salicylates and Hypoglycemia

The present review catalogues 1418 reported cases of drug-induced hypoglycemia. The main findings are that sulfonylureas (especially chlorpropamide and glyburide), either alone or with a second hypoglycemic or potentiating agent, still account for 63% of all cases; that alcohol, propranolol, and salicylate, either singly or with another hypoglycemic drug, are the next most frequent offenders (19% of the total); and that one older drug (quinine) and three new ones (pentamidine, ritodrine, and disopyramide) have caused an additional 7% of all episodes of severe hypoglycemia. The clinical factors that set the stage for drug-induced hypoglycemia are still restricted food intake, age, hepatic disease, and renal disease, both individually and even more so in combination. Drug-induced hypoglycemia continues to be so common that virtually every unconscious patient should be considered hypoglycemic until immediate estimation of the blood sugar level rules it in or out. If ruled in, the clinician should promptly start 10% intravenous glucose and plan to maintain it uninterruptedly for 1 or more days, with added glucagon, hydrocortisone, and diazoxide administration if necessary, until sustained hyperglycemia guarantees that all drug effects have worn off.

Topics: Adolescent; Adult; Age Factors; Aged; Child; Child, Preschool; Coma; Humans; Hypoglycemia; Hypoglycemic Agents; Infant; Infant, Newborn; Middle Aged; Salicylates; Sulfonylurea Compounds

Although the conditions that cause hypoglycemia in adults may also be present in infants and children, there are many entities unique to the pediatric age group. This reflects the delicate balance that exists in the newborn and young child between glucose production and utilization. During fasting in infants and children, hepatic glucose production is normally two to three times that of adults when expressed on the basis of weight. In the newborn and young infants, hypoglycemia usually presents with irritability, feeding difficulties, lethargy, cyanosis, tachypnea, and/or hypothermia rather than the typical adrenergic or neuroglucopenic symptoms seen in the adult. The hypoglycemia may be due to abnormalities in hormone secretion, substrate interconversion, or mobilization of metabolic fuels. The hypoglycemia associated with hyperinsulinemia may be transient neonatal, sustained, or drug-induced. Inborn errors of metabolism caused by enzymatic defects are responsible for hypoglycemia associated with abnormalities of production and utilization of metabolic fuels. These can involve carbohydrate, protein, and fat metabolism. In addition, there may be acquired or transient defects in carbohydrate metabolism secondary to other diseases or ingestion of certain substances. Finally ketotic hypoglycemia appears to be due to abnormalities in substrate availability. A variety of tests are useful for establishing the etiologic basis of the hypoglycemia, and the appropriate treatment depends upon the underlying cause.

Topics: Child; Endocrine System Diseases; Ethanol; Fatty Acids; Glucose; Heart Defects, Congenital; Homeostasis; Humans; Hyperinsulinism; Hypoglycemia; Infant; Infant, Newborn; Infant, Small for Gestational Age; Ketosis; Metabolism, Inborn Errors; Reye Syndrome; Salicylates

The roles of changes in cellular redox, interorgan lactate flux and balance, and quantitative aspects of lactate metabolism in the pathogenesis of lactic acidosis are discussed. Altered metabolism of pyruvate is central to the development of lactic acidosis and hyperlactatemia. Lactic acidosis occurs as a result of a relative or absolute imbalance in lactate production and utilization. Lactate utilization for oxidative purposes and for the resynthesis of glucose is essential for the maintenance of acid-base balance. Because of its role in lactate homeostasis the liver may play a central role in acid-base balance. Impairment of hepatic utilization of lactate may produce lactic acidosis.

Topics: Acidosis; Animals; Diabetic Ketoacidosis; Dichloroacetic Acid; Ethanol; Homeostasis; Humans; Hypoglycemia; Kidney; Lactates; Liver; Liver Diseases; Neoplasms; Phenformin; Renal Dialysis; Salicylates; Seizures; Vasodilator Agents

Topics: Acetohexamide; Adolescent; Adult; Aminobenzoates; Child; Child, Preschool; Chlorpropamide; Coma; Edetic Acid; Ethanol; Female; Humans; Hypoglycemia; Hypoglycemic Agents; Infant; Infant, Newborn; Insulin; Male; Manganese; Middle Aged; Nutritional Physiological Phenomena; Oxytetracycline; Propranolol; Salicylates; Sulfonylurea Compounds; Tolbutamide

Topics: Ethanol; Humans; Hypoglycemia; Insulin; Leucine; Salicylates

To compare rates and predictors of documented hypoglycaemia in type 2 diabetes patients treated with either basal insulin supported oral therapy (BOT), conventional therapy (CT) or supplementary insulin therapy (SIT) in primary care.. Data from 10,842 anonymous patients (mean age ± SD: 54 ± 8 yrs) on BOT, 2,407 subjects (56 ± 7 yrs) on CT, and 7,480 patients (52 ± 10 yrs) using SIT from 1,198 primary care practices were retrospectively analyzed (Disease Analyzer, Germany: 01/2005-07/2013). Stepwise logistic regression (≥1 documented hypoglycaemia: ICD code) was used to evaluate risk factors of hypoglycemia.. The unadjusted rates (95% CI) per 100 patient-years of documented hypoglycaemia were 1.01 (0.80-1.20) (BOT), 1.68 (1.10-2.30) (CT), and 1.61 (1.30-1.90) (SIT), respectively. The odds of having ≥1 hypoglycemia was increased for CT (OR; 95% CI: 1.71; 1.13-2.58) and SIT (1.55; 1.15-2.08) (reference: BOT). Previous hypoglycemia (OR: 11.24; 6.71-18.85), duration of insulin treatment (days) (1.06; 1.05-1.07), history of transient ischemic attack (TIA)/stroke (1.91; 1.04-3.50), and former salicylate prescriptions (1.44; 1.06-1.98) also showed an increased odds of having hypoglycemia. Higher age was associated with a slightly lower odds ratio (per year: 0.98; 0.97-0.99).. Insulin naïve type 2 diabetes patients in primary care, initiated with CT and SIT have an increased risk of hypoglycaemia compared to BOT, which is in line with previous randomized controlled trials. As hypoglycaemic events are associated with an increased mortality risk, this real-world finding is of clinical relevance.

Topics: Adult; Age Factors; Databases, Factual; Diabetes Mellitus, Type 2; Drug Prescriptions; Female; Germany; Humans; Hypoglycemia; Incidence; Insulin; Ischemic Attack, Transient; Male; Middle Aged; Primary Health Care; Recurrence; Risk Factors; Salicylates; Time Factors

Toxic induced hypoglycemia is usually caused by the anti-diabetic treatment and excessive alcohol consume. Hypoglycemia in diabetics treated with insulin or anti-diabetic oral agents is far the most studied form of hypoglycemia. Less information is available on toxic-induced hypoglycemia in non-diabetic subjects with acute exogenous poisoning.. We retrospectively studied adult non-diabetic patients admitted in Emergency Clinic Hospital of Iaşi with hypoglycemia caused by an acute poisoning, over a period of 10 years. Then we performed a prospective study in those poisoning associated with hypoglycemic risk, to assess the prevalence of toxic-induced hypoglycemia.. We identified 15,497 patients with acute poisoning in our retrospective study, 4,005 of whom presented poisoning associated with hypoglycemic risk (40% acute ethanol poisoning, 29% wild mushroom poisoning, 23% beta-blocker poisoning, 7% salicylate poisoning and 1% patients with anti-diabetic agents acute poisoning). The prospective study identified 1,034 patients with acute poisoning, 20.11% of whom had ethanol poisoning, 11.79% had beta-blocker poisoning, 5.89% had wild mushroom poisoning, 1.74% had salicylate poisoning and the rest of 60.47% had other acute poisoning, without hypoglycemic risk. Attempted suicide with anti-diabetic agents in non-diabetic subjects produced the most severe and prolonged form of hypoglycemia in acute poisoning. 23 patients in retrospective study and 6 patients in prospective study died, but in only one situation, the death was the direct consequence of hypoglycemia.. In non-diabetic subjects with acute poisoning, prevalence of toxic-induced hypoglycemia depends on the poison itself, the mechanism of poisoning, also depends on the association between toxics and the severity of toxic- induced liver disease. A useful test to assess toxic-induced hypoglycemia is standard 6 hour oral glucose tolerance test (OGTT). Factors predicting a negative outcome in toxic-induced hypoglycemia are association of toxins, cardiac and hepatic complications, and age (>65 years).

Topics: Adolescent; Adrenergic beta-Antagonists; Adult; Age Factors; Aged; Alcohol Drinking; Blood Glucose; Cyclooxygenase Inhibitors; Female; Glucose Tolerance Test; Humans; Hypoglycemia; Hypoglycemic Agents; Male; Middle Aged; Mushroom Poisoning; Prospective Studies; Retrospective Studies; Romania; Rural Health; Salicylates; Urban Health

Topics: Administration, Topical; Aged; Diabetes Mellitus, Type 2; Humans; Hypoglycemia; Male; Psoriasis; Salicylates; Salicylic Acid

We describe a case of severe refractory hypoglycemia secondary to topical salicylate intoxication. A 72-year-old man with psoriasis and end-stage renal disease was treated with a topical cream containing 10% salicylic acid. The patient presented with encephalopathy and subsequently developed hypoglycemia refractory to infusions of large amounts of glucose. A serum salicylate concentration was elevated at 3.2 mmol/L. Emergent hemodialysis was accompanied by rapid lowering of serum salicylate concentration and resolution of refractory hypoglycemia. Salicylate is well absorbed across normal and diseased skin. Salicylate markedly impairs gluconeogenesis and increases glucose utilization, resulting in hypoglycemia. To our knowledge, this is the first article on hypoglycemia due to the application of topical salicylate.

Topics: Administration, Cutaneous; Aged; Confusion; Gluconeogenesis; Humans; Hypoglycemia; Kidney Failure, Chronic; Male; Occlusive Dressings; Ointments; Psoriasis; Salicylates; Salicylic Acid; Skin Absorption

Topics: Aged; Diagnosis, Differential; Female; Frail Elderly; Hemiplegia; Humans; Hypoglycemia; Poisoning; Salicylates

Understanding of the pharmacologic principles and the pathogenesis of salicylate toxicity provides a basis for the optimization of clinical management. The role of salicylate as a scientifically proven cause of Reye's syndrome remains controversial despite epidemiologic data. The management guidelines discussed illustrate treatment details based on the pathophysiology of salicylate toxicity.

Topics: Absorption; Acidosis; Blood-Brain Barrier; Brain; Charcoal; Child, Preschool; Fluid Therapy; Gastric Lavage; Glucose; Humans; Hydrogen-Ion Concentration; Hypoglycemia; Infant; Kinetics; Nausea; Respiratory Center; Reye Syndrome; Salicylates

Topics: Acetanilides; Animals; Aspirin; Blood Glucose; Diabetes Mellitus, Experimental; Female; Hypoglycemia; Rats; Rats, Inbred Strains; Salicylates

All patients in stupor or coma should undergo blood chemistry studies, including blood gases. The anion gap and serum osmolality must be calculated in all patients. An indwelling catheter to monitor urine content and volume is essential. Electrocardiogram monitoring is indicated in all significant metabolic acidosis, especially for evaluation of intracellular potassium effect and arrhythmias. Repeated arterial monitoring of blood gases and electrolytes is essential with the use of flow sheets. Sodium lactate and Ringer's solution should never be given in an emergency care area. Large doses of insulin (100+ units intravenously) are not necessary or indicated in diabetic ketoacidosis and may be contraindicated and dangerous especially in HHNKC. Intravenous or intramuscular regular insulin after urine tests for glucose and ketones alone should not be given. Urine dilution of serum ketones is useless, and serum dilution may be grossly misleading and contraindicated: arterial studies are much more reliable.

Topics: Acidosis; Blood Glucose; Diabetic Ketoacidosis; Diagnosis, Differential; Electrolytes; Emergencies; Ethylene Glycols; Humans; Hypoglycemia; Lactates; Metabolic Diseases; Methanol; Salicylates; Uremia

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Drug-Related Side Effects and Adverse Reactions; Ethanol; Humans; Hypoglycemia; Infant; Infant, Newborn; Middle Aged; Phenformin; Propranolol; Salicylates; Sulfonylurea Compounds

A 78-year-old nondiabetic woman was admitted to the hospital with salicylate-induced hypoglycemia. Ketosis was present with a moderate metabolic acidosis and primary respiratory alkalosis. The patient's mental status improved immediately following intravenous administration of glucose. The case illustrates salicylate's hypoglycemic activity, and that the metabolic acidosis may have exacerbated symptoms of cerebral glucopenia.

Topics: Acidosis; Aged; Alkalosis, Respiratory; Aspirin; Female; Glucose; Humans; Hypoglycemia; Infusions, Parenteral; Ketosis; Salicylates

Topics: Adrenal Insufficiency; Carbohydrate Metabolism, Inborn Errors; Ethanol; Glycogen Storage Disease; Hormones, Ectopic; Humans; Hypoglycemia; Hypopituitarism; Insulin; Islets of Langerhans; Liver Diseases; Nutrition Disorders; Pancreatic Neoplasms; Salicylates; Sulfonylurea Compounds

Topics: 1-Propanol; Acute Kidney Injury; Aged; Albumins; Antidepressive Agents; Antihypertensive Agents; Benzyl Compounds; Cephaloridine; Coumarins; Digitoxin; Diuretics; Drug Interactions; Ethacrynic Acid; Guanethidine; Guanidines; Heart; Heart Block; Heart Conduction System; Humans; Hypoglycemia; Hypotension; Kidney; Pancreas; Phenylbutazone; Salicylates; Sympathetic Nervous System; Tolbutamide; Warfarin

Topics: Acetone; Biguanides; Diabetes Complications; Diabetes Mellitus; Diabetic Ketoacidosis; Diet Therapy; Glucose Tolerance Test; Glycosuria; Holidays; Humans; Hypoglycemia; Hypoglycemic Agents; Insulin; Insulin Secretion; Interpersonal Relations; Prediabetic State; Salicylates; Sports; Travel

Topics: Adipose Tissue; Animals; Blood Glucose; Diabetes Mellitus, Experimental; Fatty Acids, Nonesterified; Female; Hypoglycemia; Male; Rats; Salicylamides; Salicylates

Topics: Child Abuse; Female; Humans; Hypoglycemia; Infant, Newborn; Infant, Newborn, Diseases; Salicylates; Seizures

Topics: Aminosalicylic Acids; Animals; Anti-Inflammatory Agents; Cinnamates; Flufenamic Acid; Gibberellins; Glycolates; Hypoglycemia; Male; ortho-Aminobenzoates; Phenylacetates; Prediabetic State; Rabbits; Salicylates

Topics: Aspirin; Blood Chemical Analysis; Hypoglycemia; Infant; Insulin; Poisoning; Salicylates; Toxicology

Topics: Aspirin; Child; Glucose; Glucose Tolerance Test; Humans; Hypoglycemia; Infant; Infusions, Parenteral; Neurologic Manifestations; Pancreatic Diseases; Poisoning; Salicylates; Toxicology

Topics: Chickenpox; Child; Herpesvirus 3, Human; Humans; Hypoglycemia; Infant; Pancreatic Diseases; Salicylates