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

In spite of the continuing debate, it is possible to summarize the present state of our knowledge and to draw the following conclusions: 1. Microangiopathy of diabetes can be produced by pure insulin-deficiency in human subjects and experimental animals. 2. Evidence supports the concept that the pathology is due mainly to the deranged metabolism following insulin deprivation. 3. Repair of the insulin deficiency in animals has been shown to prevent the vascular damage associated with insulin deficiency. 4. Present methods of therapy have not been successful in preventing vascular complications in the noninsulin-dependent middle-aged diabetic patient; and, based on the findings of the University Group Diabetes Program, there is reason to believe that new methods of therapy must be realized to improve this outlook. 5. The efficacy of "compulsive control" for prevention of microangiopathy in insulin-dependent diabetic patients has not been adequately studied. Based on the results of animal experiments, the prudent physician should make every attempt to restore a normal physiological cellular environment in these patients with the expectation that this will offer the patient the best opportunity to minimize degenerative complications. Prospective observations are needed on the effects of hypoglycemic episodes which may be inevitable under these circumstances, but there is no evidence at present to suggest that mild hypoglycemia is of itself detrimental. 6. All individuals interested in the prevention of the complications of diabetes using available therapeutic methods should work to encourage a prospective clinical trial carefully designed from both an ethical and scientific point of view to obtain answers to the questions raised here.
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PMID:The role of diabetic control in diabetic retinopathy. 58 92

Spontaneous diabetes mellitus, observed in a colony of guinea pigs, parallels in many ways the syndrome known as juvenile diabetes mellitus in man: elevated blood glucose levels; reproductive dysfunction in the female; degranulation and severe cytoplasmic vacuolation of beta cells, severe fatty degeneration of acinar cells, and hyperplasia of the islets of the pancreas; and a high frequency of abnormal pancreatic secretions. Islet-cell necrosis and insulinitis usually seen in viral infections was not observed. Microangiopathy, another characteristic of juvenile diabetes mellitus in man was demonstrated as a significant increase in the thickness of the basal membranes in peripheral capillaries. A glomerular lesion encountered in some of the diabetic guinea pigs was shown to be similar to the glomerular sclerosis seen in human diabetics. Although a definitive etiologic agent was not identified, the disease was clearly contagious in origin.
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PMID:The guinea pig as an animal model of diabetes mellitus. 59 30

The importance of diabetic angiopathy for prognosis and course of diabetes mellitus, possibilities and basis of angiological therapy Complications originating from the vascular system determine life expectancy of the diabetic patient. He is particularly endangered by apoplexy, heart attack, arteriosclerosis of the lower extremities, retino- and nephropathy. Microangiopathy is a specific diabetic problem, the development of which shows a clear dependency on the quality of metabolism. Conventional therapy of circulatory problems today is less concerned with the vascular system than with the qualities of blood viscosity. In this context, viscosity is of main concern. Particularly in microcirculation viscosity is dependent on blood factors such as: haematocrit, plasmaviscosity, erythrocytes and thrombocytes. Their changed behaviour results, in the case of diabetes mellitus, in an increase in viscosity partly dependent on metabolism. A promising concept of treatment is available by pharmaceutically influencing the alteration of erythrocytes.
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PMID:[Diabetes mellitus and microcirculation. Significance of diabetic angiopathy for the prognosis and course of diabetes mellitus, possibilities and bases of angiologic therapy]. 96 91

Biopsy material obtained from the first portion of the jejunum of 56 unselected diabetics and 21 normal controls was examined under the electron microscope (in 8 cases) or with a method of stereologic morphometry. Controls were found to have a villous volume (VVi) of 50.19 +/- 10.1%. All values below 40% were interpreted as an expression of deterioration of the mucous membrane. Altogether 12.5% of the diabetics showed total atrophy, and 20% had significant reduction of VVi. These changes did not correlate with intestinal disorders or other signs of diabetes. In total atrophy histochemical changes could be demonstrated. Microangiopathy was not observed in the intestinal mucosa.
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PMID:The small intestine in diabetes mellitus. Correlation of clinical phenomena to histomorphometric findings in peroral biopsy material. 122 9

Microangiopathy is the major cause of death in Insulin Dependent Diabetes Mellitus. However, the pathogenesis of microangiopathy is still far from clear. This paper is a review of the literature on diabetic microangiopathy and discusses the current theories concerning its causes, prevention and treatment. The roles of abnormal glucose metabolism, protein glycosylation, genetic factors and puberty as well as the changes in vascular endothelium, capillary permeability and blood constituents, in the development of microangiopathy are discussed. The benefits of strict control of blood glucose concentrations are discussed along with the action of various pharmaceutical preparations such as aldose reductase inhibitors, hydroxyrutosides, pentoxifylline and free radical scavengers currently assessed in the prevention or treatment of diabetic microangiopathy.
Diabetes Res 1991 Jul
PMID:Microangiopathy in diabetes mellitus: I. Causes, prevention and treatment. 184 Oct 26

The Ticlopidine Microangiopathy of Diabetes study (TIMAD), a randomized, double-masked, placebo-controlled trial, assessed the effect of this antiplatelet agent (ticlopidine hydrochloride) in reducing the progression of nonproliferative diabetic retinopathy in 435 patients followed up for 3 years. The mean yearly increase in definite microaneurysms on fluorescein angiograms was significantly higher (P = .03) in the placebo group (1.44 +/- 4.67) than in the ticlopidine group (0.48 +/- 5.79). Significance was limited to primary analysis using a quality angiographic coefficient for definite microaneurysms in patients with at least three readable angiograms over a 3-year period. Ticlopidine was significantly beneficial to insulin-treated diabetic patients, inducing a sevenfold reduction of the yearly microaneurysm progression (0.23 +/- 6.66) compared with the placebo (1.57 +/- 5.29) (P = .03). Among insulin-treated diabetic patients, fewer had development of new vessels in the ticlopidine group than in the placebo group, at borderline statistical significance (P = .056). Overall retinopathy progression was significantly less severe in the ticlopidine group (P = .04). Adverse reactions associated with ticlopidine included neutropenia (severe in one patient) with no clinical complications, diarrhea, or rash. This study demonstrated that ticlopidine slows down the progression of nonproliferative diabetic retinopathy.
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PMID:Ticlopidine treatment reduces the progression of nonproliferative diabetic retinopathy. The TIMAD Study Group. 224 43

Microangiopathy is one of the most frequent and serious complications of diabetes. Its diagnosis is based on fundus of eye and fluorescein angiography findings, but several teams have emphasized the value of conjunctival angioscopy (CA) and peri-ungual capillaroscopy (PUC), describing suggestive anomalies: microectatic venous dilatation (V/A greater than 4.5), sludge on CA, "fish shoal" capillaries on PUC. Up to the present, however, the diagnostic value of these anomalies has not been evaluated based on data that are sensitive, specific and indicate predictive positive and negative values of a sign (Se, Sp, PPV, NPV). Anomalies of CA and PUC as a function of presence or absence of "diabetes" were studied in 114 patients with moderate hypertension, including 46 "diabetics" (33 with glucose regulation disorders and 13 non-insulin dependent diabetics). "Diabetes" was observed more predominantly in males of more advanced age and with a significantly higher global CA score (4.25 +/- 1.44 as against 2.65 +/- 1.35), and this in an increased manner as the "diabetes" was severe. Some anomalies had themselves a major orientation value with an Sp greater than 80% and an Se close to 40% (global score greater than 4; V/A greater than 4.5, microectasia, rheologic changes). For the fish shoal appearance the Sp was 73.5% and the Se 43.5%. The Sp was greater than 95% when at least 4 of the following 6 signs were present: global score greater than 4, V/A greater than 4.5, microectasia, rheologic disorders, fish shoal, gerontoxons. The more signs associated the more the Sp increased; the Se decreased from 40% for one sign to less than 10% for 4 associated signs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conjunctival and peri-ungual angioscopy in noninsulin-dependent diabetes mellitus. Informational value of observed anomalies]. 339 69

Duration of disease is the major susceptibility factor for microangiopathy. Microangiopathy does not occur without the metabolic abnormality of diabetes and there is much circumstantial evidence to implicate poor diabetic control in its pathogenesis. The rate of development and severity of complications, however, are variable even in patients with apparently similar control and about 25% of diabetics will never develop clinical evidence of microangiopathy. Studies of identical twins suggest a genetic component in the pathogenesis of retinopathy in NIDDM, and less so in IDDM, but increased capillary basement membrane thickness does not occur in the non-diabetic identical co-twins of insulin dependent diabetics. There may also be genetic heterogeneity not only of diabetes, but also of its complications, although for a given type of diabetes the prevalence of microangiopathy is often very similar in different racial groups. Associations between several different HLA molecules (particularly DR4) and microangiopathy in IDDM have been reported but not consistently confirmed. Recently the finding of an increased frequency of the B3 allotype of the fourth component of complement C4B3 in subjects with retinopathy has suggested that there is an HLA linked association. Both complement and the immunoglobulins are concerned with humoral immunity and the report of an association between a phenotype of the IgG heavy chain markers on chromosome 14 and retinopathy is of particular interest. These associations appear to be additive but independent. These reports need confirmation but provide the best evidence we have for an immunogenetic component (HLA and non-HLA linked) of the aetiology of microangiopathy, at least in IDDM. The studies of identical twins, HLA and Gm associations provide good evidence that genetic factors are involved in susceptibility to microangiopathy, at least in some diabetics, although the most relevant genes may not have been identified. Searches for better genetic markers must continue in order to identify those patients at increased risk of developing microangiopathy.
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PMID:The genetics of diabetic complications. 353 96

Type II, non insulin dependent diabetes mellitus is commonly diagnosed after the age of 45 years. For this reason it was previously called maturity onset diabetes. Type II diabetes occurring in young subjects has generally been described in selected pedigrees. The purpose of this work was to review data from all the unrelated type II diabetics (with fasting hyperglycemia) diagnosed before the age of 45 and observed in our department over the last four years. A total of 90 such patients including 44 men and 46 women were included in this study. Of 43 cases diagnosed before the age of 30, there were 30 women compared to only 16 women out of 47 cases diagnosed between 30 and 45 years (p less than 0.001). At the time of diagnosis 42 patients had a relative body weight lower than 120%. In 66,7% of the cases, one parent was a known diabetic. The rate of diabetes in the sibships was 50%. Differences in family history of diabetes were not observed in relation to age or weight at diagnosis. Comparison with a series of 150 conventional type II diabetics in whom diagnosis was made between 45 and 60 years of age showed a significantly greater frequency of obesity (86%) and fewer diabetic parent (36%). The mean apparent duration of diabetes was 14 years (range 5-42). Microangiopathy was not infrequent in these diabetic patients. Twenty-three patients had retinopathy, proliferative in 8 cases, and 3 were blind. Nine had renal insufficiency, severe in 3 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Type II diabetes in young subjects. A study of 90 unrelated cases. 359 70

We compared audiometric and clinical histories with findings in temporal bones of eight diabetics and ten normal controls matched for age and sex. The group with diabetes mellitus had significantly more hearing loss than the normal control group (p less than .01). Only patients with diabetes had microangiopathy. Patients with microangiopathic involvement of the endolymphatic sac had significantly greater hearing loss than patients without such involvement (p less than .01). Microangiopathy in the stria vascularis was highly significant in the diabetics (p less than .001); however, they did not have a significant hearing loss. Diabetic patients with basilar membrane microangiopathy had significantly lower percentages of histologically normal hair cells (p less than .05) and stria vascularis cells (p less than .05) and significantly greater hearing loss (p less than .01) than diabetic patients without such pathologic changes. Results of this study suggest that diabetic sensorineural hearing loss results from microangiopathic involvement of the endolymphatic sac and/or basilar membrane vessels.
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PMID:Diabetes mellitus and hearing loss: clinical and histopathologic relationships. 371 8


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