Case Presentation:

This was a 42–year–old Caucasian female with history of alcohol–induced cirrhosis, Roux–en–Y gastric bypass surgery who presented to the hospital for generalized weakness and severe rash. She developed symmetrical weakness in her lower extremities over several weeks. She was unable to walk after 2 weeks of the onset. She noted symmetrical numbness and tingling in both feet and hands. She also suffered from a pruritic rash on her arms that got generalized over a few days. She denied any new medications that have been started in the last few months, or any new exposures. Her home medications were bumex, lactulose and spironolactone. Her neurological examination was consistent with polyneuropathy. She had decreased muscle bulk of her intrinsic muscles of both hands. Muscle tone was normal. Strength was significantly reduced at the hip flexors and she was unable to fully dorsiflex either foot. Her reflexes were absent throughout. Gradient of distal light touch and pinprick sensation deficit up to the mid shin level was noticed. Proprioception was absent at the toes. Blanchable diffuse large erythematous patches were appreciated on her chest, abdomen, back and extremities. Electromyography and nerve conducting study were not obtained due to the severity of her skin disease. Her complete blood count and comprehensive metabolic panel were unremarkable except of chronically elevated bilirubin and mild normocytic anemia. TSH, creatine phosphokinase, hemoglobin A1C, methylmalonic acid vitamin B12, B1 and B3 levels were normal. Infectious work up including testing for HIV and viral hepatitis was unrevealing. Inflammatory markers and anti–nuclear antibody were unremarkable. Serum protein electrophoresis with immunofixation was normal. Copper and zinc levels were severely low. Skin bx showed subacute eczematous dermatitis that was likely caused by Zinc deficiency.

Discussion:

Copper deficiency is an uncommon cause of polyneuropathy. Copper is absorbed in the stomach and proximal small intestine. This makes gastric bypass surgery a major risk factor for its deficiency. Perphiral neropathy, spastic gait and sensory ataxia are common presentations. Other manifestations include anemia, neutropenia, thrombocytopenia, pancytopneia, optic neuropathy and myopathy. Treatment results typically in complete reversal of anemia and neutropenia. However, residual neurologic deficits may remain.

Conclusions:

Copper deficiency should be considered in patients with a history of gastric bypass surgery and neuropathy or new neurologic symptoms. Hospitalists should be familiar with the signs and symptoms of trace element deficiency caused by malabsorptive gastrointestinal surgeries.