Therapeutic prospects and challenges in the human genetic disorder hyperbiliverdinemia

Abstract

The epidermis, sclera, urine, and other bodily fluids have a greenish tint in hyperbiliverdinemia, a rare hepatic condition. Increased biliverdin as a result of ineffective conversion to bilirubin is the known explanation behind the onset of this disorder. The conversion of the bile pigment biliverdin to bilirubin is catalyzed by the oxidoreductase enzyme biliverdin reductase IX-α. Based on a case study, the development of hyperbiliverdinemia is reportedly caused by a novel mutation in the gene (BVRA) that encodes the protein biliverdin reductase A (enzyme) paired with a decompensated liver. Those who have been affected do not seem to experience symptoms outside of obstructive cholestasis; sometimes it is accompanied by liver failure; however, in some reports, liver failure is the only symptom faced by the affected individual. According to case reports, green jaundice occasionally goes away once obstructive cholestasis becomes resolved. This review examines jaundice, including its etiology, symptoms, and concomitant disease processes, with a focus on hyperbiliverdinemia, popularly known as “green jaundice.” Significant information regarding the therapeutics and treatment of jaundice, such as that of phototherapy and exchange transfusion, has also been discussed. Currently, there is no specific treatment for hyperbiliverdinemia; however, treating the symptoms of this disease seems to improve the affected individual's condition.