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Aaron Polliack

Publications and source records attributed to Aaron Polliack.

27 records · Page 2Linked to original sources
PubMed2002

Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis.

This case report deals with an unusual leukostatic complication in a 56-year-old woman with acute myeloblastic leukemia (AML) and extreme hyperleukocytosis (316 x 10(9)/L) who presented with acute myocardial infarction (MI). After leukopheresis the patient achieved hemodynamic stabilization and rapid neurologic recovery of encephalopathy that had also developed after the infarction. Considering the central role of WBC in the remodeling of post MI myocardial tissue, it was obvious that administration of chemotherapy with its subsequent inevitable pancytopenia could impose an increased risk for further cardiac complications including myocardial rupture. Nevertheless, cytarabine-based induction chemotherapy was initiated 3 days after admission, and she achieved prolonged complete remission. Coronary angiography disclosed segmental atherosclerosis, but the only significant obstruction was in the right coronary artery. The patient died with relapsed leukemia 7 years later without recurrence of any cardiac symptoms or signs. Autopsy disclosed segmental coronary atherosclerosis involving the LAD (60% obstruction), suggesting that atherosclerosis was a predisposing risk factor. Additional compromise to blood perfusion due to leukostasis had led to this unusual complication of AML involving a major vessel. This is the first documented case of leukostasis causing coronary artery occlusion as well as the first report of successful induction chemotherapy for AML during a myocardial infarction.

Aminoglycosides↗
PubMed2002

Heparanase expression in human leukemias is restricted to acute myeloid leukemias.

OBJECTIVE: Matrix metalloproteinases and an endo-beta-D-glucuronidase (heparanase) are enzymes that degrade the protein and carbohydrate constituents of basement membranes, thereby facilitating transendothelial migration of blood-borne cells. Heparanase activity was found to correlate with the metastatic potential of solid tumors. We evaluated heparanase expression, at the levels of gene and protein expression and activity in a variety of leukemias, and compared it with normal hematopoietic cells. MATERIALS AND METHODS: Heparanase expression was evaluated in leukocytes isolated from peripheral blood of 71 patients with myeloid and lymphoid leukemias, or non-Hodgkin's lymphoma. Analysis was performed at two levels: heparanase RNA was determined by reverse transcriptase polymerase chain reaction, and heparanase protein was evaluated by immunocytochemistry and flow cytometry. RESULTS: In eight peripheral blood samples from normal donors, heparanase RNA was detected, and protein was found within the cytoplasm of granulocytes. In mononuclear cells derived from various leukemias, heparanase RNA was expressed in 14 of 15 acute myeloid leukemia (AML) samples. In contrast, cells derived from all 33 chronic lymphoblastic leukemia, all 7 non-Hodgkin's lymphoma, 7 of 8 chronic myeloid leukemia, and 6 of 8 acute lymphoblastic leukemia patients showed no detectable expression of the heparanase RNA. Heparanase protein was detected primarily within the cytoplasm of AML cells, indicating that the enzyme is produced and stored within the cytoplasm of myeloid cells, with limited expression on the cell surface. CONCLUSION: We propose that heparanase expression is associated with the myeloid lineage and may serve as an independent marker to support the identification of AMLs.

Acute Disease↗
PubMed2002

Large-cell transformation of chronic lymphocytic leukemia and follicular lymphoma during or soon after treatment with fludarabine-rituximab-containing regimens: natural history- or therapy-related complication?

Novel therapeutic regimens containing purine analogs and monoclonal antibodies have led to significant improvement in the course of indolent lymphoproliferative diseases (LPD). Complete clinical and even molecular remissions have been achieved in an increasing proportion of patients. In parallel to their tumor cytotoxic effect, these agents are inevitably associated with prolonged immunosuppression inherent to their mechanism of antilymphocytic activity. Until now, attention has been paid mainly to opportunistic infection occurring as a result of the above drug-induced immunosuppression and less to other possible complications, such as malignancy or tumor progression in the immunocompromised host. Here we briefly report nine patients with previously treated indolent LPD in whom the onset of large-cell transformation occurred during or shortly after the initiation of regimens containing these agents before transformation occurred. One patient had received rituximab alone, three fludarabine-containing regimens and five received sequential regimens containing both agents. This

Adult↗
PubMed2002

Development and rapid dissemination of Merkel-cell carcinomatosis following therapy with fludarabine and rituximab for relapsing follicular lymphoma.

This report deals with an unusual case of a patient with follicular small cleaved lymphocytic lymphoma who developed Merkel-cell carcinoma soon after receiving chemoimmunotherapy with a fludarabine-containing regimen and rituximab. The presentation of the Merkel-cell carcinoma in this patient was atypical because of the absence of dermal involvement and the very rapid clinical progression. In the light of recent reports which suggest a possible link between the immunocompromised state and the development of Merkel-cell carcinoma, the atypical presentation seen in this patient may indeed imply a possible link between the therapy given and the development of Merkel-cell carcinoma. To the best of our knowledge, this is the first documentation of Merkel-cell carcinoma appearing in a patient soon after treatment with fludarabine and/or rituximab.

Antibodies, Monoclonal↗
PubMed2002

Large B-cell lymphoma manifesting as an invasive cardiac mass: sustained local remission after combination of methotrexate and rituximab.

Cardiac tumor is an infrequent but serious manifestation of lymphoma and optimal management has not been well defined in these rare cases. Here we describe a patient who after autologous transplant for large B-cell lymphoma, relapsed with an invasive cardiac tumor, infiltrating the full thickness of the right myocardial wall. During therapy, she developed hemodynamic collapse due to complex atrial arrhythmias and had to be treated and stabilized in the intensive cardiac care unit. Despite initial significant regression of the cardiac tumor, new extranodal sites of lymphoma soon appeared in the skin, stomach and nervous system. Because of poor compliance, she was given salvage therapy with weekly four i.v. infusions of methotrexate and rituximab followed by monthly four maintenance cycles of rituximab alone. This produced an unexpected prolonged complete remission lasting 12 months, but she then developed a fatal leukemic phase. The relapse spared the heart and no cardiac abnormality was evident clinically or by any imaging technique. To the best of our knowledge this case, unique in terms of tumor size and extent of invasion, represents the first report of the treatment of invasive cardiac lymphoma using a combination of modest chemotherapy and rituximab.

Adult↗