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At least 1,513 records · Page 84Linked to original sources
PubMed2001

An 80-year-old mitochondrial disease patient with A3243G tRNA(Leu(UUR)) gene presenting cardiac dysfunction as the main symptom.

MELAS is characterized by mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, but cardiac involvement also frequently occurs. An 80-year-old female patient had been suffering from insulin-dependent diabetes mellitus and neurosensory hearing loss. At the age of 79 she suffered metabolic acidosis with persistent drowsiness and was subsequently found to have severe cardiac dysfunction. Muscle biopsy disclosed the presence of abnormal mitochondria, and the MELAS gene mutation (A3243G of the tRNA(Leu(UUR))) was demonstrated. It is noteworthy that this mitochondrial disease patient has survived until a great age, which shows the wide clinical spectrum of MELAS, especially in the age of onset.

Aged↗
PubMed1980

Fatal coma in diabetes.

Analysis of causes of death in a population of 3,113 diabetics was carried out for a period of eight years and those patients dying of some form of diabetic coma identified. Of 1,274 deaths, only 22 (1.73%) were primarily due to coma; 7 hypoglycaemia, 8 ketoacidosis, 3 hyperosmolar coma and 4 lactic acidosis. Three of the ketoacidosis patients may have died from other causes. Most deaths occurred in patients with long-standing diabetes. In the hypoglycaemic group all were on insulin and several had been difficult to control for many years. Infection was an important precipitating factor for ketoacidosis and hyperosmolar coma. Phenformin was the cause of all cases of fatal lactic acidosis. It is reassuring that death from coma is a comparatively rare event in known treated diabetic patients.

Adult↗
PubMedDate not supplied

[Heart failure caused by myocardial hypertrophy in diabetic fetopathy].

Diabetic fetopathy is still a common clinical problem correlated with a high morbidity of the neonate. These children are often macrosome, suffer from respiratory distress syndrome due to delayed lung maturity, acidosis, hypoglycaemia, electrolyte-imbalances and polycythaemia. We describe a male neonate with diabetic fetopathy as a result of gestational diabetes of the mother. In addition to the symptoms described above, our patient clinically presented with severe hypertrophy of the right ventricle associated with intrauterine heart failure. The boy was born with serious prenatal asphyxia which made initial neonatal intensive care treatment necessary. The hypertrophic cardiomyopathy normalized within 6 weeks after birth without further treatment. Different causes of a hypertrophic cardiomyopathy (infections, metabolic disorders, neurologic affections, syndromes) could be ruled out, so that the diabetic fetopathy was the most probable cause for the condition. If we are looking at the heart only, this case-report suggests a good prognosis of septumhypertrophy as well as right ventricular hypertrophy in patients with diabetic fetopathy. The case also elucidates that not only the diabetes type I can entail serious fetal damage but also gestational diabetes can. Therefore, in suspect mothers screening for gestational diabetes should be expanded to oral glucose tolerance testing.

Adult↗
PubMed1979

Metformin: a review of its pharmacological properties and therapeutic use.

In a survey, the pharmacological and clinical documentation of metformin is presented and discussed, and the present state of knowledge relating to metformin-associated lactic acidosis is reviewed. The use of metformin in the treatment of diabetes is based on clinical experience over twenty years. It has been well documented that metformin is effective in maturity-onset diabetes both as monotherapy and in combination with a sulphonylurea. An advantage of metformin treatment is the tendency to weight reduction and the absence of significant hypoglycaemia; blood glucose levels are reduced only to normal. The disadvantages are the gastro-intestinal side effects and the potential risk of vitamin B 12 and folic acid deficiency during long-term use. Metformin-associated lactic acidosis is a very rare complication, which has mainly occured in patients with serious renal insufficiency or other contra-indications to the use of metformin. The association between phenformin and lactic acidosis has led to withdrawal of this biguanide in several countries. Metformin differs from phenformin in certain important respects, and the normal use of metformin does not involve the risk of side effects disproportionate to the intended effect. Further experimental studies are required to substantiate pharmacokinetics and metabolic effects of metformin in man.

Animals↗
PubMed2005

Improved clinical outcomes associated with metformin in patients with diabetes and heart failure.

OBJECTIVE: Metformin is considered contraindicated in patients with heart failure because of concerns over lactic acidosis, despite increasing evidence of potential benefit. The aim of this study was to evaluate the association between metformin and clinical outcomes in patients with heart failure and type 2 diabetes. RESEARCH DESIGN AND METHODS: Using the Saskatchewan Health databases, 12,272 new users of oral antidiabetic agents were identified between the years 1991 and 1996. Subjects with incident heart failure (n = 1,833) were identified through administrative records based on ICD-9 code 428 and grouped according to antidiabetic therapy: metformin monotherapy (n = 208), sulfonylurea monotherapy (n = 773), or combination therapy (n = 852). Multivariate Cox proportional hazards models were used to assess differences in all-cause mortality, all-cause hospitalization, and the combination (i.e., all-cause hospitalization or mortality). RESULTS: Average age of subjects was 72 years, 57% were male, and average follow-up was 2.5 +/- 2.0 (SD) years. Compared with sulfonylurea therapy, fewer deaths occurred in subjects receiving metformin: 404 (52%) for sulfonylurea monotherapy versus 69 (33%) for metformin monotherapy (hazard ratio [HR] 0.70 [95% CI 0.54-0.91]) and 263 (31%) for combination therapy (0.61 [0.52-0.72]). A reduction in deaths or hospitalizations was also observed: 658 (85%) for sulfonylurea monotherapy versus 160 (77%) for metformin monotherapy (0.83 [0.70-0.99]) and 681 (80%) for combination therapy (0.86 [0.77-0.96]). There was no difference in time to first hospitalization between study groups. CONCLUSIONS: Metformin, alone or in combination, in subjects with heart failure and type 2 diabetes was associated with lower morbidity and mortality compared with sulfonylurea monotherapy.

Aged↗
PubMed2001

Clozapine-associated diabetes.

Clozapine is a potent antipsychotic agent that has been marketed since 1990. Several published reports of diabetes mellitus occurring with clozapine therapy have appeared during the past 5 years. Because the risk and characteristics of clozapine-associated diabetes mellitus remain unclear, we conducted a descriptive epidemiologic study of spontaneous adverse event reports of hyperglycemia occurring in clozapine-treated patients. The Food and Drug Administration MedWatch surveillance program was queried (January 1990 through February 2001), and the results were pooled with published cases. Parameters assessed included documentation of diabetes, clinical severity, new-onset diabetes versus exacerbation of preexisting disease, demographic characteristics of patients, time to onset of hyperglycemia, and effect of drug discontinuation and rechallenge. We identified 384 reports. Of these, new-onset diabetes was diagnosed definitively in 242 patients, and 54 patients had exacerbation of preexisting disease. The mean (+/- SD) age was 40 +/- 12 years (range, 13 to 77). The male:female ratio was 2:0. Most cases appeared within 6 months of initiating clozapine therapy. One patient developed diabetes following a single 500-mg dose. There were 80 cases of metabolic acidosis or ketosis. Twenty-five patients died during hyperglycemic episodes. Forty-six patients had improved glycemic control after discontinuation or dose reduction of the drug.A causal relationship between clozapine and diabetes is suggested by the number of reports, the temporal relation to clozapine initiation, the relatively young age of the affected patients, and the prompt reversibility on withdrawal of the drug in some patients. The severity of reported cases ranged from mild glucose intolerance to diabetic ketoacidosis or hyperosmolar coma.

Adolescent↗
PubMed1994

[Management of diabetes in general practice--current requirements. 2: Oral antidiabetics and insulin therapy].

Oral antidiabetic agents continue to play an important role in the treatment of type 2 diabetes. Of decisive importance is the timing of their use, together with a knowledge of their specific properties. Acarbose, which needs to be initiated at a low, slowly increasing dose, is noted for the fact that it has virtually no systemic side effects. Metformin reduces plasma glucose levels without inducing hyperinsulinemia, and carries virtually no risk of lactic acidosis. Glibenclamide can be used either alone to treat type 2 diabetes or in combination with other oral antidiabetics or insulin. Today, intensified insulin therapy represents the optimal standard of insulin replacement. It permits meal-oriented injection of normal insulin and the use of longer-acting insulin overnight. This form of treatment is now facilitated by the possibilities of plasma glucose selfmonitoring and the use of injection aids (pen). Intensified treatment should be initiated at the time type I diabetes is diagnosed. In the case of a particularly instable metabolic situation or neuropathy, it may become necessary to use insulin pumps.

Diabetes Mellitus, Type 1↗
PubMed1988

[Alcoholic ketoacidosis. An important differential diagnosis from diabetic ketoacidosis].

Ketoacidosis developed in two patients, a woman aged 36 and a man aged 55 years, 48 and 36 hours, respectively, after a bout of drinking alcohol to excess. Both were dehydrated with hyperventilation and signs of cachexia. Other findings were polydipsia, polyuria, loss of weight and (in the woman) abdominal pain. Biochemical tests revealed a marked metabolic acidosis (pH 7.00 and 7.09, respectively), base deficit of -25 and -20 mmol/l, hyperglycaemia (210 and 297 mg/dl) and hyperkalaemia (6.3 and 6.0 mmol/l). Treatment with insulin and fluids, as well as normalization of the electrolytes, brought about rapid regression of the metabolic disorder and restoration of the carbohydrate metabolism. Both patients were discharged without medication or dietary prescription, other than abstinence from alcohol.

Acidosis↗
PubMed1995

Diabetic ketoacidosis.

This article reviews the pathogenesis of diabetic ketoacidosis (DKA) and provides a rational approach to the management of patients with DKA. The therapeutic discussion includes the use of low-dose insulin, no bicarbonate, or phosphate therapy on the majority of DKA patients, based on numerous prospective randomized studies. The article also discusses controversial subjects such as the use of hypotonic versus isotonic saline with and without colloids, hydration of subjects before insulin therapy, and admission of DKA patients to the general ward versus emergency ward versus intensive care unit. A concise, simple protocol is also presented as a suitable reference for management of patients with DKA.

Acidosis↗
PubMed1997

Pathophysiology of central nervous system complications in diabetes mellitus.

It is now generally accepted that diabetes can alter central nervous system (CNS) function. Even in the absence of overt cerebrovascular accidents or repeated hypoglycemic reactions, uncontrolled hyperglycemia is associated with cognitive changes. These changes are documented both in patients with diabetes as well as in animal models of experimental diabetes. The cognitive impairment can be ameliorated with optimization of blood glucose control. The potential causes of CNS dysfunction in diabetes can be broadly categorized as either vascular causes including changes in the blood-brain barrier and metabolic changes. The latter causes include repeated hypoglycemic episodes, hyperglycemia, hyperosmolality, acidosis, ketosis, neuroendocrine or neurochemical changes. The other contributory causes of CNS dysfunction in diabetes include the presence of hypertension, uremia, peripheral and autonomic neuropathy and multiple drug use.

Blood-Brain Barrier↗
PubMed2000

Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family.

The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnosed with chronic pancreatitis with pancreatic calcifications and pancreatic duct dilation, although she was completely asymptomatic and with no signs of steatorrhoea. She did not have gallstones and the common bile duct was normal. A possible etiopathogenic pathway for pancreatitis could be a suppressive effect of the mt 3243 mutation on the oxidative phosphorylation in affected mitochondria. Although pancreatitis and pancreatic dysfunction in association with the mt 3243 mutation, especially in patients with comorbidity of MELAS and diabetes, has previously been described as a rare manifestation, this case is specific because of the discrepancy of advanced morphological pancreatic alterations and complete lack of pancreatogenic symptoms.

Adult↗
PubMed1977

Palmitic acid concentration of amniotic fluid in diabetic pregnancy.

The fatty acid composition of total lipid and phospholipid contents was determined in the amniotic fluid of normal and diabetic pregnant patients. Disturbance of lipid metabolism which is not related to the severity of diabetes, causes difficulties in the determination of L/S ratio. The palmitic acid content of total lipid and lecithin is increased in diabetic pregnancy. The lecithin synthesis is significantly decreased as result of a transitory or prolonged acidosis.

Acidosis↗
PubMed1991

[Oxygen exchange and acid-base status in patients with diabetic angiopathy of the lower extremities with different methods of conservative treatment].

In the pathogenesis of III-IV stage diabetic angiopathy, the important place belongs to oxygen deficiency and metabolic acidosis. Introduction into the complex of treatment of the patients of hyperbaric oxygenation and endolymphatic pharmacotherapy contributes to improvement of general state of the patients, alleviation of the course of destructive processes on the extremities, rapid normalization of oxygen exchange in the organism, liquidation of the phenomena of metabolic acidosis. This results in shortening of patients' stay in a hospital and permits to avoid, or postpone performance of amputation of an extremity.

Acid-Base Equilibrium↗
PubMed1995

Diabetes mellitus carrying a mutation in the mitochondrial tRNA(Leu(UUR)) gene.

We screened 214 Japanese NIDDM (non-insulin-dependent) diabetic patients with a family history of diabetes for mutations in the mitochondrial tRNA(Leu(UUR)) gene using polymerase chain reaction-restriction fragment length polymorphism and direct sequencing. Six patients were identified as having an A to G transition at position 3243 (3243 mutation), but no patients were detected with a T to C transition at position 3271, in the mitochondrial tRNA(Leu(UUR)) gene. These two mutations were not present in 85 healthy control subjects. It was disclosed that the patients' mothers were also affected by diabetes mellitus in five of the six cases. In these six affected patients, the 3243 mutation shows variable phenotypes, such as the degree of multiple organ involvement, intrafamilial and interfamilial differences in disease characteristics, and the degree of the involvement of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) phenotype. Endocrinological examinations revealed that those diabetic patients with the 3243 mutation show not only beta-cell dysfunction, but also a defect in alpha-cell function, which is considered characteristic of diabetes with the 3243 mutation. When compared with 50 selected diabetic control subjects without the 3243 mutation, whose mothers, but not fathers, were found to have diabetes, it was established statistically that those with the 3243 mutation possess the following clinical characteristics; 1) the age of diabetes onset is lower, 2) they have lean body constitutions, and 3) they are more likely to be treated with insulin than control subjects. We suggest that diabetes with the 3243 mutation possesses phenotypes distinct from those in common forms of diabetes.

Adolescent↗