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Biomedical subjects

S S Gebhart

Publications and source records attributed to S S Gebhart.

15 recordsLinked to original sources
PubMed2000

Meeting American Diabetes Association guidelines in endocrinologist practice.

OBJECTIVE: To determine whether American Diabetes Association (ADA) guidelines can be met in the context of routine endocrinology practice. RESEARCH DESIGN AND METHODS: Charts were reviewed for a group of patients who were examined in 1998, followed for > or = 1 year, and had two or more visits during that year. Process measures and metabolic outcomes were studied for patients with type 2 diabetes, and glycemic control was assessed for patients with type 1 diabetes. RESULTS: A total of 121 patients with type 2 diabetes had a mean age of 63 years, a mean BMI of 31 kg/m2, and a mean duration of diabetes of 12 years. Many had comorbidities or complications: 80% had hypertension, 64% had hyperlipidemia, 78% had neuropathy, 22% had retinopathy, and 21% had albuminuria. Management of type 2 diabetic patients was complex: 38% used oral hypoglycemic agents alone (54% of these were using two or more agents), 31% used oral hypoglycemic agents and insulin, and 26% used insulin alone; 42% of patients taking insulin therapy injected insulin three or more times per day. Within 12 months, 74% of patients had dilated eye examinations, 70% had lipid profiles, and 55% had urine albumin screening. Of the patients, 87% had a foot examination at their last visit. Blood pressure levels averaged 133/72 mmHg, cholesterol levels averaged 4.63 mmol/l, triglyceride levels averaged 1.99 mmol/l, HDL cholesterol levels averaged 1.24 mmol/l, and LDL cholesterol levels averaged 2.61 mmol/l. Random blood glucose levels averaged 8.0 mmol/l, and HbAlc levels averaged 6.9 +/- 0.1%. A total of 87% of patients had HbAlc levels < or = 8.0%. A total of 30 patients with type 1 diabetes had mean age of 44 years, a mean BMI of 26 kg/m2, and a mean duration of diabetes of 20 years. All type 1 diabetic patients used insulin and averaged 3.4 injections a day; their average HbAlc level was 7.1 +/- 0.2%, and 80% had HbAlc levels < or = 8.0%. CONCLUSIONS: Although endocrinologists must manage patients with multifaceted problems, complex treatment regimens yield glycemic control levels comparable with the Diabetes Control and Complications Trial and allow ADA guidelines to be met in a routine practice setting.

Analysis of Variance↗
PubMed1999

Influence of diabetes mellitus on early and late outcome after coronary artery bypass grafting.

BACKGROUND: Diabetes mellitus is an established independent risk factor for significant morbidity and mortality after coronary artery bypass grafting. METHODS: The impact of diabetes on short- and longterm follow-up after coronary artery bypass grafting was studied by comparing the outcomes between 9,920 patients without diabetes mellitus and 2,278 patients with diabetes from 1978 to 1993. RESULTS: Compared with nondiabetic patients, the group with diabetes was older (62+/-10 years versus 60+/-10 years), comprised more women (31% versus 19%), had a greater incidence of hypertension (61% versus 44%) and previous myocardial infarction (51% versus 48%), had class III-IV angina more commonly (69% versus 63%), showed a higher incidence of congestive heart failure (11% versus 5%) or triple-vessel or left main disease (60% versus 50%), and had lower ejection fractions (0.54 versus 0.57) (all, p< or =0.05). Diabetic patients had a higher incidence of postoperative death (3.9% versus 1.6%) and stroke (2.9% versus 1.4%) (both, p< or =0.05), but not Q wave myocardial infarction (1.8% versus 2.9%). Diabetics had lower survival (5 years, 78% versus 88%; 10 years, 50% versus 71%; both, p< or =0.05) and lower freedom from percutaneous transluminal coronary angioplasty (5 years, 95% versus 96%; 10 years, 83% versus 86%; latter, p< or =0.05), but diabetics did not have lower freedom from either myocardial infarction (5-years, 92% versus 92%; 10-years, 80% versus 84%) or additional coronary artery bypass grafting (5-years, 98% versus 99%; 10-years, 90% versus 91%). Multivariate correlates of long-term mortality were diabetes, older age, reduced ejection fraction, hypertension, congestive heart failure, number of vessels diseased, and urgent or emergent operation. CONCLUSIONS: Diabetics have a worse hospital and longterm outcome after coronary artery bypass grafting. The increased risk in such patients can only partially be explained by other demographic characteristics.

Age Factors↗
PubMed1996

Insulin resistance associated with maternally inherited diabetes and deafness.

Maternally inherited diabetes and deafness (MIDD) is a form of diabetes associated with mutation of mitochondrial DNA (mtDNA) that occurs in 1% to 2% of individuals with diabetes. Understanding the clinical course and abnormalities in insulin secretion and action in affected individuals should allow better understanding of how this genetic defect alter glucose metabolism. We report the clinical course of three individuals with mtDNA mutations and deafness. Subjects no. 1 and 2 had diabetes not yet requiring insulin therapy, and subject no. 3, the son of subject no. 2, had normal glucose tolerance. Defective oxidative phosphorylation (OXPHOS) based on OXPHOS enzymology of skeletal muscle biopsy of subjects no. 1 and 2 showed activity of less than 5% of the tolerance level in complex III for subject no. 1 and in complexes I, I + III, and IV for subject no. 2. Assessing insulin secretion using insulin response to intravenous glucose and insulin sensitivity based on minimal model analysis of an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT), first-phase insulin secretion was abnormal in subjects no. 1 and 2 and normal in subject no. 3 (AUC, 57, 93, and 1,235 pmol/L, respectively). In contrast, all three subjects had low insulin sensitivity indices (0.04, 0.14, and 0.27 x 10-4 x min/pmol/L, respectively). Subject no. 2, who underwent three FSIGT studies over a 16-month interval, showed transient improvement in insulin release in response to modification of diet and exercise (first-phase insulin AUC, 57 pmol/min v 287 pmol/min 10 months later; fasting insulin, 97 pmol/L v 237 pmol/L 10 months later), but by 16 months, first-phase insulin release and fasting insulin had decreased (AUC, 64 and 136 pmol/L, respectively) despite higher fasting glucose. We conclude that in our subjects with MIDD, insulin resistance is present and appears to precede defects in insulin release.

Adolescent↗
PubMed1996

Insulin-resistant diabetes mellitus in a black woman with ataxia-telangiectasia.

A 24-year-old woman with ataxia-telangiectasia had traumatic arthritis, elevated serum transaminase values, polyuria, polydipsia, and a serum glucose level of 575 mg/dL. A relatively high daily dose of insulin (2.8 U/kg) was required to achieve near normoglycemia. The fasting insulin concentration was elevated. During an insulin-modified frequently sampled intravenous glucose tolerance test, the first phase of insulin release in response to the administration of glucose was blunted. The insulin sensitivity was similar to that found in individuals with non-insulin-dependent diabetes mellitus. Insulin receptor antibodies were not detected in the serum. We conclude that insulin resistance and islet beta-cell dysfunction are characteristics of diabetes mellitus in ataxia-telangiectasia. Contrary to a previous report, our findings do not support a cause-and-effect relationship between insulin receptor antibodies and insulin resistance in this disorder.

Adult↗
PubMed1992

Insulin resistance in obesity is associated with elevated basal lactate levels and diminished lactate appearance following intravenous glucose and insulin.

Lactate metabolism is altered in obesity. Increasing obesity is associated with increased blood lactate levels after an overnight fast. In contrast, we have recently shown a marked decrease in the capacity for acute lactate generation in obese subjects following an oral glucose load, which we postulated might be linked to altered insulin sensitivity. In the present study, we systematically analyzed the relationship between insulin sensitivity (the Sensitivity Index [SI] derived using the minimal model), body mass index (BMI), and glucose, insulin, and lactate levels in the basal state and following intravenous (IV) glucose and insulin administration in lean and obese subjects. The results showed that SI and BMI were inversely related, as expected. Insulin sensitivity was more tightly associated with glucose, insulin, and lactate levels (both basal and integrated) than obesity per se. A significant inverse relationship was found between SI and basal lactate levels (r = -.56). Moreover, a significant and positive relationship was found between SI and incremental lactate area under the curve (reflecting acute lactate production) (r = .41). In a multiple regression analysis to separate the independent effects of obesity (BMI) and insulin sensitivity, after adjusting for age, sex, and race, SI accounted for 34% of the variance in basal lactate and 24% of the variance in incremental lactate area. Obesity independently accounted for 10% of the variance in basal lactate and 11% of the variance in incremental lactate area, neither of which were statistically significant. We conclude that elevations in basal lactate are associated with the development of insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

A comparison of home glucose monitoring with determinations of hemoglobin A1c, total glycated hemoglobin, fructosamine, and random serum glucose in diabetic patients.

We compared four objective measures of glycemic control (fructosamine, total glycated hemoglobin, hemoglobin A1c, and random serum glucose) with home glucose monitoring records in 17 diabetic patients followed up prospectively for 4 months. There was good overall correlation between all of these objective measures and weekly mean capillary glucose values. However, considerable scatter was seen in the data such that none of the glycated protein measurements was an ideal predictor of home glucose values. For example, all markedly elevated home glucose levels (greater than 11.1 mmol/L) were associated with elevated glycated protein levels, but moderately high blood glucose levels (8.3 to 11.1 mmol/L) were associated with one or more normal glycated protein values in some patients. Similar correlations were obtained whether glycemia was estimated by 1-week or 6-week home averages. Random serum glucose level also correlated with average home glucose level; however, there was wide fluctuation within individual subjects. All three glycated protein measurements (hemoglobin A1c, glycated hemoglobin, and fructosamine) appear equally useful as a supplement to home glucose monitoring in the assessment of glycemic control. Of the three types of glycated protein assays, fructosamine, with its advantage of speed and simplicity, may offer a more cost-effective alternative.

Adolescent↗
PubMed1990

Minimal model analysis of intravenous glucose tolerance test-derived insulin sensitivity in diabetic subjects.

Although minimal model analysis of frequently sampled iv glucose tolerance tests (FSIGTs) to measure insulin sensitivity is well recognized, application has been limited by the need for endogenous insulin secretion. In the present study we determined whether use of exogenous insulin could permit minimal model assessment of insulin sensitivity (SI) to be extended to diabetic subjects. Normal volunteers had separate FSIGT assessments supplemented with both tolbutamide and insulin to accelerate glucose disappearance, while diabetics had a FSIGT supplemented only with insulin. There was a strong and highly significant correlation between the two assessments in normal subjects (r = 0.87; P less than 0.001), and the rank order of SI generally was maintained with the two assessments over a 3-fold range of SI; however, insulin-determined SI was 16% lower (3.4 +/- 0.4 vs. 4.1 +/- 0.4 x 10(-4) min/microU.microL; P less than 0.01). Diabetic subjects had markedly lower insulin sensitivity than controls (SI = 0.61 +/- 0.16; P less than 0.0001). Across all subjects, the level of fasting serum glucose was correlated inversely with both insulin sensitivity (r = -0.62; P less than 0.05) and acute insulin responses (r = -0.72; P less than 0.02); however, insulin sensitivity in diabetic subjects with little insulin secretion (0.6 +/- 0.2) was comparable to insulin sensitivity in diabetic subjects with near-normal responses (0.6 +/- 0.3). In subjects with fasting hyperglycemia, there were significant correlations between insulin sensitivity and body mass index, percent fat mass, and waist/hip ratio (all P less than 0.03). Among all female subjects, there was also a strong correlation between insulin sensitivity and upper body obesity, as measured by waist/hip ratio (r = -0.68; P less than 0.02). Model parameters also permitted glucose uptake to be estimated in diabetic vs. normal subjects at comparable hyperglycemia (11.1 mmol/L). Total glucose uptake was decreased in diabetic subjects (5.2 +/- 0.8 vs. 12.7 +/- 1.7 mg/min.kg in normals; P less than 0.001), insulin-dependent glucose uptake was diminished to a greater extent (1.3 +/- 0.4 vs. 6.2 +/- 1.2) than noninsulin-independent glucose uptake (3.9 +/- 0.5 vs. 6.4 +/- 0.9; both P less than 0.02). Administration of insulin permits minimal model FSIGT analysis to be applied to diabetic as well as normal subjects, yielding information about both insulin- and noninsulin-mediated glucose uptake as well as insulin sensitivity and insulin secretion.

Adult↗
PubMed1990

Prediction of glucose response to weight loss in patients with non-insulin-dependent diabetes mellitus.

Although diet therapy is considered the cornerstone of therapy for obese patients with non-insulin-dependent diabetes mellitus, losing weight is often difficult, and the plasma glucose concentration does not always improve after weight loss. We looked for predictors of improvement in plasma glucose levels after weight loss in 135 obese patients with non-insulin-dependent diabetes mellitus who had lost at least 9.1 kg of body weight. After weight loss there was a bimodal distribution of plasma glucose levels, allowing us to identify patients as "responders" or "nonresponders" according to whether a random plasma glucose level was above or below 10.0 mmol/L after a 9.1-kg weight loss. Fifty-five (41%) of 135 patients were responders (after a 9.1-kg weight loss, the mean +/- SEM plasma glucose level was 7.0 +/- 0.2 mmol/L). Many responders had improved plasma glucose levels after only slight weight loss. Eighty (59%) of 135 patients were nonresponders (after a 9.1-kg weight loss, the mean +/- SEM plasma glucose level was 18.3 +/- 0.6 mmol/L). Although the responder and nonresponder groups were comparable in age, sex distribution, plasma glucose levels, and body weight at initial presentation, improvement in the plasma glucose level after weight loss could be predicted by a plasma glucose level of 10.0 mmol/L or lower after 2.3-kg (62% positive predictive value) and 4.5-kg (79% positive predictive value) weight loss. We conclude that, in contrast to conventional teaching, many patients with non-insulin-dependent diabetes mellitus will not have any improvement in plasma glucose levels after a 9.1-kg weight loss. However, a substantial minority (approximately 40%) of obese patients with non-insulin-dependent diabetes mellitus have much lower plasma glucose levels with a weight loss of 9.1 kg or less. Although the plasma glucose response to weight loss cannot be forecast by initial clinical parameters, the success or failure of diet therapy can be predicted from the plasma glucose level after a weight loss of only 2.3 to 4.5 kg. Mild or moderately obese patients with non-insulin-dependent diabetes mellitus who remain hyperglycemic after a weight loss of 2.3 to 9.1 kg are unlikely to improve with further weight loss and should be considered for treatment with insulin or oral hypoglycemic agents.

Blood Glucose↗
PubMed1989

Reversible impairment of gonadotropin secretion in critical illness. Observations in postmenopausal women.

Gonadotropin levels were measured in 65 postmenopausal women admitted to the intensive care unit. Sixteen patients (25%) were hypogonadotropic as measured by luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels of 5 IU/L or less, and only 20 patients (31%) were found to have gonadotropin levels within the expected postmenopausal range (greater than or equal to 30 IU/L). No significant differences in prolactin or free thyroxine levels were found, but the cortisol level was higher and the total thyroxine level lower in the hypogonadotropic group. The patients in the hypogonadotropic group also seemed more seriously ill, with a longer duration of hospitalization, an increased total number of days in the intensive care unit, an increased number of days in the intensive care unit before gonadotropin sampling, a higher incidence of parenteral hyperalimentation, lower serum albumin levels, and higher mortality. Stimulation of the gonadotropin-releasing hormone performed on 10 patients showed a blunted response in patients with baseline LH and FSH levels of 10 IU/L or less. Of 10 patients followed up sequentially, 6 showed a rise in gonadotropin levels that paralleled recovery, 1 died with low gonadotropin levels, and 3 continued to have low gonadotropin levels 17, 34, and 82 days, respectively, after initial screening. Critically ill postmenopausal women may exhibit a marked fall in gonadotropin, LH, and FSH levels. This disease in gonadotropin levels in response to illness is reversible and results from pituitary unresponsiveness to gonadorelin hydrochloride.

Aged↗
PubMed1985

Pump-induced insulin aggregation. A problem with the Biostator.

A fall in plasma IRI despite constant C-peptide levels during prolonged insulin euglycemic clamp studies using the Biostator (Ames Division, Miles Laboratories, Elkhart, Indiana) prompted a meticulous evaluation of the Biostator's insulin delivery system. At slow infusion rates, a striking loss of immunoreactive and biologically active insulin was observed after 6 h of the Biostator run. Studies with labeled insulin indicated that the loss of insulin was not due to adsorption of insulin to the tubing since recovery of labeled insulin was close to 100%. A variety of techniques (gel filtration, polyacrylamide gel electrophoresis, centrifugation, and Coomassie Brilliant Blue protein assay) indicated that the loss of insulin activity was due to insulin coming out of solution. The insoluble nature of the immunologically and biologically inactive insulin was confirmed by centrifugation, i.e., 88% 125I-insulin precipitated into the pellet. The dependency of this loss of insulin activity on flow rate was clearly demonstrable with activity (IRI) less than 20% of expected at flow rates of 2.1 ml/h, and 30% at 4.2 ml/h. Full recovery was observed only with flow rates of 16.8 ml/h or greater. At each flow rate, IRI rose only after delivery of the effluent between the pump and exit port, demonstrating that insulin alteration occurs within the pump assembly presumably from heat-induced aggregation. Investigators employing the Biostator should carefully examine their systems for this time- and flow rate-dependent alteration of insulin. The loss of IRI at low flow rates (low-dose insulin clamp or insulin delivery during basal periods) will profoundly influence data generated from the Biostator.

Adult↗
PubMed1984

Failure of a midnocturnal insulin infusion to suppress the increased insulin need for breakfast in insulin-dependent diabetic patients.

Insulin requirements for meals were measured in eight insulin-dependent diabetic patients, using a closed-loop insulin infusion system. Patients required more insulin for breakfast than for an isocaloric lunch (35.7 +/- 5.5 mU/kcal/3 h versus 26.9 +/- 5.1 mU/kcal/3 h, P less than 0.02) or an isocaloric supper (35.7 +/- 5.5 mU/kcal/3 h versus 26.6 +/- 6.6 mU/kcal/3 h, P = 0.05). To determine whether this insulin resistance at breakfast might be due to low basal insulin levels overnight, the insulin needs for breakfast were compared after an overnight fast (day 1) and after a midnocturnal (0200 h-0500 h) insulin infusion (day 2). Breakfast insulin requirements were similar on both days (35.7 +/- 5.5 mU/kcal/3 h versus 37.7 +/- 5.1 mU/kcal/3 h, P = NS). Whereas nonobese diabetic patients required approximately 60% more insulin for breakfast than for other meals, obese diabetic patients in this study did not demonstrate insulin resistance at breakfast. These findings provide a basis for the common clinical practice of allocating more insulin for breakfast than for other meals. The absence of an increased insulin need at breakfast in our obese patients cautions against a similar algorithm for obese diabetic patients. We postulate that growth hormone may be a cause for morning insulin resistance.

Adult↗
PubMedDate not supplied

Postoperative management of diabetes mellitus: steady-state glucose control with bedside algorithm for insulin adjustment.

An algorithm was developed to determine whether an individualized insulin infusion could maintain plasma glucose in a desirable steady state after surgery. In 24 patients, insulin was provided according to a "glucose-feedback" formula to maintain plasma glucose between 120 and 180 mg/dl (6.7-10.0 mM). Initial plasma glucose was elevated, 218 +/- 16 mg/dl (mean +/- SE 12.1 +/- 0.9 mM), but reached the target range after 8 h and remained steady for the rest of the study period. Insulin requirements varied considerably, 0.5-5.0 U/h. Infusion rates were correlated with initial plasma glucose but not with previous insulin dose, HbA1c, or percent ideal body weight. Although insulin needs cannot be predicted, plasma glucose can be maintained in a desirable range after surgery via a simple formula suitable for implementation by general ward nurses.

Adult↗