Key result
ACE inhibitors significantly deplete intramonocytic zinc and enhance urinary zinc excretion in hypertensive patients.
Why the study?
The effect of chronic captopril and enalapril treatment on zinc metabolism in hypertensive patients was not well understood.
RCT (n=44)
randomly divided
p-value: p=<0.01
May warrant zinc monitoring with chronic ACE inhibitor use; leaves open need for trials on deficiency prevention in hypertension.
OBJECTIVE: To investigate the effect of chronic captopril and enalapril treatment on zinc metabolism in hypertensive patients by assessing zinc levels in serum, urine and monocytes. METHODS: Patients with newly diagnosed essential hypertension were randomly divided into two treatment groups: those treated with captopril only (n = 16) and those treated with enalapril only (n = 18). Ten healthy subjects served as controls. Prior to the start of treatment and again 6 months later, zinc was assessed in the serum, in urine collected over 24 hours, and in peripheral blood monocytes. RESULTS: Significant enhancement of 24-hour urinary zinc excretion (micrograms/24 hour) after 6 months of treatment was observed only in the captopril-treated group (p < 0.01). However, intramonocytic zinc levels decreased significantly in both of the treated groups over the same period (p < 0.01 and P < 0.04 in the captopril- and enalapril-treated groups, respectively). CONCLUSION: Treatment of hypertensive patients with captopril or enalapril may result in zinc deficiency.
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Golik et al. (1998) conducted an RCT in Essential hypertension (n=44). Captopril and Enalapril vs. Healthy subjects was evaluated on Zinc levels in serum, 24-hour urine, and peripheral blood monocytes (p=<0.01). Six months of captopril or enalapril significantly decreased intramonocytic zinc levels (P<0.01 and P<0.04), and captopril enhanced urinary zinc excretion (P<0.01) in hypertensive patients.
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