John,
The (normal) 24h urine copper excretion is higher than we've encountered in Sheffield in patients with 'true' copper deficiency (e.g. gastrectomy, zinc salts) with serum coppers ~ 2 umol/L or less. This patient's serum copper and caeruloplasmin, Cp are only marginally low, certainly consistent with alcohol-related liver disease (prothrombin time, fibrinogen?). Other less common differentials would include heterozygosity for an ATP7B or CP mutation (of no clinical significance for the individual, and not worth pursuing unless the patient were interested to have Cp checked in siblings/children).
Did the consultant recommend any 'treatment' for the presumed deficiency? More of the copper-rich foods patients with WD are asked to avoid? It is quite difficult to become copper deficient on an average UK diet (in the absence of malabsorbtion).
Bws,
Godfrey Gillett
NGH, Sheffield; UCLH WD Clinic.
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