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Clinical Chemistry, Vol 21, 582-587, Copyright © 1975 by the American Association for Clinical Chemistry
1 Department of Medicine, Wayne State University, Detroit General Hospital, Grace Hospital, Detroit; the V. A. Hospital, Allen
Park; and the Department of Human Genetics, University of
Michigan, Ann Arbor, Mich..
Clinical similarities between patients with sickle cell anemia and zinc-deficient subjects suggested a secondary zinc deficiency in sickle cell anemia. Zinc was assayed in various biological fluids and tissues by atomic absorption spectrophotometry. Zinc in the plasma, erythrocytes, and hair was decreased and urinary zinc excretion was increased in anemia patients as compared to controls. Erythrocyte zinc and daily urinary zinc excretion were inversely correlated in the anemia patients (r = -.63, P < 0.05), suggesting that hyperzincuria may have caused zinc deficiency in these patients. Carbonic anhydrase, a zinc metalloenzyme, correlated significantly with erythrocyte zinc (r = +0.94, P < 0.001). Plasma RNase activity was significantly greater in anemia subjects than in controls. We administered zinc sulfate, 660 mg per day, orally, to seven men and two women with sickle cell anemia. Two 17-year-old males gained 5 cm and 7 cm in height during 49 and 42 weeks of zinc therapy, respectively. All but one patient gained weight (0.5 kg to 4.1 kg). Five of the males showed increased growth of pubic, axillary, facial, and body hair, and in one a leg ulcer healed in six weeks on zinc and in two others some benefit of zinc therapy on healing of ulcers was noted.
Submitted on October 2, 1974
Accepted on January 29, 1975
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