Table 3.
Explanatory summary of the results
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] Decrease in TSH and TT3 or FT3 levels positively correlated to the infection severity [76, 82–85] Mild reductions of TSH and FT4 in admission to hospital [86] Normalization of thyroid function tests at follow-up post hospital discharge [82, 84, 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] Detection of SARS-CoV-1 genome sequences in hypothalamus/pituitary cells from autoptic tissues by in situ Hybridization and RT-PCR [68–70] |
83% of patients had central hypocortisolism with concomitant low or inappropriately normal ACTH levels [74] Increased PRL, LH, FSH serum levels in male patients [72, 73] |
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 |
Thrombosis and vasculitis in the adrenal vessels [65, 70] 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] Predominant vascular damage localized to the adrenals rather than the other organs [95, 96] Acute fibrinoid necrosis of adrenal arteriolae both in the parenchyma and capsule [96]. Focal inflammation [95] |
Reports of acute bilateral adrenal hemorrhage and consequent acute adrenal failure [97, 98] | |
Ovary | SARS | No detection SARS-CoV-1 RNA polymerase by immunohistochemistry and in situ hybridization [69] | |
COVID-19 | / | / | |
Testis | SARS |
Extensive destruction of testicular germ cells [105, 106] Rare spermatozoa in the epithelium and lumen of seminiferous tubules [105, 106] Peritubular fibrosis [105, 106] Massive leukocyte infiltration and IgG presence [105, 106] Conflicting evidence about the presence of SARS-CoV-1 RNA in testicular cells by in situhybridization [69, 107] |
|
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] Infiltrates of lymphocytes, macrophages and histiocytes in the interstitium [108–110] 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] Conflicting evidences about the presence of SARS-CoV-2 RNA in testicular cells by RT-PCR [108, 110] Conflicting evidence about the presence of SARS-CoV-2 RNA in semen by RT-PCR [112–116] |
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] |