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)

Periarteritis Nodosa (P.A.N.) is a systemic connective tissue disease with a variety of manifestations that includes ocular involvement in 20% of cases. The diagnosis of this condition is difficult due to the absence of any specific clinical signs or laboratory findings. However, histologic studies have demonstrated a segmental vasculitis that is often necrotic. Ocular findings frequently include choroidal involvement that is characteristic. Nevertheless, angiographic studies of this disease are extremely rare. The findings in three patients suspected of having P.A.N. are presented. Fluorescein angiography established the diagnosis of P.A.N. in two cases and ruled-out its presence in the third case. In the first case angiography demonstrated a retinal vasculitis with multiple arteriolar and capillary occlusions. There was also ischemic involvement of the choriocapillaris and a mild anterior optic nerve vasculitis. All findings resolved, leaving numerous Elschnig spots. In the second case the angiogram showed acute multifocal ischemia of the choriocapillaris. The ocular examination and fluorescein angiogram in the third case were entirely normal, thereby ruling-out P.A.N. on the basis of insufficient criteria. Acute multifocal choroidal ischemia is present in a variety of rare conditions: Toxemia of pregnancy, Disseminated Intravascular coagulopathy, Moskowitz Disease (T.T.P.), Leukemia and Malignant Hypertension. However, the presence of multifocal choroidal ischemia in the presence of a systemic connective tissue disorder strongly favors the diagnosis of P.A.N. The relative contributions of co-existent Malignant Hypertension and P.A.N. in producing choroidal ischemia are discussed. The spectrum of clinical manifestations and laboratory findings in P.A.N. as well as hypotheses concerning pathogenesis (immune-complex deposition) are described. Among all systemic vasculitis , only P.A.N., and rarely Scleroderma, feature choroidal involvement. This is possibly due to the fact that the degree of vasculitis in P.A.N. is sufficiently severe to cause clinically significant choroidal involvement.
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PMID:[Fluorescein angiography in the diagnosis of periarteritis nodosa]. 614 75

The ECG effect of amsacrine (m-AMSA) was evaluated in 12 consecutive patients with leukemia. m-AMSA induced a significant prolongation of the Q-T interval (msecs, mean +/- SE) before (448 +/- 13) and 1 hour after (512 +/- 12) treatment (P . 0.0001, paired t test), without concomitant changes in the P-R interval, QRS duration, and heart rate. This selective cardiotoxic effect appeared to be transient and was noted towards the end of the iv drug administration, but was not present 24 hours later. No cardiac arrhythmias were noted during continuous monitoring. Nevertheless, it is assumed that the prolongation of the Q-T interval may represent a state of increased vulnerability to rhythm disturbances. Special care should be taken to avoid factors that may prolong the Q-T interval (hypokalemia, ischemia, or premedication with phenothiazine) during the administration of m-AMSA.
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PMID:Acute electrocardiographic changes induced by amsacrine. 659 38

Adult T cell leukemia-derived factor (ADF) is a human homologue of thioredoxin (TRX) with many biological functions and is induced by various stimuli and stress. In the central nervous system (CNS), expression of ADF/TRX occurs in glial cells during ischemia and reperfusion. We showed that ADF/TRX was actively released from U251 astrocytoma cells upon exposure to a low concentration of H2O2. The addition of conditioned medium from H2O2-stimulated U251 cells or recombinant ADF (rADF) to the culture medium promoted the survival of neurons from embryonic mouse cortex and striatum, but the addition of mutant ADF (mADF), which has no reducing activity, did not. In addition to rADF, incubation with two other thiol compounds, 2-mercaptoethanol (2-ME) and N-acetyl-L-cysteine (NAC), also increased the neuronal cell survival rate. In contrast, L-buthionine-(S,R)-sulfoximine (BSO), which inhibited the synthesis of glutathione (GSH), decreased the neuronal cell survival rate. Intracellular GSH was increased by incubation with rADF for 24 h, as it is with 2-ME and NAC. Redox active molecules such as thiol compounds may be survival factors for central neurons in vitro, and this capacity may be supplied by endogenous molecules, such as ADF/TRX and glutathione, under certain pathologic conditions in vivo.
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PMID:Neuroprotection by glial cells through adult T cell leukemia-derived factor/human thioredoxin (ADF/TRX). 795 44

Human thioredoxin, which was previously recognized as adult T-cell leukemia-derived factor, has many physiologic activities, one of which is a radical scavenger effect. Its ability to reduce reperfusion injury was assessed in vivo in a canine lung transplantation model. In 19 dogs, left lung allotransplantation was performed after 100 minutes of warm ischemia. The function of the transplanted lung was assessed after clamping of the contralateral pulmonary artery. In the human thioredoxin group (n = 6), human thioredoxin 30 mg/kg was given to the recipients during reperfusion. In the N-acetylcysteine group (n = 5), N-acetylcysteine 150 mg/kg, known as a radical scavenger, was given in the same manner. In both groups, arterial oxygen tension was significantly higher than in the control group (n = 8). In the human thioredoxin group, peak inspiratory pressure was significantly lower than in the control group. Macroscopic and microscopic examinations showed an almost normal appearance of the lung tissues in the human thioredoxin and N-acetylcysteine groups, in contrast to the abnormal findings in the control group. Thus it would appear that human thioredoxin has a protective effect on transplanted lungs, as does N-acetylcysteine, and that its action may be a radical scavenger effect.
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PMID:Inhibition of reperfusion injury by human thioredoxin (adult T-cell leukemia-derived factor) in canine lung transplantation. 796 75

Oxygen free radicals have been implicated in the pathogenesis of ischemic cell injuries. These free radicals are normally scavenged by antioxidant enzymes. Adenosine is normally released during ischemia and protects against ischemic injuries by interacting with adenosine receptors (ARs). The mechanism underlying its cytoprotective action is unclear. In this report, we provide evidence that activation of a unique A3AR in rat basophilic leukemia cells (RBL-2H3) leads to a 2 to 3 fold increase in activity of superoxide dismutase, catalase and glutathione peroxidase and also increases in the activity of glutathione reductase. Similar increases in enzyme activity were elicited in bovine and human endothelial cells, rat cardiac myocytes and smooth muscle cells. Increases in enzyme activity were attenuated by theophylline (an antagonist of the A3AR) and by pertussis toxin, implicating a role of A3AR/Gi protein in the activation. Importantly, activation of the A3AR decreased the degree of lipid peroxidation in these cells. These data provide strong evidence that the cytoprotective action of adenosine during ischemic cell injuries is mediated, at least in part, via a novel mechanism-activation of the cellular antioxidant enzymes.
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PMID:Adenosine acts as an endogenous activator of the cellular antioxidant defense system. 800 80

The formation of reactive oxygen species (ROS) is a major factor responsible for reperfusion injury in lungs. Adult T cell leukemia derived factor (ADF), a polypeptide made of 104 amino acids, is induced by a variety of stresses including X-ray, ultraviolet, H2O2, and mitogen. ADF has a reducing activity, which catalyzes the proton transfer between thiol-radical of cystein-containing proteins. Furthermore, ADF has a protective activity of ROS which are formed by xanthine oxidase and other alternative pathways in vitro. Using a rat in vivo model of lung ischemia, we examined the protective effect of recombinant human ADF (rhADF) against ischemia reperfusion injury of the lung. Ischemia, lasting for 75 min, was induced in the left lung of rats at 23 degrees C. The lung was then reperfused. These animals were divided into two groups: group 1 (n = 6, treatment with normal saline) and group 2 (n = 6, treatment with 28 micrograms/g of rhADF). One minute after the beginning of reperfusion, arterial oxygen tension (PaO2) decreased significantly in both groups (p < 0.01), without any significant intergroup difference (55.5 +/- 9.8, 49.8 +/- 8.6 mm Hg, respectively). Twenty minutes after reperfusion, PaO2 was significantly higher (p < 0.05) in group 2 (113.0 +/- 8.1 mm Hg) than in group 1 (72.3 +/- 13.6 mm Hg). The wet/dry weight ratio was significantly higher in group 1 (7.31 +/- 0.54) than in group 2 (5.82 +/- 0.36). Histologically, lung injury tended to be milder in group 2 than in group 1. These results suggest that rhADF has a protective effect against ischemia reperfusion injury of the rat lung.
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PMID:Effect of recombinant human adult T cell leukemia-derived factor on rat lung reperfusion injury. 800 96

Invasive pulmonary aspergillosis (IPA) in the presence of hematologic malignancies is an increasingly common condition characterized by high morbidity and mortality. Plain chest films are a valuable tool for diagnosis but the radiologist must be familiar with the morphological features of the disease to interpret radiographic abnormalities and to differentiate IPA from opportunistic pneumonia. The chest films of 16 leukemia and IPA patients performed from January 1987 to September 1993 were reviewed. The natural course of infection from its early stage (nodular lesions) to the subsequent phases when eventual medullary recovery plays a critical role was thus traced. Our major finding was related to the histogenesis of primary pulmonary lesions: the most common features we observed--i.e., the spherical rather than triangular shape of necrosis areas, with no relationship to the pleura or scissural delimitation suggest that supposed ischemia from vascular infiltration cannot be the only pathogenetic factor of pulmonary injury, in spite of the well-known angioinvasivity of the fungus Aspergillus.
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PMID:[Invasive pulmonary aspergillosis in oncological hematology: its pathogenesis and correlated radiographic picture]. 819 Sep 26

Adult T-cell leukemia-derived factor (ADF), identified in the supernatant of adult T-cell leukemia (ATL) cell culture, is a human homologue of thioredoxin and consists of 104 amino acids; it has two redox-active half-cysteine residues in an exposed active center. Human thioredoxin has many biological activities, including growth promotion, cell activation, and a catalase-like radical scavenging activity. We examined the protective effect of human thioredoxin (h-thioredoxin) against reperfusion-induced arrhythmias in an isolated rat heart model with 10-min regional ischemia followed by 30-min reperfusion. Male Wistar rats were assigned to six groups: a control, a superoxide dismutase (SOD 8 x 10(4) IU/L), and a catalase group (1 x 10(6) IU/L), and three groups treated with h-thioredoxin [approximately .01 microM (TRX-I group), approximately 0.1 microM (TRX-II group), and approximately 1 microM (TRX-III group)]. In the early reperfusion period, h-thioredoxin reduced the incidence of ventricular fibrillation (VF) to 8% in the TRX-II group (p < 0.01) from the control value of 75%. SOD and catalase reduced the incidence of VF to 43 and 33%, respectively (NS). During the entire reperfusion period, the incidence of VF in the SOD group was 79%, as compared to 83% in the control group. In the catalase and TRX-II groups, the incidence of VF was significantly reduced to 42 and 25%, respectively. These findings indicate that SOD failed to protect against the reperfusion-induced arrhythmias. h-Thioredoxin exerted a protective effect against these arrhythmias; a concentration of approximately 0.1 micro was the most effective.
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PMID:Protection against reperfusion-induced arrhythmias by human thioredoxin. 885 44

Acalculous acute cholecystitis (AAC) is a well-known complication in critically ill patients. However, there is no satisfactory data regarding this complication in leukemic patients. We reviewed the medical records of 426 patients with acute or chronic leukemia retrospectively to investigate the incidence, possible pathogenetic mechanisms, and clinical course of AAC in leukemia. Six cases of AAC were identified. The incidence was 1.65% (5/302) for acute leukemias. Three out of 6 patients underwent cholecystectomy, and two recovered completely. Percutaneous cholecystostomy was performed in another patient successfully. Careful histological examinations of the surgical specimens did not reveal any specific etiopathogenetic finding. However, clinical data suggested that infectious agents and visceral ischemia may contribute to the pathogenesis of AAC in leukemia.
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PMID:Acalculous acute cholecystitis in leukemia. 975 77

To determine the clinicohematological factors predictive for the appearance of major vascular complications (MVC) in patients with essential thrombocythemia (ET), 148 consecutive such patients were retrospectively assessed for the development of MVC during a median follow-up of 58.5 months. Seventy-seven patients had vascular risk factors, and 37 a history of MVC at ET diagnosis. Forty-nine MVC were registered in 33 patients during the follow-up period. The actuarial probability of MVC was 27% at 6 years in the whole series, 35.6% for patients above 60 years, and 21.4% for patients younger than 60 years, whereas only one of the 36 patients younger than 45 years had MVC. At multivariate analysis, age >60 years, history of major ischemia and hypercholesterolemia were the variables associated with an increased MVC risk. These results suggest that all ET patients above 60 years should be treated, whereas in younger patients treatment decisions should be primarily based on the existence of risk factors for MVC.
Leukemia 1999 Feb
PMID:Major vascular complications in essential thrombocythemia: a study of the predictive factors in a series of 148 patients. 1002 86


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