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At least 1,117 records · Page 62Linked to original sources
PubMed2004

A pilot study of mitochondrial DNA point mutation A3243G in a sample of Croatian patients having type 2 diabetes mellitus associated with maternal inheritance.

In this work, patients having type 2 diabetes mellitus and diabetic mothers were tested for the presence of mitochondrial DNA point mutation A3243G. This mutation is associated with the MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), diabetes and deafness. Twenty-two diabetic persons were screened. DNA was isolated from peripheral blood lymphocytes and from swabs of oral mucosa. The mitochondrial DNA point mutation A3243G was detected using PCR-RFLP test. The mutation was detected in oral mucosal DNA of two patients (but not from lymphocyte DNA). One patient was a man with hearing and visual impairments and proteinuria; the other was a woman having proteinuria but no hearing impairment. The mutation was not detectable in oral mucosal DNA from the control persons: 20 diabetic patients having diabetic fathers and 22 healthy, nondiabetic volunteers. The incidence of mitochondrial DNA point mutation A3243G in this study of Croatian diabetic patients is in line with data in the literature.

Adenine↗
PubMed1981

Buformin concentrations in a case of fatal lactic acidosis.

A fatal case of lactic acidosis in a 84 year old diabetic woman taking buformin is reported. Buformin concentrations in serum, other body fluids and tissues were measured by gas chromatography. Serum buformin concentration at admission was 5.5 mg/l. Postmortem concentrations were: in serum 3.2 mg/l; in lung 2.8 mg/kg wet weight; in heart 3.0 mg/kg; in pericardial fluid 3.5 mg/l; in liver 5.2 mg/kg; in bile 6.3 mg/l; and in kidney 98 mg/kg.

Acidosis↗
PubMed1983

Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction.

Three Basenji dogs with renal tubular dysfunction were studied. Hyposthenuria and diminished urine concentrating ability, indicative of nephrogenic diabetes insipidus, were documented. Metabolic acidosis, hyperchloremia, and reduction in glomerular filtration rate also were detected in all dogs. In addition, an exaggerated response to the adrenocorticotropin test and hyperaldosteronism, believed to be secondary to decreased effective circulating blood volume, were detected in all 3 dogs. Thyroxine values were decreased in all dogs and could be correlated with histopathologic changes of the thyroid gland in 2 dogs. Gastropathy and hypergastrinemia were identified in 2 dogs. Diffuse lymphocytic-plasmacytic enteritis was evident in 2 dogs. It was concluded that a urine concentrating defect that may be secondary to hypercortisolism exists in Basenji dogs with renal tubular dysfunction.

Animals↗
PubMedDate not supplied

[Erythropoietin as a marker of perinatal risk].

The purpose of this study was to estimate if the erythropoietin (EPO) concentration in cord arterial blood can be an indicator of a fetal risk. We studied EPO concentration measured by enzyme immonoassay in ten patient groups: (1) control group with healthy newborns (n = 72); (2) neonates born by elective caesarean section (n = 16); (3) newborns with acidosis at birth (n = 12); (4) newborns with 1-min-Apgar < 7 (n = 8); (5) preterm neonates (n = 25); (6) newborns with gestational age > or = 242 weeks (n = 19); (7) neonates born to mothers with hypertension (n = 16); (8) newborns with signs of fetal distress in CTG (n = 29); (9) neonates born to mothers with diabetes (n = 19), divided into two subgroups: diabetes White A-D (n = 8) and gestational diabetes (n = 11); (10) neonates born to mothers with diabetes White A-D and with acidosis at birth (n = 7). The geometric mean was 26.4 mU/ml in the control group. EPO levels was found significantly increased (p < 0.01) in the following groups: (3) newborns with acidosis (52 mU/ml); (6) newborns with gestational age > or = 242 weeks (63.5 mU/ml); (8) newborns with signs of fetal distress in CTG (47.1 mU/ml); (9) neonates born to mothers with diabetes White A-D (47.7 mU/ml); (10) neonates born to mothers with diabetes White A-D and with acidosis at birth (> 64 mU/ml). We came to the conclusion that the cord arterial EPO concentration indicates a chronic fetal hypoxia and a longer duration of hypoxia before birth.

Adult↗
PubMed1987

Extreme metabolic acidosis. Case report.

A 42-year-old male patient, who suffered from insulin-dependent diabetes mellitus (IDDM) and intolerance of lactose, presented with extreme metabolic acidosis (lactic acidosis). On arrival, an arterial blood sample showed: pH 6.79, PO2 18.8 kPa, PCO2 0.9 kPa, base excess-33 mmol l-1, blood glucose 38 mmol l-1 and oesophageal temperature 30 degrees C. Apart from the uncontrolled hyperglycaemia, a fluid balance disorder elicited by diarrhoea and disturbed tissue perfusion were possible aetiological factors. The patient was treated with a low-dose insulin regimen and infusion of isotonic sodium bicarbonate with a satisfactory result.

Acidosis↗
PubMedDate not supplied

[Semi-automatic determination of blood lactate in the newborn infant of the insulin-dependent diabetic mother].

Blood lactate levels were determined by Lactate Analyzer 640 Kontron in 5 infants of diabetic mothers with pregestational insulin-dependent-diabetes, class B-C-D White, BPSP negative, in strict glycemic control all along the pregnancy. In the mothers blood lactate was found in a normal range after-delivery. In the absence of complications, the neonate of diabetic mother did not show blood lactate changes above the normal range. As well as in the neonate of non diabetic mother, blood lactate increases were found only in concomitance with respiratory acidosis. In the cases with favourable course, lactate values above 2 mmol/l were normalized in the first 24 hours after the birth. The semiautomatic determination of blood lactate supplies a good prognostic evaluation of the association between metabolic and respiratory acidosis in the neonate and should therefore be routinely used in centers for management of diabetic pregnancy.

Acidosis↗
PubMed2000

[Metformin associated lactic acidosis--case reports and literature review].

BACKGROUND: The use of metformin in the treatment of diabetes mellitus type II is increasing. The drug has several advantageous metabolic effects, and is considered safe if not used in the presence of contraindications, in particular renal failure. MATERIAL AND METHODS: We present a patient with metformin associated lactic acidosis, to remind of a potentially lethal adverse reaction. We also review the literature about incidence and risk, prognosis and treatment of the disease. RESULTS: Our patient was a 72 year old woman with diabetes mellitus type II treated with metformin, who presented with acute renal failure, severe metabolic acidosis and circulatory failure. Treatment with bicarbonate buffer and vasopressors did not improve her condition, only after hemodialysis was her situation stabilised. INTERPRETATION: Metformin associated lactic acidosis must be considered in obscure metabolic acidosis in diabetic patients. The single most important therapeutic approach appears to be immediate hemodialysis.

Acidosis, Lactic↗
PubMed1985

Metformin and the sulphonylureas: the comparative risk.

A review of the world literature until December 1982 revealed 843 cases of sulphonylurea-induced hypoglycaemia (SIH) with a mortality of 9%. There were 42 cases of metformin-associated lactic acidosis (MALA) with 18 deaths (43%); 40 of the MALA cases had documented contra-indications, especially renal impairment, and the remaining two cases were due to drug overdosage, one being a suicide. A comparative mortality risk was obtained from the Swedish Adverse Drug Reactions Advisory Committee (SADRAC) where there is accurate information regarding MALA and glibenclamide-associated hypoglycaemia. The calculated mortality risk for MALA and glibenclamide-associated hypoglycaemia showed no significant differences with values of 0.0240 and 0.0332 per 1,000 patient years, respectively. The incidence of hypoglycaemia with glibenclamide was greater than that of lactic acidosis associated with metformin (2p = 0.036). Sulphonylureas are not less dangerous than metformin and both groups of drugs should be used with care in non-insulin-dependent diabetics, especially in alderly subjects and those with impaired renal or hepatic function.

Acidosis↗
PubMed2004

[Factors affecting C-peptide level during the first year of type 1 diabetes in children].

BACKGROUND: C-peptide level is the most reliable factor evaluating the endogenous insulin secretion in patients with type 1 diabetes. OBJECTIVES: The aim of the study was to investigate whether the age at onset, gender, presence of autoantibodies and ketoacidosis at diagnosis and insulin requirement, HbA1c levels could be applied to predict the C-peptide levels in the first year of type 1 diabetes in children. MATERIAL AND METHODS: 122 type 1 diabetic children, aged: 2-18 years (average 11.2), 44 female and 78 male were studied. Fasting C-peptide levels were examined by radioimmunoassay at diagnosis, after 10 days and after 1, 2, 3, 6 and 12 months of disease. At diagnosis islet cell antibodies (ICA) were detected by indirect immunofluorescence, antibodies to glutamic acid decarboxylase (GADA) and tyrosine phosphatase antibodies (IA2A) were measured by microradioimmunoprecipitation assay. RESULTS: Age at onset was positively correlated to C-peptide levels at each evaluated point of the disease (r=0.3-0.46, p<0.0001). One year after diagnosis C-peptide levels decreased in ICA(+) (p<0.04) and GADA(+) (p<0.002) patients but not in ICA(-) or GADA(-) children. There was no significant difference between the IA2A-positive and negative subjects in the C-peptide levels at 12th month of disease. C-peptide level was also related to ketoacidosis at diagnosis, insulin requirement and HbA1c levels during the first year of type 1 diabetes. Logistic regression analysis showed that male, younger age, low pH, higher HbA1c and insulin requirement at onset were associated with decreased C-peptide level at diagnosis (p<0.00002). CONCLUSIONS: Young age, presence of diabetes-related autoantibodies and hyperglycaemia with severe acidosis at the disease onset may be associated with a decreased residual insulin secretion in type 1 diabetes in children.

Adolescent↗
PubMed1992

Biguanide-associated lactic acidosis. Case report and review of the literature.

PURPOSE: The biguanides are a class of oral hypoglycemic agents that are commonly used in the treatment of diabetes mellitus. Such agents include metformin, phenformin, and buformin. The use of phenformin was discontinued in the United States in 1976 because of probable association with lactic acidosis. However, metformin is currently in common use in many parts of the world. In this report, we describe a patient with severe lactic acidosis secondary to metformin administration, and review the literature relevant to biguanide-associated lactic acidosis. PATIENT: We describe a diabetic man with end-stage renal failure and diabetes mellitus who was hospitalized with life-threatening lactic acidosis (lactate, 10.9 mmol/L). Unbeknownst to the hospital staff, he was being treated with metformin, which had been prescribed in Indonesia. RESULTS: Arterial blood gas analysis revealed a pH of 6.76 and a bicarbonate level of 1.6 mmol/L prior to treatment. Following therapy, which included oxygen, volume expansion, other supportive therapy, and hemodialysis, the patient completely recovered and was discharged from the hospital. CONCLUSIONS: Lactic acidosis can complicate biguanide therapy in diabetic patients with renal insufficiency. We review the literature relevant to the pathogenesis and therapy of biguanide-associated lactic acidosis. Physicians who have completed their training after 1976 may not be familiar with metformin and other biguanides, but with the increasing numbers of immigrants to the United States, physicians should be aware of the potential complications of these medications.

Acidosis, Lactic↗
PubMed1996

Clinical significance of glycosylated haemoglobin (HbA1C) over fasting blood sugar for monitoring metabolic control in diabetic patients with or without complications.

Glycosylated haemoglobin was studied in 30 cases of mild to severe diabetes in the age group 12-60 years. Ten patients were keto-acidotic. Glycosylated haemoglobin and fasting blood sugar levels were studied in patients with various complications of diabetes like neuropathy, nephropathy, retinopathy, keto-acidosis, cardiac and respiratory complications. There was a significant correlation between fasting blood sugar and glycosylated haemoglobin in normal subjects as well as in diabetic patients. There was a significant correlation between levels of glycosylated haemoglobin and blood sugar over preceding 4-6 weeks. Most frequent complication being retinopathy and keto-acidosis was associated with maximum glycosylated haemoglobin with poor metabolic control.

Adolescent↗
PubMed2001

Metformin-associated lactic acidosis.

In 1995, the oral antihyperglycemic agent, metformin, was introduced in the United States for treating diabetes mellitus. Rare cases of metformin-associated lactic acidosis caused by the accumulation of the drug in patients with renal dysfunction have been described, although a detailed time course of the resulting metabolic derangements has not been reported. A case of metformin-associated lactic acidosis is presented along with key serial laboratory abnormalities observed during the treatment phase. The patient made a complete recovery following therapy with hemodialysis and supportive care.

Acidosis, Lactic↗
PubMed1987

Dichloroacetate derivatives. Metabolic effects and pharmacodynamics in normal rats.

Dichloroacetate (DCA) reduces blood glucose, lactate and lipids in diabetes or during fasting. Chronic use of DCA, however, is limited by toxicity, probably due in part to its rapid conversion to oxalate in vivo. In theory, therefore, DCA's efficacy may be retained and its toxicity minimized by controlling its rate of metabolism. We attempted to alter DCA pharmacokinetics and bioavailability by synthesizing various derivatives comprising DCA esters with polyols and DCA ionic complexes. Twenty-four hour fasted, nondiabetic rats received single, orogastric doses of saline (control) sodium DCA (100mg/kg) or the following derivatives (D1-4): the esters D1-D3: potassium tetra (dichloroacetyl) glucuronate (D1), inositol-monophosphate-tetradichloroacetate (D2), inositol-hexadichloroacetate (D3) and inositol-hexa [N-methylnicotinate] hexadichloroacetate salt (D4). Each derivative was administered at a dose that would ultimately provide 100 mg/kg DCA as the anion. All derivatives were orally effective in significantly decreasing blood glucose and lactate. D4 exerted the most potent and long-lasting glucose- and lactate-lowering effects, yet increased plasma DCA concentrations less than an equivalent dose of the sodium salt. When administered to reverse light-cycled rats, D4 markedly inhibited the incorporation of tritiated water into cholesterol and triglycerides. We conclude that derivatives of DCA retain the biological activity of the parent compound, but may exhibit different pharmacokinetics. They may eventually prove useful in the treatment of diabetes mellitus, hyperlipidemia and lactic acidosis in man.

Acetates↗