Eh. Hwang et al., ABSENT MYOCARDIAL IODINE-123-BMIPP UPTAKE AND PLATELET MONOCYTE CD36 DEFICIENCY/, The Journal of nuclear medicine, 39(10), 1998, pp. 1681-1684
Global absence of myocardial I-123-15-(p-iodophenyl)-3-(R,S)-methyl pe
ntadecanoic 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, m
ay contribute to myocardial fatty acid transport, and its deficiency h
as 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 patient
s with absent myocardial BMIPP uptake. Methods: Peripheral blood of 7
patients with global absence of myocardial BMIPP uptake (3 of 7 patien
ts in one family) and 3 control subjects were examined in flow cytomet
ric analysis. Platelet/monocyte surface CD36 was detected by using OKM
5, an anti-CD36 mouse monoclonal antibody. Results: There were no appa
rent relationships between specific clinical symptoms and absent myoca
rdial BMIPP uptake. None of the blood samples of the 7 patients were s
tained with OKM5 on the platelet/monocyte cell surface, indicating tha
t all of these patients were Type I CD36-deficient subjects. In contra
st, all the control subjects showed normal staining. Conclusion: The f
act 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.