Metformin causing

L A. Metformin causes lactic acidosis in patients with renal failure and severe congestive heart failure. It does not increase the risk of ketoacidosis and showed a reduction in cardiovascular comorbidities in a large study. It is contraindicated in patients with severe liver disease but does not cause hepatic necrosis. When used as monotherapy, metformin rarely causes hypoglycemia. 

The questions Does metformin cause lactic acidosis ... 

It is unclear whether metformin caused hemolysis directly in this case or via G6PD deficiency. Two other patients have been reported with normal G6PD activity (94,95) one had a positive Coombs test (95). 

Metformin. Metformin [657-24-9] (1,1-dimethylbiguanide), mol wt 129.17, forms crystals from propanol, mp 218—220°C, and is soluble in water and 95% ethanol, but practically insoluble in ether and chloroform. Metformin, an investigational dmg in the United States, does not increase basal or meal-stimulated insulin secretion. It lowers blood glucose levels in hyperglycemic patients with Type II diabetes but has no effect on blood glucose levels in normal subjects. It does not cause hypoglycemia. Successful metformin therapy usually is associated with no or some weight loss. 

The answer is a. (Hardman, p 1510.) Although the mechanism of action of metformin and other biguanicies is unclear, biguanides virtually never cause hypoglycemia They operate independently of pancreatic p cells but are not useful in insulin-dependent diabetes mellitus (IDDM). Some possible mechanisms of action are direct stimulation of glycolysis in peripheral tissues, increased sensitivity to insulin, and reduction of glucagon levels. 

Hypoxic states Cardiovascular collapse (shock), acute CHF, acute Ml, and other conditions characterized by hypoxemia have been associated with lactic acidosis and may cause prerenal azotemia. If such events occur, discontinue metformin. Surgicai procedures Temporarily suspend metformin for surgical procedures (unless minor and not associated with restricted intake of food and fluids). Do not restart until the patient s oral intake has resumed and renal function is normal. 

Pioglitazone - Pioglitazone when used in combination with sulfonylureas, metformin, or insulin caused an increased incidence of edema. 

Adverse gastrointestinal symptoms (nausea, vomiting, anorexia, metallic taste, abdominal discomfort, and diarrhea) occur in up to 20% of individuals taking metformin this can be minimized by starting at a low dose and slowly titrating the dose upward with food. Like phenformin, metformin can cause lactic acidosis, but its occurrence is rare except when renal failure, hypoxemia, or severe congestive heart failure is present or when coadministered with alcohol. Metformin is also contraindicated in persons with hepatic dysfunction, but it appears to be safe for use in the hepatic steatosis that often occurs with fatty infiltration of the liver in poorly controlled type II diabetics. 

Rosiglitazone is approved for use as monotherapy and in conjunction with metformin, though it is sometimes combined with a sulfonylurea or insulin. It is usually taken once or twice a day with or without food. Rosiglitazone may cause a modest increase in low-density lipoprotein and triglyceride concentrations, but it is unclear whether this effect has any clinical significance or persists in the long term. 

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

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