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

In order to evaluate a possible relation between cigarette smoking and prevalence of diabetic microangiopathy, a series of 180 consecutive patients suffering from insulin-dependent juvenile-onset diabetes mellitus with different durations of disease (60 patients each with diabetes for 10 to 19 years, 20 to 29 years, and 30 to 39 years, respectively) were examined for clinical signs of retinopathy, nephropathy, and peripheral neuropathy. The results were compared with the patients' previous and actual smoking habits. Cigarette smoking was defined as daily smoking of at least ten cigarettes for one year or more. Smoking habits of the total diabetic sample were not significantly different from those of a nondiabetic control sample. However, a decline in the number of cigarette smokers and a rising number of ex-smokers were noted with increasing duration of diabetes. In comparing smokers and nonsmokers, no difference was found in the prevalence of peripheral neuropathy, background retinopathy, and proliferative retinopathy. However, the prevalence of nephropathy (persistent proteinuria) was significantly higher (p less than 0.05) among these patients who were or had been cigarette smokers. Thus, cigarette smoking might be considered a risk factor for the development of diabetic nephropathy.
Diabetes Care
PMID:Cigarette smoking and prevalence of microangiopathy in juvenile-onset insulin-dependent diabetes mellitus. 72 38

In the case of three gastrointestinal organs - the esophagus, the stomach, and the colon - no indication for clinical transplantation is conceivable today or in future. On the other hand, experience with transplantation of the small bowel, the liver and the pancreas has already been gained, though up to now the results have been rather poor. Nevertheless, some clear indications exist which justify these transplantations in highly specialized centers. They include total loss, of the small bowel, multiple small bowel atresias, acute liver necrosis, congenital biliary atresia, Echinococcus alveolaris, in future some enzyme defects and finally, juvenile diabetes with nephropathy. Whether, and when, transplantation in these diseases becomes routine will depend on progress in immunology.
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PMID:[Organ transplantations in intestinal tract surgery: history or future?]. 76 52

Vascular responsiveness to infused angiotensin II and to norepinephrine was determined in 14 normal subjects and two groups of diabetic subjects, 16 with no clinically detectable diabetic complications and 14 with diabetic retinopathy but no clinical evidence of nephropathy. All were maintained on a 100-mEq. -Na- 100-mEq. -K diet. Serum electrolytes, 24-hour urinary sodium, creatinine clearance, and plasma renin activity did not differ significantly among the groups. Group mean baseline diastolic pressure in those with retinopathy was higher than in normal subjects but no significantly different from that of uncomplicated diabetics. The pressor dose of angiotensin II (ng./kg./min. to increase diastolic blood pressure 20 mm. Hg) for each group respectively was 11.5 +/-0.9, 12.9+/- 1.3, and 8.3 +/- 1.3, and the slope of the dose-response curve (mm. Hg rise in blood pressure resulting from the infusion of 1 ng./kg./min. following the initial increment in blood pressure) was 2.0 +/-0.2, 1.6+/-0.2, 3.3+/- 0.6. For norepinephrine, the pressor doses were 163 +/- 24, 212+/-21, and123 +/- 11 and slopes were 0.17 +/- 0.03, 0.13 +/- 0.02, and 0.20 +/-0.02. Neither diabetic group differed significantly from normal subjects. Diabetics with retinopathy were more sensitive to angiotensin II, pressor dose (P less than 0.059) and slope (P less than 0.02), and to norepinephrine, pressor dose (P less than 0.006) and slope (P =0.05) than those without complications. These data suggest that vascular reactivity is enhanced in diabetics with retinopathy.
Diabetes 1976 Apr
PMID:Vascular reactivity to angiotensin II and to norepinephrine in diabetic subjects. 77 23

This study documents the presence of marked immunofluorescence for IgG and albumin in renal extracellular membranes, especially tubular basement membranes (TBM), of patients with severe diabetic nephropathy. A comprehensive immunofluorescent analysis was carried out on kidney tissue from 83 patients--Group I: 24 living normal renal allograft donors and two infants less than one week of age. Group II: 24 patients with severe nephropathy who had juvenile onset of diabetes 16 to 30 years previously and who ranged in age from 20 to 47 years. Group III: 33 patients with severe kidney disease of varied etiologies with an age range of five to 63 years. The sections were assayed for a variety of proteins (immunoglobulins, complement components, and tissue antigens). Kidney sections of all patients with severe diabetic nephropathy were readily distinguished from kidneys of other patients and normals by the intense linear staining of the extracellular membranes, especially the tubular basement membrane for IgG and and albumin. Dual-labeled studies using FITC anti-basement membrane (BM) and tetramethyl rhodamine (TMR) antialbumin demonstrated localization of the albumin predominantly to the outer but also the inner TBM while the BM antisera reacted more intensely with the inner membrane. There is no evidence that an immunologic process is responsible for these findings. These immunofluorescent findings are specific for severe diabetic nephropathy and may reflect structural changes in the renal extracellular membranes that permit entrapment of serum proteins, possibly due to changes in permeability.
Diabetes 1976 Aug
PMID:Immunopathology of renal extracellular membranes in diabetes mellitus. Specificity of tubular basement-membrane immunofluorescence. 78 82

The results of kidney transplantation in a variety of renal diseases have been analyzed. The diseases causing end-stage kidney failure in recipients were Alport syndrome, amyloidosis, cystinosis, diabetes mellitus, Fabry disease, familial nephritis, gout, medullary cystic disease, oxalosis, and systemic lupus erythematosus. The data indicate that renal transplantation is justifiable and parallels functional results for the more common causes of end-stage renal disease in all but Fabry disease and oxalosis. Although Fabry disease did not recur in any grafted kidney, only three patients have a functioning graft one year after transplantation. From a group of ten patients with oxalosis who received a total of 14 kidneys, only one survives. In no other metabolic disease, except one instance of primary amyloidosis, did the metabolic disease notably affect the transplant as it did in oxalosis.
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PMID:Renal transplantation in congenital and metabolic diseases. A report from the ASC/NIH renal transplant registry. 80 49

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Thirty-eight patients who presented with diabetes and a changed state of consciousness satisfied the criteria for lactic acidosis. Sixteen patients were non-ketotic, and 15 of these were receiving phenformin on admission. In all but one of these 15 patients, however, additional renal or cardiovascular abnormalities, or both, could be identified, which supported a multifactorial aetiology for lactic acidosis. Advanced age and cardiovascular and renal disease are absolute contraindications to the use of phenformin in diabetics.
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PMID:Phenformin and lactic acidosis. 81 82

The controversy as to the relationship between the degree of control of diabetes and the progression of the complications of the disease has not been solved. However, in this review, various studies suggesting a relationship between the metabolic abnormality and the diabetic complications are examined. The disadvantages of the uncontrolled diabetes mellitus can be divided into two major categories-short-term and long-term. The short-term disadvantages of controlled diabetes mellitus include the following: (1) ketoacidosis and hyperosmolar coma; (2) intracellular dehydration; (3) electrolyte imbalance; (4) decreased phagocytosis; (5) immunologic and lymphocyte activity; (6) impairment of wound healing; and (7) abnormality of lipids. The long-term disadvantages of uncontrolled diabetes melitus include the following: (1) nephropathy; (2) neuropathy; (3) retinopathy; (4) cataract formation; (5) effect on perinatal mortality; (6) complications of vascular disease; and (7) the evaluation of various clinical studies suggesting the relationship of elevated blood glucose levels and complications of diabetes mellitus. It is suggested that until the question of control can absolutely be resolved, the recommendation is that the blood glucose levels should be controlled as close to the normal as possible.
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PMID:Why control blood glucose levels? 81 31

The renin-angiotensin-aldosterone system appears to function normally in uncomplicated diabetes mellitus. Alterations in this system, however, have been observed in several of the microvascular and electrolyte complications associated with this disease. Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism. PRA is low in rats with uncontrolled, nonketotic diabetes, and pressor responsiveness to angiotension II is increased in patients with diabetic retinopathy. Potential mechanisms responsible for the decreased PRA include plasma volume expansion, hyalin destruction of the juxtaglomerular cells, defective synthesis of renin, and inadequate catecholamine stimulation of renin, and inadequant cathecholamine stimulation of renin release. In diabetic ketoacidosis, PRA and aldosterone are stimulated secondary to the associated dehydration with hypovolemia. This report reviews the current status of the function of the renin-angiotensin-aldosterone system in diabetes mellitus and proposes a possible role for the altered function of this system in the pathophysiology of several diabetic complications.
Diabetes 1976
PMID:Renin-angiotensin-aldosterone system in diabetes mellitus. 82 63

Animal models of diabetes mellitus allow for the manipulation of the metabolic state and the performance of experiments that may shed light on the pathogenesis of diabetic nephropathy. Rats with long-standing chemically induced diabetes develop glomerular mesangial thickening and immunoglobulin and complement deposition. These glomerular changes are reversible on the transplantation of a kidney from a diabetic rat into a normal host and on cure of the diabetic state by pancreatic islet transplantation. Conversely, diabetic renal changes develop in normal kidneys transplanted into diabetic rats (within tow to four months) and humans (within two years). These studies suggest that nephropathy results from the diabetic state. The mesangium is thickened in diabetic rats, mice, and humans. In rats, mesangial function is the processing of macromolecules localized therein is disturbed in areas of mesangial pathology. The finding that glomerulopathy is accelerated in uninephrectomized diabetic rats and is retarded in rat kidneys "protected" by narrowing of the renal artery suggests that alterations in glomerular blood flow are related to the pathogenesis of diabetic glomerular damage. Marked hyperglycemia in animals and man leads to "glycogen nephrosis," which affects the distal tubule at the level of the macula densa of the juxtaglomerular apparatus (JGA). This could lead to disturbance of JGA blood pressure regulation. Disturned mesangial function may result from failure of macula densa cells to process macromolecules that have reached that site from the mesangium.
Diabetes 1976
PMID:Studies of diabetic nephropathy in animals and man. 82 65


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