digoxin and Hypoglycemia

Topics: Acute Kidney Injury; Airway Obstruction; Anemia, Hemolytic; Arteriovenous Fistula; Asphyxia Neonatorum; Cardiac Output; Digoxin; Ductus Arteriosus, Patent; Female; Heart Failure; Humans; Hyperthyroidism; Hypoglycemia; Infant; Infant, Newborn; Isoproterenol; Medical History Taking; Pregnancy; Pulmonary Edema; Pulmonary Valve; Sepsis; Streptococcal Infections; Tachycardia, Paroxysmal; Tricuspid Valve Insufficiency

Oleander poisoning typically results in cardiac arrhythmias, hyperkalemia, and gastrointestinal irritation, and can be fatal. Oleander extracts have also been studied experimentally as hypoglycemic agents. Here, we describe a dog with confirmed oleander toxicosis presenting with classical symptoms and also hypoglycemia. After excluding other likely causes of hypoglycemia, the finding was attributed to oleander toxicosis, which has not been previously reported in dogs. A 7-year-old female spayed Maltese was presented to the emergency service after ingesting oleander leaves. Toxicosis was confirmed by measurement of digoxin using a competitive binding immunoassay, patient level 0.7 ng/mL (0.9 nmol/L) 24-h post-ingestion. Clinical symptoms included vomiting, cardiac arrhythmia, mild hyperkalemia, and hypoglycemia. Treatment was successful with aggressive supportive care, and the dog was discharged from the hospital after 48 h and made a full recovery. This case reviews the presentation and treatment of oleander toxicity but also highlights possible effects of oleander on blood sugar in dogs. Hypoglycemia in this dog, attributed to oleander poisoning, is interesting as it supports experimental research into hypoglycemic properties of oleander extracts.

Topics: Animals; Animals, Inbred Strains; Combined Modality Therapy; Cross Reactions; Digoxin; Dog Diseases; Dogs; Emergency Treatment; Female; Hospitals, Animal; Hypoglycemia; Immunoassay; Nerium; Plant Leaves; Plant Poisoning; Treatment Outcome

Drug-drug interactions are a preventable cause of morbidity and mortality, yet their consequences in the community are not well characterized.. To determine whether elderly patients admitted to hospital with specific drug toxicities were likely to have been prescribed an interacting drug in the week prior to admission.. Three population-based, nested case-control studies.. Ontario, Canada, from January 1, 1994, to December 31, 2000.. All Ontario residents aged 66 years or older treated with glyburide, digoxin, or an angiotensin-converting enzyme (ACE) inhibitor. Case patients were those admitted to hospital for drug-related toxicity. Prescription records of cases were compared with those of controls (matched on age, sex, use of the same medication, and presence or absence of renal disease) for receipt of interacting medications (co-trimoxazole with glyburide, clarithromycin with digoxin, and potassium-sparing diuretics with ACE inhibitors).. Odds ratio for association between hospital admission for drug toxicity (hypoglycemia, digoxin toxicity, or hyperkalemia, respectively) and use of an interacting medication in the preceding week, adjusted for diagnoses, receipt of other medications, the number of prescription drugs, and the number of hospital admissions in the year preceding the index date.. During the 7-year study period, 909 elderly patients receiving glyburide were admitted with a diagnosis of hypoglycemia. In the primary analysis, those patients admitted for hypoglycemia were more than 6 times as likely to have been treated with co-trimoxazole in the previous week (adjusted odds ratio, 6.6; 95% confidence interval, 4.5-9.7). Patients admitted with digoxin toxicity (n = 1051) were about 12 times more likely to have been treated with clarithromycin (adjusted odds ratio, 11.7; 95% confidence interval, 7.5-18.2) in the previous week, and patients treated with ACE inhibitors admitted with a diagnosis of hyperkalemia (n = 523) were about 20 times more likely to have been treated with a potassium-sparing diuretic (adjusted odds ratio, 20.3; 95% confidence interval, 13.4-30.7) in the previous week. No increased risk of drug toxicity was found for drugs with similar indications but no known interactions (amoxicillin, cefuroxime, and indapamide, respectively).. Many hospital admissions of elderly patients for drug toxicity occur after administration of a drug known to cause drug-drug interactions. Many of these interactions could have been avoided.

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Anti-Asthmatic Agents; Anti-Infective Agents; Antihypertensive Agents; Case-Control Studies; Clarithromycin; Contraindications; Digoxin; Diuretics; Drug Interactions; Drug-Related Side Effects and Adverse Reactions; Female; Glyburide; Hospitalization; Humans; Hyperkalemia; Hypoglycemia; Male; Ontario; Trimethoprim, Sulfamethoxazole Drug Combination

Two women, aged 77 and 73 years, and one man, aged 71 years, were admitted because of a serious adverse drug reaction (ADR). The first woman had a probable adverse drug reaction caused by digoxin after the addition of a NSAID (diclofenac) to a combination of digoxin and other drugs (furosemide and hydroquinine). The ADR due to digoxin is an example of a pharmacokinetic interaction. The second woman had serious orthostatic hypotension because of a pharmacodynamic interaction between three different antihypertensives. In the man, the ADR was hypoglycaemia while taking glibenclamide, a second generation sulfonylurea derivative. This was probably caused by declining renal function of a transplanted kidney because of bladder cancer. Doctors should be aware of ADRs in older patients, which also can occur when no changes in medication have taken place. In old age, any decline in vitality or function can be due to an ADR.

Topics: Adverse Drug Reaction Reporting Systems; Aged; Anti-Arrhythmia Agents; Anti-Inflammatory Agents, Non-Steroidal; Antihypertensive Agents; Diclofenac; Digoxin; Diuretics; Drug Interactions; Female; Furosemide; Glyburide; Humans; Hypoglycemia; Hypoglycemic Agents; Hypotension, Orthostatic; Kidney; Male; Quinidine; Urinary Bladder Neoplasms

The effect of digoxin (0.035 mg/kg b.w., i.v.) on adrenaline-induced hyperglycemia (adrenaline: 50 micrograms/kg b.w., s.c.) and on insulin-induced hypoglycemia (insulin: 0.4 mU/kg b.w., s.c.) was studied in experiments on rabbits. Digoxin intensified the adrenaline-induced hyperglycemia at the 30th and 60th minutes of application. The hyperglycemia in this case subsided more rapidly. Digoxin alone caused on elevation of the blood sugar levels that was most pronounced at the 30th minute of introduction. These elevated levels fell to the initial value by the 180th minute. The blood sugar levels in the rabbits treated with physiological solution rose slightly. This was most noticeable at the 120th minute. Digoxin attenuated the insulin-induced hypoglycemia significantly at the 120th, 150th, and 180th minutes (p < 0.05). We suggest that the increase of the adrenaline-induced hyperglycemia and the attenuation of the insulin-induced hypoglycemia could be linked to the release of catecholamines in the acute stage of the action of Digitalis glycosides.

Topics: Animals; Digoxin; Epinephrine; Hyperglycemia; Hypoglycemia; Injections, Subcutaneous; Insulin; Rabbits

Digitalis-like factor (DLF) appears to be widely distributed throughout the body, and has been specifically localized to the mammalian hypothalamus. In this study we monitored the DLF response to insulin-induced hypoglycemia in 11 normal males. Hypoglycemia was associated with a significant increase in serum DLF activity over basal values (40 +/- 5 pg digoxin Eq/ml, mean +/- SEM) at 60 min (83 +/- 8 pg digoxin Eq/ml) and 90 min (86 +/- 10 pg digoxin Eq/ml) following insulin administration (p less than 0.01). We measured the DLF response to insulin-induced hypoglycemia in other men after infusion of hypertonic saline (n = 8) or after oral water-loading (n = 8). Saline infusion (0.06 ml 5% saline/kg BW/min for 120 min prior to insulin infusion) or water loading (20 ml/kg BW over 60 min completed 30 min before insulin infusion) alone significantly increased serum DLF (saline: 21 +/- 5 to 60 +/- 18 pg digoxin Eq/ml, p less than 0.05; water: 18 +/- 11 to 49 +/- 15 digoxin Eq/ml, p less than 0.05). DLF activity was further significantly increased within each group 60 and 90 min after administration of insulin. In the group infused with hypertonic saline, insulin caused increases of serum DLF from 60 +/- 18 at time 0 to 170 +/- 17 pg digoxin Eq/ml at peak (p less than 0.01). Similarly, in the oral water-loaded group serum DLF increased from 49 +/- 15 at time 0 to 127 +/- 24 pg digoxin Eq/ml at peak (p less than 0.01) after they received insulin.2=

Topics: Adult; Blood Glucose; Blood Proteins; Cardenolides; Digoxin; Humans; Hydrocortisone; Hypoglycemia; Hypothalamus; Insulin; Male; Radioimmunoassay; Saponins; Time Factors

Topics: Digoxin; Diuretics; Heart Failure; Humans; Hypoglycemia; Hypokalemia; Hyponatremia; Hypothermia; Magnesium; Protein-Energy Malnutrition

Topics: Acidosis; Alkalosis; Anti-Bacterial Agents; Blood Transfusion; Body Temperature; Digoxin; Diuretics; Drainage; Glucose; Heart Arrest; Heart Defects, Congenital; Humans; Hypoglycemia; Hypoproteinemia; Infant, Newborn; Intubation, Intratracheal; Isoproterenol; Parenteral Nutrition; Positive-Pressure Respiration; Postoperative Care; Serum Albumin; Thrombocytopenia; Water-Electrolyte Balance