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Mutation in the ATP7A gene may not be responsible for hypocupraemia in copper deficiency myelopathy

¹ Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA
² Department of Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic

Correspondence to:
Correspondence to:
Dr N Kumar
Department of Neurology, Mayo Clinic Bldg E-8 A, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN 55905, USA; kumar.neeraj@mayo.edu

Submitted 16 November 2005
Accepted 3 January 2006

Keywords: copper; myelopathy; ATP7A

The first 150 words of the full text of this article appear below.

The identified causes of copper deficiency in patients with copper deficiency myelopathy have included excessive consumption of zinc, a malabsorption syndrome, or a history of gastric surgery.¹ Not uncommonly the cause of copper deficiency has been unclear. We have recently reported on two patients with idiopathic hypocupraemic myelopathy who had increased copper content in biopsy specimens of the colonic mucosa.² This finding suggests impaired mobilisation of copper absorbed by intestinal epithelial cells as the probable defect in these patients. Increased copper content in the intestinal mucosa is well recognised in Menkes disease,³ the genetic basis for which are mutations in the ATP7A gene. Molecular defects at the ATP7A locus resulting in milder forms of the disease have also been described.⁴

To pursue the possibility that the hypocupraemia in idiopathic hypocupraemic myelopathy may relate to mutations in the ATP7A gene we undertook mutation analysis in one of our patients. Details of . . . [Full text of this article]

This article has been cited by other articles:

				N. Kumar Copper Deficiency Myelopathy (Human Swayback) Mayo Clin. Proc., October 1, 2006; 81(10): 1371 - 1384. [Abstract] [Full Text] [PDF]