Blood, 1959, Vol. 14, No. 6, pp. 694-707.
© 1959 American Society of Hematology, Inc.
The Macrocytosis of Hepatic Disease.
I. Thin Macrocytosis
JOHN BINGHAM 1
1 Departments of Medicine of the University of Toronto and the Toronto
Western Hospital, Toronto, Canada.
A macrocytic blood picture was present in 62 per cent of 222 patients with
various types of hepatic disease.
Three different types of macrocytes were present in the blood films: a thin
macrocyte, a target macrocyte and a thick macrocyte. Just as leukocytosis
might be described as neutrophilic, basophilic or eosinophilic according to the
predominate leukocyte present, so macrocytosis has been defined according
to the predominate macrocyte present: thin macrocytosis, target macrocytosis
and thick macrocytosis. This report deals with the first type, thin macrocytosis.
1. Thin macrocytosis is, by definition, the type of macrocytosis in which all
the macrocytes are thin macrocytes. It is the commonest type of macrocytosis
(59 per cent of all types of macrocytosis).
2. The thin macrocyte is a flattened erythrocyte. It has the same volume as
the normal erythrocyte but is broader and thinner. As the diameter of the cell
increases its thickness decreases.
3. Thin macrocytosis is caused by an alteration in erythropoiesis in the bone
marrow and not by a flattening or swelling of normal erythrocytes in the peripheral circulation, as suggested by various workers, because:
(a) Normal size erythrocytes transfused into the circulation of patients
with thin macrocytosis do not become macrocytic.
(b) Anisocytosis is increased.
(c) The nucleated red cells in the marrow are macrocytic.
4.The thin macrocyte is produced by a macronormoblastic (or rarely atypical megaloblastic) type of maturation in the bone marrow.
5. This altered erythrocyte maturation which gives rise to thin macrocytosis
is a specific response to nonspecific hepatic parenchymal cell damage. It occurs
in a significant percentage of patients suffering from all types of parenchymal
and obstructive hepatic disease. It does not occur in patients with simple fatty
liver or obstructive jaundice of short duration where hepatic cells are not
damaged. A deficiency of any known hematopoietic factor plays no part in
the etiology of this disorder.
Submitted on July 7, 1958
Accepted on October 28, 1958
