Ceruloplasmin, a crucial copper-carrying protein synthesized by the liver, plays a pivotal role in maintaining copper balance within the body. Responsible for transporting 65% to 90% of blood copper, ceruloplasmin facilitates essential physiological processes like bone development and melanin production. However, an imbalance in copper levels, as seen in conditions like Wilson disease—a rare genetic disorder—disrupts this equilibrium. In individuals with Wilson disease, the liver fails to incorporate copper into ceruloplasmin, leading to an accumulation of excess copper in the bloodstream. This surplus copper, if left untreated, can result in severe damage to vital organs such as the liver, brain, corneas, kidneys, and bones. The insidious progression of copper poisoning underscores the critical importance of timely diagnosis and intervention. To manage Wilson disease effectively, individuals are advised to avoid copper-rich foods such as liver, shellfish, mushrooms, nuts, and chocolate, while also steering clear of copper-containing dietary supplements. Additionally, testing drinking water for copper levels is recommended to further mitigate potential sources of exposure. Early detection and adherence to dietary restrictions are imperative to prevent the potentially fatal consequences of untreated Wilson disease.
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