Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with chronic myelogenous leukemia is described who developed anterior segment ischemia after extreme leukocytosis with a resultant increase in the blood viscosity. The patient's signs and symptoms resolved after therapy which normalized the white blood cell count. It is thought that the anterior segment ischemia was a result of sludging of white blood cells in the ciliary arteries. It is important to recognize that anterior segment ischemia can occur as a complication of chronic myelogenous leukemia associated with extreme leukocytosis. A new classification of anterior segment ischemia is given.
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PMID:Anterior segment ischemia: classification and description in chronic myelogenous leukemia. 29 43

Fifteen upper extremities, in 14 patients in whom incipient or actual Volkmann's ischemic contracture was present, were seen in a 5 year period. Nine patients were stuporous due to drug overdose and had laid on the extremity; two had received a recent injury of main arterial trunks; two had sudden severe compression; one with chronic myelogenous leukemia had each arm involved at different times in a bizarre autoimmune response causing massive swelling. No patient had a fracture or dislocation. Pain and tenderness, loss of sensibility, resistant muscle contracture, and rock-hard muscle compartments were warning signs. Immediate fasciotomy was done. Useful function was restored when treatment was carried out in the early stages of the ischemia.
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PMID:Volkmann's ischemic contracture due to soft tissue injury alone. 101 90

We have previously reported the occurrence of microembolic ischemia in the retina during cardiopulmonary bypass, as revealed by fluorescein angiography. This method has been extended by digital image analysis to include quantification of the extent of retinal ischemia and has been applied to a prospective comparative study of 64 patients undergoing elective coronary operations with either a bubble or a membrane oxygenator. Patients with diabetes or clinically evident cerebrovascular disease were excluded. Bypass procedures were standardized in all cases with pulsatile flow and a 40 microns arterial line filter (Pall EC Plus). Thirty patients had bypass with a bubble oxygenator (Harvey H1700) and 34 patients had bypass with a flat sheet membrane oxygenator (COBE CML). In each case retinal fluorescein angiograms were obtained preoperatively and 5 minutes before the end of bypass and were processed with a digital image analyzer (Context Vision GOP-302). Microembolic perfusion defects were identified by digital subtraction of preoperative and end-bypass angiograms and their total area was computed. Results. In the bubble oxygenator group retinal perfusion defects indicative of microembolism occurred in all 30 (100%) patients. In contrast, over half the patients in the membrane oxygenator group had normal retinal perfusion, and the prevalence of perfusion defects (44%; 70% confidence limits 34% to 54%) was significantly less than in the bubble group (p less than 0.001). In addition, those patients in the membrane group had significantly fewer lesions (median 0; 70% confidence limits 0 to 1) than patients in the bubble group (median 2; 70% confidence limits 2 to 2; p less than 0.001) and also had significantly smaller total areas of retinal ischemia (median 0 mm2; 70% confidence limits 0 to 0.16 mm2) than the bubble group (median 0.22 mm2; 70% confidence limits 0.21 to 0.27 mm2; p less than 0.001). There was no relationship between the extent of retinal ischemia and bypass time, arterial blood gas concentrations, volume of cardiotomy suction or donor blood returned to the pump, or recent medication with aspirin. Inferences. Digital image analysis of retinal fluorescein angiograms may provide a method of quantifying microembolic ischemia in the central nervous system during cardiopulmonary bypass. Flat sheet membrane oxygenation appears to provide significantly better protection against microembolic ischemia than bubble oxygenation.
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PMID:Influence of oxygenator type on the prevalence and extent of microembolic retinal ischemia during cardiopulmonary bypass. Assessment by digital image analysis. 229 66

Acral ischemia with lividity is a well-described dermatologic sign in the myeloproliferative diseases polycythemia vera and essential thrombocythemia. It has not previously been reported as a sign of chronic myelogenous leukemia (CML). We suggest the term acral lividosis to describe this clinical entity in patients with any myeloproliferative disease. We propose that the pathophysiology of acral lividosis in CML involves occlusion of small blood vessels of the skin by large, nondeformable myeloblasts, a process that has been shown histologically to occur in other organs in patients with CML. This process, called leukostasis, occurs in patients with CML who have over 50.0 X 10(9)/L (50,000/mm3) circulating myeloblasts. Patients manifest cardiorespiratory and central nervous system compromise, a clinical constellation known as the hyperleukocytosis syndrome. Acral lividosis occurred in a patient with CML in whom nearly every organ demonstrated leukostasis on autopsy.
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PMID:Acral lividosis--a sign of myeloproliferative diseases. Hyperleukocytosis syndrome in chronic myelogenous leukemia. 347 43

Both ictal nystagmus and cortical blindness may occur transiently in acute cerebral disorders and therefore escape clinical detection, particularly in confused, agitated patients. The following case report describes a young woman with chronic myelogenous leukemia who became progressively ill following bone marrow transplantation. During the course of her illness, acute ictal nystagmus developed from focal right occipital ischemia; postictally she remained cortically blind with possible visual hallucinations for 48 hours.
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PMID:Cortical blindness following ictal nystagmus. 397 48

Hydroxyurea is a cytotoxic agent used in the management of chronic granulocytic leukemia. This compound is teratogenic and embryolethal in various animal species, and has been widely used in experimental studies aimed at understanding the possible mechanisms of drug-induced malformations. Previous studies from our laboratory have demonstrated that maternal subcutaneous injections of hydroxyurea produce immediate circulatory alterations in rabbit embryos similar to those observed subsequent to uterine artery occlusion. The present study was designed to investigate the possibility that the embryolethal and teratogenic properties of hydroxyurea might be due to alterations in maternal hemodynamics, i.e., constriction of the uterine vasculature, resulting in exposure of the embryo to uterine ischemia at critical stage of in utero development. This study demonstrates that hydroxyurea significantly alters blood pressure and heart rate and produces significant uterine vasoconstriction. The resulting reductions in uterine blood flow (77%) elicited by hydroxyurea may be associated with its immediate embryotoxicity.
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PMID:Effects of hydroxyurea on hemodynamics of pregnant rabbits: a maternally mediated mechanism of embryotoxicity. 719 56

We present five patients with serious ischemia of the fingers caused by intra-arterial injection injury, trauma, rheumatoid arthritis, chronic myeloid leukemia with thrombocytosis and thoracic-outlet syndrome. The treatment consisted of thrombectomy and intra-arterial lysis if possible and intra-arterial infusion of 80 microg PGE1/24 h in combination with 25,000 U of heparin/24 h for 6-10 days. PGE1 and heparin were administered through a 3-F catheter introduced surgically into a forearm artery. In three cases a complete remission was possible, in the other two cases the therapy led to significant improvement. No side effects or complications were noticed.
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PMID:[Experience with the therapy of acute finger ischemia by high-dose intra-arterial infusion of PGE1 through a surgically introduced catheter]. 1055 Mar 45

Calcium dobesilate stabilizes blood-retinal barrier in patients with diabetic retinopathy and possesses antioxidant properties in the retinas of rats with streptozotocin-induced diabetes, exposed ex vivo to ischemia-reperfusion. Here we investigated the action of calcium dobesilate on retinal albumin leakage in streptozotocin-diabetic rats, together with relevant in vivo retinal antioxidant and permeability markers, i.e., carboxymethyl-lysine-advanced glycation end product (CML-AGE) formation and vascular endothelial cell growth factor (VEGF) overexpression. Twenty days after streptozotocin administration, diabetic rats were treated for 10 days with calcium dobesilate (100 mg/kg/day per os) or vehicle. Retinal albumin leakage, CML-AGE formation, and VEGF overexpression were evaluated by immunohistochemistry of frozen eye sections. Diabetic rats exhibited dramatic increases in: (i) retinal albumin leakage (31% of positive vessels vs. 0.2% in nondiabetic rats, P<0.008), (ii) CML-AGE retinal occurrence (40+/-3% vs. undetectable positive vessels), and (iii) retinal VEGF protein expression (14.6+/-1.1 vs. 3.5+/-0.5 VEGF-positive spots/field, P<10(-4)). Calcium dobesilate significantly reduced: (i) retinal albumin leakage (by 70%, P<0.008), (ii) retinal CML-AGEs contents (by 62%, P<0.008), and (iii) retinal VEGF expression (by 69.4%, P<0.008). In conclusion, calcium dobesilate orally given to diabetic rats markedly reduced retinal hyperpermeability, CML-AGE contents, and VEGF overexpression. These results strongly suggest that calcium dobesilate stabilizes blood-retinal barrier in diabetic retinopathy via an in situ antioxidant action. Further studies in patients are required to confirm such view.
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PMID:Reduction of retinal albumin leakage by the antioxidant calcium dobesilate in streptozotocin-diabetic rats. 1524 73

Advanced glycation end-products (AGEs) inhibit ischemia-induced angiogenesis but are potential triggers of neoangiogenesis that occurs in peritoneal dialysis (PD) patients. We investigated whether the effect of glucose and AGEs on human peritoneal mesothelial cells (HPMCs) might alter the release of vascular endothelial growth factor (VEGF) and subsequently the formation of capillary tubes by human umbilical vein endothelial cells (HUVECs). HPMCs were exposed to glucose and the glycated protein Nvarepsilon-(carboxymethyl)lysine-human serum albumin (CML-HSA) and VEGF production was measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Capillary tube formation by HUVECs in presence of HPMC supernatant or co-cultured with HPMC was investigated. AGE and VEGF levels in PD effluents from 11 patients were measured. CML-HSA stimulated VEGF production by HPMCs, P<0.001. Glucose and AGE inhibited capillary tube formation by HUVECs, P<0.001. HPMC supernatant potentiated capillary tube formation, P<0.001. In co-culture with HPMC capillary tube formation was increased, especially by HPMCs stimulated by CML-HSA, P<0.001. Anti-VEGF antibody limited this effect, P<0.001. Preincubation of HPMCs with anti-receptor for AGEs (RAGE) antibody reduced capillary tube formation, P<0.001. AGE and VEGF levels in PD effluents were increased during long dwell time, P<0.05 and P<0.001, respectively. In a co-culture system, we showed that VEGF production by HPMC favors capillary tube formation through mesothelial RAGE activation and could explain neoangiogenesis in PD patient.
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PMID:Mesothelial RAGE activation by AGEs enhances VEGF release and potentiates capillary tube formation. 1714 74

Diabetes mellitus (DM) is closely related to cardiovascular morbidity and mortality, but the specific molecular basis linking DM with increased vulnerability to cardiovascular injury remains incompletely understood. Methylglyoxal (MG), a precursor to advanced glycation end products (AGEs), is increased in diabetic patient plasma, but its role in diabetic cardiovascular complications is unclear. Thioredoxin (Trx), a cytoprotective molecule with antiapoptotic function, has been demonstrated to be vulnerable to glycative inhibition, but whether Trx is glycatively inhibited by MG, thus contributing to increased cardiac injury, has never been investigated. Cultured H9c2 cardiomyocytes were treated with MG (200 muM) for 6 days. The following were determined pre- and post-simulated ischemia-reperfusion (SI-R; 8 h of hypoxia followed by 3 h of reoxygenation): cardiomyocyte death/apoptosis, Trx expression and activity, AGE formation, Trx-apoptosis-regulating kinase-1 (Trx-ASK1) complex formation, and p38 mitogen-activated protein kinase (MAPK) phosphorylation and activity. Compared with vehicle, MG significantly increased SI-R-induced cardiomyocyte LDH release and apoptosis (P < 0.01). Prior to SI-R, Trx activity was reduced in MG-treated cells, but Trx expression was increased moderately. Moreover, Trx-ASK1 complex formation was reduced, and both p38 MAPK activity and phosphorylation were increased. To investigate the effects of MG on Trx directly, recombinant human Trx (hTrx) was incubated with MG in vitro. Compared with vehicle, MG incubation markedly increased CML formation (a glycation footprint) and inhibited Trx activity. Finally, glycation inhibitor aminoguanidine administration during MG treatment of cultured cells reduced AGE formation, increased Trx activity, restored Trx-ASK1 interaction, and reduced p38 MAPK phosphorylation and activity, caspase-3 activation, and LDH release (P < 0.01). We demonstrated for the first time that methylglyoxal sensitized cultured cardiomyocytes to SI-R injury by posttranslational modification of Trx via glycation. Therapeutic interventions scavenging AGE precursors may attenuate ischemic-reperfusion injury in hyperglycemic state diseases such as diabetes.
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PMID:Methylglyoxal increases cardiomyocyte ischemia-reperfusion injury via glycative inhibition of thioredoxin activity. 2046 May 80


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