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Effect of Triiodothyronine on Serum Copper and Basal Metabolism in Schizophrenic PatientsCorrelations with Serum p-Phenylenediamine Oxidase, Erythrocyte Sedimentation, and C-Reactive Protein
B. J. MEYER, M.B., Ph.D.;
A. C. MEYER, Ph.D.;
M. K. HORWITT, Ph.D.
AMA Arch Gen Psychiatry 1959;1(4):372-378.
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Copper, an essential trace element in the body, is associated with several enzyme systems.1 In the blood, copper is about equally distributed between the erythrocytes and the plasma. Over 90% of the plasma copper is bound to globulin.2 This copperprotein (ceruloplasmin) catalyzes the oxidation of p-phenylenediamine compounds (ppd), a property which has been employed to estimate the ceruloplasmin level in serum.3 Although serum ceruloplasmin is affected by a wide variety of stressers, it is relatively constant in unstressed mammals. The mechanisms responsible for this copper homeostasis are only partially understood. However, there are indications that various hormones may be implicated.4-8 According to Narasaka,4-6 the injection of thyroxine effects an increase in the serum copper of rabbits. Similarly, various workers reported high serum copper levels in hyperthyroid patients.4,9,10 Kasanen and Viitanen 11 studied a relatively large number of thyrotoxic patients and concluded that
. . . [Full Text PDF of this Article]
Author Affiliations
Elgin, Ill.
Biochemical Research Laboratory, Elgin State Hospital.
Footnotes
Submitted for publication Feb. 9, 1959.
Supported by grants-in-aid from the Illinois Mental Health Fund and the National Institutes of Health (A-1126-C1).
Dose was calculated as content of L-triiodothyronine in the racemic form of triiodothyronine (Trionine), as supplied by Hoffmann-La Roche, Inc., Nutley, N. J.
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