Harold E. Lebovitz

STATEMENT BY AN AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS/ AMERICAN COLLEGE OF ENDOCRINOLOGY CONSENSUS PANEL ON TYPE 2 DIABETES MELLITUS: AN ALGORITHM FOR GLYCEMIC CONTROL

This report presents an algorithm to assist primary care physicians, endocrinologists, and others in the management of adult, nonpregnant patients with type 2 diabetes mellitus. In order to minimize the risk of diabetes-related complications, the goal of therapy is to achieve a hemoglobin A1c (A1C) of 6.5% or less, with recognition of the need for individualization to minimize the risks of hypoglycemia. We provide therapeutic pathways stratified on the basis of current levels of A1C, whether the patient is receiving treatment or is drug naïve. We consider monotherapy, dual therapy, and triple therapy, including 8 major classes of medications (biguanides, dipeptidyl-peptidase-4 inhibitors, incretin mimetics, thiazolidinediones, alpha-glucosidase inhibitors, sulfonylureas, meglitinides, and bile acid sequestrants) and insulin therapy (basal, premixed, and multiple daily injections), with or without orally administered medications. We prioritize choices of medications according to safety, risk of hypoglycemia, efficacy, simplicity, anticipated degree of patient adherence, and cost of medications. We recommend only combinations of medications approved by the US Food and Drug Administration that provide complementary mechanisms of action. It is essential to monitor therapy with A1C and self-monitoring of blood glucose and to adjust or advance therapy frequently (every 2 to 3 months) if the appropriate goal for each patient has not been achieved. We provide a flow-chart and table summarizing the major considerations. This algorithm represents a consensus of 14 highly experienced clinicians, clinical researchers, practitioners, and academicians and is based on the American Association of Clinical Endocrinologists/American College of Endocrinology Diabetes Guidelines and the recent medical literature.

Stimulation of Human-Growth-Hormone Secretion by L-Dopa

Abstract The effect of L-dopa, a precursor of Central-nervous-system catecholamines, on growth-hormone secretion was studied in a group of patients with Parkinsons disease undergoing treatment with the drug. Oral doses (0.5 g) caused a significant rise in plasma growth hormone in patients initially starting therapy or on chronic therapy for as long as 11 months. The rise in plasma growth hormone persisted for 120 minutes after the administration of the drug. The L-dopa-induced rise in plasma growth hormone could not be blocked by either oral or intravenous glucose administration. The data suggest that a dopaminergic mechanism in the median eminence or a norepinephrine-sensitive site in the hypothalamus or limbic system may be involved in the regulation of growth-hormone secretion. Furthermore, patients with Parkinsons disease, on L-dopa therapy, appear to be under the influence of elevated plasma growth hormone for a substantial part of the day.

Pseudohypoparathyroidism Type II: A Possible Defect in the Reception of the Cyclic AMP Signal

Abstract A22 month old boy with grand-mal seizures and hypocalcemia, had an elevated serum concentration of parathyroid hormone, increased urinary excretion of cyclic AMP, and a marked rise in urinary cyclic AMP in response to exogenously administered parathyroid extract. However, neither the renal tubular handling of phosphate nor the serum calcium concentration responded appropriately to administered parathyroid hormone. This defect appears to represent a failure of intracellular reception of the cyclic AMP message, and the disorder might be called pseudohypoparathyroidism Type II. (N Engl J Med 289:1056–1060, 1973)

AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY - CLINICAL PRACTICE GUIDELINES FOR DEVELOPING A DIABETES MELLITUS COMPREHENSIVE CARE PLAN - 2015

The American Association of Clinical Endocrinologists/American College of Endocrinology Medical Guidelines for Clinical Practice are systematically developed statements to assist healthcare professionals in medical decision making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances. Abbreviations: A1C = hemoglobin A1c AACE = American Association of Clinical Endocrinologists ACCORD = Action to Control Cardiovascu...

Carbohydrate Metabolism in Uremia

Abstract To define more clearly the factors involved in carbohydrate metabolism in uremia, we studied blood glucose, plasma insulin, and plasma growth hormone responses after the intravenous inject...

Diagnosis and management of prediabetes in the continuum of hyperglycemia: when do the risks of diabetes begin? A consensus statement from the American College of Endocrinology and the American Association of Clinical Endocrinologists.

Alan J. Garber, MD, PhD, FACE, Yehuda Handelsman, MD, FACP, FACE, Daniel Einhorn, MD, FACP, FACE, Donald A. Bergman, MD, FACE, Zachary T. Bloomgarden, MD, FACE, Vivian Fonseca, MD, FACE, W. Timothy Garvey, MD, James R. Gavin III, MD, PhD, George Grunberger, MD, FACP, FACE, Edward S. Horton, MD, FACE, Paul S. Jellinger, MD, MACE, Kenneth L. Jones, MD, Harold Lebovitz, MD, FACE, Philip Levy, MD, MACE, Darren K. McGuire, MD, MHSc, FACC, Etie S. Moghissi, MD, FACP, FACE, and Richard W. Nesto, MD, FACC, FAHA

Does Intra-Abdominal Adipose Tissue in Black Men Determine Whether NIDDM Is Insulin-Resistant or Insulin-Sensitive?

Insulin resistance in black Americans with non-insulin-dependent diabetes mellitus (NIDDM) is found in only 60% of those with a body mass index (BMI) of <30 kg/m2, suggesting that NIDDM can occur independent of peripheral insulin resistance. When insulin resistance is present, it is not necessarily correlated with obesity. Numerous studies have shown that increased amounts of intra-abdominal adipose tissue are associated with various metabolic abnormalities. We therefore investigated whether the occurrence of insulin resistance in black NIDDM men could be explained by the pattern of body adipose tissue distribution rather than total adiposity. Twenty-two near-normoglycemic black men (fasting plasma glucose [mean ± SD] = 104 ± 10 mg/dl, HbA1c = 4.6 ± 0.78%, age 48.9 ± 9.2 years, and BMI 26.5 ± 2.4 kg/m2) were studied. The euglycemic insulin clamp with 1 mU · kg−1 · min−1 insulin infusion and D-[3-3H]glucose was used to measure insulin action. Whole-body computed tomography with 22 scans was used to determine body composition. Total body adipose tissue was 19.6 ± 7.5 1, and the percentage of body fat was 27 ± 7. Glucose disposal ranged from 2.5 to 8.1 mg · kg−1 · min−1 (10 men were insulin-sensitive and 12 were insulin-resistant). There was a strong inverse correlation between glucose disposal and the proportion of total adipose tissue in the intra-abdominal region (r = −0.78, P < 0.001), while there was no correlation between glucose disposal and total muscle volume, BMI, total adipose tissue volume, or total subcutaneous adipose tissue volume. When insulin resistance is present, it is highly correlated with an increase in the proportion of intra-abdominal adipose tissue. The data raise the possibility that insulin resistance in black NIDDM men may be a consequence of increased intra-abdominal adipose tissue mass.

Inhibition of hypoglycemia-induced growth hormone secretion by the serotonin antagonists cyproheptadine and methysergide.

Abstract Growth hormone secretion is provoked by hypoglycemia. Since hypothalamic serotonin content increases during insulin-induced hypoglycemia, the role of hypothalamic serotonin in growth hormo...

Lactate inhibition of lipolysis in exercising man

Abstract The role of rising lactate levels on substrate mobilization in exercising man is unclear. To define the role of increasing lactate levels, D,L-sodium lactate, 6 meq/kg, was infused into six exercising normal males. A mild work load was chosen that increased arterial free fatty acids (FFA) and glycerol, but did not increase lactate significantly. Infused sodium bicarbonate and sodium chloride of equal volume and osmolality served as controls. The marked rise in arterial lactate and pyruvate to 8.8 ± 0.31 μM/ml and 0.328 ± 0.023 μM/ml (mean ± SEM), respectively, resulted in a significant inhibition of the increase of plasma FFA and glycerol, which occurred during the control studies. The decreased release of these constituents could not be attributed to an “insulin effect”, since the concentration of arterial insulin decreased during exercise and was similar during each infusion period. It appears that an increase in plasma lactate or pyruvate, or both, results in a direct inhibition of exercise-mediated lipolysis in man.

Disordered Control of Thirst in Hypothalamic-Pituitary Sarcoidosis

We evaluated water metabolism in 11 patients with hypothalamic-pituitary sarcoidosis. Seven patients had abnormal water metabolism: one had partial antidiuretic hormone (ADH) deficiency, one had severe ADH deficiency, one had severe ADH deficiency and deficient thirst, one had only deficient thirst, and three had excessive thirst. In four of the five with thirst disturbances, there was loss of congruence of osmotic thresholds for thirst and ADH release. Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH. That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition.