© JAPI • VOL. 53   FEBRUARY 2005 www.japi.org 105
Original Aricle
Study of Bone Marrow Abnormalities in Patients with
HIV Disease
AK Tripathi*, Pramila Kalra**, R Misra+, A Kumar++, Neetu Gupta***
Abstract
Aim : Present work was carried out to study the bone marrow abnormalities in patients with HIV/AIDS and
to find their association with peripheral hematological abnormalities.
Methods :  Seventy four patients of HIV/AIDS were included in the study. The patients had anemia, leucopenia,
thrombocytopenia or pyrexia of unknown origin (PUO) as indications for bone marrow examination. A
complete blood count, relevant biochemical investigations, HIV RNA load and CD4 positive lymphocyte
counts were done, besides a thorough history and clinical examination. HIV positive patients were classified
as those having AIDS and those without AIDS according to NACO criteria.
Results : Majority of patients (72.9%) had AIDS. Bone marrow was normocellular in 78.95% of non-AIDS and
74.55% of AIDS, hypocellular in 5.26% of non-AIDS and 7.27% of AIDS, hypercellular in 15.79% of non-AIDS
and 18.18 % of AIDS patients. Myelodysplasia was present in 21.05% of non AIDS and 36.46% of AIDS and
the most common series affected was granulocytic (15.79% of total in non-AIDS and 30.9% in AIDS). Dysplasia
was statistically significantly associated with lower CD4 count (p = 0.031) and anemia (p = 0.013).
Myelodysplasia was apparent even before patients developed anemia (16.67%). Increased plasma cells in
bone marrow were observed in 57.89% of non-AIDS and 65.45% of AIDS, whereas decreased lymphoid cells
were seen in 36.84% of non AIDS and 60.00% of AIDS patients.
Conclusions : Myelodysplasia is found in 32.43% of cases of HIV/AIDS and is more common in AIDS than in
non AIDS patients. Granulocytic series is most commonly associated with evidence of dysplasia.
Myelodysplasia is more common in patients with CD4 count <200/µl and in patients with anemia. 54.05% of
patients had decreased lymphoid cells in bone marrow and it was more commonly seen in AIDS than in non
AIDS. ©
INTRODUCTION
Acquired Immunodeficiency Syndrome (AIDS) was
human immunodeficiency virus (HIV) was isolated from
a patient with lymphadenopathy in 1983. By 1984, HIV
was clearly demonstrated to be the causative agent of
AIDS. The dissemination of HIV-1 in humans represents
a catastrophic example of genomic transmission and
expansion. Over 60 million individuals have been
infected so far leading to nearly 20 million deaths and
20 million orphaned children.1,2 It is estimated that most
of the 16,000 individuals, newly infected each day, live
in developing countries.
Bone marrow abnormalities are found at all stages of
*Professor of Medicine and Nodal Officer (HIV Care);
**Resident; +Professor; ***Senior Research Assistant,
Department of Medicine, ++Professor, Department of
Pathology, King George’s Medical University, Lucknow, India.
Received : 19.8.2004; Accepted : 28.12.2004
HIV disease, increasing in frequency as the disease
progresses. Infection of marrow mesenchymal stem cells
with HIV has been incriminated as an important factor
causing bone marrow defects.3 As a result of HIV
infection, the marrow produces a histiocytic reaction
which varies from increased number of histiocytes to a
full blown hemophagocytic syndrome with severe
pancytopenia.4 Several defects in bone marrow
progenitor cells have been described. Reduced colony
growth factor has been demonstrated for granulocyte
macrophage progenitor cells, multipotential
hematopoietic progenitor cells, and megakaryocytic
progenitor cells as well as early erythroid progenitor
cells in most patients with AIDS.4
Marrow from HIV-infected patients is sometimes
difficult to aspirate and the trails are of decreased
cellularity. The true marrow cellularity is better
appreciated on trephine biopsy which is hypercellular
in a majority of patients.5 Although, erythroid dysplasia
has been reported to be the most common finding,
abnormal granulocytic and megakaryocytic
106 www.japi.org © JAPI   VOL. 53   FEBRUARY 2005
development are encountered in approximately one-third
of patients.6 Few studies have shown dysgranulopoiesis
to be more frequent and more accentuated than other
kinds of dyshematopoiesis.7 Intense vacuolization,
especially in the granulocytic series, is frequent.
Dyserythropoiesis may manifest as florid megaloblastic
change. This was found unrelated to serum cobalamin
and folate levels or to drug therapy with zidovudine or
folate antagonists, although these drugs may accentuate
it.8 Granulocytic dysplasia may be apparent at all stages
of maturation, with megaloblastic change, nuclear
abnormalities and Pelger cells reflecting dysfunctional
nuclear maturation.9 Erythroblasts are often bi - or
multinucleated with an irregular nuclear outline and
basophilic stippling. Abnormal sideroblasts including
ringed forms may be present. Dysplastic features in
megakaryocytes are common, occurring in one-third of
marrows and include nuclear hypolobulation and
micromegakaryocytes.10,11
Plasmacytosis has also been reported to occur in HIV
infection.12  Granulomas are an infrequent finding in
bone marrow biopsies and may be associated with a
broad spectrum of infectious and non-infectious
disorders.13
We are beginning to learn various clinical
manifestations and abnormalities in patients with HIV
disease in India. There is a possibility that the
manifestations in Indian patients may not be the same
as reported from other countries like USA and Africa.
Hence, it is imperative to methodically observe and
follow clinical and laboratory aberrations in such
patients in order to improve our diagnostic and
therapeutic skills pertinent to HIV/AIDS. Here, we aimed
at studying the bone marrow abnormalities in patients
with HIV disease and to investigate their association
with peripheral blood abnormalities.
MATERIALS AND METHODS
The study population included 74 HIV +ve
symptomatic or asymptomatic patients. HIV was
diagnosed by ELISA method as per NACO guidelines.14
The study was conducted in Department of Medicine
and Department of Pathology, King George Medical
University, Lucknow.
Inclusion criteria: HIV+ve patients who had anemia,
leucopenia, thrombocytopenia or pyrexia of unknown
origin and gave consent were included in the study.
Exclusion criteria: Patients who had chronic liver
disease or renal disease other than explained by HIV or
primary hematological abnormalities were excluded.
Detailed history was taken which mainly included
age, sex, place of residence, occupation, history of blood
or blood product transfusions, high risk behavior, fever,
weight loss, diarrhoea, oral or genital ulcerations,
bleeding diasthesis or history suggestive of systemic
involvement. All patients were subjected to thorough
physical examination both, systemic and general.
Patients were classified into two clinical groups
according to NACO criteria.14
1. AIDS: (Those patients who fulfilled diagnostic
criteria of AIDS according to NACO guidelines)
2. Non AIDS: (Asymptomatic and symptomatic, who
did not fulfill the NACO AIDS criteria)
Investigations  : Bone marrow examination was
performed for indication of anemia, leucopenia,
thrombocytopenia or pyrexia of unknown origin.
Posterior superior iliac spine was chosen as the site for
bone marrow aspiration and biopsy because of large
marrow space and least painful site. In obese and old
patients, sternum was used for bone marrow aspiration.
A smear was drawn and leishmans stained preparation
was made. Bone marrow sample was examined for
cellularity, morphology including dysplastic changes,
fibrosis, granuloma and iron stores. Other investigations
performed were hemoglobin, total leucocyte count,
differential leucocyte counts, absolute neutrophil,
lymphocyte, monocyte, eosinophil and basophil counts,
general blood picture, platelet count, reticulocyte count,
mean corpuscular volume, mean corpuscular
hemoglobin, mean corpuscular hemoglobin
concentration and total red blood cell count. CD4 and
CD8 lymphocyte counts were measured using flow
cytometry. HIV RNA load in plasma by RT PCR (SRL
Mumbai) wherever possible, were also done. Other
relevant investigations where necessary were done in
individual patient.
Statistical Analysis : The data were analysed using
mean, standard deviation, Pearson’s chi-square test,
student’t’ test, Kruskal-Wallis test, two samples
Wilcoxon Rank Sum test.
OBSERVATIONS AND RESULTS
Out of 74 patients, 19 (27.13%) were grouped as
nonAIDS and 55 (72.87%) as AIDS (NACO criteria).14
Peripheral blood examination and bone marrow
examination was done in 61 patients with anemia, 5
with leucopenia , 2 patients  with thrombocytopenia and
6 with pyrexia of unknown origin .
The commonest age group of patients was 20-40 years
with a range and of 20 to 68 years. Mean age of males
was 34.26 ± 15.25 in non-AIDS and 34.69 ± 8.00 in AIDS
and of females was 30.33 ± 5.02 in non-AIDS and 32.33
± 6.99 in AIDS group (Fig. 1, Table 1). Male to female
ratio was 4:1. Other epidemiological features are shown
in Table 1. Hematological and immunological
parameters are shown in Table 2 and 3 and there is no
statistically significant difference in hematological
parameters in both groups (AIDS and non-AIDS). The
commonest type of anemia was normocytic
normochromic seen in 88.52% (n=54) of patients,
microcytic hypochromic in 6.56 % (n=4) of patients and
macrocytic in 4.92 % ( n=3) of patients.
© JAPI   VOL. 53   FEBRUARY 2005 www.japi.org 107
As many as 78.95% of non-AIDS and 74.55% of AIDS
patients had normocellular bone marrow and 15.79% of
non-AIDS and 18.18% of AIDS patients had
hypercellular bone marrow. Bone marrow was
hypocellular in 5.26% of non-AIDS and 7.27% of AIDS
patients (Table 4).
 Myelodysplasia was found in 32.43 % of patients. It
was more common in AIDS as compared to nonAIDS
patients. As it is evident from Table 5, myelodysplasia
was commonest in granulocytic series (27.03%),
followed by erythroid (4.05%) and megakaryocytic series
(1.35%). Important dysplastic changes observed in
granulocytic series were cytoplasmic vacuolations
(60%), nuclear dysmorphism (30%), monocytoid cells
(1%) and others (1%), in erythroid series were irregular
nuclear outline and basophilic stippling (66.67%),
megaloblastoid changes (33.33%); in megakaryocytic
series were hypolobulation (100%). Out of 24 patients
showing dysplasia 20 (83.33%) had anemia, 5 (20.83%)
had leucopenia and 1 (4.17%) had thrombocytopenia.
Prevalence of dysplasia was more in patients with
advanced disease (CD4 count < 200/µl) and anemia
(Table 6). Majority of patients (83.33%) with dysplasia
had anemia, out of which, only 10% had erythroid
dysplasia. Twenty five per cent of patients with
granulocytic dysplasia had leucopenia, and all   patients
with megakaryocytic dysplasia had thrombocytopenia.
Nine (34.62%) patients showing dysplasia were on
antiretroviral therapy for at least six months.
Increased plasma cells were observed in 57.89% of
Table1 : Epidemiological parameters of patients with
HIV/AIDS
Total number of patients (N=74)
Parameter Mean ± SD
Age (male)(n=59) 34.26 ± 15.25(years)
Age (female), (n=15) 30.33 ± 5.02(years)
Commonest mode of Commercial sex worker (78%)
transmission in males
Commonest mode of From husband (96.6%)
transmission in females
Poor socioeconomic status 65.6%
Fig. 1 : Age distribution of AIDS and non-AIDS patients.
Table 2 : Values and standard deviations of peripheral
blood, immunological  and bone marrow parameters
Hematological parameters Non-AIDS AIDS
Mean ± SD Mean ± SD
 (n=19) (n=55)
Haemoglobin (gm/dl) 11.13± 1.53 10.46± 1.94
Packed cell volume (PCV) 21.91± 16.02 27.36 ± 12.40
(ml %)
Total Red Blood Cell Count 4.41 ± 0.36 3.09 ± 0.36
(TRBC) Million/mm3
Mean corpuscular volume 80.47 ± 5.62 81.81± 5.61
(MCV)(fl)
Mean corpuscular 27.36 ± 2.71 27.59 ± 1.81
Hemoglobin (MCH)(pg)
Reticulocyte count (%) 0.83 ± 0.24 0.96 ± 0.22
Erythrocyte sedimentation 20.06 ± 6.60 18.07± 4.24
Rate (ESR)(mm/hr)
Total leucocyte count 7592.06 ± 7457.23 ±
(TLC) (Cells/mm3)  1523.54  1998.02
Lymphocyte count (%) 26.37 ± 11.54 24.34 ± 10.29
Neutrophil (%) 66.57 ±12.69 69.75 ± 11.83
Eosinophil (%) 4.66 ± 7.27 2.96 ± 3.43
Monocyte (%) 1.77 ± 2.25 2.04 ± 2.35
Basophil (%) 0.6 ± 0.2 0.5 ± 0.12
Absolute Neutrophil count 5.09 ± 1.47 5.04 ± 1.71
x 109/L
Absolute lymphocyte count 2.08 ± 9.29 1.78 ± 8.36
x 109/L
Absolute eosinophil count 3.85 ± 5.69 2.20 ± 2.67
x 109/L
Platelets (Lacs/mm3) 1.91 ± 0.63 1.92 ± 0.49
CD4 count / µl 265.24 ± 97.65 177.53 ± 111.43
HIV RNA in plasma 25514.84 ± 59566.25 ±
(copies/ ml) 14080.04   29092.82
Plasma cells (%) in
bone marrow 3.89 ± 2.21 5.03 ± 2.82
Lymphoid cells (%) in
bone marrow 14.53 ± 8.39 11.14 ± 11.06
Table 3 : Peripheral blood findings in AIDS/HIV
Parameter Non-AIDS AIDS P Value
(N=19) (N=55)
Anemia 11(57.89%) 50(90.91%) 0.05
Leucopenia 1 (5.26%) 4 (7.27%) 0.417
Thrombocytopenia 0 2(3.64%) 0.11
Lymphopenia 4(21.1%) 15(27.27%) 0.05
Table 4 : Bone marrow cellularity in HIV/AIDS patients
Bone marrow Non-AIDS AIDS Total
cellularity
n% n% n%
Normocellular 15 78.95 41 74.55 56 75.68
Hypocellular 1 5.26 4     7.27 5 6.75
Hypercellular 3 15.79 10 18.18 13 17.57
Total 19 100 55 100 74 100
non-AIDS and 65.45% of AIDS patients, whereas, there
was a decrease in lymphoid cells in bone marrow of
6.84% of non-AIDS and 60.00% of AIDS patients
(Table 7).
108 www.japi.org © JAPI   VOL. 53   FEBRUARY 2005
DISCUSSION
Clinical presentation in patients with HIV/AIDS is
diverse and it may arise from involvement of almost any
body system. Hematological abnormalities are not
uncommon in HIV/AIDS. Large percentage of patients
with HIV has anemia, leucopenia and thrombocytopenia
during the course of disease. According to Paradela A et
al,15 90 % of patients are reported to have bone marrow
abnormalities during the course of disease in the form of
increased cellularity, dysplasia or granulomatous
involvement. ‘invitro’ studies have shown that HIV can
directly infect the hematopoietic and mesenchymal cells
and can influence their activity.3 The exact mechanism
of HIV induced bone marrow and peripheral blood
changes are not known, however, these are possibly due
to either direct effect of HIV, nutritional deficiencies,
opportunistic infections or bone marrow suppression
by antiretroviral therapy, and other drugs used in the
treatment of HIV infection.8
Bone marrow aspiration and biopsy is generally
needed in patients presenting with hematological
abnormalities where the cause could not be discerned.
The present study involved 74 patients of HIV / AIDS
who had anemia, leucopenia, thrombocytopenia or
pyrexia of unknown origin. Clinicoepidemiological
features are presented in Table 1 and are similar to the
data reported from India and other countries.16,17 Three
fourths (72.97%) of our patients had clinical AIDS while
the rest (27.03%) were either asymptomatic or
symptomatic but did not fit into criteria of AIDS (Table
1). This data is biased towards symptomatic HIV disease
as most patients come to hospital when they become
symptomatic.
Eighty two percent of patients had anemia and its
prevalence was significantly higher in patients with
AIDS than in non AIDS (p=0.05) (Tables 2, 3). The most
common type of anemia was normocytic normochromic,
which is in agreement with the reports in the literature.18
Macrocytic anemia is commonly reported in patients on
ART.8 Five percent (3 Patients) in our study had
Table 5 : Myelodysplasia in bone marrow in HIV patients
Dysplasia Non-AIDS AIDS Total
n (%) n (%) n (%)
No dysplasia 15 (78.95) 35 (63.64) 50 (67.57)
Granulocytic 3  (15.79) 17 (30.90) 20 (27.03)
Erythroid 1  (5.26) 2 (2.64) 3 (4.05)
Megakaryocytic 0  (0.00) 1 (1.82) 1 (1.35)
Total 19  (100) 55 (100) 74 (100)
Table 6 : Myelodysplasia and its association with peripheral blood abnormalities
Parameters Granulocytic Erythroid Megakaryocytic Significance
Haemoglobin
Normal (n=13) 2(15.38%) 1(7.69%) 1 (7.69%) p=0.01
Decreased (n=61) 18(29.51%) 2(3.28%) 0 (0.0%)
PCV
Normal (n=7) 1(14.29%) 1(14.29%) 0(0.00%) p=  0.74
Decreased (n=67) 19(28.36%) 2(2.99%) 1(1.49%)
MCV
Normocytic (n=50) 5 (30%) 2 (4%) 1 (2%) p= 0.00
Microcytic (n=23) 5 (21.74%) 0 (0.00%) 0 (0.00%)
Macrocytic (n=1) 0 (0.00%) 1 (100%) 0 (0.00%)
CD4 count
<200 (n=31) 10 (56.56%) 1 (33.33%) 0 (0.00) p= 0.03
200-350 (n=30) 6 (33.33%) 0 (0.00%) 1 (100.00%)
>350-500 (n=7) 2 (11.11%) 2 (66.67%) 0 (0.00%)
Total leucocyte count
Normal(n=69) 15(21.74%) 3(4.35%) 1(1.45%) p=0.02
Decreased(n=5) 5(100%) 0(0.00%) 0(0.00%)
Platelets
Normal(n=72) 20(27.78%) 3(4.17%) 0(0.00%)   p=0.53
Decreased(n=2) 0 0 1(50%)
HIV RNA in plasma
<30,000 (n=10) 3(30%) 1(10%) 1(10%) p=  0.54
30,000-99,000(n=49) 6(32.65%) 1(2.04%) 0 (00.00%)
>99,000 (n=15) 1 (6.66%) 0 (00.0%) 0 (0.00%)
Table 7 : Variations in lymphoid and plasma cells in  bone
marrow of HIV patients
Non-AIDS AIDS Total p value
 (n=19) (n=55) (n=74)
n (%) n (%) n (%)
Lymphoid cells
Normal 10  (52.63) 19 (34.55) 29 (39.19) chi2(2)= 3.11,
Decreased 7  (36.84) 33 (60.00) 40 (54.05) p = 0.210
Increased 2  (10.53) 3 (5.45) 5 (6.76)
Plasma cells
Normal 8 (42.11) 19  (34.55) 27 (36.49) chi2(1)= 0.35,
Increased 11  (57.89) 36 (65.45) 47 (63.51) p = 0.555
© JAPI   VOL. 53   FEBRUARY 2005 www.japi.org 109
macrocytic anemia and all were on ART. The early
diagnosis and effective management of anemia in
patients with HIV disease is of tremendous importance
as anemia in such patients may be an indicator of poor
prognosis and progression to advanced disease.6
Leucopenia was observed in 7.27 % of AIDS and 5.26 %
of non AIDS (Table 3) and all patients showed
granulocytic dysplasia, emphasizing that the latter was
a major cause for leucopenia. Lymphopenia was seen in
21.1% of nonAIDS and 27.27% of AIDS patients.
Prevalence of thrombocytopenia in patients with HIV/
AIDS has been variably reported in 13 % to 61% cases.17,18
Our study revealed a prevalence of 3.64% and it was
significantly different in AIDS and non AIDS group
(Table 3).
Bone marrow was particularly examined for
cellularity, fibrosis, dysplasia and for the evidence of
granuloma. Previous reports indicate that most of the
cases with HIV have hypercellular bone marrow.15
However present study revealed bone marrow to be
normocellular in 75.68%, hypocellular in 6.75% and
hypercellular in 17.57% patients (Table 4). The difference
is difficult to explain but it is likely to be due to different
cohort of patients included in various studies. Majority
(72.9%) of patients under study had full blown AIDS
where bone marrow could likely be normocellular or
hypocellular rather than hypercellular which is
predominant in early stages of disease.20 We have not
observed increased reticulin in any of bone marrows
examined. This is in accordance with reports by Treacy
et al. 6 Myelodysplastic changes due to HIV can explain
normocytic or macrocytic anemia which is common in
patients with AIDS. Myelodysplastic changes in bone
marrow were found in 32.43% cases as compared to 50-
90 % reported in literature.15 This difference in incidence
of dysplasia in different population of patients is
interesting to note. The underlying reason is not clear
and this needs to be addressed in future studies involving
larger number of patient. Despite the fact that
myelodysplasia in majority of patients is directly
proportionate to HIV RNA load, the incidence of
myelodysplasia is less in the study.20 Higher incidence
of dysplasia in advanced disease is probably due to
increased HIV RNA load, cytokine mediated effect of
disease and drug related changes and also effect of
infections. Myelodysplasia was significantly more
common in AIDS (36.36%) than in non-AIDS (21.05%),
(p = 0.01). Cells most commonly showing dysplasia in
our study were granulocytes (27.03%) followed by
erythroid in 4.05% and megakaryocytes in 1.35% (Table
5). Some workers have previously reported erythroid
dysplasia to be the commonest type of dysplasia whereas
others reported it in granulocytic series of cells. 15
Dysplastic changes observed   in granulocytic series were
cytoplasmic vacuolations (60%), nuclear dysmorphism
(30%), monocytoid cells (1%) and others (1%); in
erythroid series were irregular nuclear outline and
basophilic stippling (66.67%), megaloblastoid changes
(33.33%) and in megakaryocytic series were
hypolobulation (100%). Most common cause of
myelodysplasia could possibly be due to an inherent
defect of hematopoietic cells. However some patients are
diagnosed to be having secondary myelodysplastic
syndrome and important causes include drugs, alcohol,
infections like tuberculosis and malaria. Reports are
lacking on the incidence of HIV disease in patients of
myelodysplastic syndrome. Nevertheless HIV infection
should be included in differential diagnosis of patients
with secondary myelodysplasia. The myelodysplasia in
early stages may not reflect changes in peripheral blood
smear and thus may remain undiagnosed. This also
suggests that prevalence of myelodysplasia in HIV may
be much higher than what is reported. This is evident
from our observation that 7.69% of patients showing
erythroid dysplasia did not have anaemia. Dysplasia
seems to be an important factor in HIV induced
leucopenia while it may not be important for causing
anemia and thrombocytopenia that may occur due to
other factors. No such study is available which has
reported the incidence of myelodysplasia based on bone
marrow examination in all HIV/AIDS patients
irrespective of their hematological presentation.
The cause of fever was determined on bone marrow
examination in 2 out of 6 patients. One patient had
histoplasmosis and the other had evidence of tubercular
bacilli in bone marrow. Brook MG et al21 reported that
27% of marrows in HIV patients with fever revealed the
cause, commonest being mycobacteriosis in 20%.
Various studies have reported that plasma cells in
bone marrow are increased in all patients with HIV
infection.12 We observed increased number of plasma
cells in the marrow of 57.89% of nonAIDS and 65.45% of
AIDS patients (Table 7). Mean percent of plasma cells in
bone marrow sample of nonAIDS was 3.89 ± 2.21 and
5.03 ± 2.82 in AIDS (Table 2), however, this difference
was not statistically significant. Plasmacytosis was not
only confined to those with advanced disease in whom
opportunistic infections could be implied with but was
also seen in patients at an early stage who had no
concurrent infection. Increased plasma cells could thus
be a polyclonal B cell response to HIV infection and can
occur at any stage of HIV disease. Lymphoid cells were
found to be decreased in the marrow in   36.84% of non
AIDS and 60% of AIDS patients. Mean count of lymphoid
cells was 14.53 ± 8.39 percent in nonAIDS and 11.14 ±
11.06 percent in AIDS patients (Table 2). However, it is
interesting to note that decreased lymphoid cells in bone
marrow was more common in AIDS patients compared
to non-AIDS. We presume that decrease in marrow
lymphoid cells could possibly explain lymphopenia in
HIV patients. Further studies are needed to define the
diagnostic and prognostic significance of decreased
lymphoid cells in bone marrow of non-AIDS and AIDS
110 www.japi.org © JAPI   VOL. 53   FEBRUARY 2005
patients. However, we hypothesize that decrease in
marrow lymphoid cell pool is consequent upon the
destruction of lymphoid cells by HIV.
REFERENCES
1. Clark S. Experts predict global devastation due to HIV/
AIDS.  Lancet 2002;360:45.
2. Stover J, Walker N, Garnett GP. Can we reverse the HIV/
AIDS pandemic with an expanded response?  Lancet
2002;360:73-7.
3. Wang  L, Mondal D, La  Russa VF,  et al. Suppression   of
clonogenic potential of  human bone marrow mesenchymal
stem cells by HIV type 1, putative role of HIV-1 tat protein
and inflammatory cytokines. AIDS Res Hum Retroviruses
2002;18:917-31.
4. Leiderman IA, et al. A glycoprotein inhibitor of in vitro
granulopoiesis  associated with AIDS. Blood 1987;70:1267.
5. Stella CC, et al. Defective in vitro growth of hematopoietic
progenitor cells in the acquired immunodeficiency syndrome.
JClin Invest 1987;80:286.
6. Treacy M, Lai L, Costello C, et al. Peripheral blood and bone
marrow abnormalities in patients with HIV related disease.
Br J Haematol 1987;65:289-94.
7. Candido A, Rossi P, Menichella G. Indicative morphological
alterations ofbone marrow in overt AIDS.  Haematologica
1990;75:327-33.
8. Richman DD, et al. The toxicity of Azidothymidine (AZT) in
the treatment of patients with  AIDS and AIDS  related
complex. N Engl J Med 1987;317:192-97.
9. Henry K. Costello C. HIV associated bone marrow changes.
Curr Diag Pathol 1994;1:131-141.
10. Scaradavou A. HIV related thrombocytopenia.  Blood Rev
2002;16: 73-6.
11. Marandin A, Canque B, Columbel L. et al. In vitro infection
of bone marrow adherent cells by human immunodeficiency
virus type-1 (HIV-1) does not alter their ability to support
hematopoiesis.  Virology 1995;213:245-48.
12. Moller T, et al. Hematological changes associated with HIV
infection. Ugeskr Laeger 1993;155:1442-46.
13. Ryu T, Ikeda M, Okazaki Y. Myelodysplasia associated with
acquired immunodeficiency syndrome. Intern Med 2001;40:
795-801
14. National guidelines for clinical management of HIV. Ministry
of Health and Family Welfare. National testing and clinical
manifestations of HIV/AIDS pg. 6,7.
15. Paradela A, Rivas C, Fernandez -Guerrero M, Roman A.
Histopathology of bone marrow biopsy in patients  with
human immunodeficiency virus infection.  Rev Clin Esp
1996;196:9-15.
16. Rewari BB, Joshi PL. Epidemiology of HIV/AIDS with special
reference to India. Medicine Update APICON. 2003:80-85
17. Sircar AR,Tripathi AK, Chaudhary SK, Misra R. Clinical
profile of AIDS. A study at a referral hospital. JAPI 1998;46:
775-78.
18. Patwardhan MS, Golwilkar AS, Abhyanakar JR, Atre MC.
Hematological profile of HIV positive patients. Indian J Pathol
Microbiol 2002;45:147-50.
19. Mir N, Costello C, Luckit J, Lindley R. HIV disease and bone
marrow changes; a study of 60 cases.  Eur J Haematology
1989;42:339-43.
20. Katasrou C,Terpos E,Pastouris E,  et al. Myelodysplastic
features in patients with long term HIV infection and
hemophilia. Haemophilia 2001;7:47-52.
21. Brook MG, Ayles H, Harrison C, et al. Diagnostic utility of
bone marrow sampling In HIV positive patients. Genitourin
Med 1997;73:85-6.
Announcement
1st National Conference of the Indian Society for Study of Lung Cancer (NALCCON 2005).
2nd and 3rd April 2005 at PGI,  Chandigarh.
Contact : Prof. D Behera, Department of Pulmonary Medicine, PGI, Chandigarh - 160012.
E-mail : dbehera@glide.net.in