Yong, Shin Jie

ABSTRACTWith the global rollout of COVID‐19 vaccines, vaccine safety remains a priority. Emerging concerns have raised the potential risk of a long COVID‐like syndrome following vaccination, informally called long Vax and provisionally termed post‐COVID‐19 vaccination syndrome (PCVS). Our narrative review describes the putative manifestation, pathophysiology, and therapeutic approaches of PCVS based on the available evidence, mostly from case reports/series and observational studies. Our review noted that PCVS typically manifests within days to weeks post‐vaccination, with symptoms lasting months to years. PCVS may present as recognized diagnoses such as postural orthostatic tachycardia syndrome (POTS), small‐fibre neuropathy (SFN), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), or as long‐term sequelae of myocarditis, vaccine‐induced thrombotic thrombocytopaenia (VITT), or immune thrombocytopaenia purpura (ITP). Symptomatically, PCVS overlaps with long COVID, such as fatigue and brain fog, but PCVS may involve more frequent paraesthesia and less dyspnoea. We also review pathophysiological hypotheses of PCVS, focussing on the vaccine‐derived spike protein and related immune responses. Finally, we discuss potential therapies used to treat patients with PCVS or related conditions, primarily documented in case reports/series, which could guide future clinical research. Overall, PCVS remains a poorly understood condition that requires more research to elucidate its prevalence, prognosis, risk factors, and treatments.

Menstrual irregularities and abnormal uterine bleeding have been increasingly reported following severe acute respiratory syndrome coronavirus 2 infection, likely due to viral-induced endocrine disruption and immune dysregulation. A woman in her late 30s, with previously regular menses, developed persistent abnormal uterine bleeding after recovering from coronavirus disease 2019. Lab work-up over the next 2 years demonstrated high follicle-stimulating hormone, low anti-Müllerian hormone, low estrogen, and borderline antinuclear antibody titers. A pelvic ultrasound showed low antral follicle count, and she had challenges with fertility preservation. The patient was suspected of having an exaggerated immune reaction to severe acute respiratory syndrome coronavirus 2 infection with her strong family history of autoimmune disease and borderline antinuclear antibody, which may have led to an autoimmune-induced premature ovarian insufficiency. This case highlights the need to recognize post-viral menstrual irregularities and endocrine dysfunction as a potential consequence of coronavirus disease 2019. Clinicians should consider postinfectious endocrine disturbances in patients with new-onset abnormal uterine bleeding or infertility and evaluate for immune-mediated mechanisms when appropriate. Further research is needed to elucidate the long-term impact of coronavirus disease 2019 on reproductive health.