Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two children with leukemia are presented, each demonstrating an unusual aspect of anthracycline-induced cardiomyopathy. In the first patient (a 7-month-old female with acute monocytic leukemia) extremely young age and previous chemotherapy with a podophyllotoxin derivative, VP-16, may have prediposed the patient to fatal congestive heart failure at a total Daunorubicin dose of only 225 mg/m2. In the second patient, a delay of 4 1/2 years was not sufficient in preventing congestive heart failure resulting from the administration of additional anthracycline chemotherapy. We conclude that extremely young age and, possibly, prior therapy with VP-16 may be addition risk factors in the development of anthracycline cardiomyopathy. Also, we suggest that once an anthracycline agent has reached a toxic threshold for the myocardium, the heart may always be at risk to injury from additional Adriamycin or Daunorubicin therapy.
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PMID:Anthracycline cardiomyopathy in children: report of two cases. 29 72

Autoimmune hemolytic anemia often develops in patients with chronic lymphocytic leukemia, particularly elderly women. It is heralded by a drop in the hematocrit, elevation of reticulocytes, development of jaundice, or a rise in the indirect fraction of serum bilirubin. Evidence of hemolysis supports the diagnosis, and a positive result of the Coombs test confirms it. Survival time is considerably shorter in patients who have both diseases than in those with chronic lymphocytic leukemia alone. Presenting symptoms in patients with the two diseases may include weakness, dizziness, fever, or hemorrhagic phenomena. If the anemia is severe, palpitations, otic pulsations, and cardiac decompensation are common. Physical examination may show enlargement of reticuloendothelial structures. On the other hand, some patients may be essentially asymptomatic. The hemolytic process must be treated as a separate entity, as even vigorous treatment of the leukemia often does not control it. Corticosteroid therapy is preferred, with splenectomy as a second line of defense. If the patient is not a good surgical risk, chemotherapy should be considered. Transfusions are usually incompatible but should be risked if progressive congestive failure, neurologic disturbance, angina, or signs of an impending infarct are present.
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PMID:When autoimmune hemolytic anemia complicates chronic lymphocytic leukemia. 63 66

A study on 25 South African Black patients with chronic myelogenous leukaemia (CML), who were followed for 3 1/2 years, is reported. The Ph chromosome was found in 19 of 20 patients studied. Males predominated in a ratio of 2,5:1. Several unusual clinical features were encountered: significant lymphadenopathy, congestive cardiac failure and skin lesions. Patients with lymphadenopathy responded to busulphan therapy no differently from patients without lymphadenopathy. Nine patients had congestive cardiac failure, and in 7 of these a cause could not be found. Three untreated patients became pregnant, indicating that CML per se does not cause infertility. The haematological measurements were similar to those of previous reports; however, the marked splenomegaly suggests that South African Black patients present themselves for treatment rather late in the disease. The median survival time of 34 months is similar to that of previous reports of larger series from other parts of the world.
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PMID:Chronic myeloid leukaemia in South African blacks. 107 Jan 65

Cardiac pathologic findings were analyzed in 22 necropsy cases from a series of 29 patients with leukemia, aplastic anemia, or metastatic cancer who had been treated with ablative therapy followed by bone marrow transplantation. Some cardiac alterations were similar to those that occur in patients with hematologic and neoplastic diseases not treated with bone marrow transplantation, and consisted of cardiomegaly, cardiac atrophy, hemorrhage, foci of necrosis due to shock associated with sepsis or hepatic failure, myocardial abscesses secondary to systemic candidiasis or staphylococcal infection, fibrinous pericarditis, and hemosiderosis. Other cardiac alterations were more specifically related to factors associated with transplantation procedure. Six patients exhibited a distinctive interstitial reactive change characterized by the presence of (1) moderate to large numbers of Anitschkow cells, occurring alone or in small cellular aggregates and histiocytes, histiocytic cells with nuclei of the Anitschkow type, lymphoid cells, and plasma cells, and (2) nuclei of the Anitschkow type in cardiac vascular and endocardial smooth muscle, endothelial and Schwann cells, and occasional cardiac muscle cells. This alteration may have been induced by abnormal immune mechanisms, as suggested by the observation that five of the six patients with interstitial change had clinical evidence of graft-versus-host disease. Two patients developed fatal congestive cardiac failure in the early post-transplant period and exhibited myocardial damage with histologic and post-transplant period features indicative of severe acute injury. Findings in these two patients consisted of necrotic muscle cells, which exhibited multiple contraction bands, diastase-resistant PAS staining, and intracellular fibrin deposits; microthrombi, which were composed of fibrin and occasionally of fibrin and platelets; and extravasated erythrocytes and fibrin strands in the interstitium. One of the two patients also exhibited unusual nuclear alterations, which were characterized by replacement of normal chromatin by palely stained fibrous and filamentous material. Clinicopathologic analysis strongly suggested that the fatal cardiotoxicity in both patients resulted primarily from effects of high doses of cyclophosphamide, which were administered as part of a four drug regimen that provided tumor ablation and immunosuppression for bone marrow transplantation. Our findings emphasize the need for less toxic antineoplastic and immunosuppressive therapy for use in bone marrow transplantation procedures.
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PMID:Cardiac pathologic findings in patients treated with bone marrow transplantation. 110 69

Cardiac metastasis should be strongly suspected in the cancer patient with sudden onset of unexplained tachycardia, arrhythmia, or congestive heart failure. Conduction defects and low voltage on electrocardiographic examination and an enlarged heart shadow on the chest film are virtually confirmatory. Thirty-eight such patients were treated through anterior and posterior opposing portals and received 2,500-3,500 rads in 3-4 weeks, except for 6 lymphoma and leukemia patients who were controlled with lower doses (1,500-2,000 rads in 11/2-2 weeks). Primary sites and duration of improvement were as follows: breast (11/16 patients): 2-36 months; lung (2/7 patients): 1-9 months; lymphoma and leukemia (6/7 patients): 2-4 months; others (4/8 patients): 1-4 months. Overall, the clinical improvement rate was 60%, with durations of 12 to 36 months.
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PMID:Radiation therapy of cardiac and pericardial metastases. 111 76

Ischemic colitis is a disease complex that presents as a continuum of mucosal and submucosal hemorrhage, late stricture formation and frank gangrene. The exact form depends upon the degree, site and duration of the vascular occlusion, the presence of collateral vessels and the intraluminal pressure in the colon. In a study group of 19 women and seven men, the majority of whom were in the seventh to eighth decades of life, most frequent symptoms were crampy abdominal pain and abdominal distention associated with bloody diarrhea. Ischemic colitis occurred with increased colonic intraluminal pressure, generalized decreased vascular flow and embolic phenomenon. The predominating predisposing causes were atherosclerosis, shock and congestive heart failure as well as leukemia. The results of barium enema studies showed a pathognomonic condition that included thumbprinting, mucosal ulcerations and sacculations. Arteriography, generally, was not helpful, and results of sigmoidoscopy were invariably negative, since the rectum seldom is involved in ischemic colitis. Conservative treatment should include intestinal rest, low molecular weight dextran and antibiotics. Early operative intervention is recommended when conservative therapy fails or signs of peritoneal irritation become evident.
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PMID:Ischemia of the colon. 125 13

Mitoxantrone is a dihydroxyanthracenedione derivative which as intravenous mono- and combination therapy has demonstrated therapeutic efficacy similar to that of standard induction and salvage treatment regimens in advanced breast cancer, non-Hodgkin's lymphoma, acute nonlymphoblastic leukaemia and chronic myelogenous leukaemia in blast crisis; it appears to be an effective alternative to the anthracycline component of standard treatment regimens in these indications. Mitoxantrone is also effective as a component of predominantly palliative treatment regimens for hepatic and advanced ovarian carcinoma. Limited studies suggest useful therapeutic activity in multiple myeloma and acute lymphoblastic leukaemia. Regional therapy of malignant effusions, hepatic and ovarian carcinomas has also been very effective, with a reduction in systemic adverse effects. Mitoxantrone inhibits DNA synthesis by intercalating DNA, inducing DNA strand breaks, and causing DNA aggregation and compaction, and delays cell cycle progression, particularly in late S phase. In vitro antitumour activity is concentration- and exposure time-proportional, and synergy with other antineoplastic drugs has been demonstrated in murine tumour models. Leucopenia may be dose-limiting in patients with solid tumours, whereas stomatitis may be dose-limiting in patients with leukaemia. Other adverse effects are usually of mild or moderate severity although cardiac effects, particularly congestive heart failure, may be of concern, especially in patients with a history of anthracycline therapy, mediastinal irradiation or cardiovascular disease. Mitoxantrone displays an improved tolerability profile compared with doxorubicin and other anthracyclines, although myelosuppression may occur more frequently. Thus, mitoxantrone is an effective and better tolerated alternative to the anthracyclines in most haematological malignancies, in breast cancer and in advanced hepatic or ovarian carcinoma. Further studies may consolidate its role in the treatment of these and other malignancies.
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PMID:Mitoxantrone. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the chemotherapy of cancer. 171 46

Diffuse pulmonary infiltrates in the immunocompromised host in the majority represent an opportunistic infection. However, in about 25 to 30%, they represent complications of an adverse drug reaction, recurrence of the underlying disease such as leukemia or lymphoma involving the lung, or an idiopathic "fibrosis," and in a small percentage are attributable to an "unrelated" process such as congestive heart failure, pulmonary emboli, community-acquired pneumonia, and so on. In 10 to 20% of the patients, two or more of these processes occur. A pulmonary process in the immunocompromised patient is almost always fatal unless the clinician intervenes with the proper diagnosis and/or effective empiric therapy.
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PMID:Diffuse pulmonary infiltrates in the immunocompromised host. 218 78

Endomyocardial biopsy was performed on two leukemia patients who had recovered from severe congestive heart failure (CHF) due to anthracycline cardiomyopathy at 41 months and 47 months after CHF. Microscopic myocardial findings in both patients revealed that myocytes were hypertrophic, but interstitial fibrosis was not observed, suggesting a compensatory mechanism for the damaged heart muscle during the acute episode of CHF. The improvement of clinical symptoms and the normalization of cardiac function, including fractional shortening and ECG changes, is thought to have been associated with this myocardial repairing process.
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PMID:Anthracycline-induced congestive heart failure in two pediatric leukemia cases and long term follow-up. 315 69

We conducted a phase I and pharmacokinetic study of i.v. idarubicin, a new anthracycline analogue, in 42 evaluable children 1-19 years old. Twenty-seven had leukemia and 15 had various solid tumors. The drug was administered in escalating doses of 10 to 40 mg/m2/course in 3 equal fractions over 3 consecutive days at 14- to 21-day intervals. Myelosuppression and mucositis were the limiting toxicities for short-term administration. Nausea, vomiting, and elevation of liver enzymes and bilirubin were the other toxicities encountered. Peak toxicity occurred 2 weeks after drug administration with median recovery by day 24. All but 4 patients with solid tumors had prior anthracyclines. Mild cardiac function changes without clinical symptoms were observed in 17 of 35 patients measured by serial cardiac evaluations. In addition, there were 4 patients with congestive heart failure. On postmortem examination, 4 patients had changes consistent with anthracycline cardiomyopathy at a prior median total anthracycline dose of 175 mg/m2. The maximum tolerated dose for patients with solid tumors was 15 mg/m2 course in 3 divided doses. Patients with leukemia tolerated 30 mg/m2/course. Six of 15 evaluable patients with acute lymphoblastic leukemia who received greater than or equal to 30 mg/m2 idarubicin achieved a remission (M1 marrow status). The plasma clearance of idarubicin fits a 3-compartment model with a harmonic mean half-life of 2.4 min, 0.6 h, and 11.3 h for alpha, beta, and gamma phases, respectively. Idarubicinol was the only metabolite detected in the plasma and it accumulated during the 3 days of therapy. Idarubicin is similar to daunorubicin in pharmacology and toxicity. While the cardiotoxic dose still must be delineated, the complete remission achieved in multiple relapsed patients with acute lymphoblastic leukemia indicate promising activity in at least that disease.
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PMID:Phase I and clinical pharmacological study of 4-demethoxydaunorubicin (idarubicin) in children with advanced cancer. 347 21


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