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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microangiopathy is a more or less pronounced PAS deposit-located exterior to the endothelial cells of the lymphatics and the basal membrane of the capillaries. This lesion, found in various normal and pathological states, has generated numerous pathogenic hypotheses. The presence of microangiopathy in 5 groups of 50 subjects representing five different clinical conditions, subjects over 60 years old or less than 40, diabetics, latent diabetics or patients with severe coronary heart disease, together with microscopic and/or ultrastructural lesions of the connective tissue (fibroblasts, collagen and elastic fibers, ground substance) has enabled us to propose a pathogenic hypothesis applicable to any microangiopathy. The initial change, hereditary or acquired, would be fibroblastic or interstitial. It would be characterized by the accumulation of glycoproteins, proteoglyacans and soluble collagen in the interstitium. Incomplete drainage of these macromolecules would occur around the blood and lymphatic capillaries and manifest itself by a PAS deposit, the hallmark of the microangiopathy.
Atherosclerosis 1978 Mar
PMID:Hypothesis on microangiopathy of cutaneous capillaries. 66 87

Whether long-term glycemic control will prevent the chronic vascular complications of diabetes mellitus remains unknown. Microangiopathy and accelerated macroangiopathy are prevalent in both type I, or insulin-dependent diabetes mellitus, and type II, or non-insulin-dependent diabetes mellitus. Microangiopathy is predominantly responsible for the excessive morbidity and mortality in type I diabetic patients, whereas accelerated macroangiopathy directly relates to the excessive morbidity and mortality in type II diabetic patients. Institution of euglycemia for short periods will reverse preclinical, functional, renal, and retinal abnormalities, but will not reverse clinical nephropathy and retinopathy. Intensive insulin therapy, although it increases the risk of hypoglycemic encephalopathy, seems rational for type I diabetic patients without vascular complications who can recognize and respond normally to hypoglycemia. In patients with type II diabetes, sulfonylurea therapy, which is associated with fewer adverse reactions than intensive insulin therapy, may lower the risk of atherosclerosis development by correcting hyperglycemia and associated lipid abnormalities.
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PMID:Rationale for glycemic control. 390 46

By a complex biochemical, immunologic, morphohistochemical and ultrastructural study, carried out on a group of 42 obese and 38 diabetic children, comparatively with 12 normal controls, the authors arrive at conclusions which prove that obesity and diabetes mellitus carry great atherogenic risk factors. Even though the intimate atherogenesis mechanism is not perfectly known, the abnormal values of insulinemia, lipidemia and cortisolemia are certainly involved in this process. In diabetes mellitus the immunologic factor is also involved. Microangiopathy in diabetes mellitus and capillary lesions in the adipose tissue of obese children may also represent atherogenic risk factors. An efficient prophylaxis in atherosclerosis must therefore begin in childhood.
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PMID:Atherogenic risk in obese and in diabetic children. 636 4

Microangiopathy is retarded by improved blood glucose control in patients with IDDM. Whether or not this is true for macroangiopathy (atherosclerosis) has remained unclear. A total of 59 patients (44 +/- 1.5 years, previous HbA1C 9.4 +/- 0.2%, mean +/- SE) with IDDM were investigated. Of the 59 patients, 31 had been randomized to long-term intensified conventional insulin treatment (ICT), and the remaining 28 had received standard insulin treatment (ST). Blood glucose control was significantly better in the ICT patients with an HbAlc value (mean of 29 values during 10 years) of 7.1 +/- 0.1% compared with the ST patients' 8.2 +/- 0.2% (P < 0.0001). With high-frequency ultrasound, endothelial function was measured as flow-mediated dilation of the right brachial artery. The carotid arteries were scanned for plaques, intima-media thickness was measured, and arterial wall stiffness was calculated in the right common carotid artery. These measurements correlate with manifest and/or risk factors for coronary atherosclerosis. The patients in the ST group had stiffer arteries (P = 0.011) and thicker intima-media in the left common carotid artery (P = 0.009) than those in the ICT group. Patients with lower HbA1c generally had better endothelial function (P = 0.028) and less stiff arteries (P = 0.009). Better blood glucose control in patients with IDDM is related not only to less microangiopathy but also to a slower development of atherosclerosis.
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PMID:Early atherosclerosis is retarded by improved long-term blood glucose control in patients with IDDM. 877 31

Patient with diabetes mellitus is prone develop vascular lesion of blood vessels of all kinds. Microangiopathy and atherosclerosis are progressive during the illness. Following the study of Stanley I. Rapport the at all scientist on blood brain barrier permeability change in experimental conditions, also with this study blood brain barrier change in the diabetes mellitus patients was observed. In patients with diabetes mellitus the level total proteins increased in the cerebrospinal fluid.
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PMID:[Permeability of the hematoencephalic barrier by proteins in diabetes mellitus]. 1191 94

Patient with diabetes mellitus is prone to develop the vascular lesion of blood vessels of all kinds. Microangiopathy and atherosclerosis are progressive during the illness. Also with this study blood brain barrier change in the diabetes mellitus patients was observed. In patients with diabetes mellitus the level of glucose and total proteins increased in the cerebrospinal fluid. During diabetes mellitus the change of permeability blood brain barrier is evident. Blood brain barrier permeability changes in the patients with ICV as well as in the patients without ICV correlate with the values of diabetes mellitus in blood.
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PMID:[Correlation between levels of blood glucose and cerebrospinal fluid glucose and proteins in diabetes mellitus]. 1501 1

Arteriosclerosis and atheromatosis are etiologically and pathogenetically different non-physiological processes in atherosclerosis localized in the proximal segments of the arterial bed and elastic-type arteries; both affect the structure and function of the arterial wall. They cause an inflammatory reaction with subsequent compaction (sclerosing) of the walls of large and mid-size arteries, the loss of their elasticity due to structural changes in the loose connective tissue of intima-media, impaired elasticity and enhanced rigidity of the wall, inflammation, fibrosis, and increased pulse wave conduction velocity. Arteriosclerosis is initiated by long-term hyperglycemia, chemical collagen and elastin glycation by glucose and its metabolites (glycotoxins glyoxal and methylglyoxal) forming cross-links between collagen and elastin fibers. In contrast, atheromatosis as the main manifestation of atherosclerosis affects elastic-type arteries via accumulation of intimal lipids (cholesterol-esterified essential unsaturated and polyenic fatty acids, plaque formation at the sites of macrophage deposition in intima, necrotic and calcinotic foci. Atheromatosis does not affect collageous and elastic structures in the arterial wall. Arteriosclerosis and atheromatosis are two independent pathological processes in the walls of elastic-type arteries. Arteriosclerosis results from glycation of collagen and elastin chains in muscular-type arterioles, postarterioles, endothelium, and pericytes of exchangeable capillaries. Microangiopathy initiates only glycation and glycotoxin action because muscular-type arterioles have no intima, an interstitial tissue for the collection and utilization of biological "rubbish" from blood and intravascular pool of intercellular medium.
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PMID:[Glucose, glycotoxins, and protein glycation products: the role in pathogensis]. 2378 46