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Absent Myocardial Iodine-¹²³I-BMIPP Uptake and Platelet/Monocyte CD36 Deficiency

Department of Nuclear Medicine, Kanazawa University School of Medicine, Kanazawa; Division of Blood Transfusion, Kanazawa University Hospital, Kanazawa, Cardiovascular Center, Tsuruga City Hospital; Tsuruga, Japan

Correspondence: For correspondence or reprints contact: Eui-Hyo Hwang, MD, Department of Nuclear Medicine, Kanazawa University School of Medicine, 13-1 Takaramachi, Kanazawa 920-8640, Japan.

ABSTRACT

Global absence of myocardial ¹²³I-15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid (BMIPP) uptake is occasionally noted, and it reflects myocardial long-chain fatty acid uptake abnormality. CD36, a membrane glycoprotein expressed on platelet, monocyte and endothelial cells, may contribute to myocardial fatty acid transport, and its deficiency has been reported in a small subset of the population. We hypothesized that CD36 deficiency may be related to absent myocardial BMIPP uptake. Thus, we investigated CD36 expression of platelet/monocyte in patients with absent myocardial BMIPP uptake. Methods: Peripheral blood of 7 patients with global absence of myocardial BMIPP uptake (3 of 7 patients in one family) and 3 control subjects were examined in flow cytometric analysis. Platelet/monocyte surface CD36 was detected by using 0KM5, an anti-CD36 mouse monoclonal antibody. Results:There were no apparent relationships between specific clinical symptoms and absent myocardial BMIPP uptake. None of the blood samples of the 7 patients were stained with 0KM5 on the platelet/monocyte cell surface, indicating that all of these patients were Type I CD36-deficient subjects. In contrast, all the control subjects showed normal staining. Conclusion:The fact that rare Type I CD36 deficiency was observed in all patients with absent myocardial BMIPP uptake suggests that CD36 plays a role in the myocardial long-chain fatty acid uptake process in humans.

Key Words: 15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid • family • CD36 deficiency

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