Search PubMed⌕ Search

Biomedical subjects

P Raskin

Publications and source records attributed to P Raskin.

At least 91 records · Page 5Linked to original sources
PubMed1986

Effect of glycemic control on microvascular complications in patients with type I diabetes mellitus.

The relation between the control of blood glucose levels and the progression of early diabetic retinopathy and the width of skeletal muscle capillary basement membrane was studied in 54 insulin-dependent diabetic patients. After initial ophthalmologic evaluation including seven-field fundus photography and fluorescein angiography and measurement of levels of glycosylated hemoglobin and width of skeletal muscle capillary basement membrane, the patients were divided into two groups: an experimental group of 30 patients who were treated with continuous subcutaneous insulin infusion and a control group of 24 patients who continued to receive conventional treatment--usually two injections of insulin daily. After a mean follow-up period of 31.4 months, the experimental group had a significant decrease in glycosylated hemoglobin levels as compared with baseline values (mean +/- SEM, 7.2 +/- 0.3 percent versus 10.1 +/- 0.4 percent), reflecting improved control of blood glucose levels. The conventional treatment group had no change in glycosylated hemoglobin levels after a mean of 33.5 months of follow-up. With use of either a modified Early Treatment Diabetic Retinopathy Study grading system or macular microaneurysm counts, the experimental treatment group showed significantly less progression of retinopathy (p less than 0.05). The skeletal muscle capillary basement membrane width was significantly reduced only in the experimental treatment group with stable or improved retinopathy and was unchanged in the control group. There was a tendency for skeletal muscle capillary basement membrane width to increase in thickness over time in those patients whose retinopathy worsened irrespective of treatment. It is concluded that meticulous diabetic control may slow the progression of early diabetic retinopathy. Changes in skeletal muscle capillary basement membrane width may reflect the course of diabetic retinopathy.

Adult↗
PubMed1986

Increased nerve conduction in diabetics after a year of improved glucoregulation.

We studied median, ulnar and peroneal motor nerve conduction velocity (NCV) and median sensory action potential (SAP) latency and amplitude in 18 insulin-dependent diabetic patients who were begun on a continuous subcutaneous insulin infusion (CSII) program. With institution of this therapy, significant decreases in mean blood glucose and glycosylated hemoglobin occurred. After 12 months of CSII treatment, median, peroneal, and ulnar motor NCVs all increased significantly. The average NCV increase was 2.5 m/s. Median SAP amplitude and latency did not significantly change. In a second group of 12 diabetic patients with the same mean age and comparable initial NCV and SAP measures, no significant changes in motor NCVs or SAPs occurred after 12 months of conventional insulin treatment. These results indicated the need for further long-term studies of the role of strict glucose control in the prevention of diabetic neuropathy.

Adolescent↗
PubMed1986

Blood glucose control and diabetic complications.

Two hypotheses have been advanced to explain the appearance of microvascular complications in diabetic patients with glycemic control. The genetic hypothesis suggests that the development of diabetic complications is genetically determined and independent of diabetic control, whereas the metabolic hypothesis suggests that long-term hyperglycemia causes the subsequent development of small-blood-vessel complications. We review data that either support or reject these hypotheses and suggest a third unifying hypothesis.

Blood Glucose↗
PubMed1985

Islet-cell abnormalities in non-insulin-dependent diabetes mellitus.

Patients with non-insulin-dependent diabetes mellitus have enlarged islets of Langerhans, an increased number of insulin-secreting beta cells, and a "horseshoe-shaped" relationship between plasma insulin and glucose levels. To some extent, beta-cell dysfunction in patients with type II diabetes is reversible with appropriate hypoglycemic therapy. Defects in the glucagon-secreting alpha cells in patients with non-insulin-dependent diabetes mellitus include basal hyperglucagonemia, an exaggerated glucagon response to aminogenic stimuli, and hyposuppressibility of glucagon by hyperglycemia. Although peripheral resistance to insulin may play a role in type II diabetes, defects in islet-cell function clearly play a significant role as well.

Alanine↗
PubMed1985

Potassium supplementation in hypertensive patients with diuretic-induced hypokalemia.

Changes in potassium balance have been found to have variable effects on the blood pressure of animals, and the administration of potassium supplements has been reported to lower the blood pressure of normokalemic hypertensive patients. To assess the effect of potassium repletion in hypokalemic hypertension, we administered either potassium chloride, 60 mmol per day, or placebo tablets, each for six weeks, in a randomized, double-blind, crossover trial to 16 hypertensive patients who had diuretic-induced hypokalemia and who continued to take a constant amount of diuretic. We selected patients whose control serum potassium levels were below 3.5 mmol per liter. In association with an average rise in the serum potassium concentration of 0.56 mmol per liter, the mean blood pressure fell by an average of 5.5 mm Hg (P = 0.004), with at least a 4 mm Hg fall observed in 9 of the 16 patients. The fall in blood pressure correlated with a fall in plasma renin activity (r = 0.568, P = 0.043) but not with changes in plasma aldosterone levels or other variables. We conclude that short-term potassium supplementation that ameliorates diuretic-induced hypokalemia may induce a significant fall in blood pressure.

Adult↗
PubMed1985

Impaired catabolism of very low-density lipoprotein-triglyceride in a family with primary hypertriglyceridemia.

In this report, kinetic studies of plasma very low-density lipoprotein-triglyceride (VLDL-TG) were examined in five brothers (three affected and two unaffected) from a family with primary hypertriglyceridemia. Synthesis and catabolism of VLDL-TG were studied by in vivo labelling of plasma TG with 3H-glycerol, and multicompartmental analysis of the plasma die-away curves. Results of the kinetic studies revealed the following information: (1) one brother, who had the highest plasma TG level and was obese, had both overproduction and a reduced fractional catabolic rate (FCR) of VLDL-TG; (2) second brother, who had moderate hypertriglyceridemia, had a low FCR and high-normal synthesis of VLDL-TG; (3) a third, who had only mildly elevated TG, had a low FCR and normal synthesis of VLDL-TG; and (4) the two normolipidemic brothers had neither overproduction nor decreased FCR of VLDL-TG. The composition of the soluble apoproteins of VLDL was normal. The apoprotein E phenotypes were E4/3 in four brothers, and E3/2 in the fifth. We have reached the following conclusions regarding this family: (1) the common kinetic abnormality of VLDL-TG metabolism in the hypertriglyceridemic brothers was a low clearance of VLDL-TG; (2) impaired catabolism of VLDL could not be explained by the apoprotein C or E patterns; and (3) the most severe hypertriglyceridemia occurred when the decreased FCR was present in conjunction with VLDL-TG overproduction due to obesity. Thus, a moderate defect in catabolism of plasma TG appears to be responsible for one familial form of primary hypertriglyceridemia.

Adult↗
PubMed1985

The effect of long-term near normal glycemic control on mild diabetic retinopathy.

Thirty-three type l diabetics who used continuous subcutaneous infusion of insulin (CSll) and 24 diabetics on conventional treatment (maximum of two injections per day) were studied prospectively with ophthalmologic examinations, fundus photography, fluorescein angiography, and glycosylated hemoglobin (HbA1) determinations. Both groups were similar with respect to age, duration of diabetes, and length of follow-up. At entry almost all patients had only mild forms of diabetic retinopathy although three CSll patients had early proliferative retinopathy. The CSll groups achieved superior glycemic control throughout the study (mean HbA1 = 7.4% vs. 10.2%). After an average follow-up of more than 30 months, the CSll group showed significantly less progression of diabetic retinopathy as measured by macular aneurysm counts and by modified ETDRS grading. Careful control of glycemia may delay the progression of diabetic retinopathy.

Adolescent↗
PubMed1985

Effect of tolrestat on red blood cell sorbitol levels in patients with diabetes.

The effect of the aldose reductase inhibitor, tolrestat, on red blood cell (RBC) sorbitol levels was studied in 23 patients with diabetes after oral dosing with tolrestat, 25 or 100 mg b.i.d. The mean (+/- SE) RBC sorbitol levels (measured 12 hours after the preceding dose) after 3, 7, and 13 days of dosing decreased after both dose levels. After 25 mg tolrestat the RBC sorbitol levels fell from 25.1 +/- 4.0 to 20.0 +/- 5.7 nmol/gm hemoglobin (21%) and after 100 mg tolrestat the level fell from 26.7 +/- 3.7 to 11.4 +/- 1.7 nmol/gm hemoglobin (57%; P less than 0.001). This latter RBC sorbitol concentration is similar to levels in individuals without diabetes. At both dosage levels the maximum decrease in RBC sorbitol levels occurred after only 3 days of dosing. Tolrestat had no effect on plasma glucose or hemoglobin A1 concentrations. The overall mean plasma unbound drug concentration measured 12 hours after 100 mg tolrestat (11.7 +/- 3.0 ng/ml; 3.3 X 10(-8) mol/L) was similar to the median inhibitory level (3 X 10(-8) mol/L) of tolrestat for sorbitol accumulation in human RBCs incubated in a high-glucose medium. Our results demonstrate the systemic bioavailability of tolrestat and its aldose reductase inhibitory activity in erythrocytes of patients with diabetes.

Administration, Oral↗
PubMed1984

A comparative evaluation of glycosylated haemoglobin assays: feasibility of references and standards.

Four assays, high pressure liquid chromatography, colorimetric with thiobarbituric acid, affinity columns, and microcolumn cation exchange were compared for ability to discriminate between samples taken from diabetic and normal subjects; correlation with each other; stability over time at different temperatures; and reproducibility between laboratories. The most discriminatory (10 samples from a diabetic and 10 samples from a normal group) was the microcolumn cation exchange method (t = 5.25; p less than 0.001), but all were significantly different at p less than 0.005. The intra-assay coefficient of variation was 1%-6%, except for the affinity column method which was 13% in normal subjects. High pressure liquid chromatography was used as a reference and the other assays correlated well (r = 0.93-0.99). Storage at -80 degrees C, -20 degrees C, 4 degrees C, and 24 degrees C showed marked differences. The thiobarbituric acid method results were stable except for 24 degrees C. Microcolumn cation exchange was labile under all conditions. Affinity column was stable for up to 15 days, only if samples were stored as whole blood. High pressure liquid chromatography showed an increase in haemoglobin A1a + b and a decrease in the haemoglobin A1c. Haemoglobin A1c was reproducible for 4 days when stored at 4 degrees C and up to 11 days when stored at -80 degrees C. Samples exchanged between centres at 4 degrees C and performed within 5 days by high pressure liquid chromatography for haemoglobin A1 and haemoglobin A1c correlated well (r = 0.98 and 0.99). Samples exchanged between centres after storage (up to 40 days -80 degrees C) correlated (r = 0.99) by the thiobarbituric acid method.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromatography, Affinity↗
PubMed1984

The effect of diabetic control on very low-density lipoprotein--triglyceride metabolism in patients with type II diabetes mellitus and marked hypertriglyceridemia.

We examined the effect of diabetic control on very low-density lipoprotein-triglyceride (VLDL-TG) metabolism in six patients with type II (noninsulin-dependent) diabetes mellitus and marked hypertriglyceridemia. VLDL-TG transport was determined using 3H-glycerol as an endogenous precursor of VLDL-TG, and the resultant kinetic data were evaluated by multicompartmental analysis. Studies were performed in the hypertriglyceridemic diabetic subjects during poor diabetic control and again after 3 months of diabetic treatment, and the results were compared to studies in nondiabetic normolipidemic subjects and nondiabetic subjects with familial forms of hypertriglyceridemia. In the poorly controlled diabetics, mean VLDL-TG synthesis was threefold higher than in the normolipidemic subjects, and the mean fractional catabolic rate (FCR) of VLDL-TG was only one-third of the normals. With diabetic treatment, plasma triglyceride levels fell by more than 50%, but remained fourfold higher than the normals. This was associated with a decrease in mean VLDL-TG synthesis to a level similar to that observed in the genetic hyperlipidemic subjects, but still 2.6-fold higher than the normals. In addition, the mean FCR rose after diabetic control to a level slightly above that of the genetic hyperlipidemic subjects, but remained less than one-half of the normal value. However, the response of VLDL-TG kinetics to diabetic treatment was not uniform. In four subjects, control of hyperglycemia ameliorated the hypertriglyceridemia primarily by decreasing VLDL-TG overproduction. In the other two subjects, diabetic treatment had a greater effect on the FCR than an overproduction of VLDL-TG. Thus, in this select group of diabetic, hypertriglyceridemic subjects, poor diabetic control contributed to both VLDL-TG overproduction and low FCRs. Failure of diabetic treatment to restore VLDL-TG kinetic parameters to normal suggests that the hypertriglyceridemia was due not only to diabetes mellitus but also to an additional abnormality affecting lipoprotein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

The Somogyi phenomenon. Sacred cow or bull?

Posthypoglycemic hyperglycemia (Somogyi phenomenon) occurs infrequently in insulin-treated diabetic patients. When it occurs it is often in children and adolescents, or patients with a short duration of diabetes. Marked hyperglycemia (greater than 220 mg/dL) after hypoglycemia results from a large meal to relieve the symptoms of hypoglycemia. Posthypoglycemic hyperglycemia correlates with falling plasma insulin levels, rather than increasing concentrations of counterregulatory hormones, whose secretion may be defective. Asymptomatic nocturnal hypoglycemia is common but subsequent fasting hyperglycemia is not necessarily the result of "rebound." More likely, fasting hyperglycemia is due to a falling predawn insulin level. Nocturnal hypoglycemia is dealt with by a readjustment in the timing and dose of insulin. The failure of the Somogyi phenomenon to occur puts insulin-dependent diabetic patients at increased risk to potential lethal consequences of nocturnal hypoglycemia.

Adolescent↗
PubMed1983

The effect of diabetic control on the width of skeletal-muscle capillary basement membrane in patients with Type I diabetes mellitus.

We studied the relation between the control of blood glucose and the width of skeletal-muscle capillary basement membrane in 23 insulin-dependent (Type I) diabetic patients. After initial measurement of levels of glycosylated hemoglobin and width of skeletal-muscle capillary basement membrane, the patients were divided into two groups: an experimental group of 13 patients who were treated with continuous subcutaneous insulin infusion, and a control group of 10 patients who continued to receive conventional treatment--usually two injections of insulin daily. After two years, the experimental group had a significant decrease in glycosylated hemoglobin levels as compared with base-line values (mean +/- S.E.M., 7.6 +/- 0.4 vs 10.2 +/- 0.7 per cent; P less than 0.001), reflecting improved control of blood glucose, and a significant reduction in the width of skeletal-muscle capillary basement membrane (1293 +/- 68 vs. 1717 +/- 182 A; P less than 0.05). The control group of patients had no significant change in their levels of glycosylated hemoglobin or in the width of their skeletal-muscle capillary basement membranes. If changes in the capillaries in skeletal muscle parallel those in the capillaries in retinal or renal tissue, then meticulous control of blood glucose may be beneficial over time in preventing the microvascular complications of diabetes.

Adolescent↗
PubMed1982

Increased incidence and clinical correlation of persistently abnormal technetium pyrophosphate myocardial scintigrams following acute myocardial infarction in patients with diabetes mellitus.

"Persistently abnormal" technetium-99m stannous pyrophosphate myocardial scintigrams (PPi+) appear to be associated with a relatively poor prognosis after acute myocardial infarction (AMI). To assess the incidence and implications of PPi+, we performed a retrospective analysis in 29 patients with and 25 patients without diabetes mellitus who had abnormal myocardial scintigrams within 4 days of AMI and who had follow-up scintigrams at least 3 months after hospital discharge. There were no significant differences between patients with and without diabetes as regards age, incidence of transmural or nontransmural AMI, or degree of left ventricular dysfunction after AMI. Persistently abnormal PPi+ occurred more commonly in patients with diabetes than in nondiabetic patients (18 of 29, 62%, compared to 3 of 25, 12%; p less than 0.001). Patients with chronic PPi+ had more frequent cardiac complications following hospital discharge (p less than 0.005) including death, recurrent AMI, unstable angina, and intractable congestive heart failure. Postmortem analysis in two patients with diabetes and chronic PPi+ revealed marked myocytolysis. Thus, patients with diabetes mellitus have an increased incidence of post-AMI "persistently abnormal" technetium (PPi+) scintigrams and relatively poor prognosis following myocardial infarction.

Aged↗