Posters / Leukemia Research 35 (2011) S27–S142 S39

• ECOG scores remained low with higher age (69.2% of patients >84a

had ECOG-1) (Fig. 1).

• Patients < 65a and >79a received less median AZA cycles (Fig. 1).

• Patients >84a more often received AZA d1–5 (rather than d1–7)

than younger patients (Fig. 1).

• Toxicity, but not death, was more often the cause for AZA-stop in

patients >79a (Fig. 1).

• Age did not seem to significantly affect overall survival of patients

treated with AZA, neither from the timepoint of initial diagnosis

(p=.184), nor from AZA-start (p=.284) (Fig. 2).

• Interestingly, patients aged 75–79 (n =37) had by far the longest

OS as of AZA-start (677 days). Patients <65a did not fare better

than very old patients, most likely due to the fact, that younger

patients were treated more aggressively prior to AZA-start.

• All of the above lead to the conclusion, that elderly patients may

be safely treated with AZA and, allthough dose reductions to

day 1–5 were frequently made a priori, very old patients seem to

profit from AZA trestment, similarly to younger patients. Merely

patients >84 years seemed to fare worse. More detailed analysis

of response rates and reasons for death in this patient population

will be presented.

Figure 2. Effect of age on overall survival of patients treated with

azacitidine. Age does not significantly affect overall survival of

patients treated with azacitidine.

In addition, the effects of various levels of response on OS according

to age group have yet to be analized in detail and will be presented.

102

Azacytidine as a bridge to haploidentical bone marrow transplant

in a patient with hypocellular myelodysplasia with monosomy 7

S.K. Rana1, E. Das-Gupta2, N.H. Russell1. Haemato-Oncology and

Bone Marrow Transplantation, 1Clinical Haematology, 2Nottingham

University Hospitals, NHS Trust, Nottingham, UK

Background: 5-Azacytidine is increasingly becoming popular for

treating intermediate and high IPSS myelodysplasia, showing

improvement in peripheral blood values and reduced risk of

transformation to AML. The only curative treatment for MDS is

haematopoietic stem cell transplant and the use of novel therapies

is being explored as induction/bridging therapy prior to transplant.

Introduction: We report an interesting case of a gentleman with

severe aplastic anaemia who, following immunosuppressive therapy

with cyclosporine and ATG, progressed to RAEB2 MDS with a

hypocellular bone marrow and cytogenetic evidence of monosomy 7.

We were concerned that the use of intensive remission induction

therapy would render him aplastic and so elected to treat him with

azacitidine as a bridge to an allogeneic transplantation. He was

treated with 2 cycles of azacytidine, which he tolerated without

complication. This resulted in complete morphologic remission

and a major cytogenetic response with disappearance of the

monosomy 7. He went on to have a haploidentical transplant

from his son using fludarabine, cyclophosphamide and low dose

TBI conditioning. GVHD prophylaxis consisted of 2 doses of post

transplant cyclophosphamide as well as tacrolimus and MMF. He

is now nearly a year out from the transplant. He remains in

remission with good engraftment and 100% donor chimerism. His

post transplant course was uncomplicated and his only ongoing

problem is of limited cutaneous GVHD that is managed with topical

therapies.

Purpose: To evaluate the use of azacytidine as a bridging therapy

prior to allogeneic transplantation in hypocellular MDS.

Methods and Materials: Retrospective case note analysis and

literature search.

Result and Conclusion: So far there has been no consensus on the

use of Azacytidine as a bridging therapy to HSCT. The drug was used

in this case because the patient had a markedly hypocellular marrow

and we were concerned that more intensive treatment might have

resulted in delayed regeneration and prolonged cytopenias. Although

azacytidine is not the usual drug of choice to treat high grade MDS

prior to allogeneic transplantation, it may have a useful role in cases

such as this, where it has the potential to induce disease response

without the toxicities associated with intensive chemotherapy.

103

Therapy-related myeloid neoplasms following treatment with

radioiodine

T.M. Schroeder1, A. Kundgen1, N. Kroger2, U. Platzbecker3,

M. Stadler4, F. Braulke5, R.F. Schlenk6, F. Zohren1, D. Haase1,

N. Gattermann1, R. Haas1, G. Kobbe1, U. Germing1. 1Hematology,

Oncology and Clinical Immunology, University of Duesseldorf

Medical Faculty, Dusseldorf, 2Clinic for Stem Cell Transplantation,

University Hospital Hamburg Eppendorf, Hamburg, 3Hematology,

University of Dresden, Dresden, 4Hematology, Medical University of

Hannover, Hannover, 5Hematology, University of Goettingen, Gottingen,6Hematology, University of Ulm, Ulm, Germany

Development of therapy-related MDS/AML (tMDS/tAML) after

radioiodine treatment has been reported only sporadically and

is often summarized under the term radiation in the context of

tMDS/tAML. Recent data suggest, that radioiodine treatment is

associated with a 2.5-fold increased risk for the development of

tMDS/tAML and that a substantial fraction of tAML is caused by an

antecedent radioiodine therapy (Sawka et al.; Kayser et al.). Within

the Dusseldorf MDS registry, 4% of all treatment related MDS were

patients who underwent radioiodine treatment before the diagnosis

of MDS.

We report on 33pts (17 female, 16 male, median age: 62 y, range:

19–81y) who developed tMDS (n =20) or tAML (n =13) with a

median latency of 77 months (range: 6–440) after radioiodine-

therapy for benign (n =14) or malignant (n = 15) thyroid diseases

or carcinoid (n =1).

Of the 20pts with MDS 25% had RAEB II, 10% RAEB I, 20% RCMD,

10% RCMD-RS, 5% RA, 5% RARS, 15% 5q−syndrome, 5% CMML-II and

5% MDS/MPN. IPSS was low in 25% of the pts, int-1/-2 in 62% and

high in 13%. Six pts transformed into sAML within a median of 9mo

(range: 5–11) and 3 other pts progressed into an advanced MDS

subtype within 4mo (range 1–21).

Cytogenetics were available in 85% of the pts: 68% had an abnormal

karyotype including 38% with 1 and 18% with 2 aberrations and

11% with a complex or monosomal karyotype, respectively. 32% had

a favourable-, 46% an intermediate- and 22% a high-risk genetic

phenotype according to IPSS and ELN. Most frequently affected

chromosomes (chr) were chr 7 (22%), 5 (18%), 8 (14%) and 3 (11%).

Median OS of the entire cohort was 24 months.

The majority of pts was treated with best supportive care (58%).

Of 13pts receiving either induction chemotherapy (10pts) or

demethylating agents (3 pts) only 30% reached a CR. In total 10pts

received an allo-SCT, but 7 of them died either due to relapse or TRM.

Comparing this group with the non-transplant group allo-SCT did

not translate into a better OS (allo-SCT: 21mo, 95%CI 10–33mo vs.

28mo, 95%CI 2–55mo, p = .405).

In conclusion tMDS/tAML after radioiodine treatment is a

considerable late effect associated with a more advanced disease