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At least 1,135 records · Page 63Linked to original sources
PubMed1995

Cerebral metabolism of oxygen and glucose in a patient with MELAS syndrome.

We studied cerebral oxygen and glucose metabolism as well as cerebral blood flow using positron emission tomography (PET) in a case with MELAS showing dementia, diabetes mellitus, ataxia and lactic acidosis without any signs of stroke. This case, confirmed to have a point mutation at position 3243 in the transfer RNA gene of mitochondrial DNA, developed a stroke-like episode 8 months after the PET study. Uncoupling was observed between cerebral oxygen metabolism and cerebral blood flow with reduced fractional oxygen extraction ratio, indicating "hyperemia", not ischemia. The "hyperemia" may be closely related to the malfunction of mitochondria in aerobic energy production. A drastic decrease in cerebral oxygen metabolism (CMRO2) was found globally in contrast to preserved cerebral glucose metabolism (CMRglu), resulting in a remarkable decrease in the metabolic ratio (CMRO2/CMRglu). The dissociation between cerebral glucose and oxygen metabolism may be characteristic of MELAS.

Adult↗
PubMed1977

Congenital absence of islets of Langerhans.

A small-for-dates male infant who developed acute metabolic acidosis shortly after birth had diabetes and died aged 40 hours. At necropsy there was an absence of any recognizable islets of Langerhans though lymphorecticular aggregates were found. This was the fourth child of healthy unrelated parents whose first child, also a male, died at 48 hours under similar circumstances. It is suggested that both boys had the same underlying pathology and this might be a previously undescribed recessive or x-linked inherited condition.

Diabetes Mellitus↗
PubMed2000

Phenotypic heterogeneity in a Chinese family with mitochondrial disease and A3243G mutation of mitochondrial DNA.

The A3243G mutation of mitochondrial DNA (mtDNA) has been shown to be responsible for or associated with mitochondrial myopathy, encephalopathy, lactic acidosis, strokelike episodes (MELAS) syndrome, diabetes mellitus (DM) and several other neuromuscular diseases. We used polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) to identify the A3243G mtDNA mutation and an electron microscope to examine mitochondrial derangement in the muscle biopsies of a 38-year-old man suspected to have MELAS syndrome with DM. We found great variability in the clinical presentation and in the proportion of mtDNA with the A3243G mutation in the matrilineal family members of the patient. The proband had atypical MELAS syndrome, recurrent vascular headache, and DM (MELASDM), and his mother manifested chronic progressive ptosis and DM (CPPDM). Brain magnetic resonance imaging of the proband showed high signal intensity in the left temporoparieto-occipital area on T2 weighted images (T2WI). The blood lactate level ranged from 2.32 to 4.70 mmol/l, and two-hour postprandial glucose ranged from 124 mg/dl to 148 mg/dl. The blood lactate and postprandial glucose of the proband's mother were 3.15 mmol/l and 192 mg/dl, respectively. Electron microscopic examination of a muscle biopsy of the patient showed abnormal mitochondria with decreased density of cristae and membrane degeneration. No ragged-red fibers were detected in muscle upon staining with modified Gomori trichrome. The hair follicles and blood cells of the patient and his mother showed the A3243G mutation in the tRNA(Leu)(UUR) gene. The proportions of the mutant DNA in the hair follicles and blood cells of the proband were 36.8% and 35.2%, respectively, and those of the patient's mother were 28.8% and 13.9%, respectively. We conclude that the A3243G mtDNA mutation may manifest with MELASDM or CPPDM in different matrilineal members of the same family as a result of differences in random segregation of the heteroplasmic A3243G mutant mtDNA in the affected tissues of patients.

Adult↗
PubMed1988

Decrease of serum buffering capacity associated with malignant neoplasms.

We have developed a new tumor marker based on the finding that cancerous sera suppress glucose utilization by cultured macrophages. Phosphofructokinase (PFK) was identified as susceptible enzyme [Naknamura et al.: JNCI 1986; 77 (in press)]. We found a high correlation between PFK inhibition and the lower buffering capacity of cancerous sera against an ATP aqueous solution and diluted acidic solutions. Sera from healthy donors changed to the PFK-suppressive type when exposed to lactate, even when followed by elimination of lactate. Lactate in cancerous sera was 1.6 times more than in normal sera. Sera from patients who tend to show acidosis, such as those with diabetes mellitus or chronic renal failure and pregnant women, also showed a lower buffering capacity as well as a higher inhibition of PFK. Although the pH method is simpler, we recommend the application of the PFK inhibition test, because this enzyme inhibition is not simply composed of a lower buffering capacity of cancerous sera, but partially of an inactivation of the enzyme through oxidation.

Acid-Base Equilibrium↗
PubMed1998

Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy.

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.

Acute Disease↗
PubMed1999

Renal complications in patients with diabetes mellitus associated with an A to G mutation of mitochondrial DNA at the 3243 position of leucine tRNA.

The substitution of guanine for adenine at position 3243 of the leucine tRNA gene of mitochondrial DNA was originally described in association with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes). Diabetes mellitus associated with the mutation (mitochondrial diabetes) is a different phenotype from MELAS. We identified 11 patients with the mutation among 385 Japanese diabetic patients: two had MELAS and nine had mitochondrial diabetes. We present data on a male patient with mitochondrial diabetes who developed the nephrotic syndrome at the age of 23. Light microscopy revealed mesangial expansion, PAS-positive deposits and segmental sclerosis in the glomeruli. Scattered mesangial electron-dense deposits and thickening of the basement membrane were found on electron microscopy, suggesting that diabetic glomerulosclerosis accompanied by focal glomerulosclerosis (FGS). Mitochondrial diabetes may pre-dispose patients to renal complications, including forms of glomerulonephritis, such as FGS.

Adult↗
PubMed1975

A review of deaths due to suspected lactic acidosis at a large metropolitan hospital.

A review of 2,647 consecutive deaths over a 19-month period at a large metropolitan hospital revealed 27 cases (1%) to be coded as metabolic acidosis. In ten of these deaths, a presumptive diagnosis of lactic acidosis could be made. Eight of the ten were diabetic, and all eight were treated with phenformin at the time of their last admission. Although phenformin could not be incriminated as the sole cause of lactic acidosis in these cases, a contributory role of the drug seems probable. The indiscriminate use of phenformin in diabetic patients should be discouraged and the contraindications to the use of phenformin should be stressed.

Acidosis↗
PubMedDate not supplied

Metformin-associated lactic acidosis: case reports and literature review.

BACKGROUND: Lactic acidosis is a widely recognized, though rare, side effect of metformin. This paper describes five patients admitted to Chang Gung Memorial Hospital from 1 September 1998 to 31 May 2001 suffering severe lactic acidosis caused by metformin, and reviews the literature. PATIENTS: Five cases diagnosed as having meftormin-associated lactic acidosis (MALA) were discovered during the study period. Three had normal renal function before the onset of MALA and two had attempted suicide bytaking large amounts of metformin. One patient with end-stage renal disease developed MALA despite regularhemodialysis three times a week. One of the patients who had taken metformin to attempt suicide was not diabetic. RESULTS: All patients suffered severe metabolic acidosis with a high anion gap and blood lactate level. Four developed profound hypotension, and three of these also suffered acute respiratory failure. Three patients received conventional hemodialysis and two continuous renal replacement therapy. A young non-diabetic female who had taken a large dose of metformin to commit suicide died from multiple organ failure despite aggressive treatment. CONCLUSIONS: Lactic acidosis is a serious reaction to metformin, and hemodialysis (the treatment of choice) should be done urgently to prevent serious complications. MALA should be suspected in patients presenting with wide anion gap metabolic acidosis and high blood lactate, even when they are non-diabetic.

Acidosis, Lactic↗
PubMed1981

Urinary excretion of C4--C10-dicarboxylic acids and antiketogenic properties of adipic acid in ketogenic-stimulated rats due to diabetes, long-chain and short-chain monocarboxylic acids.

The urinary excretion of C4--C10-dicarboxylic acids (succinic, adipic, suberic and sebacic acids) and the antiketogenicity of adipic acid have been studied in ketogenic-stimulated rats in three biochemically different states: diabetes, fat-feeding (long-chain monocarboxylic acids) and feeding of hexanoic acid (short-chain monocarboxylic acid). In diabetic rats urinary excretions of adipic and suberic acids were elevated before the rise in urinary excretions of 3-hydroxybutyric acid, i.e. before ketosis appeared. In severe diabetic ketosis sebacic acid was below normal values, whereas the excretion of succinic acid was unaltered. Rats, in which ketosis was provoked by hexanoic acid, had preketotic high urinary excretions of adipic and succinic acids. After ketosis the excretions of succinic acid declined again whereas the excretion of adipic acid rose further, together with that of suberic acid. Moreover, when rats which were ketotic due to treatment with long-chain triacylglycerol or hexanoic acid received 500 mg of adipic acid the urinary excretion of succinic acid rose significantly. However, no changes in succinic acid excretion were seen in diabetic ketotic rats treated with the same amount of adipic acid. Exogenously administered adipic acid was strongly antiketogenic towards ketosis caused by long-chain or short-chain monocarboxylic acids, but had no effect on diabetic ketosis.

Acidosis↗
PubMed2001

Peritoneal dialysis in an infant with type 1 diabetes and hyperosmolar coma.

Hyperosmolar coma which is characterized by severe hyperglycemia in absence of chetosis is very rare in pediatric age with only 11 cases reported in the literature. The outcome of the condition is usually poor with mental retardation being the most common event. Here a case of hyperosmolar coma is described in a female of three months of age who was treated with peritoneal dialysis 11 hours after admittance to hospital. This female patient has been receiving insulin from three months of age and today at the age of 10 years she leads a normal life despite being on insulin therapy. A very low level of C-peptide (<0.3 ng/ml) clearly confirms she is affected by Type 1 diabetes. To our knowledge this is the first case report of hyperosmolar coma in a neonate with Type 1 diabetes who survived this condition without late neurological consequences.

Acidosis, Lactic↗
PubMed1979

Stopping phenformin treatment in a diabetic clinic.

Phenformin was stopped in 35 patients attending a diabetic clinic. In 4 patients where phenformin alone had been used, subsequent diabetic control was easily maintained with diet or a sulphonylurea. Thirty-one patients had been taking phenformin with a sulphonylurea and 17 (55%) later required insulin. Larger doses of a sulphonylurea were usually needed in the other patients. It is suggested that metformin is probably the biguanide of choice now and should be considered in carefully selected diabetics.

Acidosis↗
PubMed2004

Do risk factors for lactic acidosis influence dosing of metformin?

BACKGROUND: Metformin is commonly prescribed to treat type 2 diabetes mellitus, however it is associated with the potentially lethal condition of lactic acidosis. Prescribing guidelines have been developed to minimize the risk of lactic acidosis development, although some suggest they are inappropriate and have created confusion amongst prescribers. The aim of this study was to investigate whether metformin dose was influenced by the presence of risk factors for lactic acidosis. METHODS: The study was prospective, and retrieved information from patients admitted to hospital who were prescribed metformin at their time of admission. RESULTS: Eighty-three patients were included in the study, 60 of whom had a least one risk factor for lactic acidosis. Of those 60 patients, 78.3% had a dose adjustment, with renal impairment, hepatic impairment, surgery and use of radiological contrast media--the risk factors most likely to result in a dose adjustment. When dose adjustments did occur, metformin was withheld on 88.7% of occasions. CONCLUSION: Metformin dose was influenced by the presence of risk factors for lactic acidosis, although it was dependent upon the number and particular risk factor/s present.

Acidosis, Lactic↗
PubMed1982

Ventilatory response in patients with acute lactic acidosis.

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.

Acidosis↗