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Pharmacokinetics and Metabolism of ¹²³I-BMIPP Fatty Acid Analog in Healthy and CD36-Deficient Subjects

Division of Radiology, Minoh City Hospital, Minoh
Second Department of Internal Medicine and Division of Tracer Kinetics, Biomedical Research Center, Osaka University Medical School, Suita, Japan

Correspondence: For correspondence or reprints contact Tohru Yoshizumi, Division of Radiology, Minoh City Hospital, Kayano 5-7-1, Minoh City, Osaka, 562-8562, Japan.

ABSTRACT

Some have suggested that CD36, which is a multifunctional receptor with a molecular weight of 88 kDa, functions as a long-chain fatty acid (LCFA) transporter. We recently reported on a complete myocardial accumulation defect of the radiolabeled LCFA analog ¹²³I-15-(p-iodophenyl)-(R,S)-methylpentadecanoic acid (BMIPP) in patients with CD36 deficiency. In this study, we investigated the pharmacokinetics of BMIPP in patients with a myocardial accumulation defect of BMIPP accompanied by CD36 deficiency. Methods: Five patients (3 men, 2 women) with CD36 deficiency and 3 healthy men were investigated. Serial myocardial images were obtained every 70 s for 20 min (dynamic acquisition) and at 30, 60, 120, 180, and 240 min (static acquisition) after an intravenous bolus injection of 148 MBq BMIPP. Whole-body imaging was performed 60 min after injection. Plasma levels of BMIPP and its final metabolite, p-iodophenylacetic acid, at 2,5,10,30, 60,120, and 240 min after administration were determined. Results: In the CD36-deficient patients, myocardial images could not be obtained for up to 240 min after administration, and cardiac pool images showing only the cardiac chambers were obtained. The heart-to-mediastinum ratio was significantly lower in the CD36-deficient patients than in the healthy volunteers (1.71 ± 0.11 versus 2.95 ± 0.22, P < 0.05). Hepatic uptake of BMIPP was nearly double in CD36-deficient patients. The elimination of BMIPP from the circulation was retarded in the CD36-deficient patients. Conclusion: We suggest that CD36 deficiency leads to decreased myocardial accumulation of BMIPP and retardation of BMIPP elimination from the circulation. The accumulation defect is probably caused by a defect in LCFA uptake into the myocardium through CD36.

Key Words: CD36 deficiency • ¹²³I-BMIPP • long-chain fatty acids • myocardium

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