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 1,603 records · Page 89Linked to original sources
PubMed1987

Ketosis, serum carnitine and its precursor amino acids in normal and diabetic ethiopians.

In a hospital-based study in northwestern Ethiopia some clinical and biochemical features of diabetes mellitus have been assessed to contribute to the problem of classification of diabetes in a tropical country. Diabetes requiring primary insulin treatment is presented by unequivocally elevated blood glucose levels and the classic symptoms of the disease. Newly discovered cases and readmitted rural diabetics show significantly lower body mass indices and 31% have been classified as underweight. The overall frequency of ketonuria at (re)admission was 45% together with moderately elevated or high 3-hydroxybutyrate serum concentrations. The hormonal status is characterized by a reduced beta-cell function. Serum concentrations of all carnitine fractions are lower in both normal and diabetic Ethiopians when compared with Caucasoids. Carnitine precursor amino acids are normal and the complete amino acid spectrum reveales no clear-cut pattern related to protein-energy malnutrition.

Acidosis↗
PubMed2006

[Nephrotoxicity after the use of intravenous X-ray contrast media in a type 2 diabetic being treated with metformin].

Contrast media may induce nephrotoxicity, particularly in elderly patients with pre-existing renal impairment. The concomitant use of metformin may lead to lactic acidosis due to metformin accumulation. Thus, metformin should be discontinued prior to use of contrast media. We observed acute renal failure requiring haemodialysis in a 74-year-old man with non-insulin-dependent type II diabetes. The man had had an intravenous urography to examine an increased plasma creatinine level, and metformin had not been discontinued. We report the case to remind doctors of this avoidable side effect.

Acidosis, Lactic↗
PubMed2004

[Emergency landing due to a passanger with chest pain, dyspnea, and vomiting].

A 20-year old student had suffered since 3 years from diabetes mellitus type I, which was well-controlled by insulin-pump therapy. During a flight from Moscow to Los Angeles, the student all of a sudden had chest pain, dyspnea, and he vomitted repetitively--emergency landing at Zurich airport was necessary. The student presented at the emergency unit in a poor general condition with tachypnea (32/min) and tachycardia (136/min). Arterial blood gas analysis showed severe metabolic acidosis (pH 7.04), while pulmonary or cardiac disease could be ruled out. Diabetic ketoacidosis was caused by the pump running short of insulin. Treatment included rehydration and administration of insulin. Administration of insulin by an insulin-pump allows to continuously and flexibly adjust the dosage according to the requirement of the body. Interruption of insulin administration can cause, however, relatively fast ketoacidosis because exclusively short-acting insulin is used.

Adult↗
PubMed1994

Sympathetic-adrenergic activity and acid-base regulation under acute physical stress in type I (insulin-dependent) diabetic children.

To evaluate the efficacy of the acute-physical-stress response, plasma catecholamine and lactate levels, serum electrolytes, fructosamine, blood glucose and acid-base status were measured in insulin-dependent diabetes mellitus (IDDM) children and the data compared to those of healthy controls. Four groups were studied: group 1, healthy controls; group 2, newly diagnosed diabetic patients with an IDDM duration of 2-4 weeks; group 3, with an IDDM duration of 5-7 years; group 4, with an IDDM duration of 10-13 years. According to their fructosamine levels, IDDM children were in a well-controlled metabolic state. The physical stress was induced by 1.5-1.7 W/kg/10 min bicycle ergometer determined by a target pulse rate of 170/min. IDDM children exhibited pronounced lactic acidosis under stress (pH: group 2, 7.27 +/- 0.07; group 3, 7.28 +/- 0.05; group 4, 7.20 +/- 0.04, vs. group 1; 7.34 +/- 0.03). Baseline plasma norepinephrine and epinephrine levels showed a significant decrease parallel to the duration of IDDM. Stress induced an increase in the concentration of norepinephrine in each group, but the elevation was significantly higher in the IDDM children versus the controls. A significant negative correlation was found between pH and maximal plasma norepinephrine levels (y = 7.3-0.006x, r = -0.46, p < 0.02). Stress resulted in blood glucose elevation in 13 patients regardless of their pre-exercise blood glucose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1998

[Mitochondrial myopathy, deafness and type 2 diabetes mellitus with tRNALeu(UUR) point mutation in mitochondrial DNA].

BACKGROUND: A heteroplasmic A3243G point mutation in tRNALeu(UUR) gene of mitochondrial DNA (mtDNA) is found in patients with MELAS syndrome (Mitochondrial Encephalomyopathy, Lactic Acidosis and Stroke-like episodes), less frequently in patients with other dominating clinical features, such as deafness, diabetes mellitus type 2, hypertrophic cardiomyopathy, renal problems or inborn development defects. Present report describes histochemical, enzymatic and molecular biology studies of the family with clinical variant of meals syndrome. METHODS AND RESULTS: A 45-year-old woman with progressive muscle weakness, external ophtalmoplegia, perceptive deafness, ischemic heart disease, diabetes mellitus type 2 and hyperlactacidemia was metabolically investigated because the multiorgan problems indicated mitochondrial origin of the disease. Muscle biopsy revealed pronounced myopathic changes, ragged red fibers and decreased activity of respiratory chain enzymes - succinate cytochrome c reductase (< 5% control) and cytochrome c oxidase (< 10% control). Restriction fragment analysis of mtDNA from muscle, blood and hair follicles detected heteroplasmic A -> G mutation in the position 3243 of the tRNALeu(UUR) gene, which was more pronounced in muscle (28% of total mtDNA) than in blood (12%) or in hair follicles (10%). No mutation was found in blood and hair follicles of patient's mother and daughter. CONCLUSIONS: Diagnostics of mitochondrial diseases require close collaboration of clinicians with specialised laboratories. Treatment of mitochondrial disorders is only symptomatic, however, early diagnosis of the molecular defect is important for genetic counselling.

DNA, Mitochondrial↗
PubMed1995

MELAS syndrome associated with diabetes mellitus and hyperthyroidism: a case report from Taiwan.

MELAS syndrome is a form of mitochondrial myopathy with manifestations of seizure, stroke-like syndrome, lactic acidosis, ragged red muscle fibres and mitochondrial encephalopathy. The syndrome has been reported in association with a variety of endocrine and metabolic disorders including diabetes mellitus (DM), hypothalamo-pituitary hypofunction, hypothalamic growth hormone deficiency and delayed puberty. Mitochondrial DNA (mtDNA) point mutation may be the major pathological defect. However, association of MELAS syndrome with hyperthyroidism has not previously been reported. A case is reported from Taiwan of a 32-year-old woman suffering from MELAS syndrome with associated DM and hyperthyroidism. When the latter was diagnosed in April 1988, the patient underwent subtotal thyroidectomy. There was no family history of thyroid disease. Because of repeated seizures, she had computed tomography (CT) and magnetic resonance imaging (MRI) of the brain which showed focal, low-density lesions over the cerebral hemispheres. Both serum and cerebral spinal fluid lactic acid levels were elevated. Mild elevations of serum T4 and T3 and a high titre of TSH receptor antibody were still present. Hyperglycaemia was noted during hospitalization and DM confirmed by oral glucose tolerance test. Muscle biopsy showed ragged red fibres. DNA analysis showed an A-to-G transition at the 3243rd nucleotide position of the tRNA(Leu(UUR)) gene of the mtDNA from the patient. Quantitative polymerase chain reaction (PCR) and restriction analysis revealed that about 60% of the blood mtDNA was of mutant type. The patient received antithyroid drugs for hyperthyroidism, diet control for DM and anti-epileptic drugs for seizure.

Adult↗
PubMed2003

Lactic acidemia associated with metformin.

OBJECTIVE: To report 2 cases of lactic acidemia associated with the use of metformin in patients with normal renal function. CASE SUMMARY: An 82-year-old African American man and a 76-year-old white man developed an elevated serum lactic acid concentration a few weeks after initiation of metformin therapy for type 2 diabetes. After the patients discontinued metformin, the serum lactic acid concentration normalized in both cases. An objective causality assessment revealed that the adverse drug event was probably related to the use of metformin. DISCUSSION: Metformin interferes with the production and elimination of lactic acid by a variety of mechanisms that are not well understood. Few systematic data are available on changes in plasma lactic acid concentrations in patients with type 2 diabetes and normal renal function. Clinical significance of a high serum lactic acid concentration needs clarification. CONCLUSIONS: Metformin therapy can be associated with subclinical elevation of lactic acid concentration in the absence of renal insufficiency or other contraindications to using this agent in patients with type 2 diabetes. Periodic monitoring of basic metabolic panels may prevent this potentially serious complication of metformin therapy.

Acidosis, Lactic↗
PubMed1997

[Value of biguanide in therapy of diabetes mellitus].

BACKGROUND AND OBJECTIVES: Biguanides have been used in treatment of diabetes mellitus for over 30 years now. Due to frequent occurrence of lactic acidosis, particularly in patients with serious contraindications to biguanide therapy and in cases of non-compliance with dosage instructions, buformin and phenformin were taken off the market in most European countries at the end of the seventies. Metformin continued to be allowed, since the risk of lactic acidosis is 20 times less than with phenformin or buformin due to the different pharmacokinetic properties of the substance. Plenty of clinical experience has been gained with metformin, documented in a large number of reliable long-term studies. FINDINGS: Metformin lowers fasting blood glucose levels by an average of 25% (17 to 37%), postprandial blood glucose by up to 44.5% and HbA1c bei 1.5% (0.8 to 3.1%) Metformin reduces raised plasma insulin levels in cases of metabolic syndrome by as much as 30% and reduces the "insulin requirement" of type 2 insulin-treated diabetics by 15 to 32%. It has well documented effects on various rheological parameters. In overweight type 2 diabetics, metformin shows the same level of hypoglycaemic effect as all of the important sulfonylurea derivatives used in Europe. The active mechanism of these derivatives is, however, concentrated solely on reduction of blood glucose. This mechanism does not take into account the remaining risk constellation involved in insulin resistance. Biguanides, similarly to weight reduction, lead to a reduction of hyperinsulinaemia, which is by contrast exacerbated by sulfonylureas and, in particular, exogenous insulin. CONCLUSION: The risk of lactic acidosis can probably be eliminated entirely if dosage instructions and contraindications are observed carefully. The cause of such neglect in 83% of all cases was limited on renal function (serum creatinine > 1.5 mg%). Regarding morbidity and mortality from lactic acidosis, metformin therapy is no riskier than treatment with the sulfonylurea derivative glibenclamide, taking into account the incidence of fatal hypoglycaemias with the latter.

Biguanides↗
PubMed1990

The diabetic hyperosmolar state.

The diabetic hypersomolar state is defined by a serum glucose greater than 600 mg/dl and a serum osmolarity greater than 320 m Osm/L. Ketoacidosis or lactic acidosis may co-exist with DHS in the same patient. The incidence of this acute complication of diabetes is high enough (17.5 cases per 100,000 person-years) for primary care physicians to encounter a case every year or two. Predisposing factors include older age, female sex, nursing home residence, and infection. A substantial proportion of cases occur in patients with no prior history of diabetes. Common presenting signs include fatigue or weakness, polydipsia, polyuria, nausea, and alteration of consciousness. The mainstay of therapy is intravenous fluid replacement with close monitoring of glucose and electrolytes in a hospital setting. Current mortality figures are high, at 10% to 20%, and the chance of survival is adversely affected by older age, higher osmolarity, and the presence of an associated severe illness. Prevention includes screening for diabetes, educating diabetic patients and their care givers about the symptoms of hyperglycemia, prompt treatment of any infection in a diabetic person, avoidance of drugs that increase carbohydrate intolerance in diabetic people, and encouraging compliance with treatment of diabetes.

Humans↗
PubMed1990

Hormonal and acid-base regulation of phosphoenolpyruvate carboxykinase mRNA levels in rat kidney.

Metabolic acidosis (6 days NH4Cl) causes a fourfold increase in the relative abundance of mRNA encoding phosphoenolpyruvate carboxykinase in rat kidney. Streptozotocin-diabetes (6 days) also results in an increased abundance of the mRNA but this increase can be prevented if the acidosis associated with bicarbonate is corrected by treatment with bicarbonate. The results confirm that renal phosphoenolpyruvate carboxykinase is regulated primarily by changes in acid-base status and that this control is at a pretranslational step. Isolated kidney tubules in short-term incubation have been used to identify which agents regulate levels of phosphoenolpyruvate carboxykinase mRNA. The relative abundance of the mRNA was increased by glucocorticoids and hormones which act via cAMP, or by cAMP analogues directly, but was not affected by hormones acting via Ca2+. Neither incubation at pH 7.1 nor the presence of serum from acidotic rats had any effect on the level of phosphoenolpyruvate carboxykinase mRNA. It is concluded that acidosis, glucocorticoids, and cAMP independently regulate expression of renal phosphoenolpyruvate carboxykinase.

Acid-Base Equilibrium↗
PubMed2002

Acute cyanide intoxication treated with a combination of hydroxycobalamin, sodium nitrite, and sodium thiosulfate.

An 80-year-old diabetic patient was admitted to the hospital because of sudden unconsciousness and severe metabolic acidosis. His son reported the possibility of cyanide poisoning. Clinical data and the detection of cyanide in blood and gastric material confirmed this possibility. Supportive therapy and the following antidotes--sodium nitrite two doses 300 mg i.v., sodium thiosulfate 3 g i.v., and hydroxocobalamin 4 g in 24 hours--were administered immediately and the patient completely recovered in 48 hours. Our observations suggest that timely and appropriate use of antidotes for cyanide intoxication may prevent death, even in aged diabetic patients.

Acidosis↗
PubMed2005

Risperidone-associated transient diabetic ketoacidosis and diabetes mellitus type 1 in a patient treated with valproate and lithium.

UNLABELLED: A 37-year-old man treated with valproate and lithium for bipolar affective disorder since 1999 and with risperidone since March 2003 was admitted to our clinic due to metabolic acidosis. Serum glucose was 647 mg/dL and urine ketones were positive. The patient was accepted as diabetic ketoacidosis (DKA). Risperidone, valproate, and lithium were immediately stopped, and the patient was treated with insulin and i.v. fluid replacement. Serum insulin and C-peptide levels were too low, and islet cell antibody and anti-GAD antibody were positive. We accepted him as type 1 diabetes mellitus (DM type 1). After the intensive treatment of diabetes, insulin requirements decreased gradually and diabetes mellitus disappeared completely within three months. CONCLUSION: Risperidone may lead to transient DM type 1 and DKA.

Adult↗
PubMed2003

Tenofovir-related nephrotoxicity in human immunodeficiency virus-infected patients: three cases of renal failure, Fanconi syndrome, and nephrogenic diabetes insipidus.

We report 3 cases of renal toxicity associated with use of the antiviral agent tenofovir. Renal failure, proximal tubular dysfunction, and nephrogenic diabetes insipidus were observed, and, in 2 cases, renal biopsy revealed severe tubular necrosis with characteristic nuclear changes. Patients receiving tenofovir must be monitored closely for early signs of tubulopathy (glycosuria, acidosis, mild increase in the plasma creatinine level, and proteinuria).

Acidosis↗