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Results for “ACIDOSIS, DIABETIC”

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At least 883 records · Page 49Linked to original sources
PubMed1991

[Multiple causes of death in diabetics in the municipality of Recife, 1987].

In 1987, diabetes mellitus was mentioned in 492 death certificates of the population of the city of Recife, Brazil, 202 of them for males and 290 for females. Diabetes mellitus was the underlying cause of death according to 80 certificates for men and 290 for women, as a result of which premature death occurred in 16.2% of men and 11.1% of women. Multiple cause of death analysis showed that cardiovascular diseases were the most frequent underlying cause of death in individuals over 50 years of age and acute complications of diabetes mellitus in individuals under 50. Cerebrovascular diseases were the most frequent in the cardiovascular group, particularly in females. Arterial hypertension was the most frequent associated cause of death appearing in death certificates mentioning diabetes mellitus (not as the underlying cause of death), also more often in females. The acute complications of diabetes mellitus (keto-acidosis and coma) and peripheral circulatory disorders peculiar to this disease caused 23% and 30% of the deaths, respectively, in cases where diabetes mellitus was the underlying cause. Infectious and parasitic diseases were the most frequent associated causes of death according to those certificates which gave diabetes mellitus as the underlying cause.

Brazil↗
PubMed1996

Fatal lactic acidosis from imported phenformin--report of two cases.

This report describes two diabetic patients who presented with severe lactic acidosis. Both patients had been taking a medicine (phenformin) which they had obtained from China, and which has been withdrawn from Singapore since 1977. Both cases were admitted with severe metabolic acidosis and were treated with intravenous sodium bicarbonate and intensive care support with unsuccessful outcomes.

Acidosis, Lactic↗
PubMed1999

Evaluation of signals activating ubiquitin-proteasome proteolysis in a model of muscle wasting.

The ubiquitin-proteasome proteolytic system is stimulated in conditions causing muscle atrophy. Signals initiating this response in these conditions are unknown, although glucocorticoids are required but insufficient to stimulate muscle proteolysis in starvation, acidosis, and sepsis. To identify signals that activate this system, we studied acutely diabetic rats that had metabolic acidosis and increased corticosterone production. Protein degradation was increased 52% (P < 0.05), and mRNA levels encoding ubiquitin-proteasome system components, including the ubiquitin-conjugating enzyme E214k, were higher (transcription of the ubiquitin and proteasome subunit C3 genes in muscle was increased by nuclear run-off assay). In diabetic rats, prevention of acidemia by oral NaHCO3 did not eliminate muscle proteolysis. Adrenalectomy blocked accelerated proteolysis and the rise in pathway mRNAs; both responses were restored by administration of a physiological dose of glucocorticoids to adrenalectomized, diabetic rats. Finally, treating diabetic rats with insulin for >/=24 h reversed muscle proteolysis and returned pathway mRNAs to control levels. Thus acidification is not necessary for these responses, but glucocorticoids and a low insulin level in tandem activate the ubiquitin-proteasome proteolytic system.

Acidosis↗
PubMed1978

[Treatment of diabetic ketoacidosis and hyperosmolality with low dose insulin infusion (author's transl)].

Fifteen patients were treated with low-dose (5 u/hour) insulin infusion, including 10 cases of ketoacidosis, 3 cases of hyperglycemia without acidosis in severely affected diabetics, and 2 cases with hyperosmolality. The treatment was successful in all cases. Insulin was infused at a constant rate, during 12 hours as a mean value. Blood glucose fell regularly and no hypoglycemia occured. Serum potassium varied within narrow limits, and no accident related to hypokalemia was observed. The correction of ketoacidosis was delayed, as compared to that of hyperglycemia. The two elderly patients with hyperosmolality recovered quickly and completely. The method of low-dose insulin infusion seems thus effective and easily applicable, at least in an intensive care unit. Our experience prompted us to increase (10 u/h) rather than to decrease the insulin infusion rate, with the aim to obtain a faster correction of ketoacidosis.

Adult↗
PubMed1989

[Acute metabolic complications in diabetes mellitus].

The author discusses several pathologic conditions which may occur as acute metabolic complications of diabetes mellitus. Prior to the introduction of insulin in the management of the disease, these complications were the principal causes of mortality in diabetic patients.

Acidosis, Lactic↗
PubMed1989

Long term lithium therapy in Malaysia.

Ten patients on long term lithium therapy (mean four years, range 1-10.5 years) were subjected to various renal, thyroid, haematological, cardiac and endocrine tests. There was impaired urinary concentrating ability in seven subjects, which was not responsive to vasopressin stimulation, suggesting a partial nephrogenic diabetes insipidus. Nine subjects had metabolic acidosis with higher urinary pH than expected suggesting presence of acidification defect in the kidney. No significant change in renal function, thyroid function, ECG or haematological parameters were detected. Our findings concur with previous reports from the West regarding the safety of lithium administration.

Acidosis↗
PubMed1991

Fetal acidosis and hyperlacticaemia diagnosed by cordocentesis in pregnancies complicated by maternal diabetes mellitus.

Fetal blood samples were obtained by cordocentesis (ultrasound guided needle aspiration) from 28 pregnant Type 1 diabetic women between 20 and 40 weeks' gestation. Analysis of the deviations from normal values of blood pH and plasma lactate showed significant acidosis (p less than 0.001) and hyperlacticaemia (p less than 0.01) in the third trimester, but not in the second trimester. Blood PO2 and PCO2 levels did not differ significantly from normal values. The pH showed significant correlations with PO2 (r = 0.54; p less than 0.01) PCO2 (r = -0.70; p less than 0.001), lactate (r = -0.46; p less than 0.05), fetal glycosylated haemoglobin (r = -0.53; p less than 0.01), and maternal glycosylated haemoglobin (r = -0.57; p less than 0.01). Plasma lactate showed significant correlations with PO2 (r = -0.54; p less than 0.01), PCO2 (r = 0.50; p less than 0.05), and pH (r = -0.46; p less than 0.05). Neither pH nor lactate showed significant correlations with birthweight. These observations suggest that some fetuses of diabetic women are significantly acidotic and hyperlacticaemic in the third trimester. This may provide a possible explanation for the phenomenon of late intrauterine fetal death in pregnancies complicated by maternal diabetes mellitus.

Acidosis↗
PubMed1989

The hyperlactatemic effect of biguanides: a comparison between phenformin and metformin during a 6-month treatment.

To compare the chronic hyperlactatemic effect of phenformin and metformin, we performed a double-blind study in 10 non insulin-dependent diabetics without any other known hyperlactatemic condition. After a pre-study period, each patient was allocated to a 6-month treatment with phenformin (50 mg bid) or metformin (850 mg bid) in random sequence. Body weight values were not significantly different between phenformin and metformin. Diabetic control was significantly (p less than 0.001) improved by both biguanides versus pre-study, but was the same during metformin and phenformin: HbAI = 13.8 +/- 0.3 SEM% during pre-study 9.7 +/- 0.2% during phenformin, 10.2 +/- 0.2% during metformin. Mean values of plasma lactate during metformin were significantly lower versus phenformin (1.30 +/- 0.05 vs 1.64 +/- 0.05 mmol/l, p less than 0.001). Mean values of plasma lactate/pyruvate ratio during metformin were significantly lower versus phenformin (16.92 +/- 0.59 vs 22.65 +/- 0.87, p less than 0.001), but not versus pre-study (16.19 +/- 0.51). These results indicate that: 1) during a 6-month treatment with a diabetic control of similar degree phenformin produces a significantly higher hyperlactatemic effect vs metformin; 2) metformin treatment is associated with less impairment of intracellular redox state versus phenformin, and therefore should be considered advantageous in the long-term treatment of non insulin-dependent diabetics.

Acidosis, Lactic↗
PubMed1993

Phenformin-induced lactic acidosis: a forgotten adverse drug reaction.

OBJECTIVE: To document a case of severe metabolic and lactic acidosis secondary to phenformin. This adverse effect has almost been forgotten as 15 years have passed since its withdrawal from the US market. CASE SUMMARY: A 64-year-old man presented with a four-day history of left upper abdominal pain and a one-week history of constipation and diarrhea. His arterial blood gases were pH 6.7, pCO2 2.80 kPa, and pO2 12.00 kPa with 90% oxygen saturation on room air. Serum chemistries indicated an unmeasurable serum bicarbonate concentration, anion gap 52 mmol/L, lactate concentration 29.5 mmol/L, blood urea nitrogen 6.63 mmol/L, creatinine 229.84 mumol/L, and blood glucose 4.35 mmol/L. There were low levels of urine and serum ketones. In the emergency department, he required resuscitation for hypotension and bradycardia. His diagnosis was lactic and ketoacidosis secondary to phenformin. The patient was treated with NaCl 0.9%, sodium bicarbonate, insulin, and hemodialysis. Although he survived the initial insult of lactic and ketoacidosis, his hospital course was complicated and he died on hospital day 105. CONCLUSIONS: Treatment of lactic acidosis is difficult and challenging. The continued availability of phenformin in neighboring countries, and the renewed interest in biguanide therapy for treating diabetes mellitus make it an important diagnosis of exclusion in diabetic patients who present with severe acidosis. Metformin, another biguanide under investigation for the treatment of diabetes mellitus, is associated with a much lower incidence of lactic acidosis than is phenformin.

Acidosis, Lactic↗