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PubMed1983

Profound hyperglycemia and metabolic acidosis after verapamil overdose.

Verapamil, a potent calcium antagonist, possesses varied systemic effects, including smooth muscle relaxation leading to both peripheral and coronary artery vasodilation, slowed atrioventricular nodal conduction and decreased insulin release from the pancreatic B cells. Reports concerning the effects of acute intoxication with verapamil are scarce. A case is presented of a 22 year old woman who developed profound hyperglycemia and metabolic acidosis after the inadvertent overdose of thirty 80 mg tablets (2,400 mg) of verapamil. This case illustrates the need for physicians to be aware of verapamil's inhibitory effects on insulin release and to exercise special care when prescribing verapamil in patients with preexisting diabetes mellitus.

Acidosis↗
PubMed2000

Post-transplant diabetic ketoacidosis--a possible consequence of immunosuppression with calcineurin inhibiting agents: a case series.

Post-transplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus (FK506), is commonly regarded as a form of type-2 (adult-onset) diabetes mellitus. Diabetic ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type-1 diabetes mellitus. We report three patients who presented with diabetic ketoacidosis post-transplant. All three patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was a renal transplant recipient on a cyclosporine-based regimen. The other two patients were liver transplant recipients receiving either cyclosporine or tacrolimus-based immunosuppression. Both of the liver transplant recipients were found to have moderate to high serum levels of calcineurin inhibitors on presentation. The liver recipient on cyclosporine (Neoral) had a 4 hour post-dose level of 388 ng/ml and the patient on tacrolimus was found to have a trough level of 21.2 ng/ml. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibition, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post-transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type I and type II diabetes mellitus.

Adult↗
PubMed2002

High anion gap metabolic acidosis in suicide: don't forget metformin intoxication--two patients' experiences.

Lactic acidosis is a well-recognized side effect of metformin, especially in patients with renal failure. Only a few cases of deliberate self-poisoning with metformin have been described in the literature. We report two patients who took a large dose of metformin in an attempt to harm themselves and both of them presented with severe lactic acidosis. The first patient was admitted because of taking large amounts of her father's unknown drug for suicide. Arterial blood gas showed severe metabolic acidosis with high anion gap and blood lactate level which metformin intoxication was documented. She died of multiple organ failure although we provided aggressive management including continuous renal replacement therapy. The second case, a type 2 diabetic patient, was sent to the emergency department after taking 110 tablets of metformin (500 mg). Arterial blood gas showed severe metabolic acidosis with high anion gap and blood lactate level. Hypotension and consciousness disturbance occurred later. After one session of hemodialysis, she recovered completely. In our experiences, metformin intoxication should be suspected when patients presented by wide anion gap metabolic acidosis after suicide attempt by taking drugs. Hemodialysis or continuous renal replacement should be initiated as soon as possible in addition to other supportive care.

Acid-Base Equilibrium↗
PubMedDate not supplied

Reliability of serum magnesium values during diabetic ketoacidosis in children.

OBJECTIVE: To determine the prevalence of hypomagnesemia in diabetic children during diabetic ketoacidosis and following restitution of acid-base balance. METHODS: Eight consecutive diabetic children, ranging in age from 8 to 16 years, hospitalized in the pediatric intensive care unit with diabetic ketoacidosis from October 1st. through December 31st, 1995. A control group of 33 metabolically stable diabetic children, and a control group of 30 healthy children. Both control groups were similar in composition regarding age and sex to the study group. None of the patients in the study group and none of the controls had Magnesium supplementation given to them during the study period. MEASUREMENTS: Total serum Magnesium concentrations were measured from peripheral venous blood in all 71 patients. For the study group serum Magnesium was determined in a serial fashion: 1. upon admission in diabetic ketoacidosis 2. 24 hours after admission 3. 72 hours after admission RESULTS: The prevalence of hypomagnesemia was 62.4% in patients with diabetic ketoacidosis, (Group 1), 25% in patients after partial correction of ketoacidosis, (Group 2), and none in patients after resolution of ketoacidosis, (Group 3). The prevalence of hypomagnesemia was 6% for the chronic, metabolically stable diabetic control group, (Group 4), but 0% for the non-diabetic control group, (Group 5). Average serum Magnesium levels were significantly lower (p less than 0.05), in patients admitted in diabetic ketoacidosis compared to those of both the diabetic and the non-diabetic control groups. Also average serum Magnesium levels were significantly lower (p less than 0.05), in patients with corrected diabetic ketoacidosis than those of the healthy control group. But there were no significant differences (p = 0.59263) in average serum Magnesium levels between the diabetic control group and the diabetic patients after resolution of ketoacidosis. CONCLUSIONS: In this study the prevalence of hypomagnesemia was documented to be higher than the average described elsewhere for pediatric, adult, and coronary intensive care units. As hypomagnesemia is an indication of Magnesium depletion, we speculate that the transient hypomagnesemia detected in our study group is an expression of a state of Magnesium depletion that is masked by correction of acidosis and the Magnesium shifts associated with it. Consequently serum Magnesium values ought to be considered most reliable during and not after correction of diabetic ketoacidosis. Since Magnesium was not supplemented to any of our patients, the normalization of their serum values must be the result of: a. decreased glycosuria-related urinary losses b. cessation of acidosis-related urinary losses c. Magnesium shifts from intra to extracellular space The high prevalence of hypomagnesemia and the significant lower average serum Magnesium levels in children with diabetic ketoacidosis reveals the magnitude of the problem and the potential for Magnesium depletion that occurs in diabetic children.

Adolescent↗
PubMedDate not supplied

[Family incidence of latent autoimmune diabetes in adults--case report].

We describe a 37 year-old woman case of latent autoimmune diabetes in adults (LADA). She was presented with unfounded weight loss. The diagnosis of diabetes mellitus was established on twice plasma glucose measurements above 200 mg/dl. In other routine biochemical examinations we did not observe dehydratation, electrolyte depletion, acidosis. However plasma level of C peptide basal and after stimulation with glucagon was reduced. Initially, the patient responded well to sulphonylurea treatment. To test immunological pathogenesis we examine autoimmune markers of diabetes type 1. Autoimmune antibodies (GAD, IAA) were found in patients and her parents, which were until now diabetic type 2. We report this case because incidence of latent autoimmune diabetes in adults is underestimate and rarely diagnosed in clinical practice.

Adult↗
PubMed1981

Metabolic emergencies.

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.

Acidosis↗
PubMed1997

An overview of metformin in the treatment of type 2 diabetes mellitus.

Type 2 diabetes mellitus results from impaired insulin secretion and reduced peripheral insulin sensitivity. Treatment options include diet, oral antihyperglycemic agents, and insulin. Metformin, an oral biguanide, ameliorates hyperglycemia by improving peripheral sensitivity to insulin, and reducing gastrointestinal glucose absorption and hepatic glucose production. Unlike sulfonylureas, it does not stimulate insulin secretion, aggravate hyperinsulinemia, or cause hypoglycemia or weight gain (weight stabilizes or decreases). It also has beneficial effects on serum lipid profiles. In lean or overweight type 2 diabetic patients uncontrolled by diet, metformin monotherapy significantly improves glycemic control, compared with placebo, and to similar extents as sulfonylurea monotherapy. In secondary sulfonylurea failure, combination metformin-sulfonylurea treatment significantly improves glycemic control beyond that achieved with either agent along. Metformin-sulfonylurea also appears to be as effective as insulin or insulin plus sulfonylurea, suggesting that such combination therapy may obviate or substantially delay insulin therapy. Limited data suggest that metformin-insulin therapy may improve glycemic control, possibly reducing insulin requirements, in type 2 diabetic patients uncontrolled by insulin alone following secondary sulfonylurea failure. Gastrointestinal side effects are common, but usually tolerated. Lactic acidosis risk is minimal, provided that contraindications, particularly renal impairment, and prescribing guidelines are respected. Aside from elevated plasma metformin levels with cimetidine and synergistic hypoglycemia with sulfonylureas, few interactions occur. Thus, metformin is safe and effective both as monotherapy or in combination with other antihyperglycemic agents in type 2 diabetic patients requiring additional glycemic control and may be advantageous when weight control is desirable and/or hyperlipidemia exists.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

Role of metformin in treatment of diabetes mellitus.

Metformin, a biguanide antidiabetic agent that can be administered either alone or in combination with sulfonylureas, has been extensively used in Europe and Canada. The mechanism of action of metformin and other biguanides is not completely understood, but recent in vitro and in vivo studies suggest that metformin may act in part by both increasing the binding of insulin to its receptor and potentiating insulin action. Metformin, because of its chemical structure, does not interact with the liver and has a short half-life. Consequently, lactic acidosis, which is a rare complication of metformin, has not been associated with the proper use of this drug. In addition to its antidiabetic actions, metformin causes weight loss in obese diabetic patients and may be useful in managing associated lipid disorders.

Acidosis, Lactic↗
PubMed1983

Diabetic ketoacidosis in a community of suburban Osaka. Analysis of 39 episodes of ketoacidosis and related conditions.

Thirty-nine episodes of hyperglycemia and disturbance of acid-base equilibrium were classified according to the result of nitroprusside test for serum (or urine) ketones, serum electrolytes, glucose, lactate, beta-hydroxybutyrate and arterial blood pH and gas analysis into the following 6 groups; (1) diabetic ketoacidosis (DKA), (2) mild DKA, (3) DKA with mixed acid-base disturbance, (4) DKA with lactic acidosis, (5) lactic acidosis with mild ketonemia, (6) lactic acidosis. Their clinical manifestations, laboratory findings, insulin and i.v. fluid requirement in the early phase of therapy were surveyed and compared with those reported from Western countries. The fundamental problems of groups (1) to (4) were hyperglycemia and acid-base disturbance. Groups (5) and (6) were characterized by underlying serious medical illness, accompanied by lactic acidosis and hyperglycemia. All patients in groups (1) to (4) recovered but 7 of 10 patients in groups (5) and (6) died within the first 7 days. DKA with or without lactic acidosis and lactic acidosis with or without mild ketonemia appeared as two separate conditions from the standpoint of management and prognosis and were differentiated only by nitroprusside test for serum ketones. DKA with lactic acidosis and DKA without it could not be differentiated by routine blood chemistries and therapy for the two did not differ so that they were thought to be in the same spectrum of metabolic alteration.

Blood Chemical Analysis↗
PubMed2005

An acute hyperglycemia or acidosis-induced changes of indolamines level correlates with PKC-alpha expression in rat brain.

Hyperglycemia and ketoacidosis are the two most serious factors in acute metabolic complications of both type 1 and type 2 diabetes. Dysfunction of the central nervous system is a well-documented complication of diabetes. We and others have previously reported that acute or chronic diabetes in animal's results in altered brain neurotransmitter levels. In this study, we investigated the effects of acute (7 days) glucose-induced hyperglycemia and sodium acetoacetate (NaAcAc) or ammonium chloride (NH4Cl) induced acidosis on the level of indolamines (5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA)) as well as PKC-alpha expression/activity in discrete areas of rat brain. Glucose-induced (500 mg/kg, bw) hyperglycemic ( approximately 249 mg%) rats showed significant (p<0.05) increase in 5-HT levels in mid brain (MB), pons medulla (PM) and cerebellum (CB), respectively. 5-HIAA level increased in hippocampus (HC) (p<0.05) as compared to control. The rats treated with sodium acetoacetate (NaAcAc) for 7 days (60 mg/kg, bw) showed significant decrease (p<0.05) of 5-HT level in hypothalamus (HT). Whereas, the 5-HIAA level increased in MB (p<0.05). Similarly, the PKC-alpha expression as well as the enzyme activity showed significant increase in HC, MB, PM and CB under glucose-induced hyperglycemia and that changes correlated the changes of indolamines, suggesting that the hyperglycemia may be the major metabolic disorder in diabetic complications.

Acetoacetates↗
PubMed1975

Alcoholic detosis.

Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.

Acidosis↗
PubMed1978

Abnormalities of in vitro lymphocyte response to mitogens in diabetic children during acute ketoacidosis.

Cell-mediated immunity was evaluated in 11 children with diabetes mellitus; six children were evaluated during ketoacidosis and five were evaluated with ketonuria in the absence of acidosis. Five of the six ketoacidotic children had at least one positive delayed-hypersensitivity skin test. Lymphocytes from two ketoacidotic patients were unresponsive to phytohemagglutinin and pokeweed mitogen, and lymphocytes from these two patients plus a third patient were unresponsive to concanavalin A. Lymphocytes from all six patients responded to these three mitogens after one week of therapy. In the five diabetic children without ketoacidosis, lymphocyte responses were normal to all three mitogens. Similarly, the addition of glucose to normal plasma did not alter the lymphocyte transformations of three healthy nondiabetic controls. These data suggest that cell-mediated immunity may be transiently defective in children with acute diabetic ketoacidosis.

Acute Disease↗
PubMed1999

Molecular and histological evaluation of pancreata from patients with a mitochondrial gene mutation associated with impaired insulin secretion.

A mutation in mitochondrial DNA, which was originally identified in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), can be associated with a subtype of diabetes mellitus. To determine the molecular and histological basis of impaired insulin secretion in the subjects with this mutation, we studied autopsy pancreata specimens from eight subjects diagnosed as having MELAS. The 3243 bp mutation was identified in seven out of eight pancreata examined. Immunohistochemical studies demonstrated a reduction in total islet mass, and in the numbers of both B and A cells. No evidence of insulitis or apoptosis was found. These data suggested that the 3243 bp mutation may cause the reduction of islet cells, mainly through mechanisms other than autoimmune destruction.

Adolescent↗
PubMed1986

Fructose-induced hyperlactemia in hyperosmolar syndromes.

Severe hyperlactemia of 8.7, 8.6 and 7.9 mmol/l, respectively, developed in three patients with hyperosmolar syndromes (two hypernatremic, 417 and 415 mosmol/kg H2O; one hyperglycemic 437 mosmol/kg H2O) during rehydration treatment with 5% fructose in water (fructose dosage 0.5 g/kg body wt. per hour). After resolution of the electrolyte disturbances, the infusion of fructose at the same dosage increased the plasma lactate concentration in two of the patients to 4.9 and 4.0 mmol/l, indicating near normalization of hepatic lactate utilization. Thus, in addition to peripheral insulin resistance and decreased muscular glucose utilization, the hyperosmolar state is associated with a reduced tolerance to fructose. This is most likely due to an osmolality-dependent impairment of hepatic gluconeogenesis. In rehydration therapy for hyperosmolar syndromes, fructose-containing infusion solutions should no longer be used.

Acidosis↗
PubMed1975

Accumulation of 3-hydroxyisobutyric acid, 2-methyl-3-hydroxybutyric acid and 3-hydroxyisovaleric acid in ketoacidosis.

1. Urine and serum samples from patients with ketoacidosis of varying degree and etiology have been examined by gas chromatography and mass spectrometry. 2. In addition to 3-hydroxyisovaleric acid, relatively high concentrations of two analogous hydroxy acids, 3-hydroxyisobutyric acid and 2-methyl-3-hydroxybutyric acid, were found in the urine. 3. There were highly significant positive correlations between the excreted amounts of the three acids. 4. Experiments on rats with isotope-labelled compounds revealed that the acids were formed by the degradation of leucine, isoleucine and valine. 5. The accumulation of the hydroxy acids during ketoacidosis is probably caused by a similar derangement of the metabolism of all three branched-chain amino acids.

Acetates↗