A 67-year-old man from Shyanja, Western Nepal,
presented to us with the chief complaints of
anorexia alongwith fatigue, dizziness, and
palpitations. 
He was a regular smoker and alcohol
consumer.
On examination he had marked pallor,
bipedal oedema, and a blood pressure of 90/60
mm of Hg. There was no hepatosplenomegaly or
lymphadenopathy and other systems were also
unremarkable.
His investigations revealed
pancytopenia with a haemoglobin of 3.4 g%, total
leukocyte count of 3,100 with a differential
showing lymphocytes of 85% and neutrophils 15%.
Peripheral smear was normocytic, normochromic,
and platelets were reduced on smear. The
corrected reticulocyte count was 0.22%. The ESR
was 174 mm (anaemia correction was not done).
The serum urea, creatinine, protein, albumin,
fasting and post-prandial blood sugars were within
normal limits.
The bone marrow aspiration grossly revealed a
linear core, part of which was gelatinous. The total
cellularity was 5% with absence of myeloid,
erythroid, and megakaryocytic cell lineages. There
was no granuloma or abnormal cells. Reticulin
and iron stain was grade I. The background
showed diffuse gelatinous marrow involvement
classified as + + + (Fig. 1).
This patient taught us a few important lessons.
Gelatinous marrow transformation (GMT) can
be a rare but important differential diagnosis
in the evaluation of pancytopenia other than
aplastic anaemia, myelopthisic anaemias,
megaloblastic anaemias, and myelodysplastic
syndrome. Anorexia nervosa, acute febrile
states, and AIDS in younger ages (<40 years),
alcoholism and lymphomas in middle ages, and
carcinomas, lymphomas, and chronic heart
failure in older ages (>60 years) were most
commonly associated with GMT
1
. Although the
literature states that it is a non-specific,
heterogeneous indicator of a severe illness, we
reviewed the history of alcohol consumption in
our patient and found that he was a heavy
drinker of large quantities per day for several
years, and for the past few months had almost
also given up eating food. We had initially sent
him home on haematinics after 3 units of blood
transfusion and advised increased caloric and
protein intake alongwith complete abstinence
from alcohol. It was also debated at one point
of time as to whether he would merit immuno-
supression for aplastic anaemia. However, he
reported for follow up after 2 weeks with
improvement in appetite and a repeat
haemogram showed indications of marrow
recovery in the form of improvement in Hb
(6.5g) and TLC which came up to 8,900. He
was continued on the haematinics and intake
of nutritious diet and alcohol abstinence was
re-emphasised.
He came back a month later complaining of
increased giddiness. His repeat Hb was 2 gm,
TLC 2,500, Platelets 24,000. A repeat bone
marrow showed earlier findings of severe
reduction of trilinear haematopoeisis against a
background of gelatinous transformation. He
JIACM 2002; 3(3): 305-10,317
Fig. 1 : Bone marrow aspiration (see http://medind.nic.in/jac/t02/i3/jact02i3p305.pdf)

denied any further episodes of drinking
although his family and friends claimed that he
did. This time his LFT revealed evidence of mild
transaminitis alongwith hypoalbuminaemia.
There were no changes of cirrhosis on
ultrasound of abdomen. He also had fever, and
on the background of neutropenia and CXR
showing non-homogenous opacities, was
started on IV ampicillin-clavulanate in standard
adult doses. For anaemia he was again treated
with blood transfusions. He went home as soon
as his fever and giddiness subsided after 3 days.
At home he was symptom free but not for long
and he returned to us again with increasing
pallor, anorexia, and recurrent fever after one
month. He was managed aggressively as a
febrile neutropenic but succumbed to
septicaemic shock.
There is a danger of mistaking the associated
marrow aplasia of GMT as aplastic anaemia of
immune origin. A detailed evaluation of all the
above-mentioned possible causes is necessary in
a patient of pancytopenia and gelatinous
transformation of marrow with marrow aplasia.
In our patient there was a strong association with
alcoholism, so much so that every time the patient
resumed drinking it was his bone marrow, which
failed instead of his liver. Alcohol possibly played
a major role in his marrow insult compounded by
gelatinous marrow transformation due to
associated starvation. Alcohol is known to inhibit
committed haematopoeitic stem cells in vivo. The
Erythroid series is particularly vulnerable
2
. GMT
on the other hand disrupts marrow architecture
and there is fat atrophy with deposition of
mucopolysaccharides (MPS) rich in hyaluronate.
This deposition may be occurring to compensate
for the loss of fat which would have been otherwise
meeting the energy requirement. However, the
microenvironment provided by the MPS is
unsuitable for haematopoeisis resulting in marrow
failure.

References
1. Bohm J. Gelatinous transformation of the bone marrow:
the spectrum of underlying diseases. Am J Surg Pathol
2000; 24 (1): 56-65.
2. Jandl JH. Aplastic anaemia in Blood. In: Jandl JH, Blood
text book of haematology, 2nd edition, Boston: Little
Brown 1996; 214-5.