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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

If one reviews the literature with zeal, it is increasingly apparent that few organs escape recruitment when IBD is chronic or progressive. Insights into mucosal pathophysiology have helped with understanding the more frequent extraintestinal manifestations, but the mechanisms attendant to the development of less common events (e.g. acute pancreatitis, concurrent gluten sensitive enteropathy, or active pulmonary disease) remain either poorly studied or obscure. It is particularly interesting, however, to read reports of abnormal pulmonary function, generally of the obstructive type, correlated to measurements of abnormal intestinal permeability in patients with either active pulmonary sarcoid or pulmonary involvement in Crohn's disease. It has been further speculated that similarities in the mucosal immune system of the lung and intestine are responsible for evidence of bronchial hyperreactivity in patients with active IBD. Finally, it is important to recognize that extensions of the inflammatory process are not restricted to the development of organ-based events but may be responsible for some of the most frequent systemic abnormalities detected in IBD patients. It is now also well confirmed that the cytokine environment in IBD can support activated coagulation and, in some clinical situations, overt vascular thrombosis. The cerebrovascular complications of IBD are well recognized and range from peripheral venous thrombosis to central stroke syndromes and pseudotumor cerebri. Reports of focal white matter lesions in the brains of patients with IBD or an increased incidence of polyneuropathy may be other clinical examples of regional microvascular clotting. Microvascular injury appears to be more ubiquitously present, with reports ranging from a speculated primary causative role (e.g., granulomatous vasculitis in the mesenteric circulation) to the utility of nailbed vasospasm, in Crohn's disease, as a clinical marker for disease activity. It is also reported that IL-6 suppression of erythropoietin production is a major feature of the chronic anemia seen in active IBD. Moreover, the capacity of peripheral monocytes from active IBD patients to secrete TNF and IL-8 is reported predictive for the degree of therapeutic response from recombinant erythropoietin. These collected observations constitute another excellent example of the symmetry between basic science and clinical utility. It is from the context of applied basic science that many future therapies will arise. Empiricism will lose much of its appeal as clinical observations will be increasingly translated into cellular language. Already in animal models, elemental diets diminish IL-6-related acute inflammatory injury, and reductions in dietary lipid alter the antigenicity of bacteria. Provocatively, in humans, unconfirmed reports have even associated diet therapy with the resolution of uveitis and pyoderma gangrenosum. It is likely that efforts will also be made to induce oral tolerance if specific triggering proteins are discovered or to alter bowel flora if such an arcane area of investigation becomes resurgent.
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PMID:Extraintestinal considerations in inflammatory bowel disease. 880 40

While anemia is common in patients on chronic hemodialysis (HD), spontaneous erythrocytosis is rare and can be caused by either the same conditions causing erythrocytosis in the general population or any condition specific to chronic renal failure. We present a patient illustrating this latter circumstance. A 53-year-old man with diabetic nephropathy, with no known disease causing hypoxemia started HD in April 2001. Blood hemoglobin (Hgb) level was 13.7 +/- 2.8 g/dL while his kidney function was normal (1993-1996) and after 1997, with the development of chronic kidney disease, decreased progressively to a low of 10.2 g/dL in March 2001 when erythropoietin (EPO) injections were started. Erythropoietin requirements progressively decreased because of rising Hgb. Erythropoietin was discontinued in mid-2005. Blood hemoglobin continued to rise, however, to a high value of 17.6 g/dL in February 2006. At the same time, endogenous blood EPO level was 3.6 mIU/mL, a value consistent with primary polycythemia. White blood cell and platelet counts were normal. Several small renal cysts, including 1 complex cyst, were detected by ultrasonography and computer tomography in April 2006. He refused surgical treatment. He was treated with small phlebotomies (not returning the blood in the dialyzer at the end of dialysis) and monitoring of Hgb, which decreased toward the desired range. Repeated computer tomographic scans showed a slow increase in the size of the complex cyst and several other cysts. In late 2007 Hgb started rising again, and in February 2008, while the Hgb level was 16.4 g/dL, the endogenous serum EPO level was 726 mIU/mL (upper normal limit 31.5 mIU/mL). Intermittent phlebotomies were reinstituted. He subsequently developed multiple vascular catastrophes and expired from ischemic bowel disease in September 2008. Acquired cystic disease of the kidneys should be considered in HD patients who develop spontaneous erythrocytosis. The risks of acquired cystic disease include, in addition to the development of malignancy, vascular events from elevated Hgb.
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PMID:Spontaneous erythrocytosis in a patient on chronic hemodialysis. 1977 22

Anemia in the setting of chronic inflammatory disorders is a very frequent clinical condition, which is, however, often neglected or not properly treated given the problems often caused by the diseases underlying the development of anemia. Mechanistically, anemia is mainly caused by inflammation-driven retention of iron in macrophages making the metal unavailable for heme synthesis in the course of erythropoiesis, and further by impaired biological activity of the red blood cell hormone erythropoietin and the reduced proliferative capacity of erythroid progenitor cells. Anemia can be aggravated by chronic blood loss, as found in subjects with gastrointestinal cancers, inflammatory or infectious bowel disease, or iatrogenic blood loss in the setting of dialysis, all resulting in true iron deficiency. The identification of such patients is a clinical necessity because these individuals need contrasting therapies in comparison to subjects suffering from only classical anemia of chronic disorders. The diagnosis is challenging because no state of the art laboratory test is currently available that can clearly separate patients with inflammatory anemia from those with additional true iron deficiency. However, based on our expanding knowledge on the pathophysiology of inflammatory anemia, new diagnostic markers, including the iron-regulatory hormone hepcidin, and hematologic parameters emerge. Apart from traditional anemia treatments such as blood transfusions, recombinant erythropoietin, and iron, including new high-molecular-weight formulations, new therapeutics are currently under preclinical and clinical evaluation. These novel compounds aim at correcting anemia by multiple pathways, including antagonizing the inflammation- and hepcidin-driven retention of iron in the monocyte-macrophage system and thereby promoting the supply of iron for erythropoiesis or by stimulating the endogenous formation of erythopoietin via stabilization of hypoxia-regulated factors.
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PMID:Anemia of Chronic Disorders: New Diagnostic Tools and New Treatment Strategies. 2640 43