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PubMed1984

Megakaryoblastic transformation in myeloproliferative disorders.

Megakaryoblastic transformation, with cells showing characteristic morphology and ultrastructural cytochemistry, developed in two patients with agnogenic myeloid metaplasia or myelofibrosis, and in one with chronic granulocytic leukemia. From the onset of the leukemic phase, all three have followed a relatively benign clinical course, surviving for 48, 29, and 24 months, respectively; only hydroxyurea has been necessary to control thrombocytosis. This experience emphasizes that it is possible for a patient to have an improved quality of life with minimum chemotherapy. In contrast, megakaryoblastic leukemia or acute myelofibrosis, where splenomegaly and a leukoerythroblastic blood picture are typically absent, responds poorly to any form of chemotherapy, and survival is short.

Blood Cell Count↗
PubMed1984

Increased incidence of thromboembolism in stage IV breast cancer patients treated with a five-drug chemotherapy regimen. A study of 159 patients.

We report an incidence of thrombosis of 17.6% in 159 patients treated with a five-drug chemotherapy regimen (cyclophosphamide, methotrexate, 5-fluorouracil, vincristine, and prednisone) for Stage IV breast carcinoma. Chi-squared analysis of risk factors for thrombosis (ambulatory status, obesity, family history, smoking, diabetes mellitus, hypertension, liver dysfunction, thrombocytosis, and previous endocrine therapy) showed no difference between the patients who had a thromboembolic event and those who did not. Statistical analysis revealed that a significantly higher incidence of thrombosis occurred during the chemotherapy regimen than when off this regimen (P less than 0.05). Detailed coagulation studies done prospectively on 10 patients receiving the five-drug chemotherapy regimen compared with 10 control patients showed a significantly elevated Factor VIII antigen:activity ratio in the group receiving the chemotherapy regimen compared with the control group and normals. These results implicate the chemotherapeutic regimen in the pathogenesis of the increased incidence of thrombosis. The pathophysiology of thrombosis in settings such as this awaits better in vitro tests defining the "hypercoagulable state."

Adult↗
PubMed1986

Preleukemic changes in cases of nonlymphocytic leukemia secondary to cytotoxic therapy. Analysis of 105 cases.

Peripheral blood changes preceding therapy-related leukemia were studied in 105 patients who had received cytotoxic therapy, 53 for Hodgkin's disease and 52 for other cancers. Preleukemic anomalies were observed in 74.3% of the cases, appearing after a mean interval of 68.7 months after diagnosis of the initial cancer. This interval was only 57.5 months in patients aged 50 years or older and only 42.3 months in patients with Hodgkin's disease having received cytotoxic therapy for 6 months or less. The first changes most frequently observed were pancytopenia (24.8%) and isolated erythrocyte abnormalities such as anemia or macrocytosis (18.1%). Involvement of two cell lines, isolated thrombocytopenia or leukopenia, circulating immature cells, monocytosis, leukocytosis, or thrombocytosis were also observed. Therapy-related myelodysplastic syndrome was recognized in 19 patients and myelofibrosis in 3. Median duration of the preleukemic phase was 6 months; 9 months in cases of isolated erythrocyte involvement and 5 months in the other cases. Myelomonocytic or monoblastic leukemia appeared less frequently when the first sign involved erythrocytes only. Hematological surveillance thus appears necessary in all patients having received cytotoxic therapy. Bone marrow study with cytogenetic examination should be performed in cases of persistent peripheral blood abnormalities.

Adolescent↗
PubMed1986

Clinical and prognostic features of Philadelphia chromosome-negative chronic myelogenous leukemia.

Between 1965 and 1982, 105 patients with a diagnosis of Philadelphia chromosome-negative chronic myelogenous leukemia were referred to our institution with minimal or no prior therapy. The median age was 63 years and 64% were males. The overall median survival from time of referral was 14 months; 53% of patients survived 1 year and only 10% survived beyond 5 years. At the time of analysis, 92 patients (88%) were dead, 56% of deaths being preceded by a blastic crisis. Compared with Philadelphia chromosome-positive disease, patients with Philadelphia chromosome-negative chronic myelogenous leukemia were older and had a significantly higher incidence of anemia, thrombocytopenia, monocytosis, marrow blasts, decreased marrow megakaryocytes and a lower incidence of basophilia and thrombocytosis. Chromosomal abnormalities occurred in 33% of patients and consisted most frequently of trisomy 8, or an additional chromosome C, loss of the Y chromosome, or abnormalities in chromosomes #5 and #7. Of nine pretreatment characteristics significantly associated with poor survival, a multivariate analysis identified four to have independent additive prognostic significance: severe thrombocytopenia, hemoglobin levels less than 10 g/dl, increasing peripheral blasts and promyelocytes, and age 60 years or older. Monocytosis was not of prognostic significance. The derived prognostic model divided patients into three risk groups, low, intermediate, and high, with median survivals of 36, 16, and 3 months, respectively. The authors conclude that Philadelphia chromosome-negative chronic myelogenous leukemia is a distinct entity among the myeloproliferative syndromes with characteristic clinical and laboratory features and a poor prognosis. Prognostic factors and related risk categories were demonstrated within this disease entity.

Adolescent↗
PubMed1987

The relevance of reticulin stain-measured fibrosis at diagnosis in chronic myelogenous leukemia.

Although collagen myelofibrosis indicates poor prognosis in late stages of chronic myelogenous leukemia, the significance of reticulin stain-measured fibrosis in newly diagnosed patients is unknown. One hundred and thirty-eight patients with untreated or minimally treated chronic phase Philadelphia chromosome-positive chronic myelogenous leukemia had reticulin stain studies made on their bone marrows at diagnosis. Reticulin fibrosis was graded on a scale of 1 to 4. Significant (Grade 3 or 4) fibrosis was noted in 65 patients (47%). Compared with patients with mild (Grade 1 to 2) reticulin fibrosis, those with significant fibrosis had a higher incidence of splenomegaly greater than or equal to 10 cm (29% versus 49%; P = 0.02), hemoglobin less than 10 g/dl (19% versus 49%; P less than 0.01), weight loss greater than or equal to 6.75 kg (10% versus 30%; P = 0.11), marrow blasts greater than or equal to 5% (7% versus 28%; P less than 0.01), peripheral blasts greater than or equal to 3% (30% versus 46%; P = 0.09), and additional karyotypic abnormalities (1% versus 17%; P less than 0.01). The incidence of thrombocytosis was similar in the two groups. Prognostically, median survival was significantly shorter for the 26 patients with Grade 4, compared with the 39 patients with Grade 3, and the 73 patients with Grade 1 or 2 reticulin fibrosis (32 versus 49 versus 57 months; P = 0.03). Reticulin fibrosis is a useful biologic and prognostic index in newly diagnosed patients with chronic phase chronic myelogenous leukemia.

Actuarial Analysis↗
PubMed1987

Leukocytosis and large cell lung cancer. A frequent association.

In a retrospective study of 105 patients with non-small cell lung cancer during a 5-year period, 43 had leukocytosis. In 19 of the 43 patients, no clear cut etiology for the leukocytosis was apparent and it was attributed to the tumor itself. In these 19 patients, absolute neutrophilia was detected in 13, eosinophilia was present in three, and eleven exhibited concomitant thrombocytosis. Tumor-associated leukocytosis occurred predominantly, and eosinophilia exclusively, in patients with large cell pulmonary neoplasms. These results suggest an unusual myeloproliferative stimulus in this type of cancer. It may result from tumor cell production of hemopoietic growth factors such as granulocyte-macrophage colony-stimulating activity; however, additional studies are needed to elucidate the underlying mechanism(s), and to determine whether this is a peculiar characteristic of the cells that comprise large cell undifferentiated carcinoma of the lung.

Adenocarcinoma↗
PubMed1991

Clinical significance of hematologic parameters in non-Hodgkin's lymphoma at diagnosis.

Three hundred seventeen patients with non-Hodgkin's lymphoma (NHL) (54 low grade, 180 intermediate grade, 76 high grade, and seven unclassified) treated with chemotherapy were evaluated for the presence of hematologic abnormalities at diagnostic staging. Anemia was present in 42%, leukopenia in 6%, thrombocytopenia in 13%, leukocytosis in 26%, and thrombocytosis in 14% at presentation. The presence of bone marrow involvement by lymphoma was more likely to be associated with leukopenia and thrombocytopenia than the absence of bone marrow involvement. Although anemia was slightly more common in patients with bone marrow lymphoma than in those without marrow lymphoma, the difference was not statistically significant. Hematologic parameters were similar for patients with B-cell or T-cell lymphoma. Evidence of bone marrow failure with multiple cytopenias was present in 26 patients (8%). Leukoerythroblastosis was present in 2%. Circulating lymphoma was present in 9.5%. Anemic patients had a shorter survival time than nonanemic patients, whether bone marrow was involved by lymphoma or not. Survival was not affected by the presence of leukopenia or mild leukocytosis, but, in patients without marrow lymphoma, leukocytosis with a leukocyte count greater than 20 x 10(9)/l was associated with short survival length. Thrombocytopenia was associated with short survival time only in patients with bone marrow involvement by lymphoma. Patients with multiple cytopenias or leukoerythroblastosis had short survival times, but the presence of circulating lymphoma did not alter survival when compared with other patients with bone marrow involvement by lymphoma. These data suggest that hematologic evaluation at the time of diagnostic staging of NHL provides useful prognostic information that may have therapeutic implications.

Anemia, Myelophthisic↗
PubMed1992

Clonal evolution in primary 5q-syndrome.

Primary 5q-syndrome is a type of myelodysplastic syndrome characterized by refractory anemia, thrombocytosis, and hypolobulated megakaryocytes. The risk of leukemic transformation is low. A case of 5q- syndrome that occurred in a 42-year-old woman and was complicated by leukemic transformation 7 years after the initial diagnosis is reported. An additional clonal karyotypic anomaly, del(7q), was seen in the leukemic cells. The literature on leukemic and karyotypic evolution of primary 5q- syndrome is reviewed and the implication of karyotypic evolution is discussed.

Acute Disease↗
PubMed1994

Paraneoplastic cholestasis and hypercoagulability associated with medullary thyroid carcinoma. Resolution with tumor debulking.

The authors report a 69-year-old woman with a hypercoagulable state manifesting as superior sagittal sinus thrombosis, thrombocytosis, right lower extremity deep venous thrombosis, and subsequent pulmonary embolus. The liver enzyme values were elevated in a cholestatic pattern. Carcinoembryonic antigen level was markedly elevated. Evaluation revealed that her longstanding "goiter" had slowly enlarged during the past 6 years. The serum calcitonin level was markedly elevated. Subsequent biopsy revealed medullary thyroid carcinoma. Surgical debulking of the tumor and lymph nodes resulted in substantial reduction of the calcitonin and carcinoembryonic antigen levels in a matter of days. Long-term follow-up revealed normalization of cholestasis and resolution of the hypercoagulable state. Review of the literature revealed no previously reported cholestasis or hypercoagulable state associated with medullary thyroid carcinoma. The literature on paraneoplastic cholestasis, carcinoembryonic antigen production, and hypercoagulable states is reviewed.

Aged↗
PubMed1995

Philadelphia chromosome-negative chronic myelogenous leukemia with rearrangement of the breakpoint cluster region. Long-term follow-up results.

BACKGROUND: Five to 10% of patients with chronic myelogenous leukemia (CML) do not have the Philadelphia chromosome (Ph), but one-third of them have rearrangements of the breakpoint cluster region (BCR-positive). METHODS: The authors analyzed the characteristics, treatment response, and prognosis of 23 patients with BCR-positive, Ph-negative CML, and compared them with patients with Ph-positive CML, Ph-negative BCR-negative CML and chronic myelomonocytic leukemia (CMML) treated during the same period. RESULTS: Seventeen patients had early chronic phase CML, 3 had late chronic phase, 2 had accelerated phase, and 1 had blastic phase. The median age was 44 years (range, 14-71 years), median platelet count was 402 x 10(9)/l, and median leukocyte count was 86 x 10(9)/l. Fourteen of the 17 patients with early chronic phase CML received alpha-interferon; 12 (86%) achieved complete hematologic remission. Median survival in chronic phase CML was 60 months (range, 3-90+ months). Patients with Ph-negative BCR-positive CML and those with Ph-positive CML had similar characteristics and outcome. Compared with patients with Ph-negative BCR-negative CML and CMML, patients with Ph-negative BCR-positive CML and Ph-positive CML were significantly younger, had a significantly higher incidence of leukocytosis, thrombocytosis, and peripheral and marrow basophilia, and a significantly lower incidence of anemia, thrombocytopenia, marrow blast percent, and peripheral and marrow monocytosis. The median survival was 60 months for Ph-negative BCR-positive CML, 73 months for Ph-positive CML, 25 months for Ph-negative BCR-negative CML, and 9 months for CMML (P < 0.001). When analyzed adjusting for their stage, patients classified with Ph-negative BCR-positive CML. Stage I disease had a significantly better survival than did patients with Ph-negative BCR-negative CML (P < 0.02). CONCLUSIONS: Patients with Ph-negative BCR-positive CML are similar to those with Ph-positive CML and should be treated with the same approaches.

Adolescent↗
PubMed1995

Myelodysplasia. The clinical spectrum of 51 patients.

BACKGROUND: Over a 15 year period, the authors followed 51 male patients with myelodysplastic syndromes whose clinical findings, laboratory data, and evolution demonstrated a wide spectrum of disease. METHODS: The following characteristics were assessed: age at diagnosis, risk factors, clinical presentation, laboratory features, category of myelodysplasia, leukemic conversion, and overall survival. RESULTS: The clinical manifestations included hemolytic episodes in two patients, antibody-mediated thrombopenia in one, marked marrow fibrosis in two; thrombocytosis in three, and simultaneous lymphoproliferative disorders in two. There were 21 patients whose marrow was either normo- or hypocellular. Six patients presented with single cytopenia but not anemia. There were six instances of overlapping of the French-American-British classification. Eighteen patients progressed to acute leukemia and 1 to chronic myelomonocytic leukemia. CONCLUSIONS: These observations indicate that patients with myelodysplastic syndromes may have single cytopenia without anemia that progresses to acute leukemia and may, rarely, evolve into chronic myelomonocytic leukemia. The clinical aspects of these syndromes may include autoimmune phenomena and myeloproliferative features.

Adult↗
PubMed1995

The breakpoint cluster region site in patients with Philadelphia chromosome-positive chronic myelogenous leukemia. Clinical, laboratory, and prognostic correlations.

BACKGROUND: The breakpoint site of the breakpoint cluster region (bcr) has been correlated with patient characteristics, with the disease phase, and with the prognosis of patients with chronic myelogenous leukemia (CML), but the findings remain controversial. METHODS: Appropriate restriction enzymes and the 3' and universal probes were used to map the breakpoint site by Southern blot analysis into 5' and 3' breakpoints and a breakpoint in zone 3 (or fragment 2) in 362 patients in different phases of CML (238 in early chronic phase, 69 in late chronic phase, 31 in accelerated phase, and 24 in blastic phase). Standard statistical methods were used to evaluate differences in characteristics and in prognosis by the breakpoint site. RESULTS: No correlation was noted between CML phases and breakpoint site. Among patients in the early chronic phase, thrombocytosis was significantly associated with the 3' breakpoint site (P = 0.02), whereas peripheral basophilia occurred more frequently with the 5' breakpoint site (P = 0.05). Other patient and disease characteristics were similar in frequency among the breakpoint-site subgroups. There was no difference in response to alpha-interferon therapy (186 patients treated) by the breakpoint site. Survival, dated from either referral to the authors' institution or from diagnosis, was not significantly different among patients with early chronic phase CML by the breakpoint site. However, patients with a 3' deletion tended to have a shorter survival. CONCLUSION: Determination of the breakpoint site by Southern blot analysis does not help to predict prognosis of patients with CML.

Chromosomes, Human, Pair 22↗
PubMed2000

Early predictors of poor functional outcome in systemic-onset juvenile rheumatoid arthritis: a multicenter cohort study.

OBJECTIVE: To examine the ability of a previously described set of criteria to predict poor functional outcome in a large, multicenter cohort of children with systemic-onset juvenile rheumatoid arthritis (JRA). METHODS: All children who were diagnosed with systemic-onset JRA since 1980 at the Hospital for Sick Children (Toronto), since 1983 at the Isaac Walton Killam Hospital for Children (Halifax), and since 1981 at the Children's Hospital of Eastern Ontario (Ottawa) were evaluated. Patients were included in the study if they had been evaluated clinically within 6 months of diagnosis and had been followed up for at least 2 years. Patients were divided into 4 cohorts according to their length of followup: 2-4 years, 4-7 years, 7-10 years, and >10 years. Using previously described criteria for destructive arthritis in children with systemic-onset JRA, the patients were classified as either high risk or low risk for poor functional outcome based on the data from their 6-month visit. High-risk patients had active systemic disease (persistent fever or corticosteroid requirement for control of systemic disease) and a platelet count > or =600 x 10(9)/liter. Poor outcome was defined as moderate or severe disability (defined as a score of > or =0.75 on the Childhood Health Assessment Questionnaire) or disease-associated death. RESULTS: Among 122 eligible patients with systemic-onset JRA, we were able to contact 111 (91%) for outcome data. The mean followup period was 7.7 years (SD 3.7). The mean age at outcome assessment was 13.5 years (SD 5.3). There were 51 boys and 60 girls. Twenty-four patients (22%) had moderate-to-severe disability and 2 patients died; these 26 patients were considered to have had a poor outcome. We could determine risk classification for 104 patients. Twenty-four patients (23%) met the criteria for high risk at the 6-month visit. Overall, the risk of a poor functional outcome was significantly higher in the high-risk group (relative risk 3.3, 95% confidence interval [95% CI] 1.73-6.43, P = 0.0004). This risk was most marked in the cohort with > 10 years of followup (relative risk 4.3, 95% CI 1.82-10.29, P = 0.006). CONCLUSION: The presence of active systemic disease at 6 months, as characterized by fever or the need for corticosteroids, and thrombocytosis strongly predicted the development of a poor functional outcome in these patients. This was especially apparent with longterm followup. Our study validates the previously developed prognostic criteria for systemic-onset JRA.

Activities of Daily Living↗
PubMed2003

Acute leukemia and myelodysplasia in patients with a Philadelphia chromosome negative chronic myeloproliferative disorder treated with hydroxyurea alone or with hydroxyurea after busulphan.

Eighty-three patients with various chronic myeloproliferative disorders [polycythemia vera (PV), essential thrombocytosis (ET), idiopathic myelofibrosis (IMF)] were analyzed for the occurrence of acute myeloid leukemia (AML) and myelodysplasia (MDS) during treatment with hydroxyurea (HU) alone or HU following treatment with busulphan (BU). A total of 58 patients (29 PV, 14 ET, 12 IMF, 3 unclassified) had been treated with HU. Thirty-five of these patients had been treated with HU alone whereas 18 patients had received both HU and BU. The follow-up period was 7.8 years. Twenty-five patients had not been treated with HU. In this patient group, 4 patients had been treated with BU. The follow-up period was 10.5 years. In the HU-treated group (n = 58) 7 patients developed AML and 5 patients MDS. Five of the 12 patients had been treated with HU alone, and 4 patients had received both HU and BU. In the non-HU-treated group (n = 25) 1 patient with PV developed acute myeloid leukemia (AML). This patient had only been treated with phlebotomies. It is concluded that treatment with HU is leukemogenic, with an incidence of AML and MDS of approximately 14% when used alone. The incidence is markedly increased to about 30% when HU is preceded by treatment with BU. HU is not recommended for use in younger patients, in whom non-leukemogenic agents such as alpha-interferon and anagrelide should be used instead.

Acute Disease↗
PubMed2005

Every case of essential thrombocythemia should be tested for the Philadelphia chromosome.

Essential thrombocythemia (ET) and chronic myelogenous leukemia (CML) usually present with distinctive features. Citing experience with cases that overlap, the Polycythemia Vera Study Group recommends that negative tests for the Philadelphia chromosome be obtained before diagnosing ET. We describe two young women presenting with features absolutely typical for ET, including extreme thrombocytosis, no leukocytosis, no basophilia, no peripheral immature cells, and no splenomegaly. Severe thrombotic complications ensued: multiple cerebrovascular thromboemboli, pulmonary emboli, and miscarriage in one and myocardial infarction in the other. By 4 years, both developed leukocytosis, extreme basophilia, and circulating blasts, typical of accelerated CML. Cytogenetic studies were then performed, revealing the Philadelphia chromosome. Imatinib produced rapid clearing of blasts and basophils, but one woman later succumbed after allogeneic bone marrow transplant and the other has not achieved a major cytogenetic response. We conclude that CML can present in identical fashion as ET. The mandate for routine Philadelphia chromosome testing is magnified by the availability of targeted therapy and its greater efficacy in early stage disease.

Adult↗
PubMed2006

Spontaneous megakaryocytic colony formation does not discriminate between essential thrombocythemia and polycythemia vera.

Laboratory detection of spontaneous growth of colony-forming unit-megacaryocytes (CFU-MK), allowing us to distinguish essential thrombocythemia (ET) from reactive thrombocytosis, is therefore useful for the diagnostic of this myeloproliferative disorder. Whether CFU-MK assays allow us to discriminate at least partly between ET and other myeloproliferative disorders such as polycythemia vera (PV) remains, however, to be established. To gain insights about this point, we have performed CFU-MK cultures from bone marrow cells of patients diagnosed with ET (n = 42) or PV (n = 50) using a standardized collagen-based serum-free method. Spontaneous growth of CFU-MK was similarly detected in both 40/42 patients with ET and 47/50 patients with PV. These data suggest clearly that the CFU-MK assay is useful to detect not only ET, but also PV, but fails to discriminate, even partly, between these two myeloproliferative disorders.

Adolescent↗
PubMed2006

Transcriptosome and serum cytokine profiling of an atypical case of myelodysplastic syndrome with progression to acute myelogenous leukemia.

A Native American-Indian female presenting with anemia and thrombocytosis was diagnosed with myelodysplastic syndrome (MDS, refractory anemia). Over the course of 5 years she developed cytopenias and periods of leukocytosis with normal bone marrow (BM) blast counts, features of an unclassifiable MDS/MPS syndrome. The patient ultimately progressed to acute myelogenous leukemia (AML, FAB M2) and had a normal karyotype throughout her course. The episodes of leukocytosis were associated with infectious complications. Transformation to AML was characterized by a BM blast percentage of 49%. Peripheral blood and BM samples were obtained for serum protein analysis and gene expression profiling (GEP) to elucidate her disease process. An ELISA assay of the serum analyzed approximately 80 cytokines, which demonstrated that hepatocyte growth factor/scatter factor and insulin-like growth factor binding protein 1 were markedly elevated compared to normal. GEP demonstrated a unique "tumor molecular profile," which included overexpression of oncogenes (HOXA9, N-MYC, KOC1), proliferative genes (PAWR, DLG5, AKR1C3), invasion/metastatic genes (FN1, N-CAM-1, ITGB5), pro-angiogenesis genes (c-Kit), and down regulation of tumor suppressor genes (SUI1, BARD1) and anti-apoptotic genes (PGLYRP, SERPINB2, MPO). Hence, a biomics approach has provided insight into elucidating disease mechanisms, molecular prognostic factors, and discovery of novel targets for therapeutic intervention.

Aged↗
PubMed2007

Megakaryocytic blast crisis as first presentation of chronic myeloid leukemia.

We describe an extremely rare case of megakaryocytic blast crisis as first presentation of chronic myeloid leukemia. The patient had a very high platelet count and developed an ischemic stroke with seizures. She was treated with hydroxyurea, platelet apheresis, ARA-C, and idarubicin in order to obtain a prompt reduction of thrombocytosis and then with imatinib 600 mg/die PO. The therapy induced a complete hematological remission with a resolution of neurological signs within 4 weeks.

Antineoplastic Agents↗