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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
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PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

Seventy-three patients with juvenile diabetes mellitus for a mean duration of 42.9 years were retrospectively studied on a multidisciplinary basis. Only three of this group of patients were socially disabled as a result of their long-standing illness. Of all the complications, insulin-induced hypoglycemia was most common. Although diabetic retinopathy was clinically evident in about 75 per cent of patients, only 50 per cent of these seventy-three patients had a significant visual impairment. Nephropathy was apparent in 59 per cent of patients, and neuropathy was demonstrable in half of them. Significant peripheral vascular system impairment was present in 40 per cent and major cardiac complication in 20 percent.
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PMID:Juvenile diabetes mellitus after forty years. 114 May 12

To examine the impact of metabolic control on renal responses to human atrial natriuretic peptide (hANP) in type 1 diabetes mellitus, 13 patients with HbA1 less than 8.5%, nine patients with HbA1 greater than 8.5% and ten healthy volunteers were studied. According to a randomized, single-blind trial design, 0.5 and 2.0 micrograms/kg hANP-(95-126) (Urodilatin) (Bissendorf Peptide, Hannover) or placebo were given as iv bolus injections at 90-minute intervals. Patients with HbA1 greater than 8.5% differed from those with HbA1 less than 8.5% in longer diabetes duration, more prevalent retinopathy and neuropathy and increased somatomedin C levels and urinary albumin excretion (p less than 0.05). In response to hANP, patients with HbA1 greater than 8.5% had decreased responses of urinary volume and sodium excretion in comparison to patients with HbA1 less than 8.5% (p less than 0.05) in whom renal responses to hANP did not differ from controls. Despite similar hANP levels, hANP-stimulated urinary cGMP excretion in patients was higher than in controls (p less than 0.01). Impaired renal responses to hANP in diabetes patients with insufficient glycemic control apparently contribute to the mechanisms of diabetic sodium retention. Near-normoglycemia may prevent this phenomenon which is intimately involved into the pathogenesis of diabetic nephropathy.
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PMID:[Effect of metabolic control on the renal effects of human atrial natriuretic peptide-(95-126) (urodilatin) in normotensive patients with type I diabetes mellitus]. 131 42

It is a widely held view that when a patient with type I diabetes mellitus and diabetic retinopathy or neuropathy develops renal impairment the renal lesion will be diabetic glomerulonephropathy. This has been extrapolated to apply to type II diabetes. We have performed a retrospective study of the clinical data of patients with diabetes mellitus who have had a renal biopsy between November 1980 and December 1990. Seventy-one patients were biopsied, data were available on 68. Nineteen of 22 type I diabetics had diabetic glomerulopathy, two had diabetic glomerulopathy in addition to another lesion only one patient did not have diabetic glomerulopathy. Twenty-three of 46 type II diabetics had diabetic glomerulopathy alone 22 having an alternative diagnosis. Eight further patients were identified who were not known to be diabetic at the time of renal biopsy, but whose biopsies revealed diabetic glomerulopathy. These data suggest that patients with type II diabetes and renal impairment should have a renal biopsy as part of their investigation.
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PMID:Increased prevalence of renal biopsy findings other than diabetic glomerulopathy in type II diabetes mellitus. 133 73

Insulin dependent diabetes mellitus is one of the most ravaging diseases of the civilised world mainly because of its secondary complications. Even the most careful exogenous insulin administration can neither maintain an entirely physiological glucose metabolism nor prevent the development of the late complications. Today pancreatic transplantation is the only therapy leading to total normalisation of glucose and lipid metabolism in type I diabetic patients. Beside the improvement of the life quality resulted by the independence of the insulin administration and of the dietary restrictions, secondary complications as nephropathy, retinopathy and neuropathy are positively influenced. Best results can be obtained with the simultaneous procedure, grafting kidney and pancreas from the same donor. In this case the grafted pancreas can also increase the patient survival rate and the kidney graft function rate comparing with the results of the kidney transplantation alone. In conclusion simultaneous pancreatic-kidney transplantation is clearly indicated for the treatment of type I diabetic patients with end-stage kidney disease.
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PMID:[The place of pancreas transplantation in therapy]. 140 88

Selected coagulation and fibrinolytic parameters were assessed in 40 insulin dependent diabetes mellitus patients with varying degrees of metabolic control; 30 healthy subjects matched for age and sex formed the control group. Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). Regardless of the normal level of the tissue-Plasminogen Activator-related antigen, diabetic patients had tissue-Plasminogen Activator activity lower than the control group (p < 0.05). Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). Higher levels of Fibrinogen were found in patients affected by nephropathy (p < 0.005) or neuropathy (p < 0.05). These results demonstrate an impairment of the haemostatic balance in diabetic patients, that is a possible hypercoagulable state, which represents an important factor in the pathogenesis of atherosclerotic complications.
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PMID:Coagulation and fibrinolytic system impairment in insulin dependent diabetes mellitus. 144 May 30

Whether there is a diabetic osteopathy" or osteopathy in diabetes mellitus", is still unclear. Epidemiological studies show in part discrepant results: bone mass was diminished in some studies, unchanged in others--even more positive trends were reported. Increases in osteoporotic fractures were observed in smaller collectives whereas no general trends for fracturing bones were found in diabetics. There are many in part favouring, in part impairing factors to be taken into consideration: Diabetes mellitus type I is a disease including immune phenomena. As inflammation leads to bone loss (inflammation-mediated osteopenia = IMO), peak bone mass may be influenced by such a process. The lack of insulin-like growth factors may be decisive, too. Complications of diabetes mellitus include hypogonadism--this may be disadvantageous for the skeleton. Diabetic complications like retinopathy, neuropathy, and angiopathy may influence the fracture event independently from bone mass. On the other hand, diabetes mellitus type II may be somehow protected against bone loss: Increased adipose tissue in connection with the frequently seen overweight yields metabolically active steroid hormones, insulin related growth factors may stimulate bone formation (e.g. in Forestier's disease). Older diabetics do not show diminished life expectancy any more due to their regular medical care--whether this includes the risk of bone diseases, is not yet clear. It may be worth to further analyse these "positive" effects seen in bones of type II diabetics because they may be useful in osteoporosis even in non-diabetics.
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PMID:Diabetes mellitus and bone metabolism. 149 Jul

A 9-year-old girl with recently diagnosed juvenile onset diabetes mellitus presented with signs and symptoms of bilateral optic neuropathy. Leber's hereditary optic neuropathy was suspected on the basis of a strong family history. Subsequent mitochondrial DNA testing was positive. Visual recovery occurred once the diabetes was well controlled. This case suggests that such metabolic compromise that occurs in diabetes may precipitate the clinical expression of Leber's optic neuropathy.
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PMID:Evidence for a metabolic trigger for Leber's hereditary optic neuropathy. A case report. 153 94

Although neuropathy has long been recognized as a complication of diabetes, the impact of this condition has not been adequately established. The prevalence of diabetic neuropathy is virtually unknown because the published studies differ considerably with regard to definition, method of assessment, and patient selection. Furthermore, the determination of prevalence has been hampered by the fact that there is no generally accepted classification of the variety of manifestations of diabetic neuropathy. The introduction of new sensitive diagnostic methods aids in the detection of less severe stages of neuropathy, as compared with clinically based assessment, and renders the disease more prevalent. The prevalence of diabetic neuropathy in the few reported population-based studies was approximately 30%. We have evaluated the prevalence of cardiovascular autonomic neuropathy in a group of approximately 1000 diabetic patients randomly included from 21 hospitals in Germany, Austria, and Switzerland. The results of this study and those of a prospective study on the natural history of neural dysfunction during the first 5 years after diagnosis of type 1 diabetes will be presented.
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PMID:The epidemiology of diabetic neuropathy. Diabetic Cardiovascular Autonomic Neuropathy Multicenter Study Group. 156 59

A series of 1,333 patients with non-insulin dependent diabetes (NIDDM) treated with oral hypoglycaemic agents (OHAs) between 1956 and 1988 is described. In addition there were 137 patients with insulin dependent diabetes (IDDM). When last on OHAs 51% of the patients with NIDDM were free from symptoms and satisfactorily controlled; 262 patients are known to have died, 223 have had to be changed to insulin and in 41 patients it has been possible to stop OHAs as no longer being needed, usually owing to better dietary compliance. Over the 32 years, 606 patients have been lost to follow-up; this represents 6.3% per year. The rate of development of secondary failure between the first and 20th year of treatment has been about 5% per year. Patients with NIDDM treated with OHAs have been more likely to develop clinically significant neuropathy and peripheral vascular disease; they also had a higher incidence of coronary artery disease than those treated with insulin. OHAs were used in the treatment of 110 patients with IDDM in the early stages of the disease; 44% achieved satisfactory blood glucose control for at least 12 months and a few patients for as long as 10 years. Of those with IDDM treated with OHAs, 44 were under 30 years of age; 55% had well controlled blood glucose levels for more than 12 months (median 2.8 years). Side effects have not been a real problem; 27 patients reported episodes of mild hypoglycaemia, skin rashes occurred in 1% of patients on sulphonylureas, and gastrointestinal symptoms in about 4% of those on biguanide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral hypoglycaemic agents: the first thirty years. 157 84


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