This document discusses myelodysplastic syndrome (MDS), a group of stem cell diseases characterized by cytopenias, dysplasia, and risk of acute myeloid leukemia. It covers the epidemiology, etiology, pathophysiology, genetics, classification systems including FAB and WHO, clinical features, laboratory findings, bone marrow findings, immunophenotyping, and evaluation of patients with suspected MDS. Key points include that MDS occurs mainly in older adults, can be de novo or therapy-related, involves clonal stem cell mutations, and classifications are based on peripheral blood, bone marrow blasts, and cytogenetics.

1. MYELODYSPLASTIC SYNDROME
• Presented by MODERATOR
Dr ARVINDRA RAHUL DR REENA JAIN
( Asst. prof.)
Department of pathology
GRMC Gwalior
1

2. MYELODYSPLASTIC SYNDROME
• DEFINITION- The Myelodysplastic Syndromes
are a group of clonal haematopoietic stem cell
disease characterised by cytopenia(S),
dysplasia in one or more of the major myeloid
cell lines, ineffective haematopoiesis ,and
increased risk of development of ACUTE
MYELOID LEUKEMIA. There is an enhanced
degree of apoptosis which contribute to
cytopenia.
2

3. EPIDEMIOLOGY
• Myelodysplastic syndromes occur principally in
older adults with a median age of 70 years.
• Annual incidence of 3-5 /100 000 persons but
rising to >20/100 000 among those over the age
of 70 years.
• There is male predominance.
3

4. MDS Etiology
• Two etiologic categories of MDS:
• 1.) De Novo:
-benzene exposure (gasoline)
-cigarette smoking
-heavy metals ,Pesticides ,Herbicides
-viruses -Fanconi’s anemia
• 2.) Therapy related:
-Alkylating agent chemotherapy
-Radiation
4

5. Pathophysiology
• The initial hematopoietic stem cell injury
can be from cytotoxic chemotherapy,
radiation, virus, chemical exposure, or
genetic predisposition.
• A clonal mutation predominates over bone
marrow, suppressing healthy stem cells.
5

6. pathogenesis of MDS
• Mutation/Altered function of stem cell
• Altered cell formation of hematopoietic cell lineage.
• Hypercellular bone marrow with large number of abnormal
cells.
• Suppression of normal cell formation.
• Early death of these abnormal cell.
• CYTOPENIA.
6

7. GENETICS AND MDS
 CYTOGENETIC and MOLECULAR studies have a major
Role in evaluation of patients with MDS in regards to
Prognosis, Determination of Clonality, And the
Recognition of cytogenetics, Morphologic, and
Clinical correlates.
 CLONAL Cytologenetic abnormalities are observed in
Approximate 50% of MDS cases.
7

8. DELETION OF THE LONG ARM OF
CHROMOSOME 5 (5q- SYNDROME )
 Strongly associated with RA.
 5q- accounts for up to 70% of cytogenetic abnormalities
in this subtype.
 The q arm of chromosome 5 is particularly rich in genes,
which encoded haemopoietic growth factors and their
receptors. For example , IL-3 , IL-4 , IL-5 , GM-CSF and the
M-CSF receptor are located in this region.
 The potential for the loss of any or all of these genes
contribute to the disruption of ordered haematopoiesis.
8

9. Monosmy 7 and 7q-
• Most strongly associated with secondary MDS.
• Associated with the loss of a major surface
glycoprotein (gp 130) in neutrophil and
susceptibility to bacterial infection secondary
to impaired granulocyte monocyte chemotatic
activity.
9

10. Deletion of the q arm of chromosome 11
(11q-)
• Account for 20% of the chromosomal
abnormalities in RARS.
• This abnormality is associated with raised iron
stores and high ring sidroblast counts.
• The presence of the gene , which encoded the H-
subunit of ferritin at chromosome 11 , may
explain this
10

11. Abnormalities of chromosome 17 (i17q)
• It involves the loss or disruption of the Р53
tumor suppressor gene are seen in CML in
association with transformation to the blastic
phase and in up to 5% of cases of primary
MDS.
• This predisposes to certain dysplastic
features and neutrophil vaculation.
11

12. Abnormalities of Chromosome 3
• Dysmegakaryopoiesis and thombocytosis appear
to be associated with Abnormalities of
chromosome 3
12

13. The importance of indication of
chromosomal abnormalities
– To confirm diagnosis .
– To know the stage of disease.
– To know the direction of progression of disease.
– Multiple genetic abnormalities indicate late events
in MDS.
13

14. FAB CLASSIFICATION OF MDS
1. Refractory anemia
2. Refractory anemia with ring sideroblast
3. Refractory anemia with excess blasts
4. Refractory anemia with excess of blasts in
transformation
5. Chronic myelomonocytic leukemia
14

15. FAB CLASSIFICATION
subtype Peripheral blood Bone marrow
Refractory anemia RA Blast < 1 % Blasts < 5%
Ring
sideroblast<15%
Refractpry anemia
with ringed
sideroblast
RARS Blast < 1 % Blasts < 5%
Ring sideroblast>
15 %
Refractory anemia
with excess of blast
RAEB Blasts <5 % Blast 5-20 %
15

16. Continued…
subtype Peripheral
blood
Bone marrow
Refractory anemia
with exess blasts in
transformation
RAEBT Blasts > 5 % Blasts 20 -30% or
Auer rods in blasts
Chronic
myelomonocytic
leukemia
CMML Blasts <5%
Monocytes>1x109 /L
Any of above
16

17. WHO CLASSIFICATION
• Refractory cytopenia with unilineage
dysplasia(RCUD), RA, RN, RT
• Refractory anemia with ringed siderblast(RARS)
• Refractory cytopenia with multilineage
dysplasia(RCMD)
• Refractory anemia with excess blast-1(RAEB-1)
• Refractory anemia with excess blast-2(RAEB-2)
• Myelodysplastic syndrome unclassified(MDS-U)
• MDS associated with isolated del (5q)
• Childhood myelodysplastic syndrome
17

18. WHO CLASSIFICATION
DISEAE PERIPHERAL BLOOD BONE MARROW
1.Refractory cytopenia
with unilineage
dysplasia,RA,RN,RT
•Unicytopenia or
bicytopenia
•No/rare blast
Unilineage dysplasia>10%
of cells of one myeloid
lineage with <5% blasts
<15% RS(Eerthroid
precursur)
2.Refractory anemia with
ring sideroblast.(RARS)
.anemia
No blasts.
•Erythroid hyperplasia with
dyserythropoisis.
•>15% RS
•<5% blasts
3.Refractory cytopenia
with multilineage dysplasia
(RCMD)
•BI/pancytopenia
•No/rare blasts
•No Auer rods
•<1x109/LMonocytes
•Dysplasia in >10% of the
cells IN > lines2 Myeloid
•<5% blasts in the marrow
•>15% RS
•No Auer rods
18

19. 4.REFRACTORY ANEMIA
WITH EXCESS BLAST-1
(RAEB)
•<5% blasts
•Bi/ pancytopenia
•No Auer rods
•5-9 % blasts no Auer rods
•Dysplastic changes in >1
hemopoietic cell lineage.
5.REFRACTORY ANEMIA
WITH EXCESS BLASTS-2
(RAEB-2)
•5-19 % blasts
•Cytopenia
•Auer rods+-
•10-19 % blast Auer rods+_
•Myelodysplasia of >1 cell line
6.MDS UNCLASSIFIED
(MDS-U)
•NO blasts (<1 %)
•Cytopenias
•5 % blasts cytogenetic abnormality
•Granulocytic or megakaryocytic
dysplasia.
7.MDS WITH ISOLATED
DELETION OF 5q
•<1 % blast
•Anemia
•Platelate increase or
normal.
•<5 % blasts, no Auer rods
•Increase /n megakaryocytes.with
hypolobulated nuclei.
•Isolated deletion 5q
8.CHILDHOOD
MYELODYSPLASTIC
SYNDROME
•<2 % blast
•>10% neutrophills
have dysplastic change
•>10 dys. In erythroid precursors
•>10% dys.gran precursors
•Micromegakaryocytes
19

20. DIFFERENCES BETWEEN WHO AND FAB
The WHO system
• Makes use of cytogenetic findings.
• The category of RAEB-t was eliminated as it got
included within AML(>20%blasts)
• CMML was removed and put in a new category of
myelodysplastic/myeloproliferative diseases.
• Adds the subtypes 5q syndrome and
unclassifiable MDS.
• Recognizes the prognostic importance of % of
bone marrow blasts
20

21. Changes made by WHO classification
• The criteria for the diagnosis of AML was altered
(20% blasts).
.The poor prognostic significance of more than10% bone
marrow blasts, in comparison with 5-10% bone marrow
blasts is recognized andRAEB is therefore separated into
RAEB-1 and RAEB-2
. Problem relating to the classification of CMML/a CML was
resolved by creation of MDS/MPD category to which
both were assigned together with other cases with
features overlapping between MDS/MPD.
21

22. Patterns of MDS evolution
• A stable group with no increase in B.M blasts
and a normal karyotype .
• Rapid blast transformation with acquisition
of new cytogenetic changes after an initial ,
stable phase .
• Gradually increasing blast count in the
absence of new cytogenetic changes .
22

23. CLINICAL FEATURES
Clinical features depends on the cell lineage involved.
Most of the cases are asymptomatic.
 In Leucopenia-
-Bacterial infections
-Fungal infections
-Skin manifestations
 In Anemia
-Fatigue
-Weakness
-Exercise intolerance
 In Thrombocytopenia
-Bleeding disorder
-Bruising
23

24. Laboratory Finding
 Peripheral blood :
Anemia ,Neutropenia and Thrombocytopenia are the classical
findings of MDS
 Bone Marrow ASPIRATE-
Criteria… at least 500 cells to be counted and at least 30
Megakaryocytes are to be evaluated.
Dysplastic features should be present in >10 % of marrow cells.
in MDS BM Aspiration –Hypercellular BM seen.
24

25. 25

26. PERIPHERAL BLOOD FINDINGS
IN ERYTHROID SERIES
Major changes are found in the peripheral blood counts
and Morphology, and Bone marrow abnormalities also
are present.
• OVALOCYTES
• MACROCYTOSIS
• STOMATOCYTES
• ELIPTOCYTES
• TEAR DROP CELLS
• NUCLEATED RBC
• BASOPHILIC STIPPLING
• HOWELL-JOLLY BODIES
26

27. Anisopoikilocytosis in RBC and neutrophil with hypogranular
cytoplasm and hypolobular nuclei
27

28. 28

29. MYELOID SERIES
• Number of WBC,s is Variable .
• Neutropenia .
• Monocytosis .
• Increased Promyelocyte .
• Hyposegmented and hypogranular Neutrophil
(pseudopegler huet anomoly)
• Circulating metamylocytes .
• Decreased myeloperoxidase and alkaline phosphatase
activity
29

30. PEUDO-PELGER –HUET ANOMOLY
30

31. DYSMEGAKARYOPOIESIS
• Giant platelates
• Hypogranular platelets
• Agranular platelates
• Abnormal platelate function
31

32. 32

33. BONE MARROW FINDING IN MDS
• ERYTHROID SERIES
- INEFFECTIVE ERYTHROPOISIS
ERYTHROID HYPERPLASIA
RINGED SIDEROBLAST
MEGALOBLASTOID MATURATION
MULTINUCLEARITY
NUCLEAR FRAGMENTS,NUCLEAR BUDDING
CYTOPLASMIC ABNORMALITY.
33

34. Erythroid precursor with dyserythropoisis features nuclear
budding and irregular form and megaloblastoid changes
34

35. MYELOID SERIES
Defective granulation
Nuclear hypolobulation
Presence of Auer rod in in myeloid cells
maturation arrest in myeloid stage
increase in monocytoid cells
increase number of blasts < 20 %
Type1 and Type2 blast
35

36. MEGAKARYOCYTIC SERIES
REDUCED NUMBER OF MEGAKARYOCYTES
MICROMEGAKARYOCYTES
MEGAKARYOCYTES WITH LARGE, SINGLE
NUCLEI OR MULTIPLE SMALL NUCLEI
NUCLEAR HYPOLOBULATION
36

37. RINGED SIDEROBLAST WITH PERL’STAINING
37

38. 38

39. Chediak-Higashi-like Granules
• Photograph courtesy of John Scariano, University of New Mexico, Dept. of Pathology
39

40. TYPE I
• Finely dispersed nuclear
chromatin
• Prominent nucleoli
• Variable N:C ratio , agranular
cytoplasm
40

41. TYPE 2 BLAST RESEMBLE TYPE 1 BUT HAVE PRIMARY GRANULES <
20 IN NUMBER
TYPE II
41

42. 42

43. TRIPHINE BIOPSY IN BONE MARROW
Particulary useful to determine cellularity of Marrow ,
abnormal localization of immature precursors(ALIP)
,reticulin fibrosis , Megakaryocytic dysplasia ,lymphoid
aggregate and hypoplastic aggregate
Finding in MDS
1 .Proerythroblast and early normoblast are increased
2.Late normoblast decresed
3.Preponderance of early and intermediate Myeloblast
and late Normomoblast demonstrate
Dyserythropoiesis.
4.Preporedance of promyelocytes and myelocytes in the
BM.
43

44. Continued….
5.Increase monocytoid form.
6.Blasts are increased in number.
7.Clusters of >5% blasts are abnormally located in the
central part of marrow
(normally myeloblast located in peripheral part).
8.Megakaryocytes are increased in number. These are
present in Paratrabecular location.
9.Neovascularisation is increased.
44

45. IMMUNOHISTOCHEMISTRY
• ERYTHROID PRECURSORS SHOWS GLYCOPHORIN –A EXPRESSION
AND DECREASED CD71.
• MYELOID PRECURSORS MAY BE QUANTIFIED USING ANTIBODIES
FOR CD13 CD14 , CD33 ,AND CD34 .
• THERE IS DECREASE EXPRESSION OF CD11/CD18 IN NEUTROPHILS.
• MEGAKARYOCYTES MAY BE DETECTED BY THERE SPECIFICITY FOR
FACTOR 8 AND CD41 OR THE HPI-ID MONOCLONAL ANTIBODY.
• HIGH BCL2 EXPRESSION IN MDS.
• OVER EXPRESSION OF CD61 BY MEGAKARYOCYTES. 45

46. FLOW CYTOMETRY
• Erythroid abnormalities detected by
H- ferritin , CD71 ,CD105 in Glycophorin A
• Abnormal maturation pattern in granulocytes.
• For borderline dysplasia ,FC is highly suggestive
for MDS
only if aberrant features are present in all three
lineages
46

47. OTHER INVESTIGATION
. FERROKINETICS- TO ASSESS ERYTHROPOIESIS.
. HAEMOGLOBIN ELECTROPHORESIS OR HPLC, TO DETECT HbH
AND HbF
. GRANULOCYTE FUNCTION TESTS TO DEMONSTRATE DEFECTIVE
PHAGOCYTOSIS
. PLATELET FUNCTION TESTS TO DEMONSTRATE REDUCED
AGGREGATION
AND PROLONGED BLEEDING TIME.
. SERUM PROTEIN ELECTROPHORESIS TO ASSESS
IMMUNOGLOBULINS
AND DETECT PARAPROTEIN.
47

48. EVALUATION OF SUSPECTED MDS
• HISTORY
Prior exposure to CHEMOTHERAPY/RADIOTHERAPY
Recurrent infections, bleeding gums
. EXAMINATION
Pallor/ bruising
Splenomegaly
BLOOD COUNT
Hb, TLC, platelet count reticulocyte count
BLOOD FILM
Macrocytosis, cytopenia, neytrophilia, monocytosis pseudo
pelger huet anomaly,hypogranular neutrophils 48

49. CONTINUED…..
• Bone marrow aspirate
• Bone marrow trephine biopsy
• Bone marrow cytogenetics analysis
• Exclusion of reactive causes of dysplasia
• Megaloblastic anaemia
• Hiv infection
• Recent cytotoxic therapy
• Alcoholism
• Recurrent/ intercurrent infection
49

50. PROGNOSTIC FACTORS IN MDS
• LEUKEMIA BURDEN-
abnormal location of immature precursors .
.LINEAGE PENETRANCE AND SEVERITY OF MATURATION
IMPAIRMENT .
Number of cytopenia
number of dysplastic lineage
Cytopenia severity
GENETIC ABNORMALITIES
Protooncogenes mutation
DNA ploidy
CLINICAL AND PATHOLOGICAL FEATURES.
Myelofibrosis
50

51. International Prognostic Scoring System
(IPSS)
a scoring system for predicting survival and
Evolution to AML based on…..
(1) The percentage of blasts in the bone marrow
(2) Type of cytogenetic abnormalities
(3) Degree of number of cytopenias
Cytopenias- Hb<10 g/dl, neutrophil<1.8x109/L
Platelets<100x109/L
51

52. INTERNATIONAL PROGNOSTIC SCORING SYSTEM(ipss)
• IPSS :prognostic variables
• KARYOTYPE GOOD-in Normal ,del 5q alone,del 20 q alone.
INTERMIDIATE- +8 trisomy ,single karyotype anomoly,other abnormalities.
POOR- -Complex karyotype, chromosome 3 and 7 anomolies.
SCORE 0 0.5 1.0 1.5 2
%BM blast < 5 % 5-10 % 11-19 % 20- 30 %
KARYOTYPE GOOD INTERMEDIATE POOR
CYTOPENIAS 0-1 2-3 -
52

53. MORPHOLOGY FEATURES 0F SUBTYPES 0F MDS
(WHO 2008)
• WHO has defined the EIGHT tyes (with subtypes)of
MDS based on PS and BONE MARROW FINDINGS:
• REFRACTORY CYTOPENIA WITH UNILINEAGE
DYSPLASIA….INCLUDING
• A refractory anemia
• B refractory neutropenia
• C refractory thrombocytopenia.
53

54. Refractory anaemia, RCUD, RN, RT
(WHO)
• 10-20% of MDS.
• Older adults, median age- 65-70years.
PS-
• Anaemia, marked anisopoikilocytosis.
• Normochromic, normocytic/macrocytic,
• occasional hypochromia.
• Blasts are uncommon, less than 1%.
54

55. Refractory anaemia (WHO)…….
.Unilineage dysplasia must be present in 10% of
cells of one myeloid lineage.
• Bone marrow is usually hypercellular but can
be
normocellular or hypocellular.
• Ring sideroblasts are less than 15% of
erythroblasts
• and blasts are less than 5%.
• Low or intermediate IPSS scores.
• Progression to AML in 2%.
55

56. Refractory anaemia with ring sideroblasts
(WHO)
• 3-11% cases of MDS.
• PS-
Anaemia, normocytic normochromic, often
macrocytic, microcytic hypochromic, giving
dimorphic picture.
• Pappenheimer bodies may be present.
• Platelet counts increased, but not more than
450x109/L
56

57. Refractory anaemia with ring sideroblasts
• Bone marrow shows erythroid hyperplasia.
• Myeloblasts are <5% of BM nucleated cells.
• 15% or more of red cell precursors are ring
sideroblasts.
• Iron laden macrophages may be prominent.
• Very low rate of evolution to AML
57

58. REFRACTORY CYTOPENIA WITH MULTILINEAGE
DYSPLASIA (RCMD)
• Comprises about 30% of cases of MDS.
• Mostly elderly patients.
• PS-
Cytopenias (Hb<10g/dl, absolute neutrophil
count
<1.8x 109 /L and platelet count <100x 109 /L)
<1% blasts,
Auer rods not present and
monocytes are less than 1x 109 /L. 58

59. RCMD….
• Bone marrow-hypercellular
• Dysplasia in 10% of the cells in at least two
myeloid lineage.
• >15% ring sideroblasts.
• Intermediate scores according to IPSS.
• Frequency of leukemic transformation at the
end of two years in approximately 10% 59

60. REFRACTORY ANAEMIA WITH EXCESS OF
BLASTS
.It is MDS variant with 5-19% blast in the Bone
Marrow or 2-19% blasts in the peripheral blood.
Because of differences in survival and incidence of
Evolution to AML two categories of RAEB are
recognized.
RAEB-1 is defined by 5-9% blasts in the BM or 2-4 %
blast in the PB and,
RAEB-2 is defined by 10-19%blast in bone marrow or
5-9% blasts in PB.
The presence of Auer rods in blasts qualifies a case as
RAEB-2 irrespective to the blasts percentage. 60

61. RAEB ……
.The disease affects primarily individuals over 50 years
of age.it accounts for approximately 40% of all
patients with MDS.
.RAEB usually characterised by progressive BM failure
with lncreasing cytopenias, approximate 25% of
cases of RAEB-1 and 33% of patients with RAEB-2
progress to AML.
.The median survival is approximately 16 months for
RAEB-1 and 9 months for RAEB-2.
61

62. MDS UNCLASSIFIED/UNCLASSIFIABLE
• It is a subtype of MDS which initially lacks findings
appropriate for classification into any other MDS
category.
• Diagnostic criteria-
• 1. Pancytopenia in a patient who would otherwise fit
the criteria for RCUD OR
• 2. PS blasts <1% on two occasions in a patient who
would otherwise meet the criteria for RCUD and
RCMD OR
. 3. persistent cytopenia with<5% blasts in BM with
dysplasia in < 10% of cells of >1 cell lines. 62

63. MDS- U
3. Unequivocal dysplasia in not present in10%
of thecells in any lineages but a clonal
cytogeneticabnormality giving presumptive
evidence of MDS is present AND
4. PS blasts are not greater than 1%.
5. Bone marrow blasts <5%
63

64. MDS associated with isolated 5q
deletion syndrome
This is MDS associated with isolated 5q- .
Etiology- loss of tumour suppressor gene in
the deleted region.
. In the FAB classification patients with 5q-
anomaly fell into RA ,RARS or RAEB
categories.
• Patients are mainly women, usually middle
aged or elderly.
PS- Cytopenias, 1% blasts,
64

65. MDS WITH ISOLATED del(5q)…
• Bone marrow-
Hypercellular/normocellular.
• Erythroid hyperplasia.
• Megakaryocytes are increased in number and
arenormal to decreased in size with
hypolobated nuclei.
• <5% blasts.
• The rate of leukemic transformation is <10%.
65

66. 66

67. CHILDHOOD MDS
• Uncommon in children, accounts for less than 5% of
all haematopoietic neoplasms in patients less than
14 years of age.
• Refractory cytopenia of childhood (RCC) is a
myelodysplastic syndrome characterized by
persistent cytopenia with <5% blasts in the bone
marrow and <2% blasts in the peripheral blood.
• Monosomy 7 is the most common cytogenetic
abnormality (significantly higher probability of
progression).
67

68. RCC….
Dysplastic changes in at least 10% of cells of at
least two myeloid lineages.
Erythroid island with at least 20 cells maturation
arrest with excess proerythroblasts, increased
mitosis in erythroid cells.
.The detection of micromegakaryocytes is strong
indicator of RCC.
. About 75% of children with RCC show
considerable hypocellularity of the bone
marrow 68

69. OTHER TYPES OF MDS
Hypocellular MDS-
FAB group initially described MDS having a
hypercellular or normocellular bone marrow.
Subsequently it became apparent that some
cases, approximately 15% in all had
hypocellular bone marrow.
Their prognosis does not differ from MDS in
general.
D/Ds- Hypocellular AML and Aplastic Anaemia.
69

70. 70

71. THERAPY RELATED MDS
Distinctive haematological and cytogenetic
features.
Eosinophilia and basophilia are more common
Marked trilineage dysplasia, hypocellularity and
reticular fibrosis are common.
Cytogenetic abnormalities are more often
present than in de novo MDS.
Very poor prognosis.
71

72. MDS WITH MYELOFIBROSIS
• Some patients with MDS have considerable
reticulin deposition.
• It is important to distinguish these cases from
M7 AML with myelofibrosis.
• M7 AML has more than 20% blasts whereas
MDS with myelofibrosis has fewer.
. They have high incidence of complex
chromosomal abnormalities and poor prognosis
72

73. Evolution of MDS
• Patients with MDS may die of marrow failure as a
direct consequence of MDS or may die following
transformation to acute leukemia.
Myelodysplastic syndromes may evolve into other
MDS.
. Change is usually into a worse prognostic
category and very rarely into favorable.
Thus RA and RARS may evolve into either
CMML. 73

74. EVOLUTION OF MDS..
. Variation in number of monocytes can alter
classification, mainly between CMML and
RAEB and rarely ring sideroblasts disappear so
that RARS converts to RA.
• When acute leukemia supervenes it may
develop within a brief period or there may be
stepwise evolution over weeks and months.
• Acute leukemia that occurs in MDS is always
AML,but rare cases of ALL and bilineage/bi
phenotypic leukemia have been reported.
74

75. MANAGEMENT
o Chemotherapy.
o Supportive therapy, such as WBCs, RBCs,
Platelets transfusions.
o Erythropoietin , G-CSF, GM-CSF for cytopenia
o B.M transplantation in young patients.
o Antiangiogenic agents – Thalidomide
o Immuno supressive therapy 75

76. DIFFRENTIAL DIAGNOSIS OF MDS
• VITAMIN B12 AND FOLIC ACID DEFICIENCY-
can be differentiated from MDS as in it normal vit
B12 and folic acid.
. EXPOSURE TO ARSENIC AND OTHER HEAVY METALS.
.APLASTIC ANEMIA-
AA have markedly greater TNF receptor expression
than those from patients with MDS.
presence of monosomy confirm the diagnosis of MDS.
PARVO VIRUS INFECTION-
HIV INFECTION-
PAROXYMAL NOCTURAL HEMATURIA(PNH)-
IDIOPATHIC MYELOFIBROSIS- 76

77. REFERANCES
• Who fascicle
• Tejender singh hematology 4th edition
• Essential of hemathology Kawthalkar 2nd
edition
• Internet
77

78. THANK YOU…….
78