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At least 1,081 records · Page 60Linked to original sources
PubMed1992

[Alcoholic ketoacidosis].

Alcoholic ketoacidosis is seen in chronic alcoholics who have been starving for days. This was the case in the present patient who had metabolic acidosis on admission. The differential diagnoses are primarily diabetic ketoacidosis, intoxication (salicylate, methanol, ethylene glycol and fenformin), lactate acidosis, hunger-induced ketoacidosis and uraemia. Treatment should consist of intravenous glucose and correction of the dehydration with isotonic sodium chloride.

Alcoholism↗
PubMed1990

Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration.

We report a patient who developed persistent nephrogenic diabetes insipidus associated with renal tubular acidosis, renal resistance to parathyroid hormone, aminoaciduria and proximal tubule pattern proteinuria in the presence of a reduced glomerular filtration rate (19-24 ml/min). A review of the previous reports of persistent nephrogenic diabetes insipidus revealed that in all patients the glomerular filtration rate had been less than 60 ml/min at presentation. Chronic renal failure may therefore predispose to the development of persistent nephrogenic diabetes insipidus in patients receiving lithium.

Acidosis, Renal Tubular↗
PubMed1997

Possible synergistic effect of metformin and enalapril on the development of hyperkaliemic lactic acidosis.

A 71 year old hypertensive, non insulin-dependent diabetic patient with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkaliemia, normal plasma level of 3-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis, both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable under the treatment with an infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly taken by this nephropathic patient, could have played an iatrogenic role, even if the doses were low. This case highlights the importance of complying with the contraindications of these drugs, to avoid the rare but reported life-threatening complications of metformin administration.

Acidosis↗
PubMed1978

[Four cases of fatal lactic acidosis during biguanide therapy (author's transl)].

Four case reports of lactic acidosis occurring during biguanide treatment (2 with phenormin, 2 with buformin) are analysed. Three of the patients died in a toxic state of lactic acidosis, whilst the fourth patient survived lactic acidosis, but died 11 days later due to myocardial infarction. In spite of serum biguanide levels within the therapeutic range, one patient had highly toxic hepatic levels of phenformin (13,500 ng/g tissue). Two factors are essential for the treatment of lactic acidosis: 1. rapid diagnosis: history of biguanide intake; clinical symptoms; acid-base imbalance; rapid lactate determination to establish the diagnosis. 2. therapy: correction of acidosis, insulin and glucose; shock treatment; forced diuresis and/or haemodialysis. From the high numbers of biguanide-treated diabetics and the incidence of lactic acidosis in other countries it can be assumed that this toxic side effect of biguanide treatment occurs relatively frequently in Austria too, but remains largely undetected.

Acidosis↗
PubMedDate not supplied

Effect of acetazolamide on insulin sensitivity in dogs with alloxan diabetes.

The effect of acetazolamide on the sensitivity to exogenous insulin in the alloxanised diabetic dogs was studied. The administration of acetazolamide caused acidosis and insulin resistance. The liver insulinase activity of diabetic dogs after acetazolamide administration was also studied to evaluate the role of this enzyme for the destruction of exogenous insulin. It was observed that insulinase did not play role for the development of insulin resistance after acetazolamide administration.

Acetazolamide↗
PubMed2005

Pyruvate in the correction of intracellular acidosis: a metabolic basis as a novel superior buffer.

The review focuses on biochemical metabolisms of conventional buffers and emphasizes advantages of sodium pyruvate (Pyr) in the correction of intracellular acidosis. Exogenous lactate (Lac) as an alternative of natural buffer, bicarbonate, consumes intracellular protons on an equimolar basis, regenerating bicarbonate anions in plasma while the completion of gluconeogenesis and/or oxidation occurs via tricarboxylic-acid cycle in mitochondria mainly in liver and kidney, or heart. The general assumption that Lac is 'metabolized to bicarbonate' in liver to serve as a buffer has been questioned. Pyr as a novel buffer would be superior to conventional ones in the correction of metabolic acidosis. Several likely biochemical mechanisms of Pyr action are discussed. Experimental evidence, in vivo, strongly suggested that Pyr would be particularly efficient in the correction of severe acidemia: type A lactic acidosis, hypercapnia with cardiac arrest, and diabetic and alcoholic ketoacidosis in animal experiments and clinic settings. Because of its multi-cytoprotection, Pyrs not only correct acidosis, but also benefit theunderlying dysfunction of vital organs. In addition, Pyr is also a potential buffer component of dialysis solutions. However, the instability of Pyr in aqueous solutions restricts its clinical applications as a therapeutic agent. Attempts to create a stable Pyr preparation are needed.

Acidosis↗
PubMed2005

[Diabetic metabolic emergencies].

Diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome are two acute complications of diabetes that may result in high mortality. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The authors review the pathomechanism, clinical features, complications and current recommendations for management of ketoacidosis and hyperglycaemic hyperosmolar syndrome. In patients with type 2 diabetes may develop anaerobic (type A) lactic acidosis from tissue hypoxia, while aerobic (type B) lactic acidosis is a rare complication of biguanide therapy if contraindications to metformin are observed. Mortality remains very high, especially when serious comorbidities are present. Hypoglycaemia is a major factor preventing patients with both type 1 and type 2 diabetes from achieving near-normal plasma glucose targets. The authors summarize clinical presentation and therapeutic possibilities of hypoglycaemia on the basis of the literature.

Acidosis, Lactic↗
PubMed1979

[Major metabolic disturbances occur in diabetic patients whether they are obese or not (author's transl)].

The authors analyzed the effects of obesity/non-obesity in 162 epidoses of severe metabolic disturbances. Ketoacidosis and hypoglycaemics comas were more frequent in the non-obese group of diabetics, who were often insulin treated; whereas hyperosmolar coma and lactic acidosis were frequent in the obese group of diabetics, usually not treated with insulin. In the obese group both advanced age as well as a higher frequency of degenerative complications impaired the prognosis of these metabolic accidents. However the mortality rate was not significantly different in the two groups of patients. Despite the importance of the weight balance in the natural history of diabetes mellitus, it did not seem to influence the clinical aspects nor did it modify the therapeutic management of the major metabolic disturbances which occur in diabetes.

Adult↗
PubMed2005

[Effect of maternal diabetes on human and rat fetal development].

Diabetes is a genetically determined metabolic disease with fasting hyperglycemia due to relative or absolute absence of insulin. With the use of exogenous insulin, successful gestations are now possible. Nevertheless, there are still severe problems associated, such as spontaneous abortion, perinatal mortality and congenital malformations. Caudal regression syndrome, disclosure of the neural tube and cardiovascular alterations are the most common malformations. Gestational diabetes can induce increased fetal corporal fat and macrosomia with hyperinsulinemia, hypoglycemic, hypoxia, metabolic acidosis and perinatal death. During adult life, diabetic mothers' children can develop obesity, glucose intolerance and type 2 diabetes. In order to study fetuses' alterations during diabetic gestations we now have animal models of diabetes. Maternal diabetes in rats alters fetal development in a very similar manner to that of humans. Although we do not accurately know the pathogenic mechanism by which diabetes produces fetuses' abnormal development, hyperglycemia and hyperketonemia had been mentioned to have predominant roles. Hyperglycemia damages DNA and increases oxidative stress and hyperketonemia increases the rate of embryo malformations. The addition of antioxidants such as C and E vitamins can reduce this damage. During adult life, diabetic rats' cubs have alterations in glucose metabolism and in reproductive function. The understanding of mechanisms by which maternal diabetes affects fetuses development, can help us to prevent complications and improve mothers' and children's life quality.

Adult↗
PubMed2000

[Lactic acidosis: a complication of spinal cord injury in multiple trauma].

Large-dose methylprednisolone has been advocated to lessen neurologic deficits in spinal cord injury for nearly a decade despite confounding statistical results in the Second National Acute Spinal Cord Injury Study (NASCIS-2). Recent retrospective studies found lack of significant functional improvement, increases in the incidence of infectious complications and an increase in ventilated and intensive care days in steroid-treated groups. We report on five cases with severe hyperglycemia and nonketotic metabolic acidosis in otherwise non-diabetic patients with multiple blunt injuries and an associated spinal cord injury. Those adverse effects were induced by epinephrine and aggravated by methylprednisolone. We conclude that high-dose methylprednisolone should be avoided in multiple injured or otherwise compromised patients potentially needing catecholamine support.

Acidosis, Lactic↗