Cortisol and Adrenocorticotropic Hormone upon Hospitalization Can Predict SARS-CoV-2 Mortality: A Cohort Study. Int. J. Endocrinol. 2022, 2022, 4280691.
  20. Kumar, R.; Guruparan, T.; Siddiqi, S.; Sheth, R.; Jacyna, M.; Naghibi, M.; Vrentzou, E. A case of adrenal infarction in a patient with COVID 19 infection. BJR Case Rep. 2020, 6, 20200075.
  21. Elkhouly, M.M.N.; Elazzab, A.A.; Moghul, S.S. Bilateral adrenal hemorrhage in a man with severe COVID-19 pneumonia. Radiol. Case Rep. 2021, 16, 1438–1442.
  22. Sánchez, J.; Cohen, M.; Zapater, J.L.; Eisenberg, Y. Primary Adrenal Insufficiency After COVID-19 Infection. AACE Clin. Case Rep. 2022, 8, 51–53.
  23. Gagliardi, L.; Bertacca, C.; Centenari, C.; Merusi, I.; Parolo, E.; Ragazzo, V.; Tarabella, V. Orchiepididymitis in a Boy With COVID-19. Pediatr. Infect. Dis. J. 2020, 39, e200–e202.
  24. Chen, L.; Huang, X.; Yi, Z.; Deng, Q.; Jiang, N.; Feng, C.; Zhou, Q.; Sun, B.; Chen, W.; Guo, R. Ultrasound Imaging Findings of Acute Testicular Infection in Patients with Coronavirus Disease 2019: A Single-Center-Based Study in Wuhan, China. J. Ultrasound Med. Off. J. Am. Inst. Ultrasound Med. 2021, 40, 1787–1794.
  25. He, Y.; Wang, J.; Ren, J.; Zhao, Y.; Chen, J.; Chen, X. Effect of COVID-19 on Male Reproductive System—A Systematic Review. Front. Endocrinol. 2021, 12, 677701.
  26. Holtmann, N.; Edimiris, P.; Andree, M.; Doehmen, C.; Baston-Buest, D.; Adams, O.; Kruessel, J.S.; Bielfeld, A.P. Assessment of SARS-CoV-2 in human semen-a cohort study. Fertil. Steril. 2020, 114, 233–238.
  27. Ma, L.; Xie, W.; Li, D.; Shi, L.; Ye, G.; Mao, Y.; Xiong, Y.; Sun, H.; Zheng, F.; Chen, A.; et al. Evaluation of sex-related hormones and semen characteristics in reproductive-aged male COVID-19 patients. J. Med. Virol. 2021, 93, 456–462.
  28. Lebar, V.; Laganà, A.S.; Chiantera, V.; Kunič, T.; Lukanović, D. The Effect of COVID-19 on the Menstrual Cycle: A Systematic Review. J. Clin. Med. 2022, 11, 3800.
  29. Dhindsa, S.; Zhang, N.; McPhaul, M.J.; Wu, Z.; Ghoshal, A.K.; Erlich, E.C.; Mani, K.; Randolph, J.G.; Edwards, J.R.; Mudd, A.P.; et al. Association of Circulating Sex Hormones with Inflammation and Disease Severity in Patients With COVID-19. JAMA Netw. Open 2021, 4, e2111398.
  30. Li, K.; Chen, G.; Hou, H.; Liao, Q.; Chen, J.; Bai, H.; Lee, S.; Wang, H.; Li, H.; Cheng, L.; et al. Analysis of sex hormones and menstruation in COVID-19 women of child-bearing age. Reprod. Biomed. Online 2021, 42, 260–267.
  31. Ding, T.; Wang, T.; Zhang, J.; Cui, P.; Chen, Z.; Zhou, S.; Yuan, S.; Ma, W.; Zhang, M.; Rong, Y.; et al. Analysis of Ovarian Injury Associated With COVID-19 Disease in Reproductive-Aged Women in Wuhan, China: An Observational Study. Front. Med. 2021, 8, 635255.
  32. Hazzi, C.; Villemure-Poliquin, N.; Nadeau, S.; Champagne, P.O. SARS-CoV-2 Infection, A Risk Factor for Pituitary Apoplexy? A Case Series and Literature Review. Ear Nose Throat J. 2023, 1455613231179714.
  33. Khidir, R.J.Y.; Ibrahim, B.A.Y.; Adam, M.H.M.; Hassan, R.M.E.; Fedail, A.S.S.; Abdulhamid, R.O.; Mohamed, S.O. Prevalence and outcomes of hyponatremia among COVID-19 patients: A systematic review and meta-analysis. Int. J. Health Sci. 2022, 16, 69–84.
  34. Yavari, A.; Sharifan, Z.; Larijani, B.; Mosadegh Khah, A. Central diabetes insipidus secondary to COVID-19 infection: A case report. BMC Endocr. Disord. 2022, 22, 134.
  35. Facondo, P.; Maltese, V.; Delbarba, A.; Pirola, I.; Rotondi, M.; Ferlin, A.; Capelli, C. Case Report: Hypothalamic Amenorrhea Following COVID-19 Infection and Review of Literatures. Front. Endocrinol. 2022, 13, 840749.
  36. Soriano, J.B.; Murthy, S.; Marshall, J.C.; Relan, P.; Diaz, J.V. A clinical case definition of post-COVID-19 condition by a Delphi consensus. Lancet Infect. Dis. 2022, 22, e102–e107.
  37. Woodrow, M.; Carey, C.; Ziauddeen, N.; Thomas, R.; Akrami, A.; Lutje, V.; Greenwood, D.C.; Alwan, N.A. Systematic Review of the Prevalence of Long COVID. Open Forum Infect. Dis. 2023, 10, ofad233.
  38. Davis, H.E.; McCorkell, L.; Vogel, J.M.; Topol, E.J. Long COVID: Major findings, mechanisms and recommendations. Nat. Rev. Microbiol. 2023, 21, 133–146.
  39. Akanchise, T.; Angelova, A. Potential of Nano-Antioxidants and Nanomedicine for Recovery from Neurological Disorders Linked to Long COVID Syndrome. Antioxidants 2023, 12, 393.
  40. Akanchise, T.; Angelova, A. Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy. Pharmaceutics 2023, 15, 1562.
  41. Urhan, E.; Karaca, Z.; Unuvar, G.K.; Gundogan, K.; Unluhizarci, K. Investigation of pituitary functions after acute coronavirus disease 2019. Endocr. J. 2022, 69, 649–658.
  42. Nekoua, M.P.; Debuysschere, C.; Vergez, I.; Morvan, C.; Mbani, C.J.; Sane, F.; Alidjinou, E.K.; Hober, D. Viruses and Endocrine Diseases. Microorganisms 2023, 11, 361.
  43. Lazartigues, E.; Qadir, M.M.F.; Mauvais-Jarvis, F. Endocrine Significance of SARS-CoV-2’s Reliance on ACE2. Endocrinology 2020, 161, bqaa108.
  44. Steenblock, C.; Toepfner, N.; Beuschlein, F.; Perakakis, N.; Mohan Anjana, R.; Mohan, V.; Mahapatra, N.R.; Bornstei, S.R. SARS-CoV-2 infection and its effects on the endocrine system. Best Pract. Res. Clin. Endocrinol. Metab. 2023, 37, 101761.
  45. Han, T.; Kang, J.; Li, G.; Ge, J.; Gu, J. Analysis of 2019-nCoV receptor ACE2 expression in different tissues and its significance study. Ann. Transl. Med. 2020, 8, 1077.
  46. Gu, W.T.; Zhou, F.; Xie, W.Q.; Wang, S.; Yao, H.; Liu, Y.T.; Gao, L.; Wu, Z.B. A potential impact of SARS-CoV-2 on pituitary glands and pituitary neuroendocrine tumors. Endocrine 2021, 72, 340–348.
  47. Pal, R.; Banerjee, M. COVID-19 and the endocrine system: Exploring the unexplored. J. Endocrinol. Investig. 2020, 43, 1027–1031.
  48. Fitzek, A.; Gerling, M.; Püschel, K.; Saeger, W. Post-mortem histopathology of pituitary and adrenals of COVID-19 patients. Leg. Med. 2022, 57, 102045.
  49. Taieb, A.; Asma, B.A.; Mounira, E.E. Evidences that SARS-CoV-2 Vaccine-Induced apoplexy may not be solely due to ASIA or VITT syndrome’, Commentary on Pituitary apoplexy and COVID-19 vaccination: A case report and literature review. Front. Endocrinol. 2023, 14, 1111581.
  50. Nonglait, P.L.; Naik, R.; Raizada, N. Hypophysitis after COVID-19 Infection. Indian J. Endocrinol. Metab. 2021, 25, 255–256.
  51. Sheikh, A.B.; Javaid, M.A.; Sheikh, A.A.E.; Shekhar, R. Central adrenal insufficiency and diabetes insipidus as potential endocrine manifestations of COVID-19 infection: A case report. Pan. Afr. Med. J. 2021, 38, 222.
  52. Gorbova, N.Y.; Vladimirova, V.P.; Rozhinskaya, L.Y.; Belaya, Z.Y. Hypophysitis and reversible hypopituitarism developed after COVID-19 infection—A clinical case report. Probl. Endokrinol. 2022, 68, 50–56.
  53. Joshi, M.; Gunawardena, S.; Goenka, A.; Ey, E.; Kumar, G. Post COVID-19 Lymphocytic Hypophysitis: A Rare Presentation. Child Neurol. Open 2022, 9, 2329048x221103051.
  54. Misgar, R.A.; Rasool, A.; Wani, A.I.; Bashir, M.I. Central diabetes insipidus (Infundibuloneuro hypophysitis): A late complication of COVID-19 infection. J. Endocrinol. Investig. 2021, 44, 2855–2856.
  55. Falhammar, H.; Tornvall, S.; Höybye, C. Pituitary Apoplexy: A Retrospective Study of 33 Cases from a Single Center. Front. Endocrinol. 2021, 12, 656950.
  56. Langlois, F.; Varlamov, E.V.; Fleseriu, M. Hypophysitis, the Growing Spectrum of a Rare Pituitary Disease. J. Clin. Endocrinol. Metab. 2021, 107, 10–28.
  57. Hirsch, J.S.; Uppal, N.N.; Sharma, P.; Khanin, Y.; Shah, H.H.; Malieckal, D.A.; Bellucci, A.; Sachdeva, M.; Rondon-Berrios, H.; Jhaveri, K.D.; et al. Prevalence and outcomes of hyponatremia and hypernatremia in patients hospitalized with COVID-19. Nephrol. Dial. Transplant. 2021, 36, 1135–1138.
  58. Ong, W.Y.; Satish, R.L.; Herr, D.R. ACE2, Circumventricular Organs and the Hypothalamus, and COVID-19. Neuromol. Med. 2022, 24, 363–373.
  59. Iadecola, C.; Anrather, J.; Kamel, H. Effects of COVID-19 on the Nervous System. Cell 2020, 183, 16–27.e1.
  60. Haidar, M.A.; Shakkour, Z.; Reslan, M.A.; Al-Haj, N.; Chamoun, P.; Habashy, K.; Kaafarani, H.; Shahjouei, S.; Farran, S.H.; Shaito, A.; et al. SARS-CoV-2 involvement in central nervous system tissue damage. Neural Regen. Res. 2022, 17, 1228–1239.
  61. Capelli, S.; Caroli, A.; Barletta, A.; Arrigoni, A.; Napolitano, A.; Pezzetti, G.; Longhi, L.G.; Zangari, R.; Lorini, F.L.; Sessa, M.; et al. MRI evidence of olfactory system alterations in patients with COVID-19 and neurological symptoms. J. Neurol. 2023, 270, 1195–1206.
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