BACKGROUND: Copper deficiency leads to hematologic disorders like pancytopenia. In addition, myeloneuropathy was described in a few cases reports. CASE REPORT: A 71-year-old woman was hospitalized because of increasing pancytopenia and ataxic gait, that resulted in a near-complete inability to walk without assistance. Additional symptoms included arthralgia, reduced appetite and weight loss. Laboratory studies revealed a proteinuria of 3,700 mg/day. Magnetic resonance imaging of the cervical and thoracic spine revealed a wedge-shaped signal intensity in the dorsal part as a sign of damage in this area. A copper deficiency was then identified as the likely underlying cause for the low blood cell counts and neurologic deficits. In this patient, the copper deficiency may have resulted from a disturbance in absorption due to a partial gastrectomy (modified Billroth I) 10 years ago and due to urinary copper loss in view of mesangioproliferative glomerulonephritis. A therapy with copper gluconate 3 x 3 mg/day was initiated. Within 2 weeks, blood cell counts normalized and appetite became normal again; just so, arthralgia disappeared. The neurologic symptoms persisted, even though the copper substitution continued for 6 months. CONCLUSION: Copper deficiency may be a differential diagnosis for hematologic abnormalities like pancytopenia, even if a disorder of intestinal resorption or a proteinuria occurs. Myeloneuropathy is a rare complication of this deficiency. Hemograms may become normal after treatment with oral copper gluconate, but at least in the case presented here, neurologic symptomes did not show any improvement.
BACKGROUND:Copper deficiency leads to hematologic disorders like pancytopenia. In addition, myeloneuropathy was described in a few cases reports. CASE REPORT: A 71-year-old woman was hospitalized because of increasing pancytopenia and ataxic gait, that resulted in a near-complete inability to walk without assistance. Additional symptoms included arthralgia, reduced appetite and weight loss. Laboratory studies revealed a proteinuria of 3,700 mg/day. Magnetic resonance imaging of the cervical and thoracic spine revealed a wedge-shaped signal intensity in the dorsal part as a sign of damage in this area. A copper deficiency was then identified as the likely underlying cause for the low blood cell counts and neurologic deficits. In this patient, the copper deficiency may have resulted from a disturbance in absorption due to a partial gastrectomy (modified Billroth I) 10 years ago and due to urinary copper loss in view of mesangioproliferative glomerulonephritis. A therapy with copper gluconate 3 x 3 mg/day was initiated. Within 2 weeks, blood cell counts normalized and appetite became normal again; just so, arthralgia disappeared. The neurologic symptoms persisted, even though the copper substitution continued for 6 months. CONCLUSION:Copper deficiency may be a differential diagnosis for hematologic abnormalities like pancytopenia, even if a disorder of intestinal resorption or a proteinuria occurs. Myeloneuropathy is a rare complication of this deficiency. Hemograms may become normal after treatment with oral copper gluconate, but at least in the case presented here, neurologic symptomes did not show any improvement.