ABSENT MYOCARDIAL IODINE-123-BMIPP UPTAKE AND PLATELET MONOCYTE CD36 DEFICIENCY/

Citation
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
Citations number
36
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
ISSN journal
01615505
Volume
39
Issue
10
Year of publication
1998
Pages
1681 - 1684
Database
ISI
SICI code
0161-5505(1998)39:10<1681:AMIUAP>2.0.ZU;2-D
Abstract
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.