Shuzo Hirakawa

HAEMOPHAGOCYTIC SYNDROME TREATED WITH CYCLOSPORIN A: A T CELL DISORDER?

abnormal cells were CD4 + , in one case CD8 + and in four cases could be detected in both cellular subsets. Specific antibodies against CMV, HBV, EBV, HV and HTLV-I were not detected in any of these cases. The presence of atypical lymphoid cells (multilobated nuclei) can have several causes. In the case we report here, the coincidental occurrence of an adult T-cell leukaemia/ lymphoma can be ruled out by the negativity of the HTLV-I antibodies test. The presence of nuclear multilobation in the 28.6% of HIVf patients further rules out this possibility. Regarding the remarkable case described above (360 x 10’ multilobated cells per litre), the cytological picture could be attributed to the passage to peripheral blood of multilobatedcell type lymphoma cells (Pinkus’ lymphoma) (Cerezo, 1983). However, the lymph node biopsy disclosed Kaposi’s sarcoma and absence of lymphoproliferative disease. It seems also improbable that an infection by a known virus could account for the nuclear abnormalities as it has been recently described in infectious mononucleosis (Inoue, 1989). In our case the blood picture could have been due to other rarer assymptomatic viral or bacterial infections. The only positive antibody test was that for syphilis, but this disease does not normally produce this type of cellular alteration. It has also been described that keeping the blood in EDTA containing tubes can result in this particular kind of artefact (Bessis, 1972). In our cases, however, blood smears were done immediately after the blood sample was withdrawn, so the possibility of an artefact seems very improbable. We would like to propose that, at least in some cases, HIV infection per se can produce these abnormalities of the nuclear shape in peripheral blood lymphocytes, although other viral diseases cannot definitely be excluded on the basis of a negative serology in the context of AIDS. Further studies are therefore necessary to rule out the presence of genomic proteins of other types of retrovirus at intracellular level in these HIV+ patients.