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 577 records · Page 32Linked to original sources
PubMedDate not supplied

Reversible blindness associated with alcoholic ketoacidosis: pseudomethanol intoxication.

We report a case of reversible blindness associated with severe acidosis. A 49-year-old female presented with sudden onset of bilateral blindness. A work up for possible etiologic factors including computed tomography failed to reveal any abnormalities except for ethanol induced severe ketoacidosis. Methanol was not detectable in the serum despite an ethanol level of 14.76 mmol/L, effectively ruling out the diagnosis of methanol intoxication. Treatment of the acidosis led to rapid resolution of her blindness. Review of the literature revealed two case reports of reversible blindness associated with severe acidosis in diabetics. The current case underscores the necessity for a clear understanding of the role of severe acidosis as the sole causative factor of reversible bilateral blindness.

Acidosis↗
PubMed2004

[Study on mitochondrial DNA gene tRNA(Leu(UUR)) A3243G mutation in type 2 diabetes mellitus].

OBJECTIVE: To explore the prevalence and the clinical characteristics of mitochondrial gene mutation A3243G (mt tRNA(Leu(UUR)) 3243 A-->G) in patients with type 2 diabetes mellitus (DM2) in China. METHODS: Four hundred and twenty-eight cases of DM2 patients were selected randomly. One hundred and eighty-eight individuals were healthy controls. The mutation was assayed by PCR-restriction fragment length polymorphism technique. The target fragments of PCR were digested with restriction endonuclease Apa I. RESULTS: mt tRNA(Leu(UUR)) 3243A-->G gene mutation was found in 2 of 428 patients with DM2, but not found in the controls. Further investigation of the relatives of the 2 patients' families revealed that 3 members were the carriers of mt tRNA A3243G gene mutation and the patients with diabetes. In addition, one proband and her son were characterized with the syndrome of mitochondrial encephalomyopathy with lactic acidosis. The diabetes of these patients is frequently accompanied by hearing impairment or deafness with maternal inheritance. CONCLUSION: The prevalence of the mitochondrial gene A3243G mutation is 0.47% in DM2 patients in China. The data acquired in this study suggest that the clinical phenotype of these patients with A3243G should be heterogeneous.

Adult↗
PubMed2004

Metformin and lactic acidosis: cause or coincidence? A review of case reports.

OBJECTIVE: Metformin has been associated with the serious side-effect lactic acidosis. However, it remains unclear whether the use of metformin was a cause or a coincidence in lactic acidosis. DESIGN: A literature search of the Index Medicus (1959-66) and of the databases Embase, Medline, Medline Express (1966-99) was performed using the keywords metformin, biguanides and lactic acidosis. All articles of cases with metformin-induced lactic acidosis (MILA) were cross-referenced. SUBJECTS: Cases were included for analysis if they met the following criteria: serum pH < or =7.35, lactate concentration > or =5 mmol L(-1). INTERVENTION: A forum of six experts in intensive care medicine independently categorized the cases in MILA unlikely (score 0), possible MILA (score 1) or probable MILA (score 2). MAIN OUTCOME MEASURES: Statistical analysis included the paired interobserver agreement (kappa) and multivariate regression analysis. RESULTS: Of 80 reported cases, 33 were excluded because of insufficient quality. The forum scores of the remaining 47 cases were distributed normally with a mean score of 7 (range 2-10). The kappa-value was 0.041 (SD = 0.24, range -0.514, 0.427). Neither lactate concentration nor mortality correlated with serum metformin concentrations. CONCLUSIONS: Given the low interobserver agreement and the lack of any relationship between metformin levels and outcome parameters, the concept that there is a simple, causal relationship between metformin use and lactic acidosis in diabetic patients has to be reconsidered.

Acidosis, Lactic↗
PubMed1980

[Blood-level changes of lactate and pyruvate after osmotherapy with mannitol and sorbitol (author's transl)].

In 43 patients osmotherapy with Mannitol 20% and Sorbitol 40% was applied and the changes of the concentrations of lactate and pyruvate were tested in blood. The lactate level of both substances was increased. Sorbitol had the greater effect, and showed its maximum after one hour. For Mannitol the point effect was after four hours. Meanwhile Sorbitol produces an acidosis, the acid-base metabolism is unaffected after Mannitol. The pyruvate-level is not increased significantly, compared with the control group. Therefore the coefficient of lactate to pyruvate is significantly raised. These results highlight the problems of osmotherapy, if the changes of metabolism, induced by the therapy, are not considered. Lactid acidosis, previously existing or a general acidosis, shock, diabetes mellitus and hepatic dysfunctions enhance the risk of osmotherapy especially with Sorbitol.

Acidosis↗
PubMed2000

[Management of diabetes during corticosteroid therapy].

BACKGROUND: Corticosteroids are generally contraindicated in diabetic patients due to the risk of disrupting glucose control leading to acute decompensation. In some cases however, corticosteroid therapy can be beneficial if given early with a well-controlled regimen. Glucose disequilibrium after withdrawal can be anticipated with proper knowledge of the pharmacokinetics of the glucocorticoid used. FOR PATIENTS WITH TYPE I DIABETES: Ketose acidosis is a real risk in these patients. Insulin dose must be increased and the administration scheme optimized. FOR PATIENTS WITH TYPE II DIABETES: Whether oral drugs should be continued is a question of debate, excepting cases where the underlying disease might cause acute decompensation requiring insulin. Outside this situation, oral drugs can be continued at a higher dose if the fasting serum glucose is below 2 g/L. Finally, it is important to recognized steroid-induced diabetes in order to initiate proper antidiabetic measures. FOR ALL PATIENTS: The glucose curve is reproducible. Basically, the postprandial level rises, warranting repeated insulin injections. Rapid-release analogs and alpha-glucosidase inhibitors appear to be promising; biguanides affect insulin resistance.

Adult↗