Table 1.
Possible Effects of SARS-CoV-2 on the Endocrine System
| Pathology | Possible Mechanism | Effect on Hormonal Axis | Clinical Features | Management Issues and Solutions |
|---|---|---|---|---|
| Pituitary | ||||
| Central hypocortisolism and hypothyroidism | Hypophysitis resulting from infiltration by virus [41] Hypothalamic involvement [41] Destruction of ACE2 in hypothalamus [43, 44] Molecular mimicry of SARS-CoV-1 to ACTH and subsequent host defense mechanisms [46] |
Impaired ACTH/cortisol production Low thyroid hormones sometimes with low TSH |
Postviral syndromes [41] | Cosyntropin/Synacthen test TSH and free T4 If deficient, hormone replacement in physiological doses [41] |
| Hyperprolactinemia | Dopaminergic stress response [48] | Transient hyperprolactinemia | Asymptomatic | Prolactin levels may be high during acute illness. Caution on interactions of DRA with CYP450 inducing antivirals and amine based pressors/inotropes [55, 56] |
| Electrolyte imbalances | ||||
| Hypernatremia | High fever, tachypnea, gastrointestinal losses, inability to take adequate fluids [52] | Hypernatremia | Impaired level of consciousness | Monitor electrolytes Replacement Convert desmopressin to parenteral form [52] |
| Hypokalemia | Gastrointestinal losses [52] Upregulation of the RAAS by degradation of ACE2 [53, 54] |
Hypokalemia | Clinical features of hypokalemia | Monitor electrolytes Replacement |
| Adrenal | ||||
| Hypoadrenalism | Adrenal necrosis and vasculitis from direct cytopathic effect or inflammatory response [29, 59] | Hypocortisolism | Postural hypotension Persistently low blood pressure Hyperkalemia and hyponatremia |
Serum 9 am cortisol Cosyntropin test Hydrocortisone therapy |
| Thyroid | ||||
| Hypothyroidism | Destruction of follicular and parafollicular cells of thyroid [83] | Primary hypothyroidism | Hypothyroid features | High TSH and low free T4 Thyroxine replacement |
| Decreased activity of type 1 deiodinase activity, increased activity of type 3 deiodinase activity, and down-regulation of hypothalamic pituitary axis [82] | Sick euthyroidism | Clinically not significant | Difficulty in differentiating during acute illness, test TSH and free T4 following recovery | |
| Hypophysitis/ hypothalamic involvement [41] | Central hypothyroidism | Hypothyroid features | Low TSH and free T4 Thyroxine replacement |
|
| Pancreas | ||||
| Hypo-/hyperglycemia | Direct viral injury on ACE2 expressing islet cells [89] Hyperglycemia glycosylates ACE2 and viral S protein, facilitating viral entry [92] Pancreatitis [90]: direct viral injury, response to systemic inflammation, immune-mediated injury |
Possible hypoinsulinemia Stress response up-regulates cortisol, growth hormone, and adrenergic activity with hyperglycemic effects |
Hyperglycemia Mild pancreatitis: minimal or no symptoms |
Hyperglycemia predicts poor prognosis Requires frequent monitoring and titration of treatment Potential anti-COVID therapies may cause hypo- and hyperglycemia [100] |
| Parathyroid | ||||
| No direct effect | Not identified | Not identified | None | |
| Gonads | ||||
| Hypogonadism | Entry of virus into spermatogonia and somatic cells using ACE2 receptors [123, 124] Destruction of seminiferous tubules and reduced spermatozoa from immune-mediated orchitis [126] |
Impaired spermatogenesis and androgen synthesis | Male hypogonadism and subfertility | Follow-up after recovery from acute infection |