title: Diabetic microangiopathy: physiopathological, clinical and therapeutic aspects.
abstract: New evidence about diabetic microangiopathy has enabled us to identify an integrated pathogenesis of diabetic complications, including classic metabolic pathways induced by hyperglycaemia, insulin-resistance, hyperinsulinaemia, hormonal alterations and growth factors. Oxidative stress is the most important cause of endothelial damage inducing leukocyte adhesion, altered coagulation and inflammation. Adhesion molecules are a marker of endothelial damage and a potential therapeutic target. Changes in the extracellular matrix induced by TGFbeta1 and lower levels of eparan-sulfate, increased thickness of basement membranes and loss of pericytes are early events of diabetic retinopathy and diabetic nephropathy. Capillary rarefaction produced by genetic factors or by fetal undernourishment contributes to the beginning of insulin-resistance and hypertension. Psychophysical tests, electroretinogram and evoked potentials show retinal functional alterations; fundoscopy and retinal fluorescein angiography show retinal anatomic alterations. The diagnosis of diabetic neuropathy is based not only on traditional neurological examination and electroneurograms, but also on neurothesiometry for sensory testing. Medical treatment of diabetic microangiopathy is based on control of glycaemia, lipemia and blood pressure using glytazones, ACE-inhibitors, angiotensin II receptor antagonists and statins. New knowledgeabout microangiopathy pathogenesis suggests potential drugs for its therapy (ruboxistaurin, AGE-inhibitors, angiopoietin-1 and anti-VEGF, etc.), not yet on sale.
authors.affiliation: Unit of Medical Methodology and Semeiotics, Department of Internal Medicine, Cardiovascular and Nephrourological Diseases, University of Palermo, Palermo, Italy. antoniocamera@alice.it
authors.forename: A
authors.initials: A
authors.lastname: Camera
authors.forename: E
authors.initials: E
authors.lastname: Hopps
authors.forename: G
authors.initials: G
authors.lastname: Caimi
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors / Q000502:physiology; D003920:Diabetes Mellitus / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000178:diet therapy / Q000503:physiopathology; D003941:Diagnostic Techniques, Ophthalmological; D015507:Drugs, Investigational / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007249:Inflammation / Q000503:physiopathology; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D018384:Oxidative Stress; D011108:Polymers / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D019851:Thrombophilia / Q000209:etiology
chemical_list: D000959:Antihypertensive Agents; D000975:Antioxidants; D015815:Cell Adhesion Molecules; D015507:Drugs, Investigational; D017127:Glycation End Products, Advanced; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007004:Hypoglycemic Agents; D036341:Intercellular Signaling Peptides and Proteins; D011108:Polymers; C024617:polyol; D011493:Protein Kinase C