ABSTRACT
Postprandial lipemia has been associated with cardiovascular disease. The current pathophysiological concept is that postprandial remnant lipoproteins migrate into the subendothelial space and that remnants activate circulating leukocytes and endothelial cells. Activated monocytes adhere to endothelial adhesion molecules, facilitating subendothelial migration of monocytes. These cells differentiate into macrophages, with the risk of foam cell formation, due to uptake of remnants and modified lipoproteins. Evidence is emerging that specific interventions may reduce the atherogenic postprandial inflammation. Fruits rich in polyphenols, virgin olive oil, carotenoids and exercise have recently been found to reduce postprandial inflammation. Pharmaceutical interventions with fibrates or statins not only improve the overall lipid profile, but reduce postprandial inflammation as well. This review will deal with the current concept of postprandial inflammation in relation to the development of atherosclerosis and potential interventions to reduce postprandial inflammation.
Subject(s)
Cardiovascular Diseases/etiology , Hyperlipidemias/complications , Inflammation/etiology , Animals , Atherosclerosis/etiology , Atherosclerosis/prevention & control , Cardiovascular Diseases/prevention & control , Foam Cells/metabolism , Humans , Inflammation/prevention & control , Leukocytes/metabolism , Lipoproteins/metabolism , Macrophages/metabolism , Monocytes/metabolism , Postprandial PeriodABSTRACT
PURPOSE: To report on the efficacy of the somatostatin analog octreotide long-acting repeatable (LAR), in the treatment of uveitic chronic macular edema (CME). DESIGN: Case series, retrospective analysis. METHODS: In 20 patients, 20 episodes of recurrent CME during otherwise quiescent uveitis were treated with intramuscular octreotide LAR injections. Patients were included if CME control with acetazolamide or systemic and periocular steroids had failed during previous CME episodes or if contraindications existed for persistent use of these therapies. Mean outcome points were CME and visual acuity changes. Correlation of prognostic factors with these outcomes was analyzed. RESULTS: The included CME episodes occurred 7.6 +/- 1.4 years after onset of uveitis. Octreotide LAR treatment started 7.0 +/- 7.3 months after diagnosis of CME. CME decreased in 70% of episodes, after 2.7 +/- 1.3 months of treatment. After arrest of successful treatment, CME recurred instantly (27.2%) or within six months (36.4%). In 36.4% of successfully treated episodes, CME was absent for more than one year. A probable prognostic factor for success was the duration of CME before treatment. CONCLUSIONS: Octreotide LAR had an edema-reducing effect in 70% of treated CME episodes. Successful response was related to duration of CME before start of treatment. The early recurrence of CME (63.6%) after arrest of octreotide LAR advocates a long-term treatment in recent episodes of macular edema in otherwise quiescent uveitis.
