What laboratory finding would best support a diagnosis of Wilson's disease in a 30-year-old woman with tremor and hepatomegaly?

In Wilson's disease, the body fails to properly eliminate copper, leading to copper accumulation in various tissues, particularly the liver and brain. A key feature of this condition involves the synthesis and transport of copper within the body. Normally, copper is incorporated into caeruloplasmin, which is the principal copper-carrying protein in the blood.

In Wilson's disease, due to the inability to incorporate copper into caeruloplasmin effectively, there tends to be a significant decrease in serum caeruloplasmin levels. Therefore, finding a low serum caeruloplasmin concentration is a strong indicator supporting the diagnosis of Wilson's disease in a patient presenting with neurological and hepatic symptoms, as it reflects the disrupted metabolism and accumulation of copper.

The other options do not align with the characteristic biochemical disturbances seen in Wilson's disease. For instance, an increased incorporation of copper into caeruloplasmin would suggest normal copper metabolism, which is not the case in Wilson's disease. Low hepatic copper content would be atypical since patients typically have increased copper levels in the liver due to impaired excretion. A low urine copper concentration is also misleading, as Wilson's disease often results in increased urinary copper excretion once the liver becomes saturated with copper. Thus, the low