Fungal infection of the nail as well as nail bed is termed as ‘onychomycosis’. It is caused by dermatophytes, non-dermatophytic fungal species and yeasts like Candida albicans. It is traditionally treated by topical antifungals, systemic agents like ketoconazole, griseofulvin, itraconazole, fluconazole, etc. Chemical avulsion or surgical removal of nail can also be tried to treat this disease. In spite of all these treatment options available, podiatrists were always in search of an ideal drug molecule with lesser side effects and which may improve the patient compliance. This exhaustive search led to the discovery of a better antifungal agent, known as “Tavaborole.” A systematic literature search was carried out using databases such as PubMed, Cochrane Reviews, Google Scholar, etc. Detailed information about onychomycosis and tavaborole was gathered. Tavaborole is the first oxaborole antifungal agent approved by FDA in July 2014. It is marketed under the trade name “Kerydin.” It acts by inhibiting protein synthesis in the fungus. It inhibits an enzyme known as cytosolic leucyl-transfer RNA synthetase, or LeuRS, which plays a key role in fungal essential protein synthesis. Dermatitis at the site of topical application, erythema, exfoliation and ingrowing toe nail has been reported in 1% of subjects. Tavaborole may offer a promising role in the treatment of onychomycosis and may compell podiatrists to offer its use in onychomycosis. The present study describes about chemical nature, mechanism of action and two completed phase 3 clinical trial findings of Tavaborole.

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an x-linked recessive genetic disorder with mutation in the G6PD gene. Defect in the enzyme G6PD causes red blood cells (RBCs) to breakdown prematurely causing hemolytic anemia. Hemolytic anemia is also a known hematological complication associated with viral hepatitis. In such patients, hemolysis may be more severe if there is any secondary injury to RBC in the form of membrane defect, oxidative stress, or enzyme deficiency like in G6PD deficiency. Here, we present a case of an adult, not previously diagnosed with G6PD deficiency, who presented with viral hepatitis, severe hemolysis, and multiorgan failure.