LONG-TERM ENDOCRINE SEQUELAE AFTER COVID-19: CLINICAL INSIGHTS, DIGITAL HEALTH PERSPECTIVES AND PUBLIC HEALTH CHALLENGES
The COVID-19 pandemic has revealed that SARS-CoV-2 infection affects not only the respiratory system but also multiple endocrine organs, leading to a broad spectrum of long-term hormonal disturbances. This narrative review aims to summarize the current evidence on endocrine sequelae after COVID-19, emphasizing pathophysiological mechanisms, clinical manifestations, and implications for patient management. A structured literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar for studies published between January 2020 and October 2025 addressing endocrine or metabolic consequences of COVID-19. The reviewed data demonstrate that SARS-CoV-2 can impair the hypothalamic–pituitary–adrenal, thyroid, gonadal, pancreatic, and growth hormone axes through direct viral injury, immune-mediated inflammation, and chronic stress-axis dysregulation. Clinical consequences include secondary adrenal insufficiency, autoimmune thyroiditis, new-onset diabetes, hypogonadism, and menstrual disorders. While many abnormalities appear transient, a subset of patients develop persistent dysfunction requiring long-term follow-up. Tele-endocrinology and digital health solutions have emerged as valuable tools for monitoring endocrine recovery and improving access to care. However, significant research gaps remain, particularly regarding long-term prevalence, reversibility, and mechanisms of endocrine injury. Understanding and addressing these complications will require coordinated, multidisciplinary strategies that integrate clinical endocrinology, public health, and digital innovation.
Authors
- Katarzyna Bielawska
Institutions
- Grochowski Hospital (PL)
Publication Details
- Journal
- International Journal of Innovative Technologies in Social Science
- Published
- 2025-12-21
- DOI
- https://doi.org/10.31435/ijitss.4(48).2025.4194
- Primary Topic
- COVID-19 Impact on Reproduction
- Type
- article
- Field-Weighted Citation Impact
- 0.00