allopurinol and Lymphoma--Large-B-Cell--Diffuse

To identify patients with lymphoma at risk for tumor lysis after chemotherapy.. The case records of 102 patients receiving combination chemotherapy for non-Hodgkin's lymphoma (intermediate to high-grade histology) were reviewed. Patients were considered to have "laboratory tumor lysis" if two of the following metabolic changes occurred within 4 days of treatment: a 25% increase in the serum phosphate, potassium, uric acid, or urea nitrogen concentrations, or a 25% decline in the serum calcium concentration. "Clinical tumor lysis" was defined as laboratory tumor lysis plus one of the following: a serum potassium level greater than 6 mmol/L, a creatinine level greater than 221 mumol/L, or a calcium level less than 1.5 mmol/L, the development of a life-threatening arrhythmia, or sudden death.. Laboratory tumor lysis occurred in 42% of patients and clinical tumor lysis in 6%. There was no statistical difference in the frequency of either tumor lysis syndrome among lymphoma subgroups. Clinical tumor lysis occurred more frequently in patients with pretreatment renal insufficiency (serum creatinine level greater than 132 mumol/L) than in patients with normal renal function (36% versus 2%; p = 0.01). The development of azotemia correlated with high pretreatment serum lactate dehydrogenase concentrations (p < 0.01; r2 = 0.11).. Clinically significant tumor lysis is a rare occurrence in patients with lymphoma when they are receiving allopurinol. However, tumor lysis can occur in patients with all types of moderate to high-grade non-Hodgkin's lymphoma. Patients with a high serum lactate dehydrogenase level or renal insufficiency are at increased risk for metabolic complications after chemotherapy and should be closely monitored.

Topics: Acute Disease; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Blood Urea Nitrogen; Burkitt Lymphoma; Creatinine; Humans; Hyperkalemia; Hypocalcemia; L-Lactate Dehydrogenase; Leukemia, Lymphocytic, Chronic, B-Cell; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Lymphoma, T-Cell; Phosphates; Renal Insufficiency; Retrospective Studies; Risk Factors; Tumor Lysis Syndrome; Uric Acid

Topics: Allopurinol; Ampicillin; Antibody Formation; Cross Reactions; Cytomegalovirus Infections; Drug Contamination; Drug Eruptions; Drug Synergism; Erythema; Humans; Immunity, Cellular; Infectious Mononucleosis; Leukemia, Lymphoid; Lymphocytes; Lymphoma, Large B-Cell, Diffuse; Urticaria

Topics: Adult; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Breast Feeding; Chromatography, Liquid; Cyclophosphamide; Doxorubicin; Female; Humans; Infant, Newborn; Lymphoma, Large B-Cell, Diffuse; Mass Spectrometry; Milk, Human; Prednisone; Pregnancy; Pregnancy Complications, Neoplastic; Rituximab; Vincristine

Acute tumor lysis syndrome (TLS) is a life-threatening complication of cancer therapy requiring prompt recognition and aggressive management. It occurs particularly in patients with lymphoproliferative disease during potent myelosuppressive therapy. To our knowledge, acute TLS in end-stage renal disease (ESRD) patients with malignancy is extremely rare and has never been reported in English literature. We report the first case of acute TLS in an ESRD woman with diffuse large B cell lymphoma after chemotherapy. Aggressive treatments with daily hemodialysis and allopurinol rather than hydration benefit the patient. There is neither optimal therapy in treating ESRD patients with TLS nor adequate guidelines for how to adjust the chemotherapy drug in hemodialysis patients. This case provides our experience to clinician how to treat acute TLS in ESRD patients.

Topics: Acute Disease; Allopurinol; Antineoplastic Agents, Alkylating; Antineoplastic Agents, Hormonal; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Blood Cell Count; Blood Chemical Analysis; Cyclophosphamide; Dexamethasone; Enzyme Inhibitors; Female; Humans; Kidney Failure, Chronic; Lymphoma, Large B-Cell, Diffuse; Middle Aged; Renal Dialysis; Tumor Lysis Syndrome; Vincristine

Topics: Aged; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Cyclophosphamide; Dehydration; Doxorubicin; Drug Monitoring; Emergencies; Female; Fluid Therapy; Gout Suppressants; Humans; Lymphoma, B-Cell; Lymphoma, Large B-Cell, Diffuse; Nursing Assessment; Oncology Nursing; Prednisone; Risk Factors; Tumor Lysis Syndrome; Urate Oxidase; Vincristine

When differentiated into mature macrophages by the combination of all-trans retinoic acid and 1,25-dihydroxyvitamin D3, the human promonocytic cell lines U937 and THP-1 expressed inducible nitric oxide synthase (iNOS) transcripts. During their differentiation, the cells acquired the capacity to produce not only superoxide anion (O2.-) but also nitric oxide (.NO) in response to IgG (or IgE)-opsonized zymosan. The inhibitors of the iNOS pathway, aminoguanidine and NG-monomethyl-L-arginine (L-NMMA), suppressed the production of .NO and enhanced the steady-state concentration of O2.- determined. Conversely, superoxide dismutase (SOD) scavenged the O2.- released and increased the .NO-derived nitrite concentration detected. These data suggested a possible interaction between O2.- and .NO. In differentiated U937 (or THP-1) cells, IgG or IgE-opsonized zymosan induced a strong time-dependent luminol-dependent chemiluminescence (LDCL), which was abrogated by SOD and partially inhibited by aminoguanidine or L-NMMA. Since the iNOS inhibitors did not directly scavenge O2.-, LDCL determination in the presence or absence of SOD and/or iNOS inhibitors demonstrated a concomitant production of O2.- and .NO. These radicals induced the formation of a .NO-derived product(s), probably peroxynitrite (ONOO-), which was required to elicit maximal LDCL. Finally, LDCL measurement provided a convenient tool to characterize iNOS triggering and demonstrated an interaction between NADPH oxidase and iNOS products in human macrophagic cells phagocytizing opsonized-zymosan. These findings show that in activated macrophages, iNOS activity can be involved in LDCL and support the debated hypothesis of iNOS participation to the microbicidal activity of human macrophages.

Topics: Calcitriol; Cell Differentiation; Cell-Free System; Free Radical Scavengers; Guanidines; Humans; Immunoglobulin E; Immunoglobulin G; Leukemia, Monocytic, Acute; Luminescent Measurements; Luminol; Lymphoma, Large B-Cell, Diffuse; Macrophage Activation; Macrophages; Neoplastic Stem Cells; Nitrates; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; omega-N-Methylarginine; Opsonin Proteins; Phagocytosis; Superoxide Dismutase; Superoxides; Tretinoin; Tumor Cells, Cultured; Xanthine; Xanthine Oxidase; Zymosan

We describe an episode of obstructive uropathy produced by xanthine precipitation in the tubules of the kidney of a patient with histiocytic lymphoma during intensive chemotherapy, despite allopurinol therapy. Urinary oxypurine-uric acid ratio suggested a subclinical deficiency of hypoxanthine-guanine phosphoribosyltransferase. Results of an assay of this enzyme confirmed the abnormality. Both parents and three brothers of the patient had normal enzyme activity. The continued importance of adequate hydration for patients who receive allopurinol during initial periods of cancer therapy is emphasized.

Topics: Acute Kidney Injury; Adolescent; Allopurinol; Colonic Neoplasms; Humans; Hypoxanthine Phosphoribosyltransferase; Kidney Tubules; Lymphoma, Large B-Cell, Diffuse; Male; Purines; Xanthines

Topics: Adolescent; Adult; Aged; Allopurinol; Female; Hodgkin Disease; Humans; Leukemia, Lymphoid; Lymphoma; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Male; Middle Aged; Multiple Myeloma; Uric Acid

Topics: Adolescent; Antineoplastic Agents; Blood; Blood Urea Nitrogen; Drug Therapy; Geriatrics; Humans; Hyperuricemia; Leukemia; Leukemia, Myeloid; Lymphoma; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Metabolism; Neoplasms; Nitrogen; Pyrimidines; Sarcoma; Urea; Uric Acid; Uricosuric Agents; Urine; Xanthine Oxidase