Early and late endocrine complications of COVID-19

Abstract

Endocrine system plays a vital role in controlling human homeostasis. Understanding possible effects of COVID-19 on endocrine glands is crucial to prevent and manage endocrine disorders before and during hospitalization in COVID-19 infected patients, as well as to follow them up properly upon recovery. Many endocrine glands such as pancreas, hypothalamus and pituitary, thyroid, adrenal glands, testes, and ovaries have been found to express ACE2 receptors, the main binding site of the virus. Since the pandemic outbreak, various publications focus on the aggravation of preexisting endocrine diseases by COVID-19 infection or the adverse prognosis of the disease in endocrine patients. However, data on endocrine disorders, both during the phase of the infection (early complications) and upon recovery (late complications) are scarce. The aim of this review is to identify and discuss early and late endocrine complications of COVID-19. The majority of the available data refer to glucose dysregulation and its reciprocal effect on COVID-19 infection with the main interest focusing on the presentation of new onset of diabetes mellitus. Thyroid dysfunction with either low T3, low TSH or subacute thyroiditis has been reported. Adrenal dysregulation and impaired spermatogenesis in affected men have been also reported. Complications of other endocrine glands are still not clear. Considering the recent onset of COVID-19 infection, the available follow-up data are limited and therefore long-term studies are required to evaluate certain effects of COVID-19 on the endocrine glands.

Diabetic ketoacidosis (DKA) in type 1 diabetes mellitus (T1DM) temporally related to COVID-19 vaccination

“…The compromised innate immunity, an underlying chronic low-grade inflammation and an exaggerated pro-inflammatory response, characterized by increased cytokines like IL-1, IL-6, TNF-α, C-reactive protein, ferritin, and a hypercoagulable state contribute to the increasing severity in diabetics [ [9] , [10] , [11] ]. Acute hyperglycemia can upregulate angiotensin-converting enzyme 2 (ACE-2) expression facilitating viral entry, while chronic hyperglycemia can lead to low ACE-2 expression, leading to decreased degradation of angiotensin II to the vasodilatory, anti-proliferative and anti-inflammatory peptide angiotensin [ [1] , [2] , [3] , [4] , [5] , [6] , [7] ]. This response may be exaggerated after the immune response after natural infection or vaccination [ 12 ].…”

“…SARS Cov-2 infection is also associated with an adverse effect on glycemia. Proposed mechanisms include islet cell damage and acute insulinopenia after cellular entry via pancreatic ACE-2 receptor [ 13 ], cytokine storm [ 5 ], oxidative stress, overactivation of the renin-angiotensin-aldosterone system (RAAS), and dysregulated release of stress hormones like cortisol and catecholamines leading to increased insulin resistance [ 10 , 14 ].…”

“…It has been demonstrated in multiple studies that diabetes has been associated with increased risk of severe disease, acute respiratory distress syndrome (ARDS), disease progression and increased mortality rates [ 3 , 4 ]. In fact, there exists a bidirectional relationship between SARS-CoV2 infection and diabetes, with infection being associated with worsening of hyperglycemia in preexisting diabetes and new-onset hyperglycemia [ 5 ].…”

Patients With Autoimmune Thyroiditis Present Similar Immunological Response to COVID-19 BNT162b2 mRNA Vaccine With Healthy Subjects, While Vaccination May Affect Thyroid Function: A Clinical Study

“…However, no robust data deriving from a properly performed study existed so far. Decrease in T3 and TSH levels has been reported in patients affected by COVID-19 during first days ( 31 ) or weeks after the disease ( 5 – 7 ). The possible thyroid dysfunction after COVID-19 vaccination cannot be completely explained.…”

“…Since the coronavirus disease 2019 (COVID-19) pandemic outbreak, interesting data have been published on the possible thyroid complications of COVID-19 (4)(5)(6), including mainly decrease in triiodothyronine (T3) and thyroid stimulating hormone (TSH) levels, as well as subacute thyroiditis (7)(8)(9)(10)(11)(12). During this challenging period, physicians strived not only to treat new cases but also to support patients with chronic disorders.…”