Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDOSIS, DIABETIC”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources

Sudden onset of diabetes with ketoacidosis in a patient treated with FK506/tacrolimus.

We report a 43-year-old man who presented diabetic ketoacidosis 1 year after receiving kidney transplantation. He was a recipient of renal transplantation treated with metyl-prednisolone and tacrolimus regimen. The serum level of tacrolimus was 12.4 ng/ml, and he showed hyperphagia before a month of admission. A week before admission, he was aware of polydipsia, polyuria, and general fatigue. He visited our hospital and was found to have severe hyperglycemia (925 mg/dl), significant ketosis and mild metabolic acidosis (pH 7.341), although he had not been diagnosed as diabetes mellitus. He administrated in our hospital, and was treated with insulin for 5 weeks. He was not obese (BMI = 18.2 kg/m(2)) and had no family history of type 2 diabetes. He was finally treated with diet therapy alone. The 24 h urine C-peptide secretion on the third hospital day was low (8.4 microg per day). However, no autoantibodies against pancreatic islets were positive, and his insulin secretion was recovered at discharge suggesting that he was not type 1 diabetes. Although, tacrolimus has been reported to cause or worsen diabetes mellitus, the present case suggests that it could cause severe decrease in insulin secretion which leading to diabetic ketoacidosis in lean subject without previous history of diabetes mellitus.

Adult↗

A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA.

BACKGROUND: Several families have been described in which a mutation of mitochondrial DNA, the substitution of guanine for adenine (A-->G) at position 3243 of leucine transfer RNA, is associated with diabetes mellitus and deafness. The prevalence, clinical features, and pathophysiology of diabetes with this mutation are largely undefined. METHODS: We studied 55 patients with insulin-dependent diabetes mellitus (IDDM) and a family history of diabetes (group 1), 85 patients with IDDM and no family history of diabetes (group 2), 100 patients with non-insulin-dependent diabetes mellitus (NIDDM) and a family history of diabetes (group 3), and 5 patients with diabetes and deafness (group 4) for the mutation. We also studied the prevalence and characteristics of diabetes in 39 patients with a syndrome consisting of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes who were known to have the mutation and 127 of their relatives (group 5). RESULTS: We identified 16 unrelated patients with diabetes associated with the A-->G mutation: 3 patients from group 1 (6 percent), 2 patients from group 3 (2 percent), 3 patients from group 4 (60 percent), and 8 patients from group 5 (21 percent). We also identified 16 additional subjects who had diabetes and the mutation among 42 relatives of the patients with diabetes and the mutation in groups 1, 2, 3, and 4 and 20 affected subjects among the 127 relatives of the patients in group 5. Diabetes cosegregated with the mutation in a fashion consistent with maternal transmission, was frequently (in 61 percent of cases) associated with sensory hearing loss, and was generally accompanied by impaired insulin secretion. CONCLUSIONS: Diabetes mellitus associated with the A-->G mutation at position 3243 of mitochondrial leucine transfer RNA represents a subtype of diabetes found in both patients with IDDM and patients with NIDDM in Japan.

Adolescent↗

Umbilical artery resistance index in diabetic pregnancies: the associations with fetal outcome and neonatal septal hypertrophic cardiomyopathy.

AIM: To determine the incidence of an abnormal umbilical artery resistance index (UARI) in diabetic pregnancies and the relation to fetal outcome and the development of neonatal septal hypertrophic cardiomyopathy. METHODS: A case-control study with subjects comprising 50 randomly selected diabetic mothers and a matched control group of 50 non-diabetic pregnancies. Doppler studies of the UARI were carried out at least once per week, beginning from 36 weeks' gestation for both groups. Within 48 h post delivery, echocardiograms were carried out on the newborn infants to identify those with hypertrophic cardiomyopathy, particularly asymmetrical septal hypertrophy. RESULTS: The numbers of patients with abnormal UARI were similar in both the diabetic and control groups. A higher proportion of operative deliveries for intrapartum fetal distress was seen in patients with an abnormal UARI in the diabetic group. However, the groups did not differ in the numbers of infants who were small for gestational age, who had low Apgar scores or umbilical artery acidosis, and who required admission to the special care nursery. Six infants of diabetic mothers (12%) had septal hypertrophy, but none of these were associated with abnormal antenatal UARI. CONCLUSION: Diabetic pregnancy is not associated with a significantly higher incidence of abnormal UARI on Doppler study than non-diabetic pregnancy. UARI is not a useful single indicator by which to predict subsequent fetal outcome or the development of neonatal septal hypertrophic cardiomyopathy in diabetic pregnancies.

Cardiomyopathy, Hypertrophic↗

Metformin in patients with type 2 diabetes mellitus: reconsideration of traditional contraindications.

BACKGROUND: The strict limiting criteria for the use of metformin in diabetes mellitus stem largely from reports, in the 1970s, of mortality and lactic acidosis associated with phenformin. Data about metformin are less clear and are based mainly on case reports. The aim of this study was to evaluate the safety of continued use of metformin in patients with contraindications to this agent. PATIENTS: Some 393 patients with type 2 diabetes mellitus (serum creatinine 130-220 &mgr;mol/l) were studied. Among them were 266 patients with coronary heart disease (CHD), 94 with congestive heart failure (CHF), and 91 with chronic obstructive pulmonary disease (COPD), all of whom had been treated with metformin. The patients were randomized to either continue or to stop metformin and were then followed for 4 years. RESULTS: Analysis was by intention-to-treat. The patients who stopped taking metformin showed a rise in body mass index and in hemoglobin A1c significantly greater than those who continued the drug. There were no cases of lactic acidosis. Lactic acid values did not differ in the two groups and correlated only with serum creatinine and body mass index. Microvascular diabetic complications, cardiovascular events, and cardiovascular and total mortality were identical in the two groups. CONCLUSIONS: Diabetic patients who are treated with metformin and who tolerate the drug well may continue taking it, even when mild renal impairment develops, possibly up to serum creatinine levels of 220 &mgr;mol/l. There is also no apparent reason why patients with CHD, CHF, and COPD should discontinue metformin.

Journal Article↗

Metabolic effects of glucocorticoid and ethanol administration in phenformin- and metformin-treated obese diabetics.

Glucocorticoid administration for 24 hours to phenformin-treated obese diabetics increased blood lactate and lactate/pyruvate (L/P) ratio to higher levels than those found when only one drug was given. In one of 10 subjects, a metabolic acidosis with a blood lactate of 6.2 mmol developed during simultaneous administration of the two drugs. Diabetics treated with phenformin or metformin in equipotent dosages exhibited the highest blood lactate, L/P ratio, and beta-hydroxybutyrate levels during phenformin treatment, both before and during glucocorticoid administration. Ethanol administration to biguanide-treated diabetics resulted in identical increases in blood lactate and L/P ratio during phenformin and metformin treatment. These findings are consistent with the hypothesis that phenformin has a stronger inhibitory effect of gluconeogenesis than metformin. This may be one reason why lactic acidosis is seen much more often in phenformin- than metformin-treated patients.

Aged↗

[Metformin efficacious in poorly controlled diabetes mellitus type 2].

Three patients, 1 man and 2 women, aged 60, 55 and 72 years, had an insufficient glucose regulation with insulin therapy or with sulfonylurea derivatives. They started metformin therapy, after which HbA1c decreased by 0.8-1.8%. One patient had to discontinue metformin therapy due to excessive diarrhoea. Many studies have shown the beneficial effect of metformin on glucose control. The recent UK Prospective Diabetes Study has proven the effectiveness of metformin for any diabetes related endpoint. Frequent side effects of metformin are nausea, abdominal discomfort and diarrhoea. Most side effects disappear after decreasing the dosage, although in 5% of patients diarrhoea only disappears after discontinuation of metformin. Lactic acidosis is a rare, serious adverse effect of metformin, which can be prevented by carefully observing the contra-indications.

Abdominal Pain↗

Islet cell antibodies in diabetes mellitus associated with a mitochondrial tRNA(Leu(UUR)) gene mutation.

An A3243G point mutation of the mitochondrial tRNA(Leu(UUR)) gene was detected in a Caucasian family with maternal diabetes mellitus and signs of mitochondrial dysfunction such as muscular hypotonia, encephalopathy, lactic acidosis, stroke-like episodes (MELAS), neurosensory hearing loss, cardial pre-excitation, and short stature. Low levels (10 JDF) of islet cell antibodies (ICA) in insulin-treated diabetes of the mother and impaired glucose tolerance with high levels of ICA (80 JDF) in her older son indicated that mitochondrial diabetes mellitus may involve beta cell damage. Furthermore, exocrine pancreas cell damage may also occur since the stroke-like episodes of this son were combined with pancreatitis. In all family members HLA types and plasma antioxidants were determined. Normal concentrations of hydro- and lipophilic antioxidants (including ubiquinol-10) were found.

Autoantibodies↗

Glutamine-synthesizing activity in lungs of fed, starved, acidotic, diabetic, injured and septic rats.

The maximal catalytic activity of glutamine synthetase was measured in lung homogenates of the rat (being 5.46 +/- 0.29 mumol/min per g wet wt. or 31.70 +/- 2.62 nmol/min per mg of protein at 37 degrees C, in fed animals). The activity is similar to that of liver, but 16-fold higher than that in quadriceps muscles. Chronic (NH4Cl-induced) or acute (HCl-induced) metabolic acidosis had no effects on enzyme activity, but there was a marked increase in the activity of glutamine synthetase in starved (30-40%), streptozotocin-diabetic (17%), dexamethasone-treated (18-22%), laparotomized (25-27%) and septic rats (24-45%).

Acidosis↗

[Lactic acidosis].

Lactic acidosis is a metabolic disturbance characterized by an increase of the production/clearance ratio of lactate. Lactate is a catabolite of glycolysis when this takes place under anaerobic conditions. Clinically LA is characterized by: signs of acidosis, venous blood lactate greater than 5 mMol/l, arterial pH less than 7.25. LA is classified in type A, due to shock, and type B which, in turn, can be divided according to its pathogenesis in B1 correlated to particular pathologies, B2 due to exogenous substances and B3 caused by congenital metabolic diseases. LA is of particular interest in type II diabetes mellitus treated by phenformin. Current therapeutic directions, although suboptimal, are: to eliminate the causes of lactate hyperproduction by maintaining a sufficient efficiency of the cardio-vascular apparatus, to correct acidosis by using alkalinizing solutions, to remove pharmacologically or by dialysis the excess of lactate.

Acidosis↗

Insulin resistance in patients with the mitochondrial tRNA(Leu(UUR)) gene mutation at position 3243.

UNLABELLED: The point mutation at position 3243 of the tRNA Leu(UUR) of the mitochondrial DNA is associated with mitochondrial encephalomyopathy, lactic acidosis and strokes (MELAS) as well as with mitochondrial diabetes and deafness (MIDD). A defect in insulin secretion has been found in most of these patients. However, there have been controversial findings to which extent insulin resistance contributes to pathogenesis. The aim of the present investigation was to study the insulin sensitivity index (SI), insulin secretion (AIR(Glucose)) and glucose effectiveness (Sg) in patients with the 3243-mutation. MATERIAL AND METHODS: 7 patients of a large pedigree (some of the members who were not investigated had MELAS) and 3 siblings of another family in whom the 3243-mutation had been detected, as well as 23 non-related, healthy control subjects underwent a modified intravenous glucose tolerance test (Bergman's minimal model). In addition, a screening of islet cell antibodies (ICA) was performed. RESULTS: All patients except for one with known diabetes mellitus revealed normal glucose tolerance. There was no difference between patients and controls for SI, AIR(Glucose) or Sg. However, when looking at the individual results, there were 4 closely related members of the large family with very poor insulin sensitivity. The other 2 patients of this pedigree were more distantly related and extremely insulin sensitive. The siblings of the other family revealed normal or even a very good insulin sensitivity. In one patient, ICA were detected. CONCLUSIONS: The 3243-mutation does not seem to be causative for insulin resistance in our patients. Whether nuclear genes are involved and indirectly influence the expression of the 3243-mutation or, more likely, directly lead to impaired insulin sensitivity in some of our patients cannot be answered by our data. It remains open whether there is a difference in the pathogenesis of diabetes between patients with MIDD and those with MELAS.

Female↗

Modification defect at anticodon wobble nucleotide of mitochondrial tRNAs(Leu)(UUR) with pathogenic mutations of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.

The mitochondrial tRNA(Leu)(UUR) (R = A or G) gene possesses several hot spots for pathogenic mutations. A point mutation at nucleotide position 3243 or 3271 is associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes and maternally inherited diabetes with deafness. Detailed studies on two tRNAs(Leu)(UUR) with the 3243 or 3271 mutation revealed some common characteristics in cybrid cells: (i) a decreased life span, resulting in a 70% decrease in the amounts of the tRNAs in the steady state, (ii) a slight decrease in the ratios of aminoacyl-tRNAs(Leu)(UUR) versus uncharged tRNAs(Leu)(UUR), and (iii) accurate aminoacylation with leucine without any misacylation. As a marked result, both of the mutant tRNA molecules were deficient in a modification of uridine that occurs in the normal tRNA(Leu)(UUR) at the first position of the anticodon. The lack of this modification may lead to the mistranslation of leucine into non-cognate phenylalanine codons by mutant tRNAs(Leu)(UUR), according to the mitochondrial wobble rule, and/or a decrease in the rate of mitochondrial protein synthesis. This finding could explain why two different mutations (3243 and 3271) manifest indistinguishable clinical features.

Anticodon↗

Progressive nephropathy associated with mitochondrial tRNA gene mutation.

Mitochondrial DNA plays a crucial role in oxidative production of energy. Thus, defects in mitochondrial DNA can affect virtually all organ systems. The point mutation A --> G at position 3243 in the mitochondrial tRNAleu(UUR) gene is the cause of several distinct types of mitochondrial cytopathy and several clinical phenotypes, including encephalomyopathy with lactic acidosis and stroke-like episodes and maternally inherited diabetes and deafness. This mutation has been recently described also in association with kidney disease, mainly focal and segmental glomerulosclerosis. At present, little is known about the prevalence of this mitochondrial nephropathy, its clinical course and the pathogenesis of glomerular damage. We describe 2 unrelated patients, who presented with proteinuria and progressed to end-stage renal failure. Other clinical features were short stature, severe headache, hearing loss, diabetes mellitus and hypertrophic cardiomyopathy. The main histological finding was an increased number of abnormal mitochondria in tubular cells and podocytes. Analysis of mitochondrial DNA from leukocytes and urine sediment revealed heteroplasmy for the A3243G mutation in tRNAleu(UUR) gene in both patients. Recognition of the characteristic clinical and histological features of the mitochondrial A3243G mutation-associated glomerulopathy will enable correct diagnosis and better management of a disease which is likely to be underdiagnosed.

Adult↗

Non-diuretic-based antihypertensive therapy and potassium homeostasis in elderly patients.

Aging and hypertension are associated with a progressive decline in renal blood flow and renal function. As a result, physicians planning therapeutic strategies to control blood pressure need to consider these changes and how they relate to potassium homeostasis, particularly in elderly patients. Commonly used antihypertensive drugs such as beta-blockers, angiotensin converting enzyme inhibitors and potassium-sparing diuretics need to be used with increasing caution in patients with declining renal function. This is especially important in patients with diabetes who may also have type IV renal tubular acidosis, and in patients given concomitant therapy with non-steroidal anti-inflammatory drugs. Other therapies such as calcium channel blockers, particularly those that gate atrioventricular nodal conduction, also need to be used with care in people with significant renal insufficiency and hyperkalemia, as this clinical scenario may result in a greater risk of complete heart block.

Aged↗

Heterogeneous phenotypes of mitochondrial encephalomyopathy in a single kindred.

Five patients with mitochondrial disorders in a single family showed marked heterogeneity of clinical signs and symptoms. Two patients had the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes; one had blepharoptosis, seizures, and diabetes insipidus; and two had a nonspecific encephalomyopathic disorder. This family supports the concept of a "mitochondrial cytopathy."

Acidosis, Lactic↗

Skeletal carbon dioxide stores during metabolic acidosis.

These experiments were performed to examine the buffering functions of skeletal carbon dioxide during metabolic acidosis. Acidosis of several days duration was produced in rats either by inclusion of acidogenic substances in the diet or by chemical induction of diabetic ketoacidosis. Titrimetric methods were used to measure the carbon dioxide content of bone, which was divided into readily exchangeable and slowly exchangeable pools according to a model described in the text. Acid feeding resulted in a mild acidemia (blood pH greater than 7.25), whereas profound metabolic acidemia occurred during diabetic ketoacidosis (blood pH less than 7.00). Total bone carbon dioxide was reduced during both forms of metabolic acidosis. This reduction in skeletal carbon dioxide occurred within the first 24 h after the onset of metabolic acidosis, was associated with a decline in the readily exchangeable fraction of skeletal carbon dioxide, and was directly proportional to the declines in extracellular bicarbonate concentration and plasma carbon dioxide tension.

Acidosis↗

[Care of pregnant diabetic patients--results and problems].

This is a report on results and problems in taking care of pregnant diabetics in the delivering center Leipzig with special regard of women with a gestational diabetes. In the period between 1971 and 1983 a total of 314 patients were treated with manifest diabetes or a gestational diabetes. We investigated in with manifest diabetes or a gestational diabetes. We investigated in non-selected cases the morbidity of children and the perinatal mortality. The evaluation took into consideration among others the quality of metabolic guidance, the possible causes of perinatal mortality and the therapeutical indications in gestational diabetes. Depended on the changed concept of the care system we considered separately the results of two periods (first period: 1971 until 1978, 136 deliveries; second period: 1979 until 1983, 178 deliveries). We could demonstrate that a complex interdisciplinary care system can reduce the perinatal mortality and morbidity. But it is necessary to diagnose patients with a gestational diabetes earlier than actually usual.

Acidosis↗