Macroangiopathy in adults and children with diabetes: from molecular mechanisms to vascular damage (part 1).
Type 2 diabetes mellitus (T2DM) is an increasing problem in childhood; however type 1 diabetes mellitus (T1DM) remains by far the most common type of diabetes in this age group. In this review we will focus on T1DM, because this will have the greatest implication for patients diagnosed in childhood. During the atherosclerotic process, several molecular, receptorial and cellular factors provide a continous mechanism of vascular damage. In diabetic children this state seems to be enhanced and facilitated so that accelerated atherosclerosis is associated with an increased risk of cardiovascular events in respect to the non diabetic population. Hyperglycemia PER SE and associated with diabetes is an important risk factor for atherosclerosis. At present a substantial part of children with diabetes do not reach satisfactory glycemic control. Other risk factors for the development and progression of atherosclerosis may be inherited or develop in the course of the disease: hypertension, dyslipidemia, insulin resistance, obesity, cigarette smoking, physical inactivity, disturbance of platelet function, coagulation and fibrinolysis. The development and progression of atherosclerosis should be blocked at an early age, if possible. Primary prevention to all risk factors for cardiovascular disease is important and intervention is indicated if necessary. At the moment the best therapeutic strategy is to maintain metabolic control at a physiologic level and perform screening and early intervention for vascular complications.
Di Marzio
D
D
Department of Pediatrics, University of Chieti, Italy.
Mohn
A
A
Mokini
Z H
ZH
Giannini
C
C
Chiarelli
F
F
D000328:Adult; D000803:Angiotensin I / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D050197:Atherosclerosis / Q000209:etiology / Q000473:pathology; D002648:Child; D008078:Cholesterol, LDL / Q000737:chemistry / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology*; D005234:Fatty Liver / Q000235:genetics / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D013927:Thrombosis / Q000473:pathology
D008078:Cholesterol, LDL; D000804:Angiotensin II; D000803:Angiotensin I