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Biomedical subjects

Guillermo E Umpierrez

Publications and source records attributed to Guillermo E Umpierrez.

At least 19 recordsLinked to original sources
PubMed2006

Narrative review: ketosis-prone type 2 diabetes mellitus.

Several investigators have reported that more than half of African-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic features of type 2 diabetes during follow-up. These patients are usually obese, have a strong family history of diabetes, have a low prevalence of autoimmune markers, and lack a genetic association with HLA. Their initial presentation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating cause of metabolic decompensation. At presentation, they have markedly impaired insulin secretion and insulin action, but intensified diabetic management results in significant improvement in beta-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of follow-up. On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. The absence of autoimmune markers and the presence of measurable insulin secretion have proven useful in predicting near-normoglycemic remission and long-term insulin dependence in adult patients with a history of diabetic ketoacidosis. This clinical presentation is commonly reported in African and African-American persons but is also observed in Hispanic persons and those from other minority ethnic groups. The underlying mechanisms for beta-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, preliminary evidence suggests an increased susceptibility to glucose desensitization.

Adult↗
PubMed2006

Perioperative glucose control in the diabetic or nondiabetic patient.

Patients with diabetes are more likely to undergo surgery than nondiabetics, and maintaining glycemic control in subjects with diabetes can be challenging during the perioperative period. Surgery in diabetic patients is associated with longer hospital stay, higher health care resource utilization, and greater perioperative mortality. In addition, several observational and interventional studies have indicated that hyperglycemia is associated with adverse clinical outcomes in surgical and critically ill patients. This paper reviews the pathophysiology of hyperglycemia during trauma and surgical stress and will provide practical recommendations for the preoperative, intraoperative, and postoperative care of diabetic patients.

Blood Glucose↗
PubMed2005

Admission hyperglycemia and other risk factors as predictors of hospital mortality in a medical ICU population.

BACKGROUND: Tight glycemic control is recommended for patients in the ICU, as hyperglycemia is associated with increased morbidity and mortality. DESIGN: Observational cohort of patients admitted to a 12-bed, inner-city, medical ICU (MICU). SUBJECTS: A total of 1,185 of 1,506 patients from July 1, 1999, to December 31, 2002, selected based on a diagnosis other than diabetic ketoacidosis or glycemia > 280 mg/dL or < 80 mg/dL. PURPOSES: To determine if the highest serum glucose level within 24 h after ICU admission is associated with increased hospital mortality when adjusted for confounders. MEASUREMENTS: Age, gender, race, worst values within 24 h after ICU admission to construct the acute physiology and chronic health evaluation (APACHE) II score, and highest glucose within 24 h after ICU admission. Hospital mortality was the primary outcome. Admitting diagnosis, MICU length of stay (LOS), and hospital LOS were obtained. Glucose, albumin (n = 867), and lactic acid (n = 319) were stratified for analysis. ANALYSIS: Univariate analysis identified factors included in the multivariate model. RESULTS: Patients were predominantly African-American (79%) and men (56%; mean age, 49.2 years). The mean ICU admission highest glucose level was 139 +/- 43.7 mg/dL (+/- SD). MICU LOS and hospital LOS were 6.2 days and 12.9 days, respectively, and 50% of patients received mechanical ventilation. MICU and hospital mortality were 18% and 20%, respectively; standardized mortality ratio was 66%. On univariate analysis, survivors (n = 945) and nonsurvivors (n = 240) showed APACHE II score, mechanical ventilation, hypoalbuminemia, lactic acidemia, and logistic organ dysfunction system score to be hospital mortality predictors; however, the highest admission serum glucose level was not. Logistic regression estimated APACHE II score/per point (odds ratio, 1.06; 95% confidence interval, 1.02 to 1.11), mechanical ventilation (odds ratio, 3.06; 95% confidence interval, 1.34 to 6.96), severe hypoalbuminemia (< 2 g/dL) [odds ratio, 2.98; 95% confidence interval, 1.3 to 7.02], and severe lactic acidemia (> or = 8 mmol/L) [odds ratio, 7.3; 95% confidence interval, 2.14 to 24.9], but not ICU admission hyperglycemia, to be associated with hospital mortality. CONCLUSIONS: Conventional factors of disease severity, but not highest glucose value during the first 24 h after ICU admission, predict hospital mortality in an inner-city MICU.

APACHE↗
PubMed2004

Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis.

PURPOSE: To compare the efficacy and safety of subcutaneous insulin lispro with that of a standard low-dose intravenous infusion protocol of regular insulin in patients with uncomplicated diabetic ketoacidosis. METHODS: In this prospective, randomized open trial, 20 patients treated with subcutaneous insulin lispro were managed in regular medicine wards (n=10) or an intermediate care unit (n=10), while 20 patients treated with the intravenous protocol were managed in the intensive care unit. Patients treated with subcutaneous lispro received an initial injection of 0.3 unit/kg followed by 0.1 unit/kg/h until correction of hyperglycemia (blood glucose levels <250 mg/dL), followed by 0.05 to 0.1 unit/kg/h until resolution of diabetic ketoacidosis (pH > or =7.3, bicarbonate > or =18 mEq/L). Patients treated with intravenous regular insulin received an initial bolus of 0.1 unit/kg, followed by an infusion of 0.1 unit/kg/h until correction of hyperglycemia, then 0.05 to 0.1 unit/kg/h until resolution of diabetic ketoacidosis. RESULTS: Mean (+/- SD) admission biochemical parameters in patients treated with subcutaneous lispro (glucose: 674 +/- 154 mg/dL; bicarbonate: 9.2 +/- 4 mEq/L; pH: 7.17 +/- 0.10) were similar to values in patients treated with intravenous insulin (glucose: 611 +/- 264 mg/dL; bicarbonate: 10.6 +/- 4 mEq/L; pH: 7.19 +/- 0.08). The duration of treatment until correction of hyperglycemia (7 +/- 3 hours vs. 7 +/- 2 hours) and resolution of ketoacidosis (10 +/- 3 hours vs. 11 +/- 4 hours) in patients treated with subcutaneous lispro was not different than in patients treated with intravenous regular insulin. There were no deaths in either group, and there were no differences in the length of hospital stay, amount of insulin until resolution of diabetic ketoacidosis, or in the rate of hypoglycemia between treatment groups. Treatment of diabetic ketoacidosis in the intensive care unit was associated with 39% higher hospitalization charges than was treatment with subcutaneous lispro in a non-intensive care setting ($14,429 +/- $5243 vs. $8801 +/- $5549, P <0.01). CONCLUSION: Treatment of adult patients who have uncomplicated diabetic ketoacidosis with subcutaneous lispro every hour in a non-intensive care setting may be safe and more cost-effective than treatment with intravenous regular insulin in the intensive care unit.

3-Hydroxybutyric Acid↗
PubMed2004

Impaired expression and insulin-stimulated phosphorylation of Akt-2 in muscle of obese patients with atypical diabetes.

Although a pharmacological dose of insulin produces a dramatic increase in phosphorylation and activity of Akt isoforms 1 and 2 in mammalian skeletal muscle, few studies have examined the effect of physiological concentrations of insulin on the phosphorylation of Akt-1 and -2 in normal and diabetic tissue. This study examined the patterns of insulin-stimulated Akt isoform phosphorylation and protein expression in muscle biopsies obtained from obese patients with atypical diabetes immediately after a hyperglycemic crisis and again after near-normoglycemic remission. In obese patients with new-onset diabetes mellitus presenting with hyperglycemic crisis (plasma glucose 30.5 +/- 4.8 mM), in vitro stimulation of vastus lateralis muscle biopsies with 100 microU/ml (0.6 nM) insulin increased insulin receptor phosphorylation threefold and Akt-1 phosphorylation on Ser(473) twofold, whereas Akt-2 phosphorylation was not stimulated. After 10-wk intensive insulin therapy that led to near-normoglycemic remission and discontinuation of insulin therapy, both Akt-2 expression and insulin-stimulated Akt-2 Ser(474) phosphorylation doubled. Hyperglycemic crisis did not affect insulin-stimulated threonine phosphorylation of either Akt-1 or Akt-2. The decreased Akt-2 expression at presentation was accompanied by reduced GLUT4 protein expression and increased expression of enzymes counterregulatory to insulin action. Thus a physiological concentration of insulin stimulated Akt-1 and Akt-2 phosphorylation in human skeletal muscle in the absence of hyperglycemia, but Akt-2 expression and stimulation appeared to be impaired in muscle of obese patients with atypical diabetes presenting with severe hyperglycemia.

Adult↗
PubMed2004

Diabetic ketoacidosis induces in vivo activation of human T-lymphocytes.

Diabetic ketoacidosis (DKA) is an inflammatory state associated with immune responses in polymorphonuclear cells (PMN). Activation of subgroup of T-lymphocytes in PMN of DKA patients, however, is not known. We studied in vivo activation of CD4 and CD8 lymphocytes by measuring de novo growth factor receptor for insulin, IGF-1, and IL-2 in eight patients on admission and at resolution of DKA, and compared them with matched controls. The presence of these receptors was demonstrated in all patients' lymphocytes on admission, but not in control subjects. This event was associated with increased levels of thiobarbituric acid-reacting material and dichlorofluorescien, as markers of oxidative stress. Based on these new findings and works in the literature, we hypothesize that hyperglycemia/ketosis results in increased reactive oxygen species, leading to increased levels of cytokines and emergence of growth factor receptors. We propose DKA changes the T-lymphocytes to insulin sensitive tissues as a compensatory mechanism.

CD4-Positive T-Lymphocytes↗
PubMed2004

Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises.

Acute and chronic hyperglycemia are proinflammatory states, but the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks is not known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH). We studied 20 lean and 28 obese patients with DKA, 10 patients with NKH, and 12 lean and 12 obese nondiabetic control subjects. We measured 1) proinflammatory cytokines (tumor necrosis factor-alpha, interleukin [IL]-6, IL1-beta, and IL-8), 2) markers of cardiovascular risk (C-reactive protein [CRP], homocysteine, and plasminogen activator inhibitor-1 [PAI-1]), 3) products of reactive oxygen species (ROS; thiobarbituric acid [TBA]-reacting material, and dichlorofluorescein [DCF]), and 4) cortisol, growth hormone (GH), and free fatty acids (FFAs) on admission (before insulin therapy) and after insulin therapy and resolution of hyperglycemia and/or ketoacidosis. Results were compared with lean and obese control subjects. Circulating levels of cytokines, TBA, DCF, PAI-1, FFAs, cortisol, and GH on admission were significantly increased two- to fourfold in patients with hyperglycemic crises compared with control subjects, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises. Changes in CRP and homocysteine in response to insulin therapy did not reach control levels after resolution of hyperglycemia. We conclude that DKA and NKH are associated with elevation of proinflammatory cytokines, ROS, and cardiovascular risk factors in the absence of obvious infection or cardiovascular pathology. Return of these values to normal levels with insulin therapy demonstrates a robust anti-inflammatory effect of insulin.

Adult↗
PubMed2004

Treatment of diabetic ketoacidosis with subcutaneous insulin aspart.

OBJECTIVE: In this prospective, randomized, open trial, we compared the efficacy and safety of aspart insulin given subcutaneously at different time intervals to a standard low-dose intravenous (IV) infusion protocol of regular insulin in patients with uncomplicated diabetic ketoacidosis (DKA). RESEARCH DESIGN AND METHODS: A total of 45 consecutive patients admitted with DKA were randomly assigned to receive subcutaneous (SC) aspart insulin every hour (SC-1h, n = 15) or every 2 h (SC-2h, n = 15) or to receive IV infusion of regular insulin (n = 15). Response to medical therapy was evaluated by assessing the duration of treatment until resolution of hyperglycemia and ketoacidosis. Additional end points included total length of hospitalization, amount of insulin administration until resolution of hyperglycemia and ketoacidosis, and number of hypoglycemic events. RESULTS: Admission biochemical parameters in patients treated with SC-1h (glucose: 44 +/- 21 mmol/l [means +/- SD], bicarbonate: 7.1 +/- 3 mmol/l, pH: 7.14 +/- 0.09) were similar to those treated with SC-2h (glucose: 42 +/- 21 mmol/l, bicarbonate: 7.6 +/- 4 mmol/l, pH: 7.15 +/- 0.12) and IV regular insulin (glucose: 40 +/- 13 mmol/l, bicarbonate 7.1 +/- 4 mmol/l, pH: 7.11 +/- 0.17). There were no statistical differences in the mean duration of treatment until correction of hyperglycemia (6.9 +/- 4, 6.1 +/- 4, and 7.1 +/- 5 h) or until resolution of ketoacidosis (10 +/- 3, 10.7 +/- 3, and 11 +/- 3 h) among patients treated with SC-1h and SC-2h or with IV insulin, respectively (NS). There was no mortality and no differences in the length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or the number of hypoglycemic events among treatment groups. CONCLUSIONS: Our results indicate that the use of subcutaneous insulin aspart every 1 or 2 h represents a safe and effective alternative to the use of intravenous regular insulin in the management of patients with uncomplicated DKA.

Adult↗
PubMed2003

Changes in serum leptin in lean and obese subjects with acute hyperglycemic crises.

We aimed to determine the effect of insulin replacement on serum leptin concentration in lean and obese patients with diabetic ketoacidosis (DKA). We compared serial leptin levels in 52 patients with DKA, 14 obese subjects with hyperglycemia, and 52 nondiabetic control subjects. Leptin levels on admission were significantly decreased in lean and obese patients with DKA and/or hyperglycemia compared with weight- and gender-matched controls. Insulin therapy resulted in a significant increase in leptin levels within 4 h, with peak stimulation at 12 h. Leptin levels on admission and at resolution of hyperglycemia were higher in obese DKA (9.7 +/- 2 ng/ml and 26.5 +/- 5 ng/ml, respectively; P < 0.001) and obese hyperglycemia subjects (11.9 +/- 4 ng/ml vs. 24.4 +/- 2 ng/ml; P < 0.001) than in lean DKA subjects (5.3 +/- 0.3 ng/ml and 10.1 +/- 2 ng/ml; P < 0.001). We conclude that insulin treatment in patients with acute hyperglycemic crises is followed by rapid and significant increase in leptin concentration, and this increase is more discernible in obese subjects. The low serum leptin level on admission in subjects with hyperglycemic crises may be the result of impaired adipocyte glucose utilization due to insulin deficiency and/or to increased catecholamine levels.

Acute Disease↗
PubMed2003

Diabetic ketoacidosis: risk factors and management strategies.

Diabetic ketoacidosis (DKA) is the most common hyperglycemic emergency in patients with diabetes mellitus. DKA most often occurs in patients with type 1 diabetes, but patients with type 2 diabetes are susceptible to DKA under stressful conditions, such as trauma, surgery, or infections. DKA is reported to be responsible for more than 100 000 hospital admissions per year in the US, and accounts for 4-9% of all hospital discharge summaries among patients with diabetes. Treatment of patients with DKA uses significant healthcare resources and accounts for 1 out of every 4 healthcare dollars spent on direct medical care for adult patients with type 1 diabetes in the US. Recent studies using standardized written guidelines for therapy have demonstrated a mortality rate of less than 5%, with higher mortality rates observed in elderly patients and those with concomitant life-threatening illnesses. Worldwide, infection is the most common precipitating cause for DKA, occurring in 30-50% of cases. Urinary tract infection and pneumonia account for the majority of infections. Other precipitating causes are intercurrent illnesses (i.e., surgery, trauma, myocardial ischemia, pancreatitis), psychological stress, and non-compliance with insulin therapy. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA. These metabolic derangements result from the combination of absolute or relative insulin deficiency and increased levels of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Successful treatment of DKA requires frequent monitoring of patients, correction of hypovolemia and hyperglycemia, replacement of electrolyte losses, and careful search for the precipitating cause. Since the majority of DKA cases occur in patients with a known history of diabetes, this acute metabolic complication should be largely preventable through early detection, and by the education of patients, healthcare professionals, and the general public. The frequency of hospitalizations for DKA has been reduced following diabetes education programs, improved follow-up care, and access to medical advice. Novel approaches to patient education incorporating a variety of healthcare beliefs and socioeconomic issues are critical to an effective prevention program.

Acidosis↗
PubMed2003

Thyroid dysfunction in patients with type 1 diabetes: a longitudinal study.

OBJECTIVE: Cross-sectional studies have reported that the risk of thyroid dysfunction in patients with type 1 diabetes is two- to threefold higher than in the general population. However, longitudinal studies to determine the natural history of thyroid dysfunction in patients with type 1 diabetes are lacking. RESEARCH DESIGN AND METHODS: We analyzed the incidence of thyroid dysfunction over time in a cohort of 58 patients (26 men and 32 women) enrolled in the Diabetes Control and Complications Trial at the University of Tennessee Health Science Center in 1983 and prospectively followed for 18 years. Patients underwent measurement of thyroid function tests (thyroid-stimulating hormone [TSH], thyroxine, and triiodothyronine) every year and thyroid peroxidase (TPO) antibodies at 4-year intervals. RESULTS: A total of 18 patients had hypothyroidism, and 1 patient experienced transient hyperthyroidism. Two subjects developed hypothyroidism 7 and 18 years before the development of diabetes and were excluded from the analysis. The mean age of diagnosis was 19 +/- 2 years for type 1 diabetes and 29 +/- 3 years for hypothyroidism. Hypothyroidism was more common in female (41%) than in male (19%) subjects and in patients with positive TPO antibodies. Patients who were TPO positive were 17.91 times as likely to develop hypothyroidism as patients who were TPO negative (95% CI 3.89-82.54). There were no differences in BMI, lipid profile, and HbA(1c) between patients with and without thyroid dysfunction. CONCLUSIONS: This longitudinal study confirms the association between autoimmune thyroid dysfunction and type 1 diabetes. Our results indicate that all subjects with type 1 diabetes should undergo annual screening by serum TSH measurement to detect asymptomatic thyroid dysfunction, particularly those with positive TPO antibodies.

Autoimmune Diseases↗
PubMed2002

Predictors of intensive care unit and hospital length of stay in diabetic ketoacidosis.

OBJECTIVE: To determine the predictive value for prolonged intensive care unit (ICU) and hospital length of stay (LOS) in patients with diabetic ketoacidosis (DKA) of the Acute Physiology and Chronic Health Evaluation II (APACHE II) score and Logistic Organ Dysfunction System (LODS), and to identify associated characteristics. DESIGN: Prospective cohort, 18-month observation. SUBJECTS AND SETTING: All admissions to a 12-bed, inner-city, university-affiliated hospital, medical ICU from July 1999 to December 2000. MEASUREMENTS: Data for APACHE II and LODS scoring systems were collected within 24 hours of admission. Lengths of ICU and hospital stay were the primary outcomes. Prolonged ICU and hospital LOS were defined as 3 or more and 6 or more days. RESULTS: A total of 584 patients, mean age 49, 56% men, 82% African American were admitted to the ICU. At admission they had (mean +/-SD) APACHE II (18 +/- 10), LODS (5 +/- 4), and predicted mortality of 32% +/- 29%. DKA was the admitting diagnosis in 42 (7.6%) patients; they had lower APACHE II (12 +/- 6), LODS (2 +/- 1), and predicted mortality 5% +/- 5% than the general ICU population (all, P <.001). Hospital mortality in non-DKA patients was 18%; there were no deaths in patients with DKA. Among DKA patients, those with insulin noncompliance had a shorter hospital stay (2.8 +/- 1 d) than those with an underlying illness as the DKA trigger (4.8 +/- 3, P =.02). Between patients with DKA, regardless of the LOS, there were no significant differences in APACHE II, LODS, or predicted mortality. CONCLUSIONS: ICU-admitted patients with DKA are less ill, and have lower disease severity scores, mortality, and shorter length of ICU and hospital stay than non-DKA patients. Disease severity scores are not, but precipitating cause is, predictor associated with prolonged hospital LOS in patients with DKA.

APACHE↗
PubMed2002

Hyperglycemia: an independent marker of in-hospital mortality in patients with undiagnosed diabetes.

Admission hyperglycemia has been associated with increased hospital mortality in critically ill patients; however, it is not known whether hyperglycemia in patients admitted to general hospital wards is associated with poor outcome. The aim of this study was to determine the prevalence of in-hospital hyperglycemia and determine the survival and functional outcome of patients with hyperglycemia with and without a history of diabetes. We reviewed the medical records of 2030 consecutive adult patients admitted to Georgia Baptist Medical Center, a community teaching hospital in downtown Atlanta, GA, from July 1, 1998, to October 20, 1998. New hyperglycemia was defined as an admission or in-hospital fasting glucose level of 126 mg/dl (7 mmol/liter) or more or a random blood glucose level of 200 mg/dl (11.1 mmol/liter) or more on 2 or more determinations. Hyperglycemia was present in 38% of patients admitted to the hospital, of whom 26% had a known history of diabetes, and 12% had no history of diabetes before the admission. Newly discovered hyperglycemia was associated with higher in-hospital mortality rate (16%) compared with those patients with a prior history of diabetes (3%) and subjects with normoglycemia (1.7%; both P < 0.01). In addition, new hyperglycemic patients had a longer length of hospital stay, a higher admission rate to an intensive care unit, and were less likely to be discharged to home, frequently requiring transfer to a transitional care unit or nursing home facility. Our results indicate that in-hospital hyperglycemia is a common finding and represents an important marker of poor clinical outcome and mortality in patients with and without a history of diabetes. Patients with newly diagnosed hyperglycemia had a significantly higher mortality rate and a lower functional outcome than patients with a known history of diabetes or normoglycemia.

Blood Glucose↗