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At least 1,189 records · Page 66Linked to original sources
PubMed1976

Pancreatitis and severe metabolic abnormalities due to phenformin therapy.

Two elderly diabetic patients with abdominal pain were demonstrated to have complications of phenformin hydrochloride therapy. The first developed severe lactic acidosis treated with sodium bicarbonate given intravenously and followed by rebound alkalosis. The second showed severe acidosis (specimens for lactate determination were unfortunately unsatisfactory for analysis) and similar alkalotic rebound after therapy. She then developed severe pancreatitis, proved at operation, no cause for which other than phenformin was apparent. Poor renal and hepatic function predispose to these conditions by increasing serum phenformin levels and by decreasing urinary excretion of its metabolites. The acidosis should be treated judiciously with sodium bicarbonate administered intravenously. A rebound alkalosis, ensuring as the accumulated lactate is metabolized, is best treated by potassium chloride and ammonium chloride given intravenously. The mechanism by which phenformin causes pancreatitis is unknown, but termination of therapy causes cessation of the pancreatitis.

Acidosis↗
PubMed2006

[Traditional contraindications to the use of metformin -- more harmful than beneficial?].

For fear of lactic acidosis the currently listed contraindications to the use of metformin exclude a large number of people with type 2 diabetes from efficacious anti-hyperglycemic and cardioprotective treatment. Yet recent data call the traditional contraindications to metformin into question. As the incidence of lactic acidosis in patients with type 2 diabetes is the same with or without metformin therapy (about 9 per 100,000 patient years) there is no evidence that metformin therapy is associated with an increased risk of lactic acidosis. Similarly, despite disregard internationally of major metformin contraindications, there has been no corresponding increase in the incidence of lactic acidosis. Metformin treatment of elderly diabetics with multiple comorbidities and explicit contraindications has led to significantly better clinical parameters in them than in the control group without metformin; and there were no cases of lactic acidosis. The two groups did not differ with regard to progression of renal failure, patient-oriented endpoints or overall mortality. Compared with its predecessors phenformin and buformin, metformin is considerably less lipophilic and has a shorter plasma half-life; it is eliminated renally in unchanged form. In type 2 diabetics treated with metformin -- even those over 70 years of age and those in mild renal failure -- no relevant increases in lactate levels were found. In patients with lactic acidosis there was no correlation between the levels of metformin and lactate. The prognosis of lactic acidosis is determined less by the serum concentrations of metformin and lactate than by the hypoxia caused by the underlying disease and comorbidities. These findings raise doubts about the significance of metformin in the pathogenesis of lactic acidosis. On the basis of the current data, advanced age per se, mild renal impairment and stable heart failure can no longer be upheld as contraindications to the use of metformin. It should be safe to withdraw metformin the evening before radiological examinations with intravenous contrast media or surgical procedures under general anaesthesia in diabetics with normal renal function.

Acidosis, Lactic↗
PubMed2000

[An unusual cause of acute respiratory distress].

A 54-year-old patient was admitted to our ICU for ketoacidosis with acute respiratory distress (ARD). The main and unusual cause of ARD was hypophosphataemia. Patient-related risk factors for chronic hypophosphataemia were malnutrition, chronic alcoholism, and diabetes mellitus. Correction of the metabolic acidosis by insulin therapy resulted in intracellular penetration of phosphate and potassium, causing severe hypophosphataemia and hypokaliaemia responsible for ARD. This case provides an opportunity for reviewing the main causes and consequences of hypophosphataemia, and for emphasising the value of monitoring serum phosphate levels and providing supplemental phosphate in ICU patients at risk for phosphate depletion.

Alcoholism↗
PubMedDate not supplied

Case report. Fatal gas gangrene following intra-articular steroid injection.

Gas gangrene is a rare infectious disease syndrome complicating medico-surgical procedures. We describe a case of gas gangrene secondary to intra-articular steroid injection. Clostridia species and Escherichia coli were the etiologic organisms in this case. The presence of underlying diseases such as diabetes mellitus, hepatic insufficiency, and metabolic acidosis could have contributed to the fatal outcome of this patient. A high index of suspicion, early diagnosis, and appropriate treatment may improve the prognosis in gas gangrene. Although uncommon, infection is a significant complication of intra-articular steroid administration. Thus, meticulous aseptic technique should always be observed in the performance of this procedure.

Arthritis, Infectious↗
PubMed1998

Metabolic effects of aldose reductase inhibition during low-flow ischemia and reperfusion.

Several studies have shown that maintenance of glycolysis limits the metabolic and functional consequences of low-flow ischemia. Because diabetic animals are known to have impaired glycolytic metabolism coupled with increased flux through the aldose reductase (AR) pathway, we hypothesized that inhibition of AR would enhance glycolysis and thereby improve metabolic and functional recovery during low-flow ischemia. Hearts (n = 12) from nondiabetic control and diabetic rats were isolated and retrograde perfused using 11 mM glucose with or without the AR inhibitor zopolrestat (1 microM). Hearts were subjected to 30 min of low-flow ischemia (10% of baseline flow) and 30 min of reperfusion. 31P NMR spectroscopy was used to monitor time-dependent changes in phosphocreatine (PCr), ATP, and intracellular pH. Changes in the cytosolic redox ratio of NADH to NAD+ were obtained by measuring the ratio of tissue lactate to pyruvate. Effluent lactate concentrations and oxygen consumption were determined from the perfusate. AR inhibition improved functional recovery in both control and diabetic hearts, coupled with a lower cytosolic redox state and greater effluent lactate concentrations during ischemia. ATP levels during ischemia were significantly higher in AR-inhibited hearts, as was recovery of PCr. In diabetic hearts, AR inhibition also limited acidosis during ischemia and normalized pH recovery on reperfusion. These data demonstrate that AR inhibition maintains higher levels of high-energy phosphates and improves functional recovery upon reperfusion in hearts subjected to low-flow ischemia, consistent with an increase in glycolysis. Accordingly, this approach of inhibiting AR offers a novel method for protecting ischemic myocardium.

Aldehyde Reductase↗
PubMedDate not supplied

What makes cells grow larger and how do they do it? Renal hypertrophy revisited.

Hypertrophy, defined as an increase in cell size without an increase in cell number, occurs in a number of conditions, including compensatory renal growth, diabetes mellitus, protein feeding, chronic metabolic acidosis, and chronic potassium deficiency. In vitro cell culture studies have been used to characterize the mechanisms involved in the development of hypertrophy. Two mechanisms have been identified and characterized. One mechanism involves regulation of processes that are also associated with the initial events of the hyperplastic growth process, and is referred as a cell cycle-dependent mechanism. The other mechanism occurs independently of these particular cell cycle processes, but involves regulation of protein degradation by lysosomal enzymes. This latter mechanism is referred to as a cell cycle-independent mechanism. In vivo studies suggest that both compensatory renal hypertrophy following uninephrectomy and diabetes mellitus-induced hypertrophy involve the cell cycle-dependent mechanism.

Animals↗
PubMedDate not supplied

Metformin-induced lacticacidemia in patients with type 2 diabetes mellitus.

OBJECTIVE: To determine whether metformin therapy can predispose patients with type 2 diabetes and normal renal function to lactic acidosis when certain conditions are present. METHODS: We undertook this prospective cohort study in 110 consecutive patients (age range, 27 to 85 years) with normal serum creatinine levels (<1.5 mg/dL in men; <1.4 mg/dL in women), receiving metformin as monotherapy or in combination with sulfonylurea or insulin, who were undergoing assessment on a regular basis for diabetes care. Clinical evaluations were performed at 4- to 12-week intervals for up to 2 years. Serum electrolytes and creatinine as well as plasma lactic acid determinations were done in all patients, regardless of symptoms. The anion gap was calculated. RESULTS: Plasma lactic acid concentrations were normal in 47 patients (mean, 9.4 +/- 18.0 mg/dL or 1.053 +/- 0.194 mmol/L) and high in 63 patients (19.63 +/- 5.11 mg/dL or 2.208 +/- 0.569 mmol/L; P<0.001). The anion gap was increased in the high lactic acid group in comparison with the normal group (P<0.001). Comorbid conditions (for example, cardiovascular or respiratory disease) that may predispose to hypoxemia or compromise tissue perfusion were significantly more prevalent in patients in the high lactic acid group than in those with normal lactic acid values. CONCLUSION: Lacticacidemia may occur in metformin-treated patients with type 2 diabetes mellitus who have normal renal function. An increased anion gap and certain clinical symptoms may serve as clues for the presence of lacticacidemia. Progression from lacticacidemia to clinical lactic acidosis, under certain hemodynamic or respiratory adverse conditions, remains conjectural and needs further evaluation.

Aged↗
PubMed1982

[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia].

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.

Acid-Base Equilibrium↗
PubMed1978

[Lactacidosis in guanide treatment--a current disease syndrome].

It is reported on two eldery female diabetics with severe lethal lactacidosis. The clinical picture as well as the laboratory constellation leave no room for doubt about it, though only in one case the estimation of lactate could be performed. A renal insufficiency as involving factor is to be supposed in the two cases. With the help of literature the essential points of view of the clinical picture are discussed and it is referred to its origin also under influence of buformin.

Acidosis↗
PubMed2003

Historical review: concept of acid-base balance in medicine.

This paper attempts to illustrate historically how important developments in the comparatively new field of physical chemistry during the second half of the 19th century made possible the understanding of ions and acid-base phenomena in clinical and laboratory medicine. Primarily based upon the revolutionary concept of ionization by Svante Arrhenius, it was the studies of two Americans, Lawrence Joseph Henderson and Donald Dexter van Slyke, during the first two decades of the 20th century that resulted in the elucidation and clinical laboratory evaluation of two major diseases, diabetes and nephritis, and the resulting recognition of the phenomena of acidosis and alkalosis.

Acid-Base Equilibrium↗
PubMed1994

[Clinical characterization of diabetes mellitus in the families with mitochondrial encephalomyopathies].

We clinically characterized 18 diabetic patients in 7 families with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) and mitochondrial DNA mutations of tRNALEU(UUR) (3243), 5 diabetics in a family with myoclonic epilepsy and ragged red fiber (MERRF) and tRNALYS (8344) mutation and 11 diabetics in a family with chronic external ophthalmoplegia (CPEO) and multiple deletions. Insulin secretory capacities were significantly reduced in the mutant relatives, as compared with the non-mutant members. It is speculated that the mutation-induced OPHOS defects in the pancreatic beta- cells might result in insulin secretory defects.

DNA, Mitochondrial↗
PubMed1981

Somatostatin and insulin infusion in the management of diabetic ketoacidosis.

The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). Treatment with insulin only in 20 patients caused normalization of blood glucose levels within 6 hours and resolution of ketoacidosis within 5 hours. During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. Correction of acidosis is the most important problem in diabetic ketoacidosis: in the severest cases cardiovascular and cerebral complications may ensue. The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced.

Blood Glucose↗
PubMed2005

A new challenge in pediatric obesity: pediatric hyperglycemic hyperosmolar syndrome.

OBJECTIVES: To describe four adolescents with hyperglycemic hyperosmolar syndrome, an uncommon presentation of type 2 diabetes in pediatric patients. DESIGN: Case report. SETTING: Two tertiary pediatric intensive care units in university teaching hospitals. PATIENTS: Four obese adolescents with hyperglycemic hyperosmolar syndrome associated with type 2 diabetes mellitus. INTERVENTIONS: Isotonic fluid resuscitation and insulin. MEASUREMENTS AND MAIN RESULTS: Two of the four patients died. The first patient died within the first 24 hrs of hyperglycemic hyperosmolar syndrome presumably due to hypovolemic shock. The second patient, who died, developed rhabdomyolysis and multiple-system organ failure after a prolonged intensive care unit stay. The third and fourth patients were discharged from the hospital in good health. None of the patients had cerebral edema on head computed tomography, despite differences in fluid and insulin management. CONCLUSIONS: Pediatric patients with hyperglycemic hyperosmolar syndrome have a high mortality rate and may experience multiple complications such as rhabdomyolysis and hypovolemic shock. Treatment strategies to reduce mortality are unclear and warrant further investigation.

Acidosis↗