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 739 records · Page 41Linked to original sources
PubMed1992

Metformin-induced lactic acidosis: report of a case.

Lactic acidosis associated with diabetic patients receiving metformin therapy is rare but may cause significant morbidity and mortality. In nearly all reported cases of metformin-associated lactic acidosis, contraindications to its use were noted, especially renal insufficiency. We describe a 59-year-old diabetic man treated with metformin for more than three years. During the third year of use, he experienced progressive renal function impairment, and during the final month of use, he became azotemic. He was maintained on continuous ambulatory peritoneal dialysis. Several days prior to admission, he suffered from epigastralgia, nausea and vomiting, followed by progressive dyspnea which was Kussmaul in nature. Profound hypotension developed and he sank progressively into a coma. Wide-anion gap metabolic acidosis without ketonemia was detected. His blood lactate level was elevated and metformin-induced lactic acidosis was substantiated. An elevated plasma metformin level of greater than 50 mg/mL was determined later by high-performance chromatography. Rigorous treatment including bicarbonate therapy, bicarbonate hemodialysis and vasoactive agents as well as supportive measures were provided. With a return of pH to normal, the hypotension resolved and his consciousness level slowly improved. Our patient survived this disastrous event, but some neurologic sequelae remained. In order to avoid this life-threatening metabolic disturbance, patients with any contraindications should not be prescribed metformin.

Acidosis, Lactic↗
PubMed1984

The regulation of phosphate-activated glutaminase activity and glutamine metabolism in the streptozotocin-diabetic rat.

The activity of phosphate-activated glutaminase was increased in the kidney, liver and small intestine of rats made diabetic for 6 days with injection of streptozotocin (75 mg/kg body wt.). Insulin prevented this increase in all three tissues. Treatment with NaHCO3, to correct the acidosis that accompanies diabetes, prevented the increase in renal glutaminase activity, but not that in liver or small intestine. Chemically induced acidosis (NH4Cl solution as drinking water) or alkalosis (NaHCO3 solution as drinking water) increased and decreased, respectively, glutaminase activity in the kidney, but were without significant effect on the activity in liver and small intestine. The increase in glutaminase activity in the small intestine during diabetes was due to an overall increase in the size of this organ, and was only detectable when activity was expressed in terms of whole organ, not mucosal scrapings or isolated enterocytes. Prolonged diabetes (40 days) resulted in an even greater increase in the size and glutaminase activity of the small intestine. Despite this marked increase in capacity for glutamine catabolism, arteriovenous-difference measurements showed a complete suppression of plasma glutamine utilization by the small intestine during diabetes, confirming the report by Brosnan, Man, Hall, Colbourne & Brosnan [(1983) Am. J. Physiol. 235, E261-E265].

Animals↗
PubMed2006

[Metformin-associated lactic acidosis].

OBJECTIVE: The aims of this review are to precise the pathophysiological mechanisms leading to biguanide-associated lactic acidosis, to give elements of diagnosis, and to underline the precautionary conditions for prescribing these drugs by an improvement in physicians and patient's education. DATA SOURCES: A PubMed database research in English and French language reports published until December 2005. The keywords were: lactic acidosis, metformin, biguanide, diabetes mellitus. DATA EXTRACTION: Data in selected articles were reviewed, clinical and basic science research relevant informations were extracted. DATA SYNTHESIS: Metformin, which is an oral antidiabetic agent, is the only one biguanide available in France. It acts by enhancing the sensitivity to insulin by a decrease in the hepatic glucose production and an increase in its peripheral use. In term of glycemic control, it has the same efficiency than the other hypoglycemic agents. It represents the treatment of choice for overweight type 2 diabetic patients because of its beneficial effects on the weight loss and on the cardiovascular complications. The incidence of metformin-associated lactic acidosis is very low when contra-indications and appropriate rules for prescribing this drug are respected. The relationship between metformin and lactic acidosis remains largely controversial. In practical, we can distinguish three situations which have different prognosis. In the first case, metformin seems to be responsible for lactic acidosis because of self-poisoning or accidental overdose, and prognosis is good. In the second case, the association between metformin and lactic acidosis is coincidental rather than causal, and may be induced by an underlying organ failure. In the last case there is a cause of lactic acidosis which is worsened by a precipitating factor leading to metformin accumulation. The 2 latter situations are very severe as mortality rate is about 50%. Symptomatic treatments and renal replacement therapy which allows metformin removal are the curative treatment. Prevention is essential. It requires the respect of metformin contraindications and a better education of physicians and patients for a safe prescription. CONCLUSION: Due to its beneficial effects, metformin is the gold standard treatment for overweight type 2 diabetic patients. The essential precautionary conditions for prescribing metformin as well as the respect of its contra-indications permit largely to prevent lactic acidosis. This complication is serious when it is associated with intercurrent illnesses and metformin accumulation. The curative treatment is based on renal replacement therapy. Prevention only rests on the respect of the contra-indications. Education of physicians and patients concerning the rules of prescription remains essential.

Acidosis, Lactic↗
PubMed1988

Intracellular pH regulation in papillary muscle cells from streptozotocin diabetic rats: an ion-sensitive microelectrode study.

Intracellular pH regulation was studied in papillary muscle from STZ-induced diabetic rat hearts. In control bicarbonate solution there was no difference between the steady-state pHi values recorded from diabetic or normal papillary muscle. The addition of insulin had no effect on the pHi of either group. The amplitude of NH4+-induced alkalinization and the time course of recovery from alkalinization were similar in both normal and diabetic muscles. In both preparations, the recovery from alkalinization was similarly delayed by the disulfonic stilbene DIDS. This suggests the participation of a Cl-/HCO3- exchange in the recovery from alkalosis in rat myocardial cells that is not changed by diabetes. On the other hand, the amplitude of the acidification induced by the withdrawal of NH4+ was markedly increased in diabetic papillary muscles as compared to normal muscles. Moreover, there was a marked slowing down of the recovery from acidosis in the diabetics. The amplitude of NH+4 withdrawal-induced acidification was increased equally by amiloride in both normal and diabetic muscles. These findings suggest that diabetes is associated with a change in the activity of the amiloride-sensitive Na+/H+ exchange.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

[Splenic infarct, lactate acidosis, and pulmonary edema as manifestations of a pheochromocytoma].

The case of a 45-year-old woman with pheochromocytoma, who presented with severe abdominal pain and headache, diabetes mellitus, lactic acidosis and pulmonary edema, is described and discussed. Spleen infarction, not so far described as an ischemic complication of pheochromocytoma, was seen in computer tomography. After medical pretreatment with labetalol, a pheochromocytoma (2 x 2 cm) of the left adrenal gland was removed. The postoperative course was uneventful.

Acidosis, Lactic↗
PubMed2001

Use of base in the treatment of severe acidemic states.

Severe acidemia (blood pH < 7.1 to 7.2) suppresses myocardial contractility, predisposes to cardiac arrhythmias, causes venoconstriction, and can decrease total peripheral vascular resistance and blood pressure, reduce hepatic blood flow, and impair oxygen delivery. These alterations in organ function can contribute to increased morbidity and mortality. Although it seemed logical to administer sodium bicarbonate to attenuate acidemia and therefore lessen the impact on cardiac function, the routine use of bicarbonate in the treatment of the most common causes of severe acidemia, diabetic ketoacidosis, lactic acidosis, and cardiac arrest, has been an issue of great controversy. Studies of animals and patients with these disorders have reported conflicting data on the benefits of bicarbonate, showing both beneficial and detrimental effects. Alternative alkalinizing agents, tris-hydroxymethyl aminomethane and Carbicarb, have shown some promise in studies of animals and humans, and reevaluation of these buffers in the treatment of severe acidemic states seems warranted. The potential value of base therapy in the treatment of severe acidemia remains an important issue, and further studies are required to determine which patients should be administered base therapy and what base should be used.

Acidosis↗