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At least 469 records · Page 26Linked to original sources
PubMed1998

[Decompensated diabetes mellitus and hyperchloremic metabolic acidosis: a case with both pathologies].

Diabetic ketoacidosis is manifested by elevated blood glucose levels, ketosis and metabolic acidosis with increased anion gap. A transitory hyperchloremic acidosis, with normal anion gap, can appear. We report a 21 years old female with a type 2 diabetes mellitus, admitted to the emergency room of a general hospital with hyperglycemia, absence of ketonemia, severe hypokalemia and hyperchloremic metabolic acidosis. Initially, she was diagnosed and treated as a severe diabetic ketoacidosis. Normal blood glucose levels were rapidly achieved but electrolyte and acid base alterations persisted, leading to the suspicion that another associated condition was causing the acidosis and hypokalemia. Urinary pH and anion gap measurement, the study of renal acidification and a bicarbonate overload test lead to the diagnosis of a distal renal tubular acidosis, secondary to a Sjögren syndrome, that was confirmed with a Schirmer test and positive anti Ro antibodies. In this diabetic patient, the acute hyperglycemia intensified the hypokalemia of her distal renal tubular acidosis and unchained the acute metabolic condition.

Acidosis, Renal Tubular↗
PubMed2002

Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus.

BACKGROUND: Metformin is an oral anti-hyperglycemic agent used in the treatment of type 2 diabetes mellitus. The results of the UK Prospective Diabetes Study indicate that metformin treatment is associated with a reduction in total mortality compared to other anti-hyperglycemic treatments. Metformin, however, is thought to increase the risk of lactic acidosis, and is considered to be contraindicated in many chronic hypoxemic conditions that may be associated with lactic acidosis, such as cardiovascular, renal, hepatic and pulmonary disease, and advancing age. OBJECTIVES: To assess the incidence of fatal and nonfatal lactic acidosis with metformin use compared to placebo and other glucose-lowering treatments in patients with type 2 diabetes mellitus. A secondary objective was to evaluate the blood lactate levels for those on metformin treatment compared to placebo or non-metformin therapies. SEARCH STRATEGY: A search was performed of the Cochrane Controlled Trials Register and the Database of Abstracts of Reviews of Effectiveness (up to 4/2000), Medline (up to 11/2000), Embase (up to 11/2000), Oldmedline, and Reactions (up to 5/2000), in order to identify all studies of metformin treatment from 1966 to November 2000. The Cumulated Index Medicus was used to search relevant articles from 1959 to 1965. The search was augmented by scanning references of identified articles, and by contacting principal investigators. Date of latest search: November 2000. SELECTION CRITERIA: Prospective trials in patients with type 2 diabetes that lasted longer than one month were included if they evaluated metformin, alone or in combination with other treatments, compared to placebo or any other glucose-lowering therapy. Observational cohort studies of metformin treatment lasting greater than one month were also included. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials to be included, assessed study quality and extracted data. The incidence of fatal and nonfatal lactic acidosis was recorded as cases per patient-years, for metformin treatment and for placebo or other treatments. The upper limit for the true incidence of cases in the metformin and non-metformin groups were calculated using Poisson statistics. In a second analysis lactate levels were measured as a net change from baseline or as mean treatment values (basal and stimulated by food or exercise) for treatment and comparison groups. The pooled results were recorded as a weighted mean difference (WMD) in mmol/L, using the fixed effects model for continuous data. MAIN RESULTS: Pooled data from 176 comparative trials and cohort studies revealed no cases of fatal or nonfatal lactic acidosis in 35,619 patient-years of metformin use or in 30,002 patients-years in the non-metformin group. Using Poisson statistics with 95% confidence intervals the upper limit for the true incidence of metformin-associated lactic acidosis was 8.4 cases per 100,000 patient-years, and the upper limit for the true incidence of lactic acidosis in the non-metformin group was 9 cases per 100,000 patient-years. There was no difference in lactate levels, either as mean treatment levels or as a net change from baseline, for metformin compared to placebo or other non-biguanide therapies. The mean lactate levels were slightly lower for metformin treatment compared to phenformin (WMD -0.75 mmol/L, 95% CI -0.86 to -0.15). REVIEWER'S CONCLUSIONS: There is no evidence from prospective comparative trials or from observational cohort studies that metformin is associated with an increased risk of lactic acidosis, or with increased levels of lactate, compared to other anti-hyperglycemic treatments if prescribed under the study conditions, taking into account contra-indications.

Acidosis, Lactic↗
PubMed1984

Idiopathic hypergammaglobulinaemia associated with nephrogenic diabetes insipidus and distal renal tubular acidosis.

Renal tubular dysfunction may be recognized in patients suffering from urinary light chain disease or non-myelomatous hypergammaglobulinaemia. We report a patient who has the combination of distal renal tubular acidosis and nephrogenic diabetes insipidus in association with hypergammaglobulinaemia due solely to increased IgG. We postulate that the abnormalities of distal nephron function resulted from cell-mediated immune damage.

Acidosis, Renal Tubular↗
PubMed1994

Acquired nephrogenic diabetes insipidus secondary to distal renal tubular acidosis and nephrocalcinosis associated with Sjögren's syndrome.

A 52-year-old woman was referred to our hospital because of 16-year history of polyuria and polydipsia. Hyposthenuria, hyperchloremic metabolic acidosis and the inabilities to acidify the urine after acid-loading test and to concentrate the urine in responses to water-deprivation and antidiuretic hormone administration allowed us to diagnose renal tubular acidosis and nephrogenic diabetes insipidus. Radiographic examinations revealed bilateral nephrocalcinosis. The patient was also found to have clinical and laboratory findings characteristic for Sjögren's syndrome. Thus the longstanding, poorly monitored distal renal tubular acidosis associated with Sjögren's syndrome was considered to result in very rare renal complications-nephrocalcinosis and nephrogenic diabetes insipidus. In patients with renal tubular acidosis and/or nephrogenic diabetes insipidus of unknown etiology, therefore, Sjögren's syndrome should be considered as one of primary disorders.

Acidosis, Renal Tubular↗
PubMed2002

End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes.

BACKGROUND: Patients with diabetic ketoacidosis (DKA) hyperventilate, lowering their alveolar (PACO(2)) and arterial carbon dioxide (PaCO(2)). This ventilatory response lessens the severity of their acidemia in a predictable way. Because end-tidal CO(2) (ETCO(2)) closely approximates PaCO(2), measured ETCO(2) levels should allow for predictions about the presence and severity of acidosis in diabetic patients. OBJECTIVES: 1) To evaluate the relationship between measured serum bicarbonate (HCO(3)) and ETCO(2) measured via nasal capnography in children with suspected DKA; and 2) to assess the ability of capnography to predict DKA. METHODS: Children being evaluated in a pediatric emergency department for suspected DKA (known or suspected diabetes presenting with hyperglycemia with or without ketonuria) were enrolled in a cross-sectional, prospective, observational study. Prior to the availability of venous HCO(3) results, ETCO(2) values were measured using a Nellcor NPB-70 Handheld Capnograph. RESULTS: Forty-two patients were enrolled. Linear regression analysis revealed a significant relationship between HCO(3) and ETCO(2) (R(2) = 0.80, p < 0.0001). Mean ETCO(2) was 37 torr (95% CI = 35.5 to 37.9 torr) in the children without DKA and 22 torr (95% CI = 17.4 to 26.9 torr) in the children with DKA (p < 0.0001). An ETCO(2) cut-point of <29 torr correctly classified the most patients (95%), with a sensitivity of 0.83 (95% CI = 0.52 to 0.98) and a specificity of 1.0 (95% CI = 0.88 to 1.0). No patient with an ETCO(2) of > or =36 torr had DKA, for a sensitivity of 1.0 (95% CI = 0.74 to 1.0). CONCLUSIONS: End-tidal CO(2) is linearly related to HCO(3) and is significantly lower in children with DKA. If confirmed by larger trials, cut-points of 29 torr and 36 torr, in conjunction with clinical assessment, may help discriminate between patients with and without DKA, respectively.

Adolescent↗
PubMed1980

Hereditary and acquired abnormalities in erythrocyte phosphofructokinase activity: the close association with altered 2,3-diphosphoglycerate levels.

Specific deficiency of erythrocyte phosphofructokinase (PFK) activity in Type VII glycogenosis presents a good model for the analysis of the relationship between 2,3 diphosphoglycerate (2,3 DPG) level and glycolysis in erythrocytes since glycolytic flow is partially blocked at the regulatory step. Enzymatic analyses of glycolytic intermediates of erythrocytes from a patient with Type VII glycogenosis demonstrated that 2,3 DPG is markedly decreased in parallel with fructose-1,6-phosphate (FDP). In acidosis including diabetic ketoacidosis and uremic acidosis a fall in 2,3 DPG is also associated with a marked reduction in FDP. On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG. These data indicate a close relationship between 2,3 DPG level and PFK activity in erythrocytes. At least in acidosis and alkalosis the alteration in 2,3 DPG level may well be explained by changes in PFK activity caused mainly through allosteric mechanism. In addition, twelve cases with hereditary PFK deficiency in muscle and erythrocytes reported in the world are reviewed and discussed briefly.

Alkalosis↗
PubMedDate not supplied

[Blood lactate semiautomatic estimation during acidotic diabetic coma (author's transl)].

Blood lactate levels were determined by Lactate Analyzer 640 Kontron during the course of 7 cases of hyperglycemic hyperosmolar diabetic coma, with severe acidosis and more or less marked ketosis. In 5 cases lactate values were found in normal range; slight increases around 2 mmol/l were rapidly corrected following standard coma treatment. One of these cases presented with extreme acidosis and relatively mild hyperglycemia, with differential problems in regard to lactic acidosis. In 2 cases, the former with alcoholic cirrhosis, the latter with myocardial infarction, blood lactate was markedly increased; in the second case, full clinical recovery was accompanied by normalization of lactate levels. A previous biguanide treatment could be ruled out as a cause of lactic acidosis. Thus the association of lactic acidosis and diabetic ketoacidosis seems to be unusual in the absence of concurrent serious conditions. The semiautomatic determination of blood lactate, because of its remarkable prognostic importance, should be included among the routine procedures for the emergency treatment of diabetic coma.

Adult↗