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

The natural history of patients with glucose intolerance was observed in 334 patients during a period of 18 years. Glucose tolerance testing (100 g orally) was characterized by measurement of induced insulin secretion. Diabetic complications of retinopathy, sensory neuropathy, and renal disease developed only in the group of patients in whom the induced serum insulin peak fell below 60 mu U/ml. Preservation of an insulin secretory reserve that permitted serum insulin peaks of 60 muU/ml or greater was not associated with development of these complications or symptoms of insulin deficiency despite the presence of an equal degree of fasting hyperglycemia and glucose intolerance. A critical amount of insulin secretory reserve distinguishes between two qualitatively distinct clinical syndromes: true diabetes mellitus (the development of signs and symptoms of insulin deficiency) and the syndrome of pure resistance to insulin (signs and symptoms of hyperglycemia in the setting of adequate or excessive insulin secretion, frequently with obesity, but without diabetic complication).
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PMID:Insulin secretion in the diagnosis of adult-onset diabetes mellitus. 67 27

The-Polarographic method was applied to the study of free oxygen tension (PO2) in the subcutaneous cellular tissue and the muscle of the arm in 104 patients suffering from diabetes mellitus without any concomitant pathology of the lungs and in 25 healthy persons. At the period of decompensation of diabetes mellitus (in the patients without any concomitant diseases of the lungs) PO2 was decreased in the subcutaneous cellular tissue by the average of 42% in comparison with the norm, and in the skeletal muscle of the arm--by 38%. The most frequently (and more significant) was tissue hypoxia in complicated diabetes, particularly in ketacidosis. Effective treatment led to an elevation of PO2 in the tissues of the great majority of the patients; in some of the patients it became normal.
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PMID:[Tissue oxygenation and tissue hypoxia in diabetes mellitus]. 82 79

Diabetic complications may result from chronic glycosylation of protein within cells and in the extracellular matrix. Prevention of glycosylation with aminoguanidine has forestalled complications in experimental diabetes.
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PMID:Glycosylation of proteins and microangiopathy. 134 43

Diabetic complications such as retinopathy and nephropathy affect the quality of life of diabetic patients. The aim of this study was to find out whether there are differences in the development of these complications associated with the age at onset of diabetes and the different effects of diabetes onset before, during or after puberty. Therefore, we tested the hypothesis whether onset of insulin dependent diabetes in puberty was connected with an increased risk of developing diabetic microangiopathy. We found a significantly increased risk in patients with diabetes onset in puberty up to a diabetes duration of 20 years if compared with diabetes onset before but not with that after puberty. It seems that diabetes onset before puberty delays the development of early diabetic complications and that changes of the hormonal status during puberty may be responsible for an earlier development of retinopathy. After about 20 years of diabetes there are no significant differences between the groups. Our results emphasize the necessity of early ophthalmological diagnosis and adequate metabolic control, especially in patients with diabetes onset during or after puberty, in order to prevent or delay the development of diabetic complications.
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PMID:Different frequencies of diabetic complications in insulin-treated patients with diabetes of comparable duration, in relation to age at onset of diabetes. 146 16

Renal failure is an important cause of morbidity and mortality in diabetic patients, who account for up to 25 per cent of new patients entering renal replacement therapy. Between 1980 and 1989, 651 patients with renal failure were treated at King's College Hospital, of whom 177 (27 per cent) had diabetes. Of these 177 patients 148 had diabetic nephropathy (65 non-insulin-dependent), while the rest had other renal diseases. Of the non-insulin-dependent diabetics, 45 per cent (29 of 65) were Asian or Afro-Caribbean compared to only 12 per cent (10/83) of the insulin-dependent diabetics. Ninety-two patients (62 per cent) have received a renal transplant with actuarial patient survival of 82 per cent at 1 year and 61 per cent at 4 years. Both patient and graft survival have been improved by the introduction of cyclosporin A. Continuous ambulatory peritoneal dialysis is the main form of dialysis and has allowed increasing numbers of patients to be dialysed, especially older individuals with non-insulin-dependent diabetes. Rehabilitation is best in those with functioning transplants: 21 patients (19 with functioning grafts) have survived for longer than 5 years. Diabetic complications before and after renal replacement therapy are described. Cardiovascular disease is especially common and may limit the success of renal replacement therapy.
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PMID:Renal replacement for diabetic patients: experience at King's College Hospital 1980-1989. 148 48

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

Estimates of the cost of diabetes should take into account the development of complications. Patient records identified from the 1987 National Hospital Discharge Survey were used to evaluate the risk of hospitalization due to late complications. Hospitalization for diabetic nephropathy reached a peak of 6.74/1000 between the ages of 45 and 54 years, compared to 0.14 to 1.80/1000 in controls. Diabetic patients less than or equal to 45 years of age were 46 times more likely to be hospitalized due to neuropathy. The risk of cardiovascular complications is high, with a greater incidence of arterial than venous disorders. Diabetic patients were 22 times more likely to be admitted for skin ulcers/gangrene, 15 times more likely due to peripheral vascular disease, and 10 times due to atherosclerosis. The risk of cerebrovascular accident and heart disease was 6 to 10 times greater in diabetic patients. Seventy-five per cent of diabetic cardiovascular disorders are myocardial infarction or chronic ischaemia. Hospitalization from renal complications occurs at younger ages than in the general population. Ophthalmic complications increase with age. Diabetic complications account for 2% of the total hospital admissions in the US in 1987. The total cost of the treatment of late diabetic complications was estimated at +5091 million (cardiovascular 74%; renal diseases 10%; nephropathy 3.6%; ophthalmic disorders 1.5%; other unspecified diseases 10%).
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PMID:The cost of hospitalization for the late complications of diabetes in the United States. 182 50

Beta-thromboglobulin (BTG) and fibrinopeptide A (FpA) were studied in 68 non-insulin dependent diabetic patients (NIDD) aged 32-81 with a mean duration of diabetes of 9 +/- 0.8 SEM years and 44 healthy controls, comparable for age and sex. Diabetic patients were subdivided into subsets according to the presence of microvascular disease, macrovascular disease or the absence of these lesions. Patients with microangiopathy (micro- and/or macrovascular disease) had higher HbA1 (a-c) (p less than 0.01), higher blood pressure (p less than 0.05) than both healthy controls and uncomplicated diabetics. Plasma BTG was higher in diabetic patients than in healthy controls (p less than 0.02), and was higher in complicated than in non-complicated diabetic subjects. Fpa was higher in complicated than in non-complicated diabetes (p less than 0.05). No differences were observed between the two subsets of complicated patients. In conclusion, we have shown that increased plasma- and platelet-BTG levels are present in non-insulin dependent diabetic subjects, with normal renal function and that plasma BTG is higher in patients with than in those without vascular disease. Fibrinopeptide A, a sensitive marker of in vivo fibrin formation, was significantly increased in NIDD with vascular complications.
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PMID:Beta-thromboglobulin and fibrinopeptide A in diabetes mellitus as markers of vascular damage. 240 34

The natural history of brittle diabetes is unknown. We have followed up 13 patients with disabling brittle diabetes unresponsive to continuous subcutaneous insulin infusion (CSII) for 3-6 yr. All were young, C-peptide deficient females. One patient has died (of hypoglycaemia). In the others, disruption of life has generally lessened, but only one patient is currently considered metabolically stable. Insulin treatment regimens have included long-term intravenous insulin infusions and intraperitoneal insulin, but all but four have now reverted to subcutaneous injections. Eleven patients intermittently required greater than 200 U/day of insulin and two have needed greater than 1,000 U/day. Insulin dosages have fallen significantly during follow-up (from 6.8 +/- 3.1 to 1.4 +/- 0.3 U/kg/day). Diabetic complications, initially present in only 2 cases (1 cataract, 1 proliferative retinopathy), have now developed in 5 others (2 background retinopathy, 1 proliferative retinopathy, 1 mixed peripheral neuropathy and 1 intermittent proteinuria). Psychosocial disturbance and non-compliance were common. We conclude that brittleness generally seems to improve, which probably explains the scarcity of older brittle patients. However, these patients are at considerable risk from diabetes, its complications and its treatment.
Diabetes Res 1988 Jan
PMID:The natural history of brittle diabetes. 304 51

Some patients do not fall neatly into the categories of Type 1 (insulin-dependent), Type 2 (non-insulin-dependent) or maturity onset diabetes of young people diabetes. The pedigree and characteristics of the family reported here illustrate this problem. Nine cases of diabetes are known in 4 out of 5 generations, with onset between 17-70 years. Treatment was with insulin in 5 (onset 17-29 years), tablets in 3 (onset 32-70 years), and in one diabetes occurred before the insulin era. Plasma C-peptide was 0.04-0.52 nmol/l (fasting) and 0.35-1.33 nmol/l (peak stimulation with glucagon). HLA typing, available in 7 diabetic patients showed DR2 or DR7 in all, DR4 in 2 and DR3 in none. Pancreatic islet cell antibodies were absent at diagnosis in the most recently diagnosed patient. Diabetic complications remain absent in two insulin-treated patients (duration 28 and 24 years), but have occurred extensively in the remainder. The form of diabetes in this family is therefore characterised by (a) strong family history (possible autosomal dominant with variable penetrance), (b) widely variable age of onset, (c) a variable degree of B cell reserve (d) no association with HLA DR3/4 and the presence of DR2 or DR7 and (e) no protection from complications.
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PMID:Familial diabetes mellitus with variable B cell reserve; analysis of a pedigree. 330 4


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