**Core Concept**
Wilson's disease is a genetic disorder characterized by impaired copper excretion due to mutations in the ATP7A gene, leading to copper accumulation in the liver, brain, and kidneys. It is caused by defective copper transport and metabolism, resulting in copper toxicity despite normal or low serum ceruloplasmin levels.

**Why the Correct Answer is Right**
In Wilson's disease, urinary copper excretion is typically **elevated**, not reduced. The normal value is usually >100 µg/day, and in patients with Wilson’s disease, it often exceeds 100 µg/day due to impaired biliary excretion and increased renal copper retention. Thus, stating urinary copper excretion <100 µg/day is false and represents the exception. The disease is autosomal recessive (A), serum ceruloplasmin is usually <20 mg/dL (B), and zinc acetate therapy is used to inhibit copper absorption in maintenance (D).

**Why Each Wrong Option is Incorrect**
Option A: Incorrect because Wilson’s disease is indeed autosomal recessive, not dominant or X-linked.
Option B: Incorrect because serum ceruloplasmin is typically reduced (<20 mg/dL) in Wilson’s disease due to impaired copper binding.
Option D: Incorrect because zinc acetate is used as maintenance therapy to block copper absorption in the gut, especially in patients with normal or mildly reduced ceruloplasmin.

**Clinical Pearl / High-Yield Fact**
Remember: **Low ceruloplasmin + high urinary copper = Wilson’s disease**. A key exam trap is that urinary copper is *increased*, not decreased — this is the most common mistake.

✓ Correct Answer: C. Urinary copper excretion < 100 µg/day