ABSTRACT
Currently, humanity is suffering from a highly contagious and infectious novel coron-avirus disease. Due to the unavailability of any specifically approved therapy to eradicate this pathogenic virus, day by day, it is claiming more and more lives of humans. Observing the current scenario, human civilization seems to be in dangerous situation, and the development of a potential vaccine against this invisible enemy may take some more time. It was observed that the individual immune system plays an important role in the fight against the novel coronavirus. Additionally, the innate immune system of the host acts as the first line of defense against invading pathogenic virus-es. The host innate immune cells can detect and detoxify the evading viruses. Thus, boosting the innate immune response via targeting activator or inhibitory immune check points pathways for en-hancing T-cell immune response may potentially help the patients to fight against this deadly virus. The aim of this editorial is to discuss in brief about the pathogenesis of COVID-19, the role of innate immunity and autophagy during viral clearance.Copyright © 2021 Bentham Science Publishers.
ABSTRACT
Background: Since COVID-19 vaccination was introduced, various adverse effects have been linked to the vaccines. In patients with hypopituitarism, adrenal insufficiency due to the side reactions including fever of COVID-19 vaccination is concerned. Clinical Case: A 33-year woman was on medical therapy including hydrocortisone (HC) for panhypopituitarism arising from surgical treatment of a pituitary adenoma in 2006. She received a COVID-19 vaccination on day X-3. On day X-2, she developed fever in the morning and became unconscious in the evening. She was brought to our hospital by her family at night on day X. She had fever of 40.5°C, low blood pressure, and Glasgow Coma Scale (GCS) of 11. Her neck was supple and she had no quadriplegia. A COVID-19 PCR test was negative. Blood tests showed elevated white blood cell count (8900/μL;reference range: 3300–8600/µL) and C-reactive protein (138.3 mg/l;reference range: 0-1.44 mg/l). Blood glucose (81 mg/dL), ACTH (<3. 00 pg/mL;reference range: 7.2–63.3 pg/mL), and cortisol (1.9 μg/dL;reference range: 2.9–19.4 µg/dL) were low. Serum electrolytes were normal. A computed tomography scan showed no abnormality. Adrenal insufficiency was suspected, and she received HC intravenously. Her blood glucose and blood pressure increased, but her disorientation persisted. Lumbar puncture with cerebrospinal fluid (CSF) examination revealed slightly elevated cell counts (8 μ/L;reference range ≤4 μ/L) with average protein and glucose levels. Magnetic resonance imaging (MRI) of the brain revealed abnormal hyperintensity in the splenium of the corpus callosum on diffusion-weighted images and decreased apparent diffusion coefficient in the lesion, suggesting clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). During her hospital stay, she received a 7-day course of meropenem and acyclovir for suspected meningoencephalitis. Her consciousness disturbance improved to GCS of 15 on day X+1 and her fever decreased on day X+2. HSV and VZV PCR tests were negative on CSF examination, and antibiotics and antivirals were discontinued on day X+7. On day X+8, brain MRI showed complete resolution of the corpus callosum lesion. She discharged on day X+18 without any neurological sequelae. Conclusions: For most vaccines, the incidence rates of encephalitis are low at 0.1–0.2 per 100,000 vaccinated individuals (1). The present patient developed fever and adrenal insufficiency after COVID-19 vaccination, and her prolonged disturbance of consciousness after HC administration led to the diagnosis of MERS. MERS should be considered in patients with adrenocortical insufficiency who show delayed recovery from unconsciousness with HC administration after COVID-19 vaccination. Reference: (1) Huynh W, Cordato DJ, Kehdi E, Masters LT, Dedousis C. Post-vaccination encephalomyelitis: literature review and illustrative case. J Clin Neurosci. 2008 Dec;15(12): 1315-22.Presentation: No date and time listed