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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, hemodynamic and radiologic signs of pericardial effusion are reviewed. From the symptomatic point of view low pressure (lax) pericardial effusion and compressive effusion (tamponade) are to be distinguished. Echocardiography is today the preferred method for study of patients with suspected pericardial effusion. This technique also provides insight into ventricular performance and is therefore helpful in the differential diagnosis of cardiomegaly due to pericardial effusion, heart failure or both. In our material uremic pericarditis, malignant tumors and leukemia were the predominant causes of pericardial effusion.
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PMID:[Diagnosis and differential diagnosis of pericardial effusion]. 13 71

Two patients with Wegener's granulomatosis have been treated with chlorambucil and prednisolone continuosly for 3 and 5 years, respectively. This treatment was effective in controlling the disease, but bone marrow toxicity with severe pancytopenia developed in both cases. Both patients died from thrombocytopenia with haemorrhagic pericarditis. In one case, the diagnosis of acute myeloid leukaemia was established from the appearance of myeloblasts in the peripheral blood and from characteristic bone marrow morphology. In the other case this diagnosis was strongly suspected on the basis of the bone marrow morphology alone. It is proposed that this development of acute leukaemia in two patients with a primary non-neoplastic disease may result from a direct carcinogenic action of chlorambucil in humans.
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PMID:Acute myeloid leukemia appearing in two patients after prolonged continuous chlorambucil treatment for Wegener's granulomatosis. 106 90

Thirty-six consecutive patients with cancer who met the classical criteria for fever of unexplained origin (FUO) were identified. A total of 18 patients had infections including all 12 with leukemia, four of 12 with Hodgkin's disease, and two with solid tumors. Fungal infections were found in nine: histoplasmosis, three; candidiasis, three; and aspergillosis, systemic sporotrichosis, or cryptococcal meningitis, one each. Six patients had unresolved pyogenic infections and one had tuberculous pericarditis. Two others had viral etiologies. Granulocytopenia was significantly more common in the FUO patients with documented infections. Clinical or laboratory abnormalities suggesting involvement of a specific organ or organ system provided important clues indicating infections. Morphological examination of biopsy specimens, with cultures, was the best method for diagnosis. In 18 patients, 12 with lymphomas and 6 with solid tumors, only the neoplasm appeared responsible for the fever. In these patients there was a paucity of abnormalities indicating organ system involvement with infection. Regardless, physicians' diagnostic efforts should not be deterred in such patients. Repeated thorough evaluations for infection are warranted.
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PMID:Infections or neoplasm as causes of prolonged fever in cancer patients. 106 64

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

A nine years old female child with malnutrition who showed, six months before admission, a number of clinical manifestations consistent with leukemia. The outstanding clinical manifestation during her hospital stay was that of pericarditis with effusion, which was found associated with pericardial leukemic infiltration. The final picture was that of cardiorespiratory failure associated, both to leukemic infiltration of these organs, as to that of postoperative hemorrhage.
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PMID:[Acute leukemia with cardiac infiltration]. 125 21

The myelodysplastic syndromes (MDS) are a group of therapeutically refractory anemias resulting from a clonal stem cell disorder often associated with cytogenetic abnormalities. Immunologic abnormalities and occasionally vasculitis have been reported although no series has characterized an associated arthritis. All cases of MDS diagnosed in 1990 by bone marrow biopsy and followed up at the authors' institution were reviewed. Of the 28 consecutive patients, 8 had acute seronegative inflammatory arthritis temporally related to the initial discovery of cytopenia. Five patients had a symmetric polyarthritis resolving only with use of steroids or upon evolution to leukemia, and 3 had episodes of oligoarthritis with systemic features including fever, pleuritis, pericarditis, and hemolytic anemia. Arthrocenteses in 2 cases did not show crystals or infection. Serological studies were nondiagnostic. The arthritis and systemic features responded to steroids in all 5 treated patients. Inflammatory arthritis appears to be common in MDS. Most compelling is the apparent bone marrow response to steroids in 2 cases, possibly identifying a treatable subgroup.
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PMID:Seronegative inflammatory arthritis in the myelodysplastic syndromes. 162 80

The treatment of patients with relapsed or refractory acute myeloid leukemia (AML) with high dose cytosine arabinoside (ara-C) results in short-lived complete response rates of 30-50%. We have previously shown that entry of myeloid leukemic cells into S phase can be accelerated in vitro through the use of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), resulting in enhancement of ara-C-mediated cytotoxicity. In order to evaluate the in vivo biological and clinical effects of this strategy in patients with high risk AML, we treated three patients with either refractory or relapsed disease with a continuous infusion of rhGM-CSF (0.45 micrograms/kg/h aglycoprotein) for 18 h, followed by the institution of high dose ara-C and continuation of rhGM-CSF throughout the 4 day duration of ara-C treatment. Prior to therapy, no patient had detectable levels of circulating rhGM-CSF, and there was no evidence of GM-CSF receptor occupancy in leukemic myeloblasts. After 18 h of rhGM-CSF therapy, all patients had biologically active levels of circulating rhGM-CSF (7.9-12.0 ng/ml), and two patients showed a significant degree of leukemic GM-CSF receptor occupancy without evidence of GM-CSF receptor down-regulation. A significant rise in the S phase fraction of leukemic myeloblasts was observed at 18 h of rhGM-CSF treatment in all three patients (29-56% increment). The toxicity of combined rhGM-CSF/ara-C therapy included pericarditis and cerebellar degeneration in one patient, fever and mild renal dysfunction in two patients, and mild hepatic dysfunction in all three patients. Each patient showed a transient rise in the absolute neutrophil and blast count during rhGM-CSF/ara-C administration, followed by profound, but clinically tolerable, myelosuppression. No patient developed clinical evidence of leukostasis. There was one death related to pericardial tamponade, one death related to refractory disease, and one clinical and cytogenetic remission. These results suggest that exogenously administered rhGM-CSF is capable of rapidly mobilizing leukemic cells into S phase in vivo and theoretically should be useful in overcoming kinetic resistance to ara-C. Clinical trials of this regimen in patients with high risk AML who are not already pharmacologically resistant to ara-C are warranted.
Leukemia 1991 Mar
PMID:Simultaneous administration of granulocyte-macrophage colony-stimulating factor and cytosine arabinoside for the treatment of relapsed acute myeloid leukemia. 182 36

A 28-year-old man was admitted to our hospital because of cardiac tamponade and pleural effusion. Although his peripheral blood picture was normal, his pericardial fluid contained a lot of myeloblasts with Auer bodies and a diagnosis of acute myeloblastic leukemia (M2) was made from the finding of bone marrow smears. The pericarditis was successfully treated with instillation of mitoxantrone into the pericardial space after drainage. He responded well to the systemic chemotherapy and achieved a complete remission. Although 27 cases of leukemia complicated with cardiac tamponade have so far reported, only three cases gave normal findings of the peripheral blood on admission. Leukemic pericardial effusion with cardiac tamponade in very rare as an initial manifestation of AML. The efficacy and safety of pericardial infusion of mitoxantrone were demonstrated in this patient.
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PMID:[Cardiac tamponade as an initial manifestation of acute myeloblastic leukemia]. 232 85

Pericardial exudate and/or spread of the tumour to the pericardium occurs frequently in leukaemia and malignant lymphomata. Metastases to the pericardium may be demonstrated at autopsy in 50% and 20-25%, respectively. In the majority of cases no symptoms from the heart occur. In cases with significant pericardial effusion or constrictive pericarditis, urgent treatment is indicated. Pericardiocentesis is carried out in cases of cardiac tamponade. Irradiation has frequently a rapid and dramatic effect in cases of massive tumour infiltration in the pericardium. Long-term treatment depends on the malignant haematological disease concerned. Meticulous diagnostic investigation is therefore indicated in every case with cardiac symptoms. This has frequently therapeutic consequences, reduces the morbidity and prolongs survival. Two cases of acute pericardial effusion with haemodynamic consequences are reviewed in this article. The haematological diagnoses were acute myeloid leukaemia and malignant lymphoma (diffuse large-cell non-Hodgkin's lymphoma), respectively.
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PMID:[Pericardial involvement in leukemia and malignant lymphoma]. 240 59

Pitfalls in the clinical diagnosis of the aetiology of acquired tricuspid incompetence in children were exemplified in five patients. In three of them acute staphylococcal endocarditis, the cause of the valve defect, was obscured during life by co-existing sickle cell haemoglobinopathy, acute leukaemia and rheumatic mitral valvulitis, respectively. The fourth and fifth patients had clinical features suggestive of right ventricular endomyocardial fibrosis but necropsy revealed that the tricuspid incompetence was caused by dilated cardiomyopathy and constrictive pericarditis respectively. This series illustrates the need to suspect bacterial endocarditis if a child presents with signs of infection and valvular incompetence, and also dispels the widespread belief that pericardial constriction does not cause tricuspid incompetence.
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PMID:Acquired tricuspid incompetence in children: pitfalls in the clinical diagnosis of its aetiology. 619 11


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