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)

Although peripheral vascular thrombic events are recognized as a serious extra-intestinal complication of inflammatory bowel disease, the occurrence of cerebral vascular events in association with acute exacerbations of this group of diseases is rare. In this article, relevant literature is reviewed and three children, 5, 12, and 13 years of age, who presented with clinical and magnetic resonance imaging evidence of an acute cerebrovascular event in association with an acute exacerbation of their inflammatory bowel disease are described. Except for the presence of anemia, hematologic and coagulation studies were unremarkable, and a search for evidence of a systemic vasculitis proved negative.
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PMID:Cerebral vascular events associated with ulcerative colitis in children. 1130 Dec 30

Anaemia, thrombocytosis are common secondary changes in inflammatory bowel disease (IBD), reflecting the clinical severity of the IBD cases, too. On the other hand, increased platelet function, fibrinolytic abnormalities, hypercoagulation of IBD patients predispose to thromboembolic events, and they may as well contribute to the local microcirculatory alterations leading to IBD itself. Reduced FXIII levels have been observed in IBD, which seems to be correlated with mucosal repair and might have therapeutic importance, too. Genetic thrombophilia received much attention recently, however, much less is known how frequent they are in IBD, what their clinical significance is, do they modify the clinical course itself. A short, concise review about links between haematology and IBD is given.
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PMID:[Hematologic aspects of inflammatory bowel diseases]. 1137 89

Many patients with chronic diseases such as chronic renal failure, chronic inflammatory bowel disease and rheumatoid arthritis are anaemic. Recently congestive heart failure (CHF) has also been found to be associated with anaemia. In all these diseases this anaemia or chronic disease is at least partially due to excessive production of cytokines and leukotrines that interfere both with the effect of erythropoietin (EPO) at the bone marrow and the release of stored iron in the reticuloendothelial system. Treating this anaemia with subcutaneous EPO and IV iron improves the weakness, fatigue, cachexia, nutritional state, mood, cognitive function and quality of life. In the case of CHF it also improves cardiac function and patient functional class, prevents deterioration of renal function and markedly reduces hospitalization. Very few agents in medicine improve so many aspects of the patient so well and so quickly. Unfortunately (for the suffering patient) this anaemia is often ignored and goes untreated.
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PMID:The pathological consequences of anaemia. 1142 23

The use of hematopoietic growth factors has increased rapidly during the last decade. Among the growth factors available, erythropoietin (EPO) was the first growth factor to be used clinically. To date, EPO has shown activity in the treatment of the tumor-associated anemia and for correction of tumor hypoxia, however, when compared with transfusion of erythrocytes EPO treatment did not significantly prolong survival in cancer patients in any published study so far. Recently, novel extramedullary EPO receptors have been identified leading to a better understanding of the molecular mechanisms of action of EPO. Results from these experiments and from several clinical studies suggest that EPO treatment may be beneficial for patients with (chronic) infections (HIV, inflammatory bowel disease, septic episodes) and for treatment of the fatigue syndrome following cancer chemotherapy. In addition, EPO may also improve stem cell engraftment following high-dose chemotherapy and can increase survival rates of patients with aplastic anemia and myelodysplastic syndrome. Currently, new EPO derivatives, synthetic fusion proteins and gene therapeutic studies are under clinical investigation suggesting that the EPO-induced effects may be increased significantly by these agents in the future.
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PMID:[Possible new indications for erythropoietin therapy]. 1156 47

We examined the therapeutic effects of the inflammatory cell infiltration inhibitor IS-741 (N-(2-((ethylsulfonyl)amino)-5-(trifluoromethyl)-3-pyridinyl)-cyclohexanecarboxamide monosodium salt monohydrate) on a rat colitis model. As a result of its effects on leukocyte infiltration, IS-741 inhibits cell adhesion, alleviates symptoms and signs of pancreatitis and multiple organ failure and demonstrates a life-saving effect in a model of severe acute pancreatitis. A rat model was prepared by inducing colitis with 3% dextran sodium sulfate (DSS) and maintaining pathology with 1% DSS. Repeated oral administration of IS-741 at 1, 10 or 100 mg/kg per day was conducted for 2 weeks (during treatment with 1% DSS). IS-741 at each dose decreased the area of erosion in the large intestine, thickening of the wall of the large intestine and anemia caused by melena. Some effects of IS-741 were nearly equivalent to those of the control compound salazosulfapyridine. Furthermore, IS-741 markedly alleviated inflammatory cell infiltration into the intestinal wall. IS-741 improved lesions in a rat DSS model by inhibiting leukocyte infiltration, suggesting the possibility of clinical application of this drug for IBD.
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PMID:Efficacy of the inflammatory cell infiltration inhibitor IS-741 on colitis induced by dextran sulfate sodium in the rat. 1170 14

Arthritis occurred in 23 of 136 (17 per cent) children and teenagers with inflammatory bowel disease, in 18 of 86 (21 per cent) patients with ulcerative colitis, and 5 of 50 (10 per cent) with granulomatous bowel disease. Eighteen children had peripheral arthritis which characteristically affected only a few large joints and was of brief duration and benign outcome. Five boys had spondylitis which was progressive and inseparable clinically from ankylosing spondylitis. Occurrence of joint manifestations was not associated with severity of bowel disease. Anemia and growth retardation occurred frequently. Mucocutaneous lesions were associated with peripheral arthritis but not with spondylitis. No patient had iridocyclitis. The possibility of bowel disease should be considered in children presenting with arthritis, particularly if gastrointestinal complaints, mucocutaneous lesions, anemia, or growth retardation are associated with pauciarticular arthritis. Peripheral arthritis is benign and regresses with improvement of underlying bowel disease but spondylitis is progressive and requires recognition and management for prevention of deformity.
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PMID:Arthritis associated with inflammatory bowel disease in children. 1211 46

Anemia is frequently observed in patients suffering from chronic inflammatory disorders. Recent in vitro data suggest that Th2 cytokines, such as IL-10, could be involved in its pathogenesis. We analyzed 1) changes in hemoglobin values in 329 patients with chronic active Crohn's disease receiving the anti-inflammatory cytokine IL-10 as part of a randomized, double-blind, placebo-controlled study, 2) serum iron parameters in a subgroup of these patients (n = 54), and 3) the in vitro effects of IL-10 on ferritin transcription and translation in human monocytic cells (THP-1) by means of Northern blot and immunoprecipitation after metabolic labeling. Patients receiving higher doses of IL-10 developed anemia and presented with a dose-dependent increase of ferritin and soluble transferrin receptor levels, an indicator of iron restriction to erythroid progenitor cells. According to our in vitro data, hyperferritinemia may result from direct stimulation of ferritin translation by IL-10 in activated monocytic cells, most likely by cytokine-mediated reduction of the binding affinity of translational repressors, iron-regulatory proteins, to the 5'-untranslated region of ferritin mRNA. In patients, all observed changes were most pronounced at the end of therapy (day +29), and thereafter hemoglobin levels and serum iron parameters returned to baseline levels within 4 wk of follow-up. Our data demonstrate that IL-10 causes anemia in patients with inflammatory bowel disease which may be referred to the induction of imbalances in iron homeostasis by the cytokine, leading to hyperferritinemia and limited iron availability to erythroid progenitor cells, a condition typically seen in the anemia of chronic inflammation.
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PMID:Role of IL-10 for induction of anemia during inflammation. 1216 51

Although the etiology of inflammatory bowel disease (IBD) is unknown, there is increasing evidence for the pivotal role played by tumor necrosis factor-alpha (TNF-alpha). Recent work has shown an increased concentration of TNF-alpha in both the bowel wall and in the stools of patients with IBD, and in children with that disease there are increased serum levels. Coincidental studies have shown that IL-10 knockout mice have increased levels of TNF-alpha and are known to develop a syndrome of stunted growth, anemia, bloody diarrhea, and colon tumors that mimics IBD. By injecting monoclonal antibodies intraperitoneally into IL-10 knockout mice, we were able to demonstrate significant histologic improvement of inflammation that correlates well with a resolution of diarrhea and rectal bleeding. This finding is consistent with a role for anti-TNF-alpha in the pathogenesis of IBD and suggests that this model may be of use for examining the effects of anti-TNF-alpha antibody administration.
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PMID:Murine monoclonal anti-tNF antibody administration has a beneficial effect on inflammatory bowel disease that develops in IL-10 knockout mice. 1218 21

Ulcers of the small bowel are rare, and in most cases are due to infections, inflammatory bowel diseases, malignancies or drugs. When none of these causes is recognized, they are classified as 'nonspecific' or idiopathic. Such lesions are uncommon, and in most cases present with occlusion. A case of a middle-aged woman with iron deficiency anemia due to occult bleeding, with negative gastroscopy and colonoscopy is presented. The diagnosis of a small bowel pathology resembling Crohn's disease was made by small bowel follow through and small intestine contrast ultrasonography. An ileal ulcer was identified at surgery, and after resection the patient experienced a stable recovery from the anemia without ulcer recurrence. Neither histology nor clinical or biochemical features suggested the diagnosis of an inflammatory bowel disease. Other possible causes were unlikely and the lesion was therefore diagnosed as idiopathic. This report also focuses on the need and the modality to investigate the small bowel in iron deficiency anemia patients.
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PMID:Iron deficiency anemia caused by nonspecific (idiopathic) small bowel ulceration: an uncommon presentation of an uncommon disease. 1252 74

The anemia of chronic disease is a common disorder that afflicts patients with a wide variety of inflammatory conditions including arthritis, malignancies, infections, and inflammatory bowel disease. It results in significant morbidity and may be severe enough to require blood transfusions. The pathogenesis of anemia of chronic disease is not fully understood, but poor maintenance of red blood cell mass has been observed at three levels: 1) iron is not efficiently recycled from reticuloendothelial macrophages to erythroid precursors, 2) erythroid precursors respond poorly to erythropoietin, and 3) red blood cell survival is decreased. Whether each of these changes is related to the same effector of the inflammatory process is unknown. We have had the opportunity to investigate severe anemia of chronic disease in an unusual group of patients with glycogen storage disease type 1a. We found that anemia was directly related to the presence of large hepatic adenomas that inappropriately produced a new peptide hormone, hepcidin. Hepcidin has recently been identified as part of the innate immune response and is a key regulator of cellular iron egress. Based on our findings in this patient group, we propose a central role for hepcidin in anemia of chronic disease, linking the inflammatory process with iron recycling and erythropoiesis. We present a hypothesis based on our findings.
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PMID:2002 E. Mead Johnson Award for Research in Pediatrics Lecture: the molecular biology of the anemia of chronic disease: a hypothesis. 1259 2


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