Key result
Telmisartan treatment for 20 weeks dose-dependently increased 18F-FDG levels in the blood of mice (0.15 vs 0.09 in high-dose vs control, P<0.0083), which reversed 3 weeks after cessation.
Why the study?
Does telmisartan alter 18F-FDG biodistribution and renal excretion in male C57BL/6J mice?
Does telmisartan alter 18F-FDG biodistribution and renal excretion in male C57BL/6J mice?
Telmisartan treatment significantly increases 18F-FDG levels in blood and organs in mice, suggesting a potential increase in background activity on PET imaging in patients treated with ARBs.
Potential ARB interference with 18F-FDG PET warrants imaging caution; leaves open translation from mice to patients.
UNLABELLED: Angiotensin II receptor blockers (ARBs) are a common treatment for hypertensive patients but affect renal function. In this study, the effects of ARB on (18)F-FDG distribution and excretion were examined in mice treated with telmisartan at different doses. METHODS: Male C57BL/6J mice were given telmisartan (low-dose group, 0.33 mg/kg/d; moderate-dose group, 0.66 mg/kg/d; high-dose group, 3 mg/kg/d) mixed in a high-fat diet for 20 wk. Mice on a telmisartan-free diet served as the control. At designated time points, the mice were injected with (18)F-FDG (18.5 MBq/mouse, n = 5-10/time point for each group) to examine its biodistribution. Autoradiography using kidney sections was performed to visualize (18)F-FDG excretion. Plasma blood urea nitrogen (BUN) and creatinine levels were also measured to evaluate renal function. RESULTS: Twenty-week telmisartan treatment significantly and dose-dependently increased (18)F-FDG levels in the blood (percentage injected dose per gram of tissue normalized by animal body weight: low, 0.13 ± 0.03 [P < 0.0083]; moderate, 0.15 ± 0.01 [P < 0.0083]; high, 0.15 ± 0.03 [P < 0.0083], vs. control, 0.09 ± 0.01). Significantly increased (18)F-FDG levels in organs were observed in mice in the moderate- and high-dose groups but not in the low-dose group. The plasma BUN and creatinine levels also dose-dependently increased, but they were within the reference ranges (for BUN: low, 27.00 ± 4.42 mg/dL; moderate, 28.40 ± 2.70 mg/dL; high, 39.22 ± 6.91 mg/dL [P < 0.0083], vs. control, 22.40 ± 2.80 mg/dL. For creatinine: low, 0.28 ± 0.11 mg/dL; moderate, 0.40 ± 0.07 mg/dL [P < 0.0083]; high, 0.51 ± 0.09 mg/dL [P < 0.0083], vs. control, 0.18 ± 0.04 mg/dL). The blood (18)F-FDG level positively correlated with plasma BUN (r = 0.48, P < 0.01) and creatinine (r = 0.61, P < 0.01) levels. The (18)F-FDG levels in the blood and organs returned to baseline 3 wk after cessation of telmisartan treatment. Autoradiography indicated that renal (18)F-FDG excretion was attenuated by telmisartan treatment and was reversed after treatment cessation. CONCLUSION: (18)F-FDG levels in the blood and organs were significantly increased by telmisartan treatment, indicating a potential increase in background activity on PET imaging of patients treated with ARBs. Our findings indicate the need for a careful assessment of (18)F-FDG uptake in patients treated with ARBs. A brief cessation of ARB treatment may be a potential method to avoid these effects and solve this problem.
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Zhao et al. (2013) studied this question. Telmisartan vs. Telmisartan-free diet was evaluated on 18F-FDG levels in the blood (p=<0.0083). Telmisartan treatment for 20 weeks dose-dependently increased 18F-FDG levels in the blood of mice (0.15 vs 0.09 in high-dose vs control, P<0.0083), which reversed 3 weeks after cessation.
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