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At least 1,171 records · Page 65Linked to original sources
PubMed1997

Metformin.

Metformin, a dimethylbiguanide, was first synthesized in 1929 and was shown to be a potent hypoglycemic agent. It was rediscovered in 1957 and was widely used in Europe to treat obese type II patients. Metformin resurfaced in the 1980s and was shown to increase insulin sensitivity; this has led to its introduction to clinical practice in the United States for the first time. The small risk of lactic acidosis is now well documented and appropriate therapeutic guidelines have been established. Metformin is a sage and effective drug for management of non-insulin-dependent diabetes mellitus.

Acidosis, Lactic↗
PubMed1995

[Lactic acidosis induced by phenformin: a still forgotten iatrogenic complication].

Phenformin, a drug used in the treatment of diabetes mellitus frequently associated with potentially fatal cases of lactic acidosis, has been removed from market in the USA and several European countries. However, cases of lactic acidosis are still reported in countries where phenformin is available, either because well-known contraindications for its use are not observed, or because the prodromic syndrome of the lactic acidosis is not diagnosed. This study describes two cases of lactic acidosis, the treatment used and the final outcome. The authors point out that plainly evident contraindications were ignored in both cases, while the prodromic syndrome remained unrecognized even by specialists. The management of lactic acidosis continues to be a challenge. There is no optimal treatment and early recognition is essential. The authors call for greater attention in the use of phenformin and its eventual removal from market, especially in the light of alternative therapies which prove to be equally valid and easier to administer.

Acidosis, Lactic↗
PubMed2001

Adverse reactions to iodinated contrast media.

Adverse reactions to iodinated contrast media (ICM) are more likely to develop in patients with asthma, a history of allergy or contrast reaction and in those who are debilitated or medically unstable. These reactions can be divided into renal and general, and the latter are subdivided into acute and delayed. Acute general reactions can be minor, intermediate or severe. Fatal reactions are rare. The introduction of low-osmolality agents has caused an overall reduction in the number of non-fatal contrast reactions. Prompt recognition and treatment of acute adverse side effects to ICM is invaluable and may prevent a reaction from becoming severe. Familiarity with cardiopulmonary resuscitation is essential for successful management of life-threatening reactions. Contrast-media-induced renal impairment can be reduced with the use of low-osmolality contrast media and extracellular volume expansion. The use of ICM in diabetic patients receiving metformin should be carried out with care to avoid metformin-induced lactic acidosis. However, this problem is mainly observed in patients with diabetic nephropathy.

Acidosis, Lactic↗
PubMed1999

Cardiac abnormalities in diabetic patients with mutation in the mitochondrial tRNA(Leu(UUR)) gene.

An A-to-G transition at position 3243 of the mitochondrial DNA is known to be a pathogenic factor for mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), diabetes and cardiomyopathy. This mutation causes dysfunction of the central nervous system in MELAS. Because the heart, as well as the brain and nervous system, is highly dependent on the energy produced by mitochondrial oxidation, these tissues are more vulnerable to mitochondrial defects. Cardiac abnormalities were assessed in 10 diabetic patients associated with this mutation using echocardiography and 123I-metaiodobenzylguanidine (MIBG) scintigraphy, and compared with 19 diabetic patients without the mutation. Duration of diabetes, therapy, control of blood glucose and diabetic complications, such as diabetic retinopathy and nephropathy, were not different between the 2 groups. Diabetic patients with the mutation had a significantly thicker interventricular septum (16.8+/-3.7 vs 11.0+/-1.6mm, p<0.001) than those without the mutation. Fractional shortening was lower in diabetic patients with the mutation than those without it (30.7+/-7.0 vs 42.5+/-6.6, p<0.001). MIBG uptake on the delayed MIBG image was significantly lower in diabetic patients with the mutation than in those without the mutation (mean value of the heart to mediastinum ratio: 1.6+/-0.2 vs 2.0+/-0.4, p>0.05). In conclusion, left ventricular hypertrophy with or without abnormal wall motion and severely reduced MIBG uptake may be characteristic in diabetic patients with a mutation in the mitochondrial tRNA(Leu(UUR)) gene.

3-Iodobenzylguanidine↗
PubMed2005

Intraretinal pH in diabetic cats.

PURPOSE: To examine intraretinal extracellular H+ concentration([H+]o) in diabetic cats. METHODS: Double-barreled H+-selective microelectrodes were used to measure [H+]o as a function of retinal depth ([H+]o profiles) in four cats with different stages of diabetic retinopathy. Profiles from "normal"and "damaged" areas of the retina were compared to profiles previously obtained from healthy cats. RESULTS: In the healthy retina, [H+]o is generally highest in the middle of the retina and decreases toward the choroid and the vitreous. In 48 % of the profiles from diabetic animals with visible retinopathy, the inner retinal gradient was reversed so that the vitreous was more acidic than the middle of the retina. The profiles with reversed inner retinal gradients were classified as damaged. On the average, the inner retina tended to be 0.07-0.08 pH units more acidic in diabetic animals than in healthy normoglycemic animals, but of similar acidity to healthy hyperglycemic animals. In areas with damaged inner retinal gradients, net H+ production in the outer retina was also impaired. CONCLUSIONS: While the number of animals is small, we conclude that the [H+](O) distribution varied from normal to damaged in the same retina. Diabetes seems to lead to an acidification of the inner retina that appears to be at least partly related to hyperglycemia and which may be important in the progression of retinopathy.

Acidosis↗
PubMed1996

Protein turnover in the hypertrophying kidney.

To establish whether altered proteolysis contributes to the increase in protein content in hypertrophying kidneys, we studied protein turnover in proximal renal tubules isolated from rats with three forms of renal hypertrophy, diabetes mellitus (DM), ammonium chloride-induced acidosis and compensatory renal growth (CRG). We found that in DM and in chronic acidosis the normal balance in protein turnover is altered due to attenuated proteolysis and accelerated protein synthesis. Together this favors an increase in kidney protein content. In contrast, in CRG, the increase in protein content is entirely due to increased protein synthesis. Thus, the changes in protein turnover leading to the net gain in kidney protein content in renal hypertrophy depends on the cause of hypertrophy.

Acidosis↗
PubMedDate not supplied

[Coma in type 2 diabete mellitus on metformin treatment].

Non traumatic coma in diabete mellitus has two origins : hypo- or hyperglycemia. Coma with hyperglycemia can be due to ketoacidosis, hyperosmolar state or lactic acidosis. The present observation reports on a type 2 diabete mellitus patient presenting with a coma while the patient was on metformin and glibenclamide treatment. On admission, biologicals tests showed major acidosis, hyperglycemia and hyperosmolarity. No metformine accumulation was demonstrated by analytical measure. In this case, the association of hyperosmolar state and metabolic acidosis prove the difficulty of the differential diagnosis.

Aged↗
PubMed1983

Carbohydrate and lipid metabolism in type I diabetics during exhaustive exercise.

During an exhaustive graded bicycle spiroergometer test, several arterial blood samples were taken from six type I diabetics and seven normal controls for determination of catecholamines and parameters of carbohydrate and lipid metabolism. In both groups during exercise, glucose remained unchanged, and lactate associated metabolic acidosis was compensated by respiratory gas exchange. Diabetics showed an impaired exercise-induced response of adrenaline and noradrenaline (62 +/- 8 to 176 +/- 24 and 98 +/- 6 to 612 +/- 175 pg X ml-1), respectively, compared to controls (55 +/- 6 to 1213 +/- 720 and 95 +/- 17 to 1710 +/- 506 pg X ml-1). Free glycerol increased to an equivalent extent in both groups. Simultaneously produced free fatty acids decreased at high work loads in diabetics. In addition to insulin deficiency and impaired catecholamine secretion, diabetics showed high values of growth hormone, ACTH, and cortisol. These may be responsible for the high values of free glycerol and free fatty acids. At maximum the FFA values decreased in both groups, although levels of lactate and pyruvate were high. It is suggested that insulin deficiency is the reason for the disturbed hormonal and metabolic response to exhaustive exercise and reduces physical fitness in diabetics.

Adult↗
PubMed1979

Low-dose versus high-dose insulin therapy for diabetic ketoacidosis.

The effects of low-dose continuous insulin therapy were compared to those of high-dose subcutaneous and intravenous insulin therapy in six episodes of diabetic ketoacidosis. Time for correction of acidosis, ketosis, and hyperglycemia were similar for both regimens. The high-dose method required more exogenous glucose and supplemental potassium to avoid hypoglycemia and/or hypokalemia during treatment. Levels of cortisol, human growth hormone, and glucagon, initially elevated in most patients, showed a progressive decline with both modes of therapy. Plasma insulin remained remarkably stable during both treatment regimens, but remained within the physiologic range only in patients receiving low-dose therapy. Our study suggest that either modality is effective in the treatment of diabetic ketoacidosis.

Adult↗
PubMed1988

Lactic acidosis due to metformin therapy in a low risk patient.

A 55 year old diabetic women treated with chlorpropamide and metformin for three years presented with acute oliguric renal failure and lactic acidosis from which she died. The plasma metformin level was very high suggesting that the lactic acidosis was caused by the drug. There were no contraindications to metformin therapy and renal function was normal three months previously. This case demonstrates that lactic acidosis can occur as a result of metformin therapy in the absence of pre-existing risk factors.

Acidosis, Lactic↗
PubMed1985

Rhinocerebral mucormycosis in a diabetic ketoacidotic patient.

A 51-year-old, ketoacidotic diabetic with the rare neurological complications of rhinocerebral mucormycosis is reported. The clinical presentation was characterized by initial severe frontal headache, rapid visual loss with complete external ophthalmoplegia and intracranial spread by invasive fungal growth. Its course and fungostatic therapy with amphotericin B and ketoconazole are described and the literature reviewed.

Acidosis↗
PubMed1970

Serum lipid levels in hyperosmolar non-ketotic diabetic coma.

Levels of serum lipids were measured in two patients with hyperosmolar non-ketotic diabetic coma. Each lipid fraction was raised in a patient with severe hyperglycaemia and the degree of disturbance was less in a patient with moderate hyperglycaemia. The studies suggest that a block in the hepatic uptake of free fatty acids is not the explanation for the lack of ketosis.

Acidosis↗