Parviz Rabbani

Experimental zinc deficiency in humans.

Abstract The effects of a mild zinc-deficient state in humans were studied. Four male volunteers received restricted zinc intake for several weeks under strict metabolic conditions. As a result of ...

Oral Zinc Therapy for Wilson's Disease

Wilsons disease is an inherited disorder of copper accumulation that is fatal if untreated. Because penicillamine, the established treatment, is toxic in a substantial number of patients, we studied the efficacy of zinc treatment. We induced a negative or neutral copper balance in five out of five patients with Wilsons disease who were receiving no therapy other than zinc. Zinc acetate was given every 4 hours during the day, and the patient was not allowed to eat for 1 hour before and 1 hour after each dose. Oral zinc therapy, used according to our regimen, may now be considered in the treatment of patients with penicillamine intolerance. However, it is premature to convert patients to zinc therapy if they tolerate penicillamine well. The efficacy of zinc therapy in the initial removal of the copper burden in acutely ill patients with Wilsons disease has not yet been evaluated.

Effect of Oral Zinc Therapy on Gonadal Function in Hemodialysis Patients: A Double-Blind Study

Zinc deficiency may account for the persistence of gonadal dysfunction in a majority of uremic men despite adequate dialysis. Twenty stable patients having hemodialysis three times a week completed a double-blind trial using either 50 mg of elemental zinc as zinc acetate (10 patients) or placebo (10 patients), orally. At the end of the 6-month study period, a significant increase in the mean (+/- SE) plasma zinc (75 +/- 2 micrograms/dL to 100 +/- 2 micrograms/dL, p less than 0.001), serum testosterone (2.8 +/- 0.3 ng/dL to 5.2 +/- 0.5 ng/mL, p less than 0.001), and sperm count (30 +/- 3 million/mL to 63 +/- 5 million/mL, p less than 0.001) occurred in the zinc-treated group, but not in those receiving the placebo. The zinc-treated group also had a significant fall in serum luteinizing hormone (92 +2- 10 mIU/mL to 49 +/- 26 mIU/mL, p less than 0.005) and follicle stimulating hormone (45 +/- 9 mIU/mL to 25 +/- 7 mIU/mL, p less than 0.05), not seen in the placebo group. Patients receiving zinc had an improvement in potency, libido, and frequency of intercourse not found in the placebo group. These results suggest that zinc deficiency is a reversible cause of gonadal dysfunction in patients having regular hemodialysis.

Testicular androgen binding protein in zinc deficient rats

Abstract Zinc deficiency in rats and humans is characterized by an increase in serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and decrease in serum testosterone level and spermatogenesis. The possibility that an abnormality in the androgen binding protein may be responsible for decreased spermatogenesis in zinc deficiency was investigated. White male rats weighing approximately 220 gm were allotted to three groups: zinc-deficiency (Zn-D), Pair-fed (PF), and Ad-libitum fed controls (Ad-Lib). Androgen binding protein (ABP), total protein, testosterone, and dihydrotestosterone (DHT) were assayed in testicular cytosol by established techniques. Testosterone, DHT, and DHT binding protein sites per pair of testes were reduced in Zn-D in comparison to PF and Ad-Lib controls (p

Zinc treatment of Wilson's disease.

Excerpt To the editor: We are disturbed by some statements in the editorial by Dr. Deiss (1) in the issue in which our paper on zinc treatment of Wilsons disease (2) appeared. First, Dr. Deiss mis...