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Biomedical subjects

D S Bell

Publications and source records attributed to D S Bell.

At least 91 records · Page 5Linked to original sources
PubMed1990

Screening for slight albuminuria: a comparison of selected commercially available methods.

Slight albuminuria predicts clinically significant nephropathy in patients with insulin-dependent diabetes mellitus (IDDM) and early death in patients with non-insulin-dependent diabetes mellitus (NIDDM). This study compares four commercially available methods for measuring low concentrations of urinary albumin. We tested random spot urine specimens from 50 nondiabetic volunteers and 100 diabetic patients. This specimen was chosen to simplify collection in an outpatient setting. Two screening methods were evaluated for their ability to detect urinary albumin in the range of 15 to 200 mg/L. Sensitivity and specificity were 100% and 54.7%, respectively, for the Ames Micro-Bumintest; and 95.5% and 91.5%, respectively, for the Sclavo Albumin Screen. The high number of false-positive results made the Micro-Bumintest unacceptable. The Albumin Screen yielded fewer false-positive results, but also produced some false-negatives. Two quantitative methods, a radioimmunoassay (RIA) and a turbidimetric assay (the SPQ Microalbumin), yielded results that agreed well with each other.

Albuminuria↗
PubMed1990

Risk factors for gestational diabetes in black population.

In a long-term longitudinal study of gestational diabetes mellitus in Black women, risk factors that were identified were age, obesity, a family history of diabetes, and the presence of hypertension. Poor predictors were a history of a previous large-for-date infant, parity, and age at first pregnancy. The prevalence of smooth muscle and nuclear autoantibodies was higher in gestational diabetic subjects. Gestational diabetic subjects who required insulin for glycemic control were more obese, had a lower frequency of the Bf-F phenotype and a higher frequency of the Bf-F1 phenotype, and had a lower frequency of the type 2 allele at the polymorphic locus adjacent to the insulin gene. Restriction-fragment-length polymorphisms flanking the insulin and apolipoprotein A-I and C-III genes, although not associated with gestational diabetes mellitus, may be associated with hyperlipidemia and subsequent atherosclerosis.

Adult↗
PubMed1989

Hypertension in the person with diabetes.

Hypertension is more common in persons with both insulin-dependent and noninsulin-dependent diabetes. Pathophysiologic mechanisms that result in an increased prevalence of essential hypertension in noninsulin-dependent diabetes, premature diastolic hypertension in insulin-dependent diabetes, and systolic hypertension in both forms of diabetes are described. Aggressive treatment of the hypertension associated with diabetic nephropathy will result in a deceleration of renal decompensation. The commonly used antihypertensives that successfully treat hypertension in the non-diabetic population often have unacceptable side effects in the diabetic population. Rational approaches to the treatment of diabetic hypertension in general and in circumstances unique to the hypertensive diabetic individual are described.

Antihypertensive Agents↗
PubMed1988

Factors associated with discontinuation of continuous subcutaneous insulin infusion.

Fifty-five patients who had been started on continuous subcutaneous insulin infusion (CSII) more than 1 year previously were surveyed to determine the difference between those who had continued and those who had discontinued CSII. These retrospective results were used to determine characteristics that predict a suitable candidate for CSII which could be tested in a future prospective study and would guide our clinical choice of candidates for CSII. Twenty patients had discontinued CSII (Group D) and 35 patients had continued CSII (Group C). Group D contained younger patients, more likely to be women who had had a shorter duration of diabetes, more frequent antecedent episodes of diabetic ketoacidosis (DKA), and more frequent doctor visits. The major rationale for starting CSII in Group D was poor control with keotacidosis whereas Group C started CSII for poor control with hypoglycemia. The reasons for stopping CSII in Group D were interference with lifestyle (40%), needle site abcesses (40%), psychological rejection (10%), and poor insulin absorption (10%). Group D patients had a significantly higher incidence of psychological rejection of CSII, dermatological problems, and needle site abcesses. For patients in Group D, glycosylated hemoglobin levels during CSII were similar to those prior to CSII. Group C patients had improved glycosylated hemoglobin levels and were more satisfied with CSII despite a slightly higher incidence of pump runaway. Group C patients had a trend toward more frequent hypoglycemia while on CSII; however, in patients who had reported severe hypoglycemia before starting CSII, there was a significant decline in the frequency of severe hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Abscess↗
PubMed1987

Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer's disease.

The formation of clusters of altered axons and dendrites surrounding extracellular deposits of amyloid filaments (neuritic plaques) is a major feature of the human brain in both aging and Alzheimer's disease. A panel of antibodies against amyloid filaments and their constituent proteins from humans with Alzheimer's disease cross-reacted with neuritic plaque and cerebrovascular amyloid deposits in five other species of aged mammals, including monkey, orangutan, polar bear, and dog. Antibodies to a 28-amino acid peptide representing the partial protein sequence of the human amyloid filaments recognized the cortical and microvascular amyloid of all of the aged mammals examined. Plaque amyloid, plaque neurites, and neuronal cell bodies in the aged animals showed no reaction with antibodies to human paired helical filaments. Thus, with age, the amyloid proteins associated with progressive cortical degeneration in Alzheimer's disease are also deposited in the brains of other mammals. Aged primates can provide biochemically relevant models for principal features of Alzheimer's disease: cerebrovascular amyloidosis and neuritic plaque formation.

Aging↗
PubMed1987

Rapid insulin initiation in non-insulin-dependent diabetes mellitus.

Three insulin-initiation regimens were compared in 43 severely hyperglycemic non-insulin-dependent diabetic patients: a "standard" regimen (Lente insulin once daily), a "rapid" regimen (a mixture of regular and Lente insulins twice daily), and a "rapid/intravenous" regimen (the "rapid" regimen preceded by overnight intravenous infusion of regular insulin). The mean serum glucose level fell more rapidly in both groups receiving "rapid" regimens, reaching less than 200 mg/dl in 3.0 days with the "rapid" regimen compared with 5.9 days with the "standard" regimen (p less than 0.005). Duration of hospitalization was similarly reduced (6.4 versus 9.9 days, p less than 0.0001) as was the cost of hospitalization. In contrast to the "rapid" regimens, symptomatic hypoglycemia was common and adequate glycemic control was rare with the "standard" regimen. Thus, rapid initiation of insulin therapy with 0.5 to 0.6 units/kg per day of a mixture of regular and intermediate-acting insulins given twice daily is effective, safe, and reduces the cost of hospitalization in patients with non-insulin-dependent diabetes mellitus who require insulin treatment.

Adult↗
PubMed1987

Effect of insulin therapy on lipoproteins in non-insulin dependent diabetes mellitus (NIDDM).

Thirty patients with NIDDM and severe hyperglycemia (fasting plasma glucose greater than 200 mg/dl) were initiated on insulin therapy. Lipoprotein concentrations were measured by the Vertical Autoprofile procedure before insulin therapy and 1, 3, 6 and 26 weeks after insulin initiation. Patients were divided into 4 phenotypes based on their pretreatment lipoprotein profile: HyperVLDL (elevated VLDL), HyperLDL (elevated LDL), HyperVLDL-LDL (elevated VLDL and LDL), and non-hyperlipidemic. There were no differences in the initial fasting plasma glucose, Hgb Alc, or fasting free insulin concentrations between the groups. Both the HyperVLDL and HyperLDL groups had significantly lower HDL-C concentrations that the non-hyperlipidemic group and the HyperVLDL-LDL group had significantly higher IDL-C than any of the other groups. Insulin therapy resulted in similar decreases in fasting plasma glucose and increases in fasting free insulin concentrations in all 4 groups. HDL-C increased in all 4 groups. The most marked improvements in HDL-C were seen in the non-hyperlipidemic (+37%) and HyperLDL (+42%) groups while the HyperVLDL group had only an 18% increase. VLDL-C fell in all groups but in the HyperVLDL group it fell dramatically to almost normal levels within the first week, whereas it took 6 weeks for the HyperVLDL-LDL group to reach its VLDL-C nadir and this was still significantly higher than normal. LDL-C improved modestly in only the HyperLDL patients after 6 weeks of insulin therapy. There were no statistically significant changes in either the IDL-C or Lp(a)-C in any of the groups during insulin therapy. The changes in HDL-C and IDL-C were negatively correlated with the fasting plasma glucose and Hgb Alc but not with the free insulin concentration. We conclude that: 1) Insulin therapy can cause dramatic improvements in HDL-C and VLDL-C while it has only a mild suppressive effect on LDL-C and no statistically significant effect on IDL-C or Lp(a)-C. The degree of improvement in the lipid profiles varied considerably between the different lipid phenotypes. 2) The hyperlipidemic phenotypes seen in these patients appear to be determined primarily by factors other than the degree of hyperglycemia and hypoinsulinemia.

Blood Glucose↗
PubMed1985

Complications of diabetes. Prevalence, detection, current treatment, and prognosis.

The late complications associated with diabetes mellitus affect the eye (retinopathy and cataract), the kidney (diabetic glomerulosclerosis), the nerves (mononeuropathies, distal symmetric polyneuropathy, and autonomic neuropathy), and the large blood vessels (coronary artery, cerebrovascular, and peripheral vascular disease). With the exception of large blood vessel disease, evidence in animals and humans has suggested that the development of diabetes-associated complications is related to metabolic abnormalities associated with hyperglycemia. Although the exact mechanism by which hyperglycemia causes damage in individual tissues is unknown, a number of potentially pathogenic mechanisms have been proposed. These include increased activity of the polyol pathway, disturbance in the metabolism of myo-inositol and its phospholipid derivatives, abnormal permeability of the small blood vessels, and excessive glycosylation of various proteins. With the introduction of potent aldose reductase inhibitors, the role of increased activity of the polyol pathway (and related abnormalities in myo-inositol metabolism) in the pathogenesis of diabetes-associated complications can be clarified.

Adult↗