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PubMed1998

Clinical risk associated with contrast angiography in metformin treated patients: a clinical review.

Recently, concern has been expressed about the hazards of lactic acidosis following the use of intravascular iodinated contrast agents in patients taking metformin. In response the Royal College of Radiologists have issued guidelines for the management of these patients. We have reviewed the reported cases of lactic acidosis and identified that in all cases underlying renal impairment existed. To examine this further we reviewed the notes of 33 in-patients receiving metformin who underwent contrast angiography in our hospital. Twenty-nine patients had a normal serum creatinine prior to the procedure and none had a rise following angiography. Four patients had an abnormal serum creatinine prior to angiography, all four patients showed significant deterioration and all four patients died, two from unrelated causes and two from acute renal failure and acidosis. These data strongly highlight the hazards of intravascular contrast radiology in diabetic patients with pre-existing renal impairment. We have failed to find evidence in support of the Royal College of Radiologists recommendation; instead we recommend that in those patients taking metformin with evidence of renal impairment metformin should be stopped and diabetic control obtained using alternative therapy before proceeding with angiography. Patients with normal renal function taking metformin are not at risk of lactic acidosis following the use of iodinated contrast agents for angiography.

Acidosis, Lactic↗
PubMed2005

Control of muscle protein kinetics by acid-base balance.

PURPOSE OF REVIEW: Abnormalities of acid-base balance accompany many pathological conditions. Acidosis is associated with several diseases such as chronic renal failure, diabetic ketosis, severe trauma and sepsis, and chronic obstructive respiratory disease, which are often associated with muscle wasting. There is evidence that acidosis can induce muscle protein catabolism and it could therefore be an important factor contributing to loss of muscle protein in these conditions. This review aims at outlining the effects of acid-base balance abnormalities on muscle protein metabolism, and will in particular summarize and evaluate the most recent studies on the impact of pH on control of muscle protein metabolism. RECENT FINDINGS: Acidosis has been shown to promote muscle protein catabolism by stimulating protein degradation and amino acid oxidation. This effect is achieved through up-regulation of the ubiquitin-proteasome pathway - one of the major enzyme systems for protein degradation. Recent studies in animals and humans have also shown that acidosis inhibits muscle protein synthesis. Little is known about the mechanisms by which acidosis depresses protein synthesis, or of the impact of alkalosis on protein metabolism. SUMMARY: Increasing evidence suggests that acidosis promotes muscle protein wasting by both increasing protein degradation and inhibiting protein synthesis. Correction of acidosis may therefore help to preserve muscle mass and improve the health of patients with pathological conditions associated with acidosis.

Acid-Base Equilibrium↗
PubMedDate not supplied

A novel mutation in the mitochondrial 16S rRNA gene in a patient with MELAS syndrome, diabetes mellitus, hyperthyroidism and cardiomyopathy.

Using RNase protection analysis, we found a novel C to G mutation at nucleotide position 3093 of mitochondrial DNA (mtDNA) in a previously reported 35-year-old woman exhibiting clinical features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome together with diabetes mellitus, hyperthyroidism and cardiomyopathy. The patient also had an A3243G mutation in the tRNA(Leu(UUR)) gene and a 260-base pair duplication in the D-loop of mtDNA. The fibroblasts of the patient were cultured and used for the construction of cybrids using cytoplasmic transfer of the patient's mtDNA to the mtDNA-less rho(0) cells. RNA isolated from the cybrids was subjected to RNase protection analysis, and a C3093G transversion at the 16S rRNA gene and a MELAS-associated A3243G mutation of mtDNA were detected. The novel C3093G mutation together with the A3243G transition were found in muscle biopsies, hair follicles and blood cells of this patient and also in her skin fibroblasts and cybrids. The proportion of the C3093G mutant mtDNA in muscle biopsies of the patient was 51%. In contrast, the mutation was not detected in three sons of the proband. To characterize the impact of the mtDNA mutation-associated defects on mitochondrial function, we determined the respiratory enzyme activities of the primary culture of fibroblasts established from the proband, her mother and her three sons. The proportions of mtDNA with the C3093G transversion and the A3243G transition in the fibroblasts of the proband were 45 and 58%, respectively. However, the fibroblasts of the proband's mother and children harbored lower levels of mtDNA with the A3243G mutation but did not contain the C3093G mutation. The complex I activity in the proband's fibroblasts was decreased to 47% of the control but those of the fibroblasts of the mother and three sons of the proband were not significantly changed. These findings suggest that the C3093G transversion together with the A3243G transition of mtDNA impaired the respiratory function of mitochondria and caused the atypical MELAS syndrome associated with diabetes mellitus, hyperthyroidism and cardiomyopathy in this patient.

Adult↗
PubMedDate not supplied

[Semi-automatic determination of blood lactate during hypoglycemic treatment with biguanides].

Blood lactate levels were determined by Lactate Analyzer 640 Kontron in 67 adult insulin-independent diabetics during hypoglycemic treatment with usual therapeutical doses of phenformin. In 5 cases were found lactate values above 2 mmol/l and, in consideration of accompanying conditions prone to lactic acidosis, the drug was discontinued. However, the mean value of blood lactate in diabetics treated with phenformin was not significantly different from that found in a group of insulin-treated diabetics. The semiautomatic determination of blood lactate is proposed as a rapid screening of possible candidates for lactic acidosis during biguanide treatment.

Autoanalysis↗
PubMed1999

Metformin-associated lactic acidosis: a rare or very rare clinical entity?

AIMS: Lactic acidosis is a well recognized complication of biguanide therapy which is potentially serious. Although the prevalence of metformin-associated lactic acidosis (MALA) is much lower than that associated with phenformin, it is still being reported sporadically which raises concerns for the practising clinicians. We review the currently available world-wide data of the prevalence of MALA, the risk factors for its development and the current practical guidelines on the use of metformin to minimize the risk of this potential hazard. METHODS: An extensive literature search was conducted from both Medline and Ovid (1965-98) using the following keywords: 'Type 2 diabetes mellitus', 'oral hypoglycaemic drugs', 'biguanides', 'metformin-associated lactic acidosis' and 'renal impairment'. RESULTS: MALA was found to be a very rare clinical entity, being 20 times less common than phenformin-associated lactic acidosis. Amongst all the risk factors, renal impairment appears to be the major precipitating factor for the development of MALA in metformin-treated patients. We also found cases of MALA where no precipitating factors were identified and the underlying mechanism in these cases remains unclear. Practical recommendations of metformin use to minimize the risk of MALA have been listed based on previous reports. CONCLUSIONS: The low prevalence of MALA is comparable to the prevalence of sulphonylurea-induced hypoglycaemia. Metformin has many beneficial metabolic effects in the management of Type 2 diabetes mellitus. Provided that the recommended guidelines for metformin use are strictly adhered to, its widespread use would be safe and the incidence of MALA will be further reduced.

Acidosis, Lactic↗
PubMed2004

Alcoholic ketoacidosis associated with multiple complications: report of 3 cases.

We report 3 patients with alcoholic ketoacidosis (AKA). All had a history of excessive intake and abrupt termination of alcohol. They showed tachypnea, tachycardia, abdominal tenderness, and epigastralgia. Metabolic acidosis with an increased anion gap, decreased PaCO2 and ketonemia were present. One patient whose ratio of 3-hydroxybutyric acid to acetoacetic acid was 4.0 was associated with diabetic ketoacidosis. All patients were successfully hydrated with electrolyte, glucose and thiamine. Complications such as liver dysfunction, lactic acidosis, acute pancreatitis, Wernicke's encephalopathy, rhabdomyolysis and heart failure were present. Attention should be paid to multiple complications in the treatment of AKA.

Acidosis↗
PubMed1990

[Lactic acidosis associated with metformin].

Lactic acidosis is an extremely rare but serious complication of treatment with metformin. In order to avoid lactate acidosis, it is important to select patients correctly and to ensure that contraindications such as cases of renal involvement, advanced age and chronic alcoholism are observed prior to treatment with metformin. In addition, it is necessary to carry out meticulous follow-up control of the patients with annual investigations of renal and hepatic functions and clinical assessment approximately four times per annum with the object of revealing commencing symptoms of diabetes and ischaemic conditions. In this manner, the majority of cases of lactate acidosis can be avoided.

Acidosis, Lactic↗
PubMed2002

[Pitfalls and precautions concerning the use of conventional oral antidiabetic drugs].

The main pitfalls regarding the use of sulphonylureas and metformin in type 2 diabetic patients are described and illustrated by a clinical case. Advices are given in order to avoid the occurrence of severe hypoglycaemic episodes with sulphonylureas and to minimise the risk of lactic acidosis with metformin. These drugs, when used appropriately with respect of contra-indications, have an excellent safety profile and remain the basis of the treatment of type 2 diabetes.

Acidosis, Lactic↗
PubMedDate not supplied

Mixed acid-base abnormalities in diabetes.

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.

Acid-Base Equilibrium↗
PubMed1978

Reduction of beta-galactosidase in the ketotic Chinese hamster kidney.

Kidneys from normal, diabetic-nonketotic and ketotic Chinese hamsters were homogenized, fractionated and assayed for beta-glucosidase, and beta-galactosidase activities. The kidneys of the ketotic animals were enlarged but the protein content in each subcellular fraction was similar in all three groups of animals. beta-Glucosidase was found chiefly in the soluble fraction and no difference was observed in these animals. beta-Galactosidase was distributed in both cytoplasmic and particulate fractions; difference in the specific activity of beta-galactosidase between control and ketotic animals was found in nuclear, lysosomal-mitochondrial, microsomal and soluble fractions.

Acidosis↗
PubMed1999

Inhibition of Na+-H+ exchanger protects diabetic and non-diabetic hearts from ischemic injury: insight into altered susceptibility of diabetic hearts to ischemic injury.

It has been previously suggested that alterations in sodium homeostasis, leading to calcium overload may play a part in the mediation of cardiac ischemic injury. It has been demonstrated that the Na+-H+ exchanger plays an important role with regard to the regulation of intracellular sodium during ischemia and reperfusion and that inhibition of the Na+-H+ exchanger during ischemia protects hearts from ischemic injury. Studies using chemically-induced diabetic animals have suggested that the cardiac Na+-H+ exchanger in the diabetic heart is impaired and is responsible for limiting the increase in sodium during ischemia. The extent to which the Na+-H+ exchanger contributes to increases in intracellular sodium during ischemia in diabetic hearts is unclear as direct measurements of exchanger activity have not been made in genetically diabetic hearts. Therefore, this paper aims to address the following issues: (a) is the Na+-H+ exchanger impaired in a genetically diabetic rat heart: (b) does this impairment result in lower [Na]i or [Ca]i during ischemia; and (c) does Na+-H+ exchanger inhibition limit injury and functional impairment in diabetic hearts during ischemia and reperfusion? These issues were examined by inhibiting the Na+-H+ exchanger with ethylisopropylamiloride (EIPA) in isolated perfused hearts from both genetically diabetic (BB/W) and non-diabetic rats. Levels of intracellular sodium, intracellular calcium, intracellular pH and high energy phosphates (using 23Na,19F, 31P NMR spectroscopies, respectively) during global ischemia and reperfusion were also measured. The impact of diabetes on Na+-H+ exchanger activity was assessed by measuring pH recovery of these hearts after an acid load. Creatine kinase release during reperfusion was used as a measure of ischemic injury. This study demonstrated that the Na+-H+ exchanger is impaired in diabetic hearts. Despite this impaired activity, inhibition of Na+-H+ exchanger protected diabetic hearts from ischemic injury and was associated with attenuation of the rise in sodium and calcium, and limitation of acidosis and preservation of ATP during ischemia. The data presented here favor the use of Na+-H+ exchanger inhibitors to protect ischemic myocardium in diabetics. Also, the data provides possible mechanisms for the altered susceptibility of diabetic hearts to ischemic injury.

Acidosis↗
PubMed2006

Maternally inherited diabetes and deafness in a North American kindred: tips for making the diagnosis and review of unique management issues.

CONTEXT: Mutations in mitochondrial DNA are rare etiologies of adult-onset diabetes mellitus (DM) that merit identification to 1) prevent iatrogenic lactic acidosis, 2) prompt appropriate screening of affected patients and their families, 3) provide genetic counseling, and 4) provide an opportunity to investigate strategies for preventing diabetes. OBJECTIVE: The objective of this study is to raise awareness of this rare form of adult-onset nonobese DM so that these patients are identified and provided with appropriate care. PATIENTS: We describe a kindred in which four of seven siblings have adult-onset DM and sensorineural hearing loss with a confirmed genetic mutation at position 3243 in the tRNA. Two other siblings in this kindred demonstrate different phenotypes of mitochondrial disease. INTERVENTION: The proband was treated with coenzyme Q10 for 1 yr. OUTCOME MEASURES: Outcome measures included stress thallium exercise testing and audiometry testing. RESULTS: After 1 yr of treatment of with coenzyme Q10, repeat stress thallium testing demonstrated improvement in the exercise tolerance of the proband from 7-12 min. Audiometry testing did not demonstrate a change in the rate of hearing decline. CONCLUSION: Maternally inherited diabetes and deafness is a rare cause of DM that is important to diagnose because of the unique management issues and associated comorbidities. This work highlights clues to the identification of this rare monogenic form of adult- onset diabetes.

Adult↗