Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocytic sarcoma (GS) is a rare extramedullary tumor composed of myeloblasts and other granulocytic precursors. GS is mostly associated with myeloproliferative disorders, myelodysplastic syndromes and acute myeloid leukaemia. These tumors arise in the absence of leukaemia, at its initial diagnosis or at the time of recurrence. The most common sites of involvement are bone, skin, soft tissue and lymph node. Reports of GS in testis are very rare. We report an unusual case of GS in a patient with megakaryoblastic leukaemia arising in the left testis after four months in complete remission attained with low doses of Ara-C and granulomonocytic stimulating factor.
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PMID:[Testicular granulocytic sarcoma as a form of relapse in a patient with acute megakaryoblastic leukemia]. 974 Dec 36

We report two cases of cytarabine (Ara-C) induced pericarditis. The first patient was a 61-year-old man with de novo acute myelogenous leukemia (AML) with trilineage myelodysplasia (M2). Fever and pericardial effusion developed after treatment with low-dose Ara-C and etoposide (VP16) during the patient's second leukemic relapse. The second patient was a 65-year-old man with myelodysplastic syndrome (MDS) transformed into AML (M2). He achieved a complete remission after treatment with low-dose Ara-C and VP16. However, during consolidation chemotherapy consisting of oral cytarabine ocfosfate and VP16, fever and pericardial effusion developed. In both cases, pericardiocentesis revealed exudative effusion with many neutrophils. Neither bacterial nor fungal infection was demonstrated. Chest symptoms and fever were resolved by methylprednisolone pulse therapy and pericardial drainage. Both patients were given a diagnosis of pericarditis caused by allergic reaction to Ara-C. We also report on 6 other patients with Ara-C syndrome who have been encountered by our hospital.
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PMID:[Cytarabine-induced pericarditis]. 986 24

Thirty-one patients (20 male and 11 female; median age 51 years (16-79)) with high-risk acute myeloblastic leukemia (AML) (20 refractory AML and 11 secondary AML (s-AML) (four to myelodysplastic syndrome, five to chemo/radiotherapy, one to aplastic anemia and one blastic chronic myelogenous leukemia (B-CML)) were treated with CBDCA (300 mg/m2/day x 5 days in continuous i.v. infusion) plus intermediate-dose Ara-C (500 mg/m2/day x 3 days in rapid i.v. infusion). Nine patients (29%) achieved CR (five s-AML (three myelodysplastic syndromes, one CML and one ALL) and four refractory AML) and 11 patients had resistant disease. There were 11 early deaths (35%). Median disease-free survival of the nine responders was 4 months. The main toxicity was hematological, febrile episodes took place in nearly all the patients (96%). The CBDCA plus Ara-C regimen showed an evident antileukemic activity in high-risk leukemia. However, the lack of long-term disease-free survivors shows the need for innovative postremission strategies. The high initial response rate seen in AML secondary to myelodysplastic syndromes (MDS) warrants further investigation of CBDCA in combination regimens for MDS patients.
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PMID:Carboplatin plus cytarabine in the treatment of high-risk acute myeloblastic leukemia. 1002 88

Ten patients with acute leukemia (AL) in early relapse after allo-BMT were treated with a modified MEC (mitoxantrone, etoposide and Ara-C) regimen followed by donor PBPC collected after mobilization with G-CSF. Seven patients achieved CR or had normal hemopoietic reconstitution: two had an early relapse at days +53 and +48, two patients died from acute GVHD at days +31 and +96, one died of interstitial pneumonia at day +55, and two patients experienced long-term survival. One patient with refractory disease and nodal involvement who did not respond to the first BMT had overt expansion of the leukemia at day +36; one patient with Ph+ ALL and one with ANLL evolving from MDS, both with skin involvement, had blast cells in peripheral blood at day +27 and +26, respectively. Transient cytopenia occurred in all patients; a normal granulocyte and platelet count was achieved within 3 weeks in all patients but one; acute GVHD occurred in six patients, and four had chronic GVHD. This approach is feasible in patients in early relapse after allo-BMT. It assists prompt re-establishment of normal donor hematopoiesis avoiding the prolonged cytopenia observed after donor lymphocyte infusion in AL patients relapsed after allo-BMT.
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PMID:Chemotherapy and donor peripheral blood progenitor cells for acute leukemia in early relapse after allogeneic bone marrow transplantation. 1021 92

A 65-year-old woman was admitted to our hospital with arthritis and agranulocytosis. She had given a diagnosis of acute myelogenous leukemia (FAB classification M1) a year ago and treated with 3 cycles of cytarabine and anthracycline or etoposide for 4 months, achieving complete remission state. Her bone marrow aspirate revealed normocellularity with normal karyotype (46, XX [20]) without apparent dysplastic feature at this time. She received autologous peripheral blood stem cell transplantation subsequently after conditioning regimen consisted of granulocyte colony-stimulating factor, busulfan, Ara-C and etoposide. Three months later, she started to manifest low grade fever, polyarthralgia and agranulocytosis and she admitted to our hospital after nine months. Bone marrow aspirate revealed marked hypocellularity with dysplastic features in three series of hematopoietic cells. Arthritis was dramatically improved after administration of prednisolone, but low granulocyte count continued. Bone marrow aspirate revealed karyotypic abnormality with monosomy 7 and we diagnosed her as myelodysplastic syndrome. Chemotherapy-induced myelodysplasia has been reported so far. This case would represent secondary myelodysplastic syndrome after chemotherapy. We could not clarify the etiology for polyarthritis but could be one of the paraneoplastic syndrome. We should note subsequent occurrence of myelodysplasia when planning treatment schedule.
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PMID:[Myelodysplastic syndrome after autologous peripheral blood stem cell transplantation for adult acute myelogenous leukemia]. 1042 26

We examined the bone marrow of 109 patients with myelodysplastic syndrome (MDS) at the time of diagnosis and during the course of the disease by means of Southern blot analysis and/or cytogenetic studies to detect and evaluate clonal markers, their implications for the prognosis of the disease, and the response to treatment. The patients either were enrolled in an EORTC study and received low-dose Ara-C with (n=31) or without (n=21) growth factors, according to the study protocol, or were treated supportively (only one patient received regular chemotherapy for concomitant lymphoma). Full or at least partial remission was achieved by 34% of the treated patients (n=54). In 57% (53 of 93) of all patients a clonal marker of either kind was detected by Southern blot analysis and/or cytogenetic examination. Clonal chromosomal aberrations were found in 45% (35 of 77) of the cases examined at diagnosis, with solitary del(5q) aberrations occurring in 10% of the cases and complex aberrations in 18%, trisomy 8 or monosomy 7 being a frequent finding. Of all patients, 49% (28 of 57) were characterized by one or more gene rearrangements (e.g., Ig-JH, TcR-beta, M-bcr, GM-CSF, G-CSF, or IL-3) at diagnosis. In five of 21 cases (24%) studied in hematological remission of the disease chromosomal aberrations were still detectable, and in seven of 23 (30%) a gene rearrangement persisted. We also found six cases with multiple clones exhibiting different susceptibilities to treatment and thereby indicating the oligoclonal character of this disease. Clinical evaluation revealed that the prognosis of the respective patients was directly related to the particular clonal markers detected at diagnosis: Risk groups were subdivided according to the karyotypes, with a solitary del(5q) aberration meaning a favorable, a normal karyotype an intermediate, solitary aberrations without del(5q) a poor, and complex karyotypes a very poor prognosis. We showed that densitometry helps to increase the sensitivity of Southern blot analysis by quantifying the amount of altered DNA, which often increases shortly before or at progression of MDS. Overall, there was a high level of concordance of both clonality examinations with the clinical course of the disease and the response rate. Therefore, we recommend cytogenetic studies and Southern blot analysis to detect clonal markers at diagnosis of MDS, to detect oligoclonality and clonal evolution, or to quantify the amount of clonal DNA, which appears to be a sensitive tool for evaluating the prognosis and response to therapy in MDS.
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PMID:Cytogenetic and Southern blot analysis to demonstrate clonality and to estimate prognosis in patients with myelodysplastic syndromes. 1066 17

Fifty-six patients older than 65 (median age: 77, range: 65-91) were treated in our general hospital, between January 1991 and November 1995 with the diagnosis of AML. Twenty-five were de novo AML (45%). The other cases which were considered as secondary AML (sAML) occurred after: myelodysplastic syndromes (19 cases: 34%), myeloproliferative disorders (7: 13%) or therapy of malignancies (5: 9%). Distribution of FAB subtypes was: M0: 4, M1: 8, M2: 14, M4: 10, M4eo: 1, M5: 10, M6: 1, unclassified: 8. Twenty-seven patients (48%) (de novo: 18, sAML: 9) received conventional "3 + 5" or "3 +7" induction chemotherapy +/- consolidation and maintenance (group 1). Low-dose Ara-C was given in eighteen cases (32%) (group 2), miscellaneous single agents were prescribed in seven cases and two patients received only supportive care. Sixteen early deaths (ED) (<1 month) occurred (29%). Distribution of age, WHO-PS, hyperleukocytosis, ED and median survival (MS) (3 months) was equivalent in de novo and sAML. Fifteen CR were achieved including twelve patients from group 1 (no difference between age <75 versus >75 years) and three from group 2. The MS of CR patients was 13 months. Eleven patients survived more than one year (de novo: 8). M5 subtype, fever >38 degrees C, high LDH level, WHO-PS>2, CR non achievement were predictive of reduced survival. Besides conventional induction, investigational therapies currently remain the best antileukemic modalities. Age per se should not be an exclusion criteria for treatment. Our data underline the high frequency of sAML in the community. Of note, this common type AML is largely excluded from many trials.
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PMID:De novo and secondary acute myeloid leukemia in patients over the age of 65: a review of fifty-six successive and unselected cases from a general hospital. 1070 52

A 72-year-old woman was given a diagnosis of severe aplastic anemia, and treated with anabolic steroid and cyclosporin A starting in October 1996. Because this treatment was ineffective, anti-thymocyte globulin (ATG) therapy was started in September 1997. In May 1998, chromosome analysis revealed transformation to myelodysplastic syndrome (MDS), refractory anemia with excess of blasts with monosomy 7 in 60% of metaphase cells. The patient showed gradual hematologic improvement and became transfusion independent. Despite progression to acute myeloid leukemia (FAB-M6) with monosomy 7 in 100% of metaphase cells in December 1998, the hemoglobin level recovered to 13.2 g/dl. In May 1999 the blasts increased rapidly and transformation to acute myelomonocytic leukemia (FAB-M4) was diagnosed. The patient was treated with low-dose Ara-C and aclarubicin with no improvement and died in August 1999. This case demonstrated the transformation of severe aplastic anemia to acute myeloid leukemia via MDS with monosomy 7 associated with transfusion independence after immunosuppressive therapy. These findings suggested a close relationship between aplastic anemia and hypoplastic MDS and the possibility of hematologic improvement based on the growth advantage of abnormal clones.
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PMID:[Transformation of severe aplastic anemia to myelodysplastic syndrome with monosomy 7 in a patient who achieved transfusion independence after immunosuppressive therapy]. 1084 67

We examined the differentiation-inducing effect on freshly isolated myeloid leukemia cells in liquid suspension culture by combined treatment with granulocyte colony-stimulating factor (G-CSF) plus low-dose cytosine arabinoside (Ara-C; 5-10 ng/ml) in 25 patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) in leukemic transformation. Culture with G-CSF alone showed leukemic cell growth stimulation in 15 out of the 25 cases (60%) and induction of cell differentiation in 19 out of the 25 cases (76%), respectively. In 23 cases (92%), either growth stimulation and/or differentiation induction of leukemia cells was observed in response to G-CSF. This suggests that most myeloid leukemia cells are able to respond to G-CSF stimulation. In addition, treatment of cells with low-dose Ara-C alone resulted in the enhancement of myeloid specific antigens expression in 16 cases (64%). Treatment of leukemia cells with higher concentrations of Ara-C (over 50 ng/ml) alone resulted in cytocidal effects but not in the induction of differentiation. Furthermore, 15 cases (60%) showed pronounced myeloid differentiation of leukemia cells after combined exposure to G-CSF plus low-dose Ara-C as compared with cells treated with either G-CSF or Ara-C alone. The enhanced effect of differentiation induction by combining G-CSF plus low-dose Ara-C was also observed in a murine myeloid leukemia cell line WEHI-3B in vitro. These data suggest that treatment with G-CSF plus low-dose Ara-C is capable of inducing differentiation of leukemic cells in vitro, and also appears to be useful for the differentiation-based therapy of patients with AML and MDS.
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PMID:Combination of granulocyte colony-stimulating factor and low-dose cytosine arabinoside further enhances myeloid differentiation in leukemia cells in vitro. 1097 97

Standard antileukemic chemotherapy induces complete remission in approximately half of patients with high-risk (HR) myelodysplastic syndrome (MDS). Intensification of induction therapy by the use of intermediate- or high-dose cytosine arabinoside in combination with fludarabine, idarubicin, or topotecan seemingly improved complete response (CR) rates, particularly in patients with poor prognosis karyotypes. The various high-intensity regimens appear to be comparable in inducing CR, although some are better tolerated with low mortality even in advanced-age populations with MDS. The encouraging early results with new agents, eg, topoisomerase inhibitors (topotecan) and hypomethylating agents (5-azacytidine), have been disappointing because long-term follow-up has shown continuous relapses. Regardless of the intensity of chemotherapy, remissions are short, even with continuation of intensive postremission therapy. Long-term disease-free survival remains dismal. In a large population with HR MDS treated with high-dose chemotherapy, only 5% of patients were alive at 3 years, and a majority of survivors were the younger patients with diploid karyotype refractory anemia with excess blasts in transformation. Further intensification of either induction chemotherapy or postremission therapy is unlikely to improve results with current drug combinations. With these results at hand, the role of intensive chemotherapy in the management of MDS remains controversial. Because CR status is associated with clinical benefits and possibly better survival, induction of CR should remain an important aim for HR MDS. The intensive combination chemotherapy may be integrated as an initial part of the management of HR MDS, as an alternative for patients not eligible for allogeneic bone marrow transplantation (BMT). Regimens with low early mortality, eg, topotecan plus intermediate dose Ara-C, could also be used to reduce tumor load prior to allogeneic BMT. Induction of CR should be attempted with the most effective and best tolerated regimens, particularly, but not only, in younger patients with good performance status regardless of karyotype. Postremission therapy remains a major challenge. It should involve either allogeneic BMT or investigational approaches to eliminate or control the minimal residual disease with different mechanisms In elderly patients, allogeneic "minitransplant" is an investigational alternative seeking to exploit graft-versus-tumor reaction. New agents, such as farnesyl transferase inhibitors (ras inhibitors), drug-antibody conjugates (Myelotarg), thalidomide, arsenic trioxide, maintenance chemotherapy with hypomethylating agents, or oral topoisomerase inhibitors along with agents modulating factors affecting growth and differentiation, should be explored to maintain remission with minimal compromise of quality of life. Although prognostic scoring systems such as the new International Prognostic Scoring System (IPSS) do not predict for initial response, IPSS continues to predict survival in patients treated with high-dose chemotherapy. Although activity of new agents could be rapidly assessed in single-arm pilot studies, the final merit of high-dose chemotherapy could be assessed only in well-designed randomized trials with patients assigned according to risk-based classification and evaluated for response by generally accepted and standardized criteria.
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PMID:Intensive chemotherapy for patients with high-risk myelodysplastic syndrome. 1103 61


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