Thelansis

 Wilson Disease (WD) is an inherited disorder characterized by an abnormality in copper metabolism. It results from specific mutations in the ATP7B gene, which encodes a protein called ATP7B responsible for copper transportation and regulation. This gene mutation can occur as homozygous or compounds heterozygous mutations. ATP7B plays a vital role in excreting excess copper into bile and facilitating the synthesis of ceruloplasmin, a key copper-transporting protein in the bloodstream. The liver serves as the primary site for managing dietary copper, and in individuals with WD, impaired ATP7B function leads to copper accumulation within liver cells, causing liver-related issues. ·        The prevalence of Wilson's disease varies across regions, with around 31 to 37 cases per 100,000 individuals in EU countries, 48 to 59 cases in the USA, and 33 cases per 1,000,000 individuals in Japan.   Thelansis’s “Wilson Disease (WD) Market Outlook, Epidem...

 Wilson Disease (WD) is an inherited disorder of copper metabolism. The disease is caused by homozygous or compounds heterozygous mutations (the presence of two different mutant alleles) in ATP7B, which encodes transmembrane copper-transporting ATPase 2 (widely known as ATP7B), which mediates the excretion of copper into bile and delivers copper for the functional synthesis of ceruloplasmin (the major copper-transporting protein in the blood) diagnostic methods, ideal treatment regimens, efficacy evaluation standards and prognostic indicators for NPC. The liver is the site of metabolism for dietary copper; in WD, defective ATP7B function leads to copper overload in hepatocytes, which is associated with liver pathology. ·        Wilson disease (WD) prevalence ranges between 31 to 37 cases per 1,00,000 individuals in EU countries, 48 to 59 cases in the USA, and 33 cases per 1,000,000 individuals in Japan. ·        The gl...