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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological examinations in the lungs in patients with diabetes mellitus of different degrees of severity and duration (28 autopsy observations) were carried out. Diabetic microangiopathy in the lungs was found to involve the capillaries of alveolar septa and arterioles as well as pleural arterioles, and is manifested by plasmorrhagia, insudation, thickening of basal membranes and hyalinosis of the vessels. Moreover, intraseptal nodules, granulomas in small artery walls, focal proteinosis develop in the lungs followed by sclerosis of the microcirculatory bed vessels and centrilobular emphysema. All these comprise a favourable background for the development of pneumonias which, along with pulmonary-cardiac insufficiency are one of the most frequent causes of death of patients with diabetes mellitus.
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PMID:[Changes in the lungs in diabetes mellitus]. 712 37

Diabetic microangiopathy is in its developed form a serious complication for patients with diabetes, in particular diabetes type 1. An important aspect of prevention of organ damage is early assessment of factors which accelerate the development of microangiopathy. In the submitted paper the authors draw attention assessment of plasma fibrinogen, thrombocyte aggregation in relation to renal functions in type 1 diabetics as well as other indicators which promote the development and acceleration of diabetic nephropathy. In patients with diabetic nephropathy a correlation was found between fibrinogen and thrombocyte aggregation as well as between the rate of urinary albumin excretion, systolic and median blood pressure which are risk factors which increase the mortality of patients with type 1 diabetes.
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PMID:[Fibrinogen and diabetic microangiopathy]. 924 73

A reasonable interpretation of the present evidence indicates that diabetes, when a complication of periodontitis, acts as a modifying and aggravating factor in the severity of periodontal infection. Diabetics with periodontitis who were young and poorly controlled, those who were long-duration diabetics, especially those over 30 years old, demonstrated more attachment loss, bone loss, and deeper probing pocket depths than their nondiabetic controls. It seems that the earlier the onset of diabetes and the longer the duration, especially without consistent control, the more susceptible the individual will be to periodontal disease. Consequently, once a diabetic contracts periodontal disease, it is usually more destructive. Although plaque scores of diabetics may be comparable to or even less than those of nondiabetics, diabetics often exhibit higher gingival index scores. The elevation of this particular clinical parameter is indicative of the microangiopathy associated with diabetes. Diabetic microangiopathy contributes to compromised delivery of nutrients to surrounding tissues and poor elimination of metabolic waste products. The complications associated with diabetes such as macroangiopathy, microangiopathy (i.e., retinopathy), ketoacidosis, and hyperglycemia result in impaired wound healing, immunosuppression, and susceptibility to bacterial infection. Individuals ages 30 to 40 suffering from diabetic retinopathy had significantly more gingival inflammation than controls or diabetics without complications. Collagen metabolism is defective in diabetics and is one component underlying delayed wound healing. Animal studies have been instrumental in elucidating the details of delayed wound healing. Hyperglycemia was associated with increased collagenase and protease activity in the gingiva of rats. Vascular wound healing in rats, particularly new re-endothelialization across vascular anastomoses, was significantly impaired. Diabetic abnormalities in immune response include impaired neutrophil chemotaxis, phagocytosis, and adhesion. Decreased neutrophilic chemotactic response seems to be attributable to protein factors in diabetic serum that competitively bind neutrophil receptors, thereby preventing complement-mediated phagocytosis. Because diabetics are not able to eliminate circulating immune complexes (CIC) effectively, serum CIC levels are elevated. There are microbiological differences in the characteristic flora of NIDDM patients and IDDM patients with periodontitis. These differences are not associated with diabetic impaired immune response. Ultimately, bacterial plaque is the primary etiology of periodontal diseases. Evidently, the host's response to bacterial plaque and ability to heal following surgery is altered by diabetic disease. Therefore, a thorough history regarding onset of diabetes, duration, and diabetic control would prove useful in the clinical management of diabetics presenting for treatment of periodontal disease.
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PMID:Periodontal disease, diabetes, and immune response: a review of current concepts. 947 64

Diabetic microangiopathy has been implicated as a fundamental feature of the pathological complications of diabetes including retinopathy, neuropathy, and diabetic foot ulceration. However, previous studies devoted to examining the deleterious effects of elevated glucose on the endothelium have been performed largely in primary cultured cells of macrovessel origin. Difficulty in the harvesting and maintenance of microvascular endothelial cells in culture have hindered the study of this relevant population. Therefore, the objective of this study was to characterize the effect of elevated glucose on the proliferation and involved signaling pathways of an immortalized human dermal microvascular endothelial cell line (HMEC-1) that possess similar characteristics to their in vivo counterparts. Human dermal microvascular endothelial cells (HMEC-1) were grown in the presence of normal (5 mM) or high D-glucose (20 mM) for 14 days. The proliferative response of HMEC-1 was compared under these conditions as well as the cAMP and PKC pathways by in vitro assays. Elevated glucose significantly inhibited (P < 0.05) HMEC-1 proliferation after 7, 10, and 14 days. This effect was not mimicked by 20 mM mannitol. The antiproliferative effect was more pronounced with longer exposure (1-14 days) to elevated glucose and was irreversible 4 days after a 10-day exposure. The antiproliferative effect was partially reversed in the presence of a PKA inhibitor, Rp-cAMP (10-50 microM), and/or a PKC inhibitor, Calphostin C (10 nM). HMEC-1 exposed to elevated glucose (20 mM) for 14 days caused an increase in cyclic AMP accumulation, PKA, and PKC activity but was not associated with the activation of downstream events such as CRE and AP-1 binding activity. These data support the hypothesis that HMEC-1 is a suitable model to study the deleterious effects of elevated glucose on microvascular endothelial cells. Continued studies with HMEC-1 may prove advantageous in delineation of the molecular pathophysiology associated with diabetic microangiopathy.
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PMID:Antiproliferative effect of elevated glucose in human microvascular endothelial cells. 982 95

A 30-year-old female complained of lancinating pain in the bilateral thighs for 10 days. The patient had a 22-year history of insulin-dependent diabetes mellitus. Physical examination revealed swelling of the bilateral lower extremities. There was exquisite tenderness on palpation over the medial thighs, with marked increase in pain on hip and knee flexion. Muscle strength of quadriceps, hamstrings, and hip adductor was decreased due to muscle pain. Pedal pulses were palpable bilaterally. Roentogenograms of the left femur revealed calcification of the left femoral arterial wall. Venogram revealed no obstruction with normal drainage. Complete blood cell count showed left shift of the neutrophils, markedly accelerated erythrocyte sedimentation rate, prolonged prothorombin time of 9 sec (normal 11.7 sec), C-reactive protein of 7.3 mg/dl and serum creatine kinase level of 175 IU/L. FBS was 225 mg/dl and Hb A 1 c was 16.4%. An MR imaging of the thighs revealed high signal intensities in the bilateral adductor muscles on T 2-weighted images. The symptoms resolved spontaneously over a three week period. From the course of the illness and MR imaging, the patient was diagnosed having diabetic muscle infarction (DMI), a rare complication of diabetes mellitus. To our knowledge, this is the first reported case of DMI in Japan. Diabetic microangiopathy and hypercoagulability are thought to be responsible for inducing DMI. Because the diagnosis can be made from the characteristic clinical and the typical MR imaging findings, muscle biopsy is not always necessary to obtain the diagnosis of DMI.
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PMID:[Bilateral diabetic infarction of the thigh adductor muscles in a diabetic female patient-- A case report and review of the literature]. 1039 Oct 74

Diabetic microangiopathy is characterized by increased prorenin concentrations. In the present study, we evaluated plasma prorenin concentrations in a large group of adolescents with onset of diabetes during childhood to determine whether increasing prorenin levels may predict the development of persistent microalbuminuria. Ninety-seven young diabetic patients were studied; they were divided according to the presence of persistent microalbuminuria, at the end of follow-up, into group A and group B (patients who did not develop and who developed persistent microalbuminuria, respectively). One hundred and two healthy subjects, matched for age and sex, were also selected. Patients were followed up for at least 10 years. At the beginning of the study there were no significant differences in prorenin levels between either the two diabetic groups or the healthy controls. During follow-up, an increase in plasma prorenin started at 4 years and became statistically significant (P<0.01) 3 years before the onset of persistent microalbuminuria. No correlation was found between plasma prorenin levels and HbAlc percentages. In conclusion, an increased concentration of prorenin in plasma precedes the elevation of albumin excretion rate (AER) and, therefore, can be useful for identifying patients with onset of diabetes during childhood at risk of developing incipient nephropathy later in life.
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PMID:Plasma prorenin levels may predict persistent microalbuminuria in children with diabetes. 1126 77

Pieces of the aorta and heart coronary arteries taken at autopsy of 100 patients who had died of insulin-dependent and non-insulin-dependent diabetes mellitus were studied histologically and immunohistologically. Atherosclerosis was more pronounced in diabetes mellitus patients than in patients with normal glycemic indices. Atherosclerosis was most severe in non-insulin-dependent diabetes. Diabetic microangiopathy of the vasa vasorum of large arteries promotes development of atherosclerosis.
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PMID:[Mechanisms of development of diabetic macroangiopathy]. 1139 87

Diabetic microangiopathy produces widespread small vessel impairment which particularly affects renal glomeruli functions. Microalbuminuria is the earliest marker of microangiopathic kidney disease and has also recently been recognised as a marker of macroangiopathic cardiovascular involvement. To determine correlations between daily microalbuminuria, local microangiopathic kidney damage, systemic macroangiopathic involvement and functional brain microcirculation, 70 Type 2 diabetic subjects who were diagnosed more than 5 years ago underwent carotid (to determine index of macro- and microangiopathy) and interlobar kidney artery color Doppler (to determine microangiopathic involvement), transcranial Doppler (to determine alterations in brain vasomotor reserve), and evaluation of daily albumin excretion rate. All the indices of microcirculatory involvement in the kidney, brain and small vessels downstream-from the carotid arteries were closely related (for all p<0.001) but never correlated with the macroangiopathy index. Daily microalbuminuria correlated with all the micro- (p<0.0001) and macroangiopathic (p<0.005) Doppler indices. These findings confirm that microangiopathy is the main cause of the diabetic increase in the albumin excretion rate and support the view that microalbuminuria can be considered a powerful biomarker of widespread macroangiopathy. Our results suggest microalbuminuria may also identify cerebrovascular diabetic involvement, as it predicts both macroangiopathic carotid alteration and microvascular brain impairment.
Diabetes Nutr Metab 2004 Dec
PMID:Microalbuminuria, brain vasomotor reactivity, carotid and kidney arterial flow in Type 2 diabetes mellitus. 1588 25

Microvascular insufficiency represents a major cause of end-organ failure among diabetics. Prevention at early stage of disease is therefore necessary and is a focus of current investigations. Progression of diabetes is complicated by endothelial cell apoptosis as well as occlusion of arteriole and capillary leading to microvascular rarefaction. This favors the formation of non-healing limb ulcers and limits the benefit of revascularization. Recent study indicated that reduction of platelet derived growth factor (PDGF) expression was indeed critical, in causing functional and morphological vascular changes, namely the dissociation of pericytes from the capillaries in muscles. Diabetic microangiopathy is a result of pericytes dissociation from reduced PDGF as well as vessel rarefaction from reduced number of endothelial progenitor cells (EPCs) and EPC dysfunction. Since blood vessels develop through the assembly of these two principal cell types--endothelial cells and pericytes/smooth muscle cells, prevention of diabetic microangiopathy requires interventions targeting at both cell types in a complementary and synergistic manner. An improved recruitment of EPCs will help repair of injured endothelium while molecular targeting with PDGF will enhance pericytes recruitment. EPCs modified with PDGF therefore hold promise as the next generation of agents for prevention of microangiopathy.
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PMID:Endothelial progenitor cells transfected with PDGF: cellular and molecular targets for prevention of diabetic microangiopathy. 1684 33

Diabetic microangiopathy is responsible for an important rate of morbidity and mortality related to the disease. Endothelial damage seems to be the triggering factor in the pathogenesis of microvascular complications. Diabetes mellitus and other metabolic diseases are associated to endothelial dysfunction, the most precocious known marker of atherosclerosis. Changes on microvascular reactivity are present in patients with diabetes mellitus, as well as in individuals with risk factors for this disease. Evaluation of endothelial and microvascular functions is possible using different invasive or preferentially non-invasive methods. Adequate control of diabetes mellitus might postpone or perhaps even prevent the microvascular disease. Microvascular dysfunction, when seen only by changes on microvascular reactivity, could be ameliorated with correction of risk factors or drug treatment.
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PMID:[Microcirculation in diabetes: implications for chronic complications and treatment of the disease]. 1750 27


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