COVID-19 and Chronic Fatigue Syndrome: An endocrine perspective, by Rashika Bansal, Sriram Gubbi, Christian A Koch in Journal of Clinical & Translational Endocrinology 3 Dec 2021 [doi.org/10.1016/j.jcte.2021.100284]
Research abstract:
Patients recovering from COVID-19 may have persistent debilitating symptoms requiring long term support through individually tailored cardiopulmonary and psychological rehabilitation programs. Clinicians need to be aware about the likely long-term complications and their diagnostic assessments to help identify any occult problems requiring additional help.
Endocrinological evaluations should be considered as part of the armamentarium in the management of such individuals with diligent cognizance about the involvement of the hypothalamo-pituitary-adrenal (HPA) axis, adrenals, and thyroid.
An uncanny resemblance has been observed between the long-COVID syndrome and clinical features of CFS, though this is not an unfamiliar concept.
The endocrine connection to Long-COVID syndrome:
ACE2 receptors, the route of entry of the SARS-CoV-2 virus into the human body, are expressed (https://www.proteinatlas.org/ENSG00000130234-ACE2/tissue) in the hypothalamus, pituitary, adrenal gland, thyroid, testes, and pancreatic islets leading to the involvement of the endocrine system during and after the recovery of the disease.
Longitudinal and postmortem studies conducted on SARS-CoV patients provide some guidance on the extent of endocrine gland involvement. On postmortem examination, SARS-CoV RNA was found in the pituitary gland, parathyroid, pancreas and adrenal gland (39).
In another study, both parafollicular and follicular cells were found to be apoptotic explaining the low serum triiodothyronine and thyroxine levels and the osteonecrosis of the femoral head associated with patients of SARS-CoV (40).
Evidence of hypocortisolism was found in 39% of sixty-one survivors of SARS prospectively recruited for hormonal derangements 3 months after recovery (41).
Nonetheless, information about the adverse effects on endocrine function by the SARS-CoV-2 virus remain limited [42], [43].
