Disease relevance of Leukostasis

• Neutropenia and leukostasis observed in diseases associated with activation of the contact phase system may be the result of PMN aggregation by plasma kallikrein [1].
• Thus, pronounced vascular leukostasis, vasculitis, and T-cell and monocyte infiltration of the tubulointerstitium led to a severe damage of the allograft under therapy with CyA and NOS-B [2].
• The irreplaceable image: Cerebral leukostasis manifesting as multifocal intracerebral hemorrhage [3].
• High-voltage irradiation and hydroxyurea for pulmonary leukostasis in acute myelomonocytic leukemia [4].
• In particular, administration of steroid and the use of CHDF may improve the status of pulmonary leukostasis in leukopenic pneumococcal infection [5].

High impact information on Leukostasis

• Fatal complement-induced leukostasis after diatrizoate injection. Principles of clinicopathologic diagnosis [6].
• A case of fatal radiographic contrast medium (RCM)-induced pulmonary granulocyte aggregation (leukostasis) showed massive elevation of the postmortem histamine level [6].
• ICAM-1 blockade with a mAb prevents diabetic retinal leukostasis and vascular leakage by 48.5% and 85.6%, respectively [7].
• In the model of pulmonary leukostasis, the presence of omega-oxidation products of LTB4 indicated metabolic integrity of the trapped PMNs [8].
• Pulmonary histology in rabbits and sheep confirmed the presence of intracapillary leukostasis after the plasma infusions, whether or not sulfinpyrazone had been administered previously [9].

Chemical compound and disease context of Leukostasis

• Pretreatment with gadolinium chloride (GdCl3), which reduces KC function, attenuated the liver leukostasis and NPS elicited by gut I/R [10].
• The platelet activating factor (PAF) antagonist, WEB2086, and a tumor necrosis factor (TNF)-alpha-specific antibody were also effective in attenuating the gut I/R-induced leukostasis and NAD(P)H autofluorescence [10].
• In the model of pulmonary leukostasis, no nonenzymatic LTA4-derivatives were detected, coincident with a predominance of cysteinyl-LT [11].
• In diabetic rats, treatment with the antioxidant alpha-lipoic acid normalized the amount of leukostasis but not retinal blood flow [12].
• In contrast, treatment with D-alpha-tocopherol and protein kinase-C beta-isoform inhibition (LY333531) prevented the increases in leukostasis and decreases in retinal blood flow in diabetic rats [12].

Biological context of Leukostasis

• The leukostasis is accompanied by the up-regulation of intercellular adhesion molecule-1 expression in the retina [13].
• The leukostasis syndrome associated with very high blast cell counts in adults with acute leukemia can be avoided by the use of hydroxyurea in the manner described [14].
• Using a cationic liposomal carrier, this same antisense oligonucleotide (but not the sense control) instilled into the pulmonary vasculature at the time of preservation reduced subsequent graft ICAM-1 expression and graft leukostasis and markedly improved oxygenation, pulmonary blood flow, and graft survival [15].

Anatomical context of Leukostasis

• Gliclazide, a sulphonylurea, was reported to reduce leukocyte adhesion to endothelial cells in hyperglycaemia in vitro, thus suggesting possible selective efficacy of this sulphonylurea in preventing leukostasis in diabetic patients [16].
• Integrin-mediated neutrophil adhesion and retinal leukostasis in diabetes [17].
• Anti-ICAM-1 did not affect sinusoidal leukostasis; however, it effectively inhibited postischemic leukocyte adherence to the venular endothelial lining (217 +/- 38 cells/mm2, p < 0.01) [18].
• Nisoldipine significantly reduced the FMLP-induced leukostasis in coronary capillaries (P < 0.05) [19].
• The magnitude of the attenuation of leukostasis with nisoldipine was remarkably similar in both models, suggesting a direct effect of this agent on the blood rather than on the blood vessels [19].

Gene context of Leukostasis

• As a consequence of PPAR-gamma activation, pulmonary leukostasis was decreased and oxygenation and overall survival were improved [20].
• VEGF-induced increases in ICAM-1 may promote retinal leukostasis in diabetic eyes [21].
• Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis [22].
• Soluble TNF induced leukostasis in wt and TNFRp75-/- mice but not in TNFRp55-/- mice [23].
• Pretreatment of LDLr(-/-) mice with gadolinium chloride, which reduces Kupffer cell function, attenuated the hepatic leukostasis, NPS, and hepatocellular injury elicited by I/R [24].

Analytical, diagnostic and therapeutic context of Leukostasis

• METHODS: Retinal leukostasis and BRB breakdown were simultaneously quantified by combining concanavalin A lectin (ConA) perfusion labeling with a fluorophotometric dextran leakage assay [25].
• Electron microscopy of the lungs, liver, and spleen in the test group showed severe damage, with endothelial disruption, capillary or sinusoidal occlusion, leukostasis, and neutrophil degranulation [26].
• Treatment of acute promyelocytic leukemia with all-trans retinoic acid: successful control of hyperleukocytosis and leukostasis syndrome with leukaphereses and hydroxyurea [27].
• Among the treatment and control groups, there was no evidence of pulmonary leukostasis as determined by mean alveolar septal wall granulocytes per high power field or mean lung myeloperoxidase activity per gram of tissue [28].

References