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COMBINED ESTERASES IN ACUTE MYELOMONOCYTIC LEUKAEMIA

The finding by Scott et al (2983) of double esterase in bone marrow cells of patients with
myelodysplastic syndromes is of interest. This has previously been reported by our group
(Tavassoli et al, 1979) in patients with acute myelomonocytic leukaemia. When marrow
cells from patients with acute nonlymphoblastic leukaemias were sequentially stained for
naphthyl AS D chloracetate-reacting (chloracetate esterase, a granulocytic marker) and
a-naphthyl butyrate-reacting (nonspecific esterase, a monocytic marker) enzymes, three
groups could be identified: true granulocytic leukaemias stained only with chloracetate
esterase, pure monocytic leukaemia gave a positive reaction with a-naphthyl butyratereacting esterase, but in a third group, comprising almost half the patients, leukaemic cells
contained both esterases in the same cells in varied proportions. This group was felt to
represent true myelomonocytic leukaemia. We proposed combined esterase staining as the
basis for identification of myelomonocytic leukaemia. Compared to this cytochemical
method, Wright-Giemsa staining appears to over-estimate the incidence of myelomonocytic
leukaemia. In our experience, the double esterase-positive myelomonocytic leukaemia often
developson the background of a pre-existing myelodysplastic syndrome, a finding supporting
the work of Scott et al. Compared to this cytochemical method, Wright-Giemsa staining
appears to overestimate the incidence of myelomonocytic leukaemia.
I do not agree with Scott et al that these cells are pure granulocytes. To the contrary, the
presence of double esterase in a single cell supports the common origin of granulocytes and
monocytes and although the cells may lack some receptor characteristics of monocytes, this
is essentially a negative finding and could be attributed to dysplasia. It should not detract
from the fact that the esterase enzyme is truly monocyte-derived by biochemical analysis.
V A Medical Center,
University of Mississippi Medical Center,
Jackson, MS 39216. U.S.A.

MEHDITAVASSOLI

REFERENCES
S c m , C.S., CAHILL,A., BYNOE,A.G., AINLEY,M.J.,
HOUGH,D. & ROBERTS,B.E. (1983) Esterase
cytochemistry in primary myelodysplasticsyndromes and megaloblastic anaemias. British
Journal of Haematologg, 55, 4 1 1 4 1 8 .

TAVASSOLI,
M.. SHAKLAI.M. & CROSBY,W.H.
(1979) Cytochemical diagnosis of acute myelomonocytic leukemia. American Journal of Clinical Pathology, 72, 59-62.

AUTOIMMUNE HAEMOLYTIC ANAEMIA AND APLASTIC CRISIS

I read with interest the revision of Davis (1983) about the role of parvovirus in the aplastic
crisis in haemolytic anaemias. It has been demonstrated recently that the virus infects the
late erythroid progenitors, blocking in vitro erythroid colony formation (Young et al, 1984).
This mechanism could explain the aplastic crisis in children with congenital haemolytic
anaemias.

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179

Davis (1983) suggests that in adults with haemolytic anaemias and aplastic crisis it is
unlikely that parvovirus could have played a role in the development of aplasia.
I have had the opportunity to study two patients suffering from a n autoimmune
haemolytic anaemia who developed an aplastic crisis after several years of treatment with
immunosuppressive drugs. One of these cases has already been reported in detail (Celada et al,
1977).The bone marrow of these patients during the episode of reticulocytopenia, showed a
hyperplasia with a predominance of erythroid cells. Iron stains showed macrophages
containing abundant haemosiderin and 98% of erythroblasts in one and 80% in the other
patient showed typical features of ring sideroblasts.Despite treatment with corticoids, folate,
vitamins Blz and B6,as well as transfusions with type specific red cells when compatible blood
could be obtained, both patients died at 3 and 5 weeks, respectively, after the start of the
reticulocytopenia.
These observations as well as others previously reported (Buchanan et aZ, 1976: Conley et
al, 1982; Crosby & Rappaport, 1956; Harley L? Dods, 1959; Hegde et al, 1977; Seewann,
1979) show that in some patients with autoimmune haemolytic anaemia episodes of
unexplainable reticulocytopenia were associated with an intensively erythroid marrow. It
appears that some agent is able to block the late erythroid progenitors in these patients. At the
present there are no evidences for the role of a virus in the development of the aplastic crisis in
these immunosuppressed patients. However, a viral hypothesis needs to be considered and in
future cases the presence of agents like parvovirus needs to be evaluated.
Department of Immunology, I M M l 1 ,
Research Institute of Scripps Clinic,
1 0 6 6 6 North Torrey Pines Road,
La JoZZa, CaZi;fornin 9203 7 , U.S.A.

ANTONIOCELADA

REFERENCES
BUCHANAN,G.R., BOXER, L.A. & NATHAN, D.G.
(1976) The acute and transient nature of
idiopathic immune hemolytic anemia in childhood. Journal of Pediatrics. 88, 780-783.
CELADA,A.. FARQUET,J.J. 81MULLER,
A.F. (1977)
Refractory sideroblastic anaemia secondary to
autoimmune haemolytic anaemia. Acta Haematologica. 58, 2 13-2 16.
CONLEY,C.L., LIPPMAN. S.M.. NESS. P.M., PETZ,
L.D., BRANCH,D.R. & GALLAGHER,M.T. (1982)
Autoimmune hemolytic anemia with reticulocytopenia and erythroid marrow. New England
Journal of Medicine. 306, 281-286.
CROSBY,W.H.&RAPPAPORT.
H. (1956)Reticulocytopenia in autoimmune hemolytic anemia.
Blood, 11, 929-936.
DAVIS,L.R. (1983) Aplastic crisis in haemolytic
anaemias: the role of a parvovirus-like agent.

British Journal of Hematology. 5 5 , 391-393.

HARLEY,J. 81 DODS, L. (1959) Some acquired
haemolytic anaemias of childhood. Australian
Annals of Medicine, 8, 98-108.
HEGDE,U.M., GORWN-SMITH.
E.C. & WORLLEDGE,
S.M. (1977) Reticulocytopenia and absenceof
red cell autoantibodies in immune haemolytic
anaemia.
British Medical Journal, ii,
1444-1447.
SEEWANN.
H.L. (1979) Subakute idiopathische
autoimmunhamolytische Anamie mit protrahierter aplastischer Phase und erythramischer
Reaktion. Wiener Medizinische Wochenschrift,
129, 180-183.
YOUNG, N.S.. MORTIMER,P.P., MOORE, J.G. &
HUMPHRIES,R.K. (1984) Characterization of a
virus that causes transient aplastic crisis. lournu1 of Clinical Investigation, 7 3 , 224-230.