Introduction
Methods
Results and discussion
Systematic search results
Endocrine links to SARS and COVID-19 pathophysiology | Reference number | Author (Year) |
---|---|---|
Similarities between SARS-CoV-2 and other beta-coronaviridae | [5] | Chen Y (2020) |
[10] | Hoffmann M (2020) | |
[21] | Siddell SG (2005) | |
[22] | Cavanagh D (1995) | |
[23] | Kandeel M (2018) | |
[24] | Risco C (1996) | |
[25] | Ruch T (2012) | |
[26] | Neuman BW (2011) | |
[27] | Chan JFW (2020) | |
[28] | Rabaan AA (2020) | |
[29] | Xu J (2020) | |
[30] | Li W (2003) | |
[31] | Matsuyama S (2010) | |
[32] | Shulla A (2011) | |
[33] | Zhang C (2020) | |
[34] | Zhou P (2020) | |
[35] | Fehr AR (2015) | |
ACE2 and TMPRSS2 expression in endocrine tissues | [11] | Chen Y (2020) |
[12] | Lazartigues E (2020) | |
[63] | Hamming I (2004) | |
[64] | Chi M (2020) | |
[100] | Reis FM (2011) | |
[101] | Jing Y (2020) | |
[102] | Goad J (2020) | |
[103] | Wang Z (2020) | |
[104] | Fan C (2020) | |
ACE2 expression and COVID-19 treatments | [36] | Malek Mahdavi A (2020) |
[37] | Xiang Z (2020) | |
[38] | Young MJ (2020) | |
[39] | Hanff TC (2020) | |
[40] | Marshall RP (2000) | |
[41] | Marshall RP (2004) | |
[42] | Mastruzzo C (2002) | |
[43] | Okada M (2009) | |
[44] | Wang R (1999) | |
[45] | Keidar S (2007) | |
[46] | Mizuiri S (2015) | |
[47] | Imai Y (2008) | |
[48] | Xu J (2017) | |
[49] | Panarese A (2020) | |
Coronavirus infections and potential damage systems to endocrine glands | [65] | Ding Y (2003) |
[66] | Guo Y (2008) | |
[67] | Yao XH (2020) | |
[77] | Conti P (2020) | |
[99] | Giannis D (2020) | |
Hormonal regulation of TMPRSS2 expression and its role in susceptibility to COVID-19 infection | [50] | Jin J (2020) |
[51] | Bertram S (2013) | |
[52] | Asselta R (2020) | |
[53] | Li MY (2020) | |
[54] | Stopsack KH (2020) | |
[55] | Thebault R (2020) | |
[56] | Bennett CL (2002) | |
[57] | Wambier CV (2020) | |
[58] | Montopoli M (2020) | |
[59] | Chen J (2020) | |
[60] | Dasinger JH (2016) | |
[61] | Mishra JS (2016) | |
[62] | Klein SL (2012) |
Endocrine gland/system | Reference number | Author (Year) | Infection | Kind of study |
---|---|---|---|---|
Hypothalamus/Pituitary | [68] | Zhang QL (2003) | SARS | Pathology |
[69] | Ding Y (2004) | SARS | Pathology | |
[70] | Gu J (2005) | SARS | Pathology | |
[71] | Wei L (2010) | SARS | Pathology | |
[72] | Ye YX (2004) | SARS | Clinical | |
[73] | Wang W (2003) | SARS | Clinical | |
[74] | Leow MK (2005) | SARS | Clinical | |
[75] | Zhou L (2020) | COVID-19 | Case report | |
[76] | Li T (2020) | COVID-19 | Clinical | |
Thyroid | [67] | Yao XH (2020) | COVID-19 | Pathology |
[70] | Gu J (2005) | SARS | Pathology | |
[74] | Leow MK (2005) | SARS | Clinical | |
[76] | Li T (2020) | COVID-19 | Clinical | |
[78] | Wei L (2007) | SARS | Pathology | |
[79] | Wang W (2003) | SARS | Clinical | |
[82] | Chen M (2020) | COVID-19 | Clinical | |
[83] | Chen T (2020) | COVID-19 | Clinical | |
[84] | Gao W (2020) | COVID-19 | Clinical | |
[85] | Lui DTW (2020) | COVID-19 | Clinical | |
[86] | Khoo B (2020) | COVID-19 | Clinical | |
[87] | Brancatella A (2020) | COVID-19 | Case report | |
[88] | Ippolito S (2020) | COVID-19 | Case report | |
[89] | Asfuroglu K E (2020) | COVID-19 | Case report | |
[90] | Ruggeri RM (2020) | COVID-19 | Case report | |
[91] | Brancatella A (2020) | COVID-19 | Case report | |
[92] | Lania A (2020) | COVID-19 | Clinical | |
[93] | Muller I (2020) | COVID-19 | Clinical | |
Adrenal gland | [65] | Ding Y (2003) | SARS | Pathology |
[68] | Zhang QL (2003) | SARS | Pathology | |
[70] | Gu J (2005) | SARS | Pathology | |
[94] | Zinserling VA (2020) | COVID-19 | Pathology | |
[95] | Freire S M (2020) | COVID-19 | Pathology | |
[96] | Iuga AC (2020) | COVID-19 | Pathology | |
[97] | Frankel M (2020) | COVID-19 | Case report | |
[98] | Álvarez-T J (2020) | COVID-19 | Case report | |
Ovary | [69] | Ding Y (2004) | SARS | Pathology |
Testis | [69] | Ding Y (2004) | SARS | Pathology |
[70] | Gu J (2005) | SARS | Pathology | |
[105] | Xu J (2006) | SARS | Pathology | |
[106] | Wang DW (2003) | SARS | Pathology | |
[107] | Zhao JM (2003) | SARS | Pathology | |
[108] | Yang M (2020) | COVID-19 | Pathology | |
[109] | Achua JK (2020) | COVID-19 | Pathology | |
[110] | Li H (2020) | COVID-19 | Clinical/Pathology | |
[111] | Ma L (2020) | COVID-19 | Clinical | |
[112] | Pan F (2020) | COVID-19 | Clinical | |
[113] | Song C (2020) | COVID-19 | Clinical | |
[114] | Paoli D (2020) | COVID-19 | Case report | |
[115] | Holtmann N (2020) | COVID-19 | Clinical | |
[116] | Li D (2020) | COVID-19 | Clinical | |
[117] | Vishvkarma R (2020) | COVID-19 | Sistematic review | |
[118] | Corona G (2020) | COVID-19 | Position statement |
Similarities between SARS-CoV-2 and other beta-coronaviridae
Effect of hormones on human susceptibility to coronavirus infection
Glucocorticoid and vitamin D
Sex hormones
Effect of coronavirus on the endocrine system
ACE2 and TMPRSS2 expression in endocrine tissues
Mechanisms of potential damage on endocrine glands induced by coronavirus infection
Endocrine gland/system | Infection | Pathological features | Endocrine function |
---|---|---|---|
Thyroid | SARS | Derangement of the follicular architecture [78] High levels of apoptosis (by Tunel), in both follicular epithelium and in interfollicular region [78] Interfollicular fibrosis [78] Absence of calcitonin-positive cells [78] | FT3 and FT4 levels significantly lower than control group [79] FT3 and FT4 levels decreased, respectively, by 94% and 46%, during the acute phase of illness [79] FT3 and FT4 levels decreased, respectively, by 90% and 38% during the convalescence phase of illness [79] |
COVID-19 | No abnormalities in thyroid follicular cells [67] Interstitial lymphocytic infiltration [67] | During recovery, TSH and FT3 levels were significantly lower in patients than in healthy subjects [82] Mild reductions of TSH and FT4 in admission to hospital [86] Clinical, biochemical and ultrasound evidences of subacute thyroiditis during recovery phase [87‐92] Low TSH and FT3 levels associated with normal/elevated FT4 [93] | |
Hypothalamus/Pituitary axis | SARS | Focal cell damage and reduction of TSH-positive, ACTH-positive and GH-positive cells by IHC [71] Increased number of PRL-, LH-e and FSH-positive cells by IHC [71] | 83% of patients had central hypocortisolism with concomitant low or inappropriately normal ACTH levels [74] |
COVID-19 | Presence of SARS-CoV-2 in the cerebrospinal fluid of patients [75] | Decrease of GH and IGFBP-3 levels [76] 34% of patients displayed isolated low TSH values [82] | |
Adrenal Gland | SARS | Hybridization in situ detected SARS-CoV-1 genome sequences in autoptic tissues [68] | |
COVID-19 | Infiltration of CD3+ and CD8+ lymphocytes in different layers of cortex and in surrounding tissue [94] Small groups of proliferating cells with enlarged clear nuclei [94] Acute fibrinoid necrosis of adrenal arteriolae both in the parenchyma and capsule [96]. Focal inflammation [95] | ||
Ovary | SARS | No detection SARS-CoV-1 RNA polymerase by immunohistochemistry and in situ hybridization [69] | |
COVID-19 | / | / | |
Testis | SARS | ||
COVID-19 | Sertoli cells: variable degree of swelling, vacuolation and cytoplasmic rarefaction, detachment from tubular basement membranes and sloughing into lumens of the intratubular cell mass [108] Reduced number of Leydig cells [108] Thinning of seminiferous tubules with a significant high number of apoptotic cells and IgG inside [110] Oligozoospermia and significant increase of semen leucocyte number in 39.1% and 60.9% of COVID-19 patients, respectively [110] | Significant increase in serum LH, while T/LH and decrease of FSH/LH ratios [111] Not significant changes in serum testosterone levels between patients and control groups [111] |