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178

Correspondence

COMBINED ESTERASES IN ACUTE MYELOMONOCYTIC LEUKAEMIA

The finding by Scott t

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

t

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 butyrate-

reacting 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.

do not agree with Scott t 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

Scm,

C.S.

CAHILL . BYNOE

A.G.

AINLEY .J. TAVASSOLI .. SHAKLAI.M. CROSBY

W.H.

1979)Cytochemical diagnosis

of

acute myelo-

monocytic leukemia. American

Journal

of Clini-

cal Pathology, 72, 59-62.

HOUGH

D. ROBERTS .E.

1983) Esterase

cytochemistry in primary myelodysplasticsyn-

dromes and megaloblastic anaemias. British

Journal of Haematologg, 55 4 1 1 4 1 8 .

AUTOIMMUNE HAEMOLYTIC ANAEMIA A N D 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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Correspondence 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 an autoimmune

haemolytic anaemia who developed an aplastic crisis after several years of treatment with

immunosuppressive drugs. Oneof these cases has already been reported in detail (Celadaet 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 s 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: Conleye t

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 developmentof 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 I m m u n o l o g y I M M l 1

Research Institute

of

Scripps Clinic

1 0 6 6 6 Nor th Torrey P ines Road

La JoZZa CaZi;fornin9 2 0 3

7

U.S.A.

ANTONIOCELADA

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BUCHANAN

.R. BOXER L.A. NATHAN

D.G.

British Journal of Hematology. 5 5 391-393.

(1976) The acute and transient nature

of HARLEY

.

8

DODS

L. (1959) Some acquired

idiopathic immune hemolytic anemia in child- haemolytic anaemias

of

childhood. Australian

hood. Journal

of

Pediatrics. 88, 780-783. Annals of Medicine 8, 98-108.

CELADA

A.. FARQUET

.J.

8 MULLER,

.F.

(1977)

HEGDE U.M.

GORWN-SMITH..C. WORLLEDGE,

Refractory sideroblastic anaemia secondary to S.M. (1977) Reticulocytopenia and absenceof

autoimmune haemolytic anaemia. Acta Haema- red cell autoantibodies in immune haemolytic

tologica. 5 8 2 13-2 16. anaemia. British Medical Journal ii,

CONLEY

C.L. LIPPMAN S.M.. NESS. P.M. PETZ, 1444-1447.

L.D.,

BRANCH

D.R. GALLAGHERM.T. (1982) SEEWANN..L. (1979) Subakute idiopathische

Autoimmune hemolytic anemia with reticulo- autoimmunhamolytische Anamie mit protra-

cytopenia and erythroid marrow. New England hierter aplastischer Phase und erythramischer

Journal of Medicine. 306 281-286. Reaktion. Wiener Medizinische Wochenschrift

CROSBY

W.H.&RAPPAPORT.

.

(1956)Reticulocy- 129, 180-183.

topenia in autoimmune hemolytic anemia. YOUNG N.S.. MORTIMER P.P., MOORE J.G.

Blood

11

929-936.

HUMPHRIES .K. (1984) Characterization

of

a

DAVIS

L.R. (1983) Aplastic crisis in haemolytic virus that causes transient aplastic crisis. lour-

anaemias: the role

of

a parvovirus-like agent.

nu1

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Clinical Investigation 7 3

224-230.