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leukostasis/хипоксия
Линкът е запазен в клипборда
Страница 1 от 45 резултата
Pulmonary leukostasis: role of perfusion lung scan in diagnosis and follow up.
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A patient with hyperleukocytic myelomonocytic leukemia who presented to the emergency room with sudden pleuritic chest pain and dyspnea is reported. Clinical manifestations included dyspnea tachypnea and hyperventilation. Blood gas analysis revealed hypoxemia, hypocarbia, and respiratory alkalosis.
[Leukostasis syndrome in a case of chronic lymphocytic leukemia].
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The leukostasis syndrome is rare complication of leukemias with extremely high white cell counts. It occurs most frequently in chronic myelosis or acute leukemias and is exceptional in chronic lymphocytic leukemia (CLL). A severe leukostasis syndrome was observed in a case of CLL with peripheral
[Postoperative pulmonary leukostasis responsible for fatal respiratory distress].
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A case is reported of a 78-year-old woman with a history of chronic leukemia and who developed after emergency appendicectomy a fatal respiratory distress syndrome related to pulmonary leukostasis. Clinically, the patient had fever, dyspnea and severe hypoxaemia. Chest x-ray showed diffuse pulmonary
Management of life-threatening pulmonary leukostasis with single agent imatinib mesylate during CML myeloid blast crisis.
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Pulmonary leukostasis is a rare but serious and often fatal complication of chronic myeloid leukemia (CML) in blast crisis and acute myeloid leukemia. Treatment options are limited for these patients. Imatinib mesylate (STI-571, Gleevec, Novartis) is a potent and selective inhibitor of the BCR-abl
Respiratory failure due to pulmonary leukostasis following chemotherapy of acute nonlymphocytic leukemia.
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Four patients with acute nonlymphocytic leukemia and leukocyte counts of more than 200,000/mm3 developed respiratory distress due to pulmonary leukostasis within 10-48 hours after initiation of chemotherapy. Clinically, the patients manifested fever, dyspnea, tachypnea, diffuse pulmonary rales,
[Therapeutic leukapheresis in a leukostasis syndrome complicating chronic lymphoid leukemia].
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A 50 year old man with chronic lymphocytic leukemia (CLL) and extreme hyperleukocytosis (600 x 10(9)/liter) presented with a respiratory distress syndrome, congestive heart failure with cardiomegaly, endotoxic shock and anuria. Examination revealed nodes in all areas and hepatosplenomegaly;
Hypoxemia during hemodialysis.
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Decrease in arterial oxygen tension has been reported during hemodialysis.(1-3) The etiology of the hypoxemia has not been clearly demonstrated. Intravascular leukostasis,(1) pulmonary arterial microembolization,(3) and loss of CO(2) through the dialyzer are some of the explanations given for this
Hypoxemia during hemodialysis: a critical review of the facts.
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The literature describing the fall in PaO2 during dialysis is intensively and critically reviewed. This phenomenon is related to both the type of membrane used (cellulosic v noncellulosic membrane), and to the composition of the dialysate (acetate v bicarbonate). It appears that a
Relative contribution of intrinsic lung dysfunction and hypoventilation to hypoxemia during hemodialysis.
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Two mechanisms have been proposed to explain hemodialysis (HD)-induced hypoxemia: reversible lung damage due to intrapulmonary leukostasis as a consequence of the contact of blood with the dialyzer membrane, or alveolar hypoventilation due to the loss of carbon dioxide through the dialyzer. To
Leukopenia and hypoxemia. Unrelated effects of hemodialysis.
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Hemodialysis-induced hypoxemia has been attributed to membrane-related complement activation leading to pulmonary leukostasis and to hypoventilation secondary to carbon dioxide losses via the dialyzer. We have separately assessed the role of membrane- and dialysis-related factors by using different
Hepatic leukostasis and hypoxic stress in adhesion molecule-deficient mice after gut ischemia/reperfusion.
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The concept that leukocyte-endothelial cell adhesion (LECA) is a major determinant of the tissue injury elicited by ischemia/reperfusion (I/R) is largely based on studies employing adhesion molecule-specific monoclonal antibodies. The objective of this study was to assess the contribution of LECA to
T-lymphocytes contribute to hepatic leukostasis and hypoxic stress induced by gut ischemia-reperfusion.
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Although neutrophils have been implicated in the hepatic injury elicited by gut ischemia/reperfusion (I/R), the contribution of other leukocyte populations to this injury process remains unclear. The objective of this study was to determine whether lymphocytes contribute to gut I/R-induced
Reversible respiratory failure due to intravascular leukostasis in chronic myelogenous leukemia. Relationship of oxygen transfer to leukocyte count.
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In a 49 year old man with blast crisis and massive leukocytosis due to chronic myelogenous leukemia, severe hypoxic respiratory failure developed despite a normal chest film. Correction of hypoxemia was observed after reduction of the white blood cell count by hydroxy-urea therapy. A similar episode
Activation of plasma complement by perfluorocarbon artificial blood: probable mechanism of adverse pulmonary reactions in treated patients and rationale for corticosteroids prophylaxis.
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Perfluorocarbons have shown promise as clinical blood substitutes. Although early experience in Japan with one such product--Fluosol-DA--has been uncomplicated, we observed an adverse pulmonary reaction in the first American patient to receive it and know of similar reactions in two other Americans
Effect of hydroxyl radical scavenging on endotoxin-induced lung injury.
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The release of oxygen radicals, in particular the hydroxyl radical, from sequestered neutrophils produces acute lung injury after a number of insults. Our purpose was to determine whether hydroxyl radical, OH., is responsible for the lung injury from endotoxin characterized by (1) pulmonary
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