Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Churg-Strauss syndrome, or allergic granulomatous angiitis, is an uncommon vasculitic syndrome. We describe a 53-year-old man with Churg-Strauss syndrome and subsequent opportunistic cytomegalovirus enterocolitis. During intensive care, including steroid-pulse therapy, the patient developed rapidly progressive anemia caused by active bleeding from his small intestine, resulting in resection of 20 cm of ileum. Diagnosis of Churg-Strauss syndrome was confirmed both by characteristic clinical features and by histology. Histologic examination also revealed multiple shallow ulcers accompanied by cytomegalovirus infection. Characteristic angiitis was found in the ileum with normal-like mucosa, and it was not necessarily associated with ileal ulcers. This finding suggests that cytomegalovirus infection may be one of the causes or exacerbating factors for ileal ulcers in Churg-Strauss syndrome, although ulcers of the intestine have usually been considered to be caused by ischemia resulting from angiitis.
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PMID:Ileal ulcers and cytomegalovirus infection in a case of Churg-Strauss syndrome. 1591 42

Ischemic preconditioning is a powerful endogenous phenomenon in which brief periods of a sub-toxic ischemic insult induce robust protection against future, lengthy, lethal ischemia. The cardioprotective effects of ischemic preconditioning are manifest in all species studied so far, including humans. The ability to reproduce the cardioprotective effects of ischemic preconditioning with pharmacological agents raises the possibility that a drug may ultimately be introduced into clinical practice to treat human hearts undergoing ischemia/reperfusion. This chapter focuses on erythropoietin (Epo), a drug that has already been approved for humans and is in current use for the treatment of anemia associated with chronic renal failure, HIV infection, cancer patients on chemotherapy, and to reduce allogenic blood transfusion in surgery patients. Several recent studies have suggested that this cytokine possesses properties far beyond its capacity to produce red blood cells such as the ability to protect tissues including brain, kidney and heart against injury caused by ischemia/reperfusion. Cardioprotection conferred by Epo has been shown to be equal in magnitude to that conferred by ischemic preconditioning. However, the underlying mechanisms by which Epo protects the heart against injury caused by ischemia remain unknown.
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PMID:Erythropoietin mimics ischemic preconditioning. 1592 56

We examined the association between anemia (hemoglobin < or =12 g/dl) and 6 indexes of heart rate variability (HRV) as measured by 24-hour ambulatory electrocardiography in a cross-sectional study of 874 outpatients who had stable coronary heart disease. Of 90 participants who had anemia, 29% to 41% had low HRV, defined as the lowest quartile of each HRV index, compared with 23% to 25% of the 784 participants who did not have anemia (comparison p values <0.05 for all HRV indexes except high-frequency power). With the exception of high-frequency power, each 1 g/dl decrease in hemoglobin was associated with increased odds of having low HRV. This association remained strong after adjustment for potential confounding variables, including ischemia, left ventricular mass, left ventricular ejection fraction, and diastolic dysfunction. Thus, anemia is associated with low HRV in ambulatory patients who have stable coronary heart disease. Low HRV could potentially mediate the association of anemia with increased cardiac risk.
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PMID:Relation of anemia to low heart rate variability in patients with coronary heart disease (from the Heart and Soul study). 1595 May 76

The recently identified acute-phase response antimicrobial peptide hepcidin has been postulated to maintain iron homeostasis by modulating iron absorption at both the intestinal and macrophage levels. Hepcidin has also been reported to be responsible for anemia associated with chronic inflammatory diseases, and in anemia in patients with hepatic adenomas. Since Kupffer cells are known to be the primary contributor to early-phase ischemia-reperfusion injury in the liver and iron is known to modulate Kupffer cell production of proinflammatory cytokine and reactive oxygen species, we investigated hepcidin in vivo expression in the well-established rat partial-liver ischemia-reperfusion model. We found that both liver ischemia alone and liver ischemia-reperfusion significantly induced serum and liver hepcidin levels. Furthermore, currently proposed mediators of in vivo hepcidin expression, such as interleukin-6, signal transducers and activators of transcription-family transducers, and CCAAT/enhancing binding protein-alpha do not appear to modulate hepcidin expression in the liver ischemia-reperfusion acute inflammatory model. In this study we report the first in vivo evidence of liver ischemia and liver ischemia-reperfusion modulation of hepcidin expression. In conclusion, in the well-characterized liver ischemia-reperfusion model of acute inflammation, mechanism(s) other than interleukin-6 signal transduction via signal transducers and activators of transcription-3 may be responsible for hepcidin induction.
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PMID:Ischemia-reperfusion of rat liver modulates hepcidin in vivo expression. 1597 3

Treatment of diastolic heart failure is divided into acute and chronic management. During acute management, the focus should be treatment of the presenting syndrome, including correction of volume overload, treating hypertension, alleviating ischemia, and controlling tachyarrhythmias. Therefore, acute treatment should include several components: treating volume overload with sodium restriction and diuretics; treating ischemic heart disease with antiplatelet therapy, anticoagulants, and beta blockers; treating hypertension aggressively, using multiple agents if necessary; and treating atrial tachyarrhythmias such as atrial fibrillation with rate-controlling agents, such as beta blockers and possibly nondihydropyridine calcium channel blockers such as diltiazem and verapamil. Antiarrhythmic agents with or without electrical cardioversion may be necessary. Thoroughly evaluate and manage extracardiac precipitants such as anemia and renal failure. Chronic management should also focus on precipitating factors, for which adequate control of hypertension is paramount. Patient education regarding dietary and medication compliance and lifestyle changes is also important. If ischemic heart disease is present, aggressive anti-ischemic therapy is necessary, including revascularization when indicated.
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PMID:Treatment of heart failure with a normal ejection fraction. 1600 62

Erythropoietin (EPO), the principal hematopoietic cytokine produced by the kidney and the liver in fetuses, regulates mammalian erythropoiesis and exhibits diverse cellular effects in non-hematopoietic tissues. The introduction of recombinant human EPO (rhEPO) has marked a significant advance in the management of anemia associated with chronic renal failure. At the same time, experimental studies have unveiled its potential cardioprotective actions. As with other preconditioning agents, administration of exogenous rhEPO can confer myocardial protection against ischemia-reperfusion injury, in terms of reduction in cellular apoptosis and necrosis as well as improvement in myocardial functional recovery. The purpose of this study is to review current information regarding the various protocols used to investigate the effects of rhEPO administration as well as its cardioprotective properties. We also address the potential mechanisms underlying the protective effects of EPO. A better understanding of these mechanisms is essential for the development of clinical applications and the design of novel therapeutical strategies.
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PMID:Erythropoietin and myocardial protection: what's new? 1601 30

There is little objective to guide the therapy of patients with diastolic heart failure. Because of the similarities of pathophysiology abnormalities in diastolic and systolic heart failure, it is a reasonable inference to suggest that the proven therapy for systolic heart failure may also be of benefit in patients with diastolic heart failure. Treatment of underlying or exacerbating conditions in diastolic heart failure, such as hypertension, left ventricular hypertrophy, ischemia, diabetes, anemia, obesity and pulmonary disease is an important means of managing diastolic heart failure. Control of systolic blood pressure is effective in improving and preventing the development of diastolic heart failure. Treatment of diastolic heart failure is most effective when it is associated with hypertension. Production of systolic arterial pressure acutely reduces pulmonary congestion, ischemia, and chronically may lead to regression of left ventricular hypertrophy. Patients with diastolic heart failure in the absence of hypertension are very difficult to treat.
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PMID:Therapy for diastolic heart failure. 1611 17

After monotherapy with gemcitabine in low dose in long infusion, promising results in a variety of advanced chemoresistant tumors have been reported. In a previous phase I trial on heavily pre-treated patients, maximum tolerated dose (MTD) of gemcitabine in a 6 h infusion was 250 mg/m. The objective of our phase I-II trial was to test the combination of gemcitabine in a 6-h infusion and cisplatin in the treatment of advanced non-small cell lung cancer (NSCLC). Eligible patients were chemonaive, had locally advanced or metastatic NSCLC, Eastern Oncology Cooperative Oncology Group performance status 0-2 and normal organ function. Treatment consisted of gemcitabine in a 6-h infusion on days 1 and 8, and cisplatin at 75 mg/m on day 2 of a 3-week cycle. During phase I of the trial, the dose of gemcitabine was escalated from 130 to 170, 210 and 250 mg/m. After establishing dose-limiting toxicity (DLT) and MTD of the combination, the trial continued as phase II. Altogether, 61 patients were enrolled, of whom 54 had stage IV disease. In phase I of the trial, groups of six, seven, eight and eight patients were treated at the four dose levels of gemcitabine. In phase II, the remaining 32 patients all received gemcitabine at 250 mg/m. Serious toxicity included a patient with grade 5 ventricular arrhythmia and another with grade 4 cerebrovascular ischemia; four patients had grade 3 anemia. Reversible thrombocytosis with platelets over 500 was recorded in 32 patients; 42 patients had grade 2 alopecia. In general, tolerance to this treatment was good. One patient had complete response and 27 had partial responses, for a 28 of 61 (46%) response rate. Median progression-free survival, median survival and 1-year survival were 6 months, 9.5 months and 40%, respectively. We conclude that this treatment has an acceptable, yet distinct, toxicity profile; routine thromboprophylaxis is recommended. In our population of chemonaive patients, no DLT has been encountered. Due to the remarkable response rate, further research is warranted.
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PMID:Phase I-II trial of low-dose gemcitabine in prolonged infusion and cisplatin for advanced non-small cell lung cancer. 1622 56

Zebrafish (Danio rerio) have advantages over mammals as an animal model for investigating developmental toxicity. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (dioxin, TCDD), a persistent global contaminant, is the most comprehensively studied developmental toxicant in zebrafish. The hallmark responses of TCDD developmental toxicity manifested in zebrafish larvae include edema, anemia, hemorrhage, and ischemia associated with arrested growth and development. Heart and vasculature development and function are severely impaired, and jaw malformations occur secondary to inhibited chondrogenesis. The swim bladder fails to inflate, and the switch from embryonic to adult erythropoiesis is blocked. This profile of developmental toxicity responses, commonly referred to as "blue sac syndrome" because the edematous yolk sac appears blue, is observed in the larval form of all freshwater fish species exposed to TCDD at the embryonic stage of development. Components of the aryl hydrocarbon receptor/aryl hydrocarbon receptor nuclear translocator (AHR/ARNT) signaling pathway in zebrafish have been identified and functionally characterized. Their role in mediating TCDD toxicity has been determined using morpholinos to specifically knockdown the translation of zfAHR1, zfAHR2, zfARNT1, and zfARNT2 mRNAs, respectively, and a line of zfARNT2 null mutant zebrafish has provided further insight. These studies have shown that zfAHR2 and zfARNT1 mediate TCDD developmental toxicity. In addition, the growing use of molecular and genomic tools for research on zebrafish have led to advances in our understanding of the mechanism of TCDD developmental toxicity at the molecular level, including the recent finding that toxicity is not mediated by increased cytochrome P4501A (zfCYP1A) expression.
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PMID:Understanding dioxin developmental toxicity using the zebrafish model. 1633 42

It has been well established that erythropoietin (EPO) can limit myocardial ischemia/reperfusion injury in a variety of acute settings. However, despite EPO being used chronically to treat anemia the infarct limiting effects of long term treatment (chronic) have never been fully investigated. In this study we examined the effects of a 3 week treatment of EPO (5,000 IU/Kg) in male Sprague Dawley rats in limiting myocardial infarction after 35 min ischemia and 2 h reperfusion in an in vitro isolated heart perfusion model. Treating the animals 'once a week' failed to limit infarct size significantly compared to a saline control (54.1% +/- 3.5 v 52.3% +/- 4.4), whereas a '3 times a week' regime succeeded in significantly reducing infarct size (36.2% +/- 3.2 v 52.3% +/- 4.4, p < 0.05). To demonstrate that the effect was not due to improved oxygen supply caused by a raised hematocrit level, we also administered EPO 24 h prior to ischemia/reperfusion. This treatment again reduced infarct size compared to a saline control (39.9% +/- 4.4 v 58.4% +/- 5.0, p < 0.05). To examine the mechanism of protection we used the PI3K inhibitor wortmannin and the nitric oxide synthase inhibitor L-NAME to try to abrogate EPO mediated protection. Where wortmannin failed to block the effects of EPO (31.7% +/- 6.0 v 36.2% +/- 3.2), L-NAME did abrogate protection (51.6% +/- 5.6 v 36.2% +/- 3.2, p < 0.05). We demonstrate that chronic EPO treatment limits infarct size and that it does so in a nitric oxide dependent manner.
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PMID:Chronic erythropoietin treatment limits infarct-size in the myocardium in vitro. 1638 95


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