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At least 847 records · Page 47Linked to original sources
PubMed1976

Can phenformin-induced lactic acidosis be prevented?

Although patients taking phenformin are more likely to develop lactic acidosis in the presence of renal, cardiovascular, or hepatic disease, criteria for safe use of the drug are not well established. Eight diabetics died of lactic acidosis in Nottingham in 1972-5 and all were taking phenformin in therapeutic doses. Six had attended the diabetic clinic within a month of their terminal illness. Two patients had appreciable renal impairment and should not have been given phenformin. Four had hypertension and minimal evidence of renal disease, while in two no predisposing factor was identified. There are so many contraindications to the use of phenformin that it is doubtful whether patients on the drug can be monitored adequately. We suggest that phenformin should be withdrawn from general use.

Acidosis↗
PubMed1975

Phenformin-associated lactic acidosis; a review.

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.

Acidosis↗
PubMed1976

Phenformin-associated metabolic acidosis.

We report 18 consecutive phenformin-treated diabetic patients admitted to this Medical Service acutely ill with metabolic acidosis. Lactic acidosis was anticipated, and documented, in all. Also, however, though most of the patients had only weakly positive, or even negative, serum reactions with the nitroprusside reagent, all were found to have coexisting ketoacidosis, plasma 3-hydroxybutyrate averaging 7.1 mmol/L. +/- 3.9 (S.D.). This finding suggest that treatment of these patients should include insulin, and often also glucose, because most do not have marked hyperglycemia and some have hypoglycemia. The lactic acidosis in the nine patients who survivied was, on average, less severe than in the nine who died, but the difference was not statistically significant. Surivival correlated closely with the absence of shock on arrival. Only eight patients had a identifiable acute illness other than the metabolic acidosis. The other 10 patients had no discernible cause for the acute illness apart from their treatment with phenoformin. This finding raises serious doubts about whether phenformin should be used to treat patients with diabetes.

Acidosis↗
PubMed2003

Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Venous blood gas in adult patients with diabetic ketoacidosis.

A short cut review was carried out to establish whether venous blood gas measurement accurately demonstrates the degree of acidosis in patients with diabetic ketoacidosis. A total of 27 papers were found using the reported search, of which two presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these best papers are tabulated. A clinical bottom line is stated.

Blood Gas Analysis↗
PubMed2000

Characteristics of Caucasian type 2 diabetic patients during ketoacidosis and at follow-up.

OBJECTIVE: To analyse among adult Caucasian patients hospitalised for diabetic ketoacidosis the relative frequency of patients with type 2 diabetes and their characteristics. RESEARCH DESIGN: A retrospective review of adult patients presenting with diabetic ketoacidosis was conducted between 1993 and 1996. Patients with typical type 1 diabetes were classified according to age of onset < 35 years, insulin-dependence and BMI < 25 kg/m2; patients who did not meet these criteria were further classified on the basis of a basal and stimulated C-peptide and the detection of antibodies to glutamic acid decarboxylase (GADA) and to islet cells (ICA). RESULTS: 43 patients presenting with an episode of diabetic ketoacidosis were divided into two groups, A and B. Group A consisted of 19 patients, 17 patients classified as patients with typical type 1 diabetes and 2 patients with diabetes post-pancreatectomy. The other patients were the subjects of our study (group B; n = 20, 4 lost to follow-up). 13 patients (65% of group B = B I) were diagnosed with type 1 diabetes (median basal C-peptide: 0.15 nmol/l) and 7 patients (35% of group B = B II) with type 2 diabetes (median basal C-peptide of 1 nmol/l). Higher body mass index (BMI), shorter duration of diabetes, smaller anion gap and worse glycaemic control were found to be significantly different between groups B I and II on admission (p < 0.05). After a median follow-up of 18 months, patients in group B II had a better metabolic control than those in B I and 5 of the 7 patients were treated without insulin. CONCLUSION: Diabetic ketoacidosis is more common than previously thought in patients with type 2 diabetes, occurring in 16% of all cases. Distinctive features at presentation are the degree of acidosis, the duration of diabetes, BMI and HbA1c. However, the basal plasma C-peptide value remains the best discriminating factor.

Adult↗
PubMed1979

Diabetic ketoalkalosis.

The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.

Alkalosis↗