IMMUNOHISTOCHEMICAL ANALYSIS OF LYMPHOCYTES IN POSTMORTEM STUDY OF THE HEART FROM FATAL CASES OF THE EOSINOPHILIA-MYALGIA-SYNDROME AND OF THE TOXIC OIL SYNDROME

Citation
T. Hayashi et Tn. James, IMMUNOHISTOCHEMICAL ANALYSIS OF LYMPHOCYTES IN POSTMORTEM STUDY OF THE HEART FROM FATAL CASES OF THE EOSINOPHILIA-MYALGIA-SYNDROME AND OF THE TOXIC OIL SYNDROME, The American heart journal, 127(5), 1994, pp. 1298-1308
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00028703
Volume
127
Issue
5
Year of publication
1994
Pages
1298 - 1308
Database
ISI
SICI code
0002-8703(1994)127:5<1298:IAOLIP>2.0.ZU;2-X
Abstract
Inflammatory lesions of coronary arteries and cardiac neural structure s are postmortem histopathologic features of both the eosinophilia-mya lgia syndrome (EMS) and the toxic oil syndrome (TOS). The inflammation is primarily lymphocytic. For further definition of the lymphocytes, immunohistochemical analysis was carried out in the hearts of three vi ctims of EMS and four victims of TOS. Many CD45RO+ T cells, OPD4+ help er/inducer T (Th) cells, and CD20+ B cells were observed in these neur ovascular lesions, notably in the conduction system and the coronary c hemoreceptor. T cells were prominent in EMS around nerves, ganglia, an d sometimes around arteries. B cells and Th cells, however, were more prominent in TOS around arteries. The percentage of T cells in EMS (59 .6 +/- 2.4%) was significantly higher than in TOS (45.0 +/- 4.2%), whe reas that of B cells was significantly higher in TOS (27.7 +/- 4.4%) t han in EMS (17.5 +/- 1.3%) (p < 0.01, respectively). There was no sign ificant difference between the syndromes in the percentages of Th cell s. Therefore cytotoxic/suppressor T cells are more prominent in EMS th an in TOS. These findings suggest that (1) cellular immune mechanisms are involved in cardioneuropathy in victims of both EMS and TOS; (2) c ell-mediated cytotoxicity directed against chemoreceptor neural struct ures and sinus nodal myocytes is prominent in EMS; and (3) some humora l factors may also be involved in the pathogenesis of TOS.