Globally, acute respiratory illnesses are the most commonly manifesting illness in all age group. The disease mostly affects the upper respiratory tract (URT) and is self-limiting. However, a small percentage progresses to lower respiratory tract infections (LRTI). The most important causative agents of severe LRTIs are bacteria and viruses. Various viruses can cause respiratory tract infections, being the most essential belonging to the Orthomyxoviridae, Paramyxoviridae, Picornaviridae, coronaviruses, and adenoviruses. Quercetin is classified as a flavonoid compound and was previously known to have antiviral, antibacterial, antioxidant, and anti-inflammatory activities. Some preclinical studies highlight quercetin could also interfere with coronavirus infection and modulate the release of pro-inflammatory cytokines. Since there is no comprehensive compilation addressing the antiviral activities of quercetin and its derivatives, this narrative review provides a summary of the preclinical evidence of their antiviral activities on respiratory illnesses induced by viruses other than coronaviruses. The literature research was performed in PubMed, Scopus, and Google Scholar. The results explain that quercetin has a wide range of actions in viral-induced respiratory illnesses including, but not limited to suppressing pro-inflammatory cytokines and chemokines, promoting antioxidant-related genes expression, blocking viral entry and replication, accelerating viral clearance, reducing the accumulation of alveolar macrophages, and reducing goblet cells marker and mucin gene expression.

Introduction: Fahr’s syndrome (FS) is a rare neurodegenerative disorder characterized by bilateral and symmetrical calcification of basal ganglia and other brain structures. In contrast to Fahr’s disease, FS is distinguished by the association of secondary etiology. The diagnosis is confirmed by neuroimaging studies such as a head computer tomography (CT) scan or magnetic resonance imaging, which displays the calcification of basal ganglia and other structures in a bilateral and symmetrical pattern. Case Report: A 63-year-old female with a previous history of total thyroidectomy and ischemic stroke presented to our hospital with altered mentation and recurrent generalized tonic-clonic seizures. Laboratory evaluation revealed hypocalcemia, hypokalemia, and hypoparathyroidism. Imaging with head CT was consistent with FS, demonstrating bilateral, symmetrical, and extensive calcification of basal ganglia, corona radiata, and cerebellar hemispheres with ventricular enlargement. Conclusion: Our case represents a long-term consequence of untreated post-surgical hypoparathyroidism, which led to secondary FS. Long-term hypocalcemia and low calcium/phosphate ratio are associated with basal ganglia calcification in patients with hypoparathyroidism. Maintenance of eucalcemic and euphosphatemic state is essential as the preventive measure for metastatic calcification. There is currently no definitive treatment for FS, with adjunctive symptomatic treatments to reduce the clinical manifestations.

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Aim: To describe a rare case of Fahr’s syndrome (FS) associated with chronic post-surgical hypoparathyroidism and hypocalcemia. Case Presentation: A 63-year-old female with a previous history of total thyroidectomy and hemiplegia presented to our hospital with altered mentation and recurrent generalized tonic-clonic seizures. Laboratory evaluation revealed hypoparathyroidism, hypocalcemia, and hypokalemia. Head computed tomography (CT) scan was consistent with FS, demonstrating extensive, bilateral, and symmetrical calcified deposits in the brain, predominantly in basal ganglia, corona radiata, and cerebellar hemispheres. The association with post-surgical hypoparathyroidism and relevant biochemical indices determined the suspected etiology of the pathologic process of ectopic calcification. Discussion: FS is a rare, neurodegenerative disorder characterized by abnormal bilateral ectopic calcified deposits in the basal ganglia and other brain structures. FS presents with a wide variety of neurological and psychiatric manifestations. The diagnosis is confirmed by neuroimaging studies such as a head CT scan or magnetic resonance imaging, which displays the calcification of BG and other structures in a bilateral and symmetrical pattern. Biochemical analysis may adjunctively identify the underlying risk factor of the disease. Conclusion: Our case represents a long-term severe consequence of untreated post-surgical hypoparathyroidism, which has consequently led to irreversible secondary FS. Maintenance of eucalcemic and euphosphatemic states is essential to prevent the progression of ectopic cerebral calcification.