Lactate can be viewed as a metabolic dead end in that it can only be produced or utilized via pyruvate. Lactate production is determined primarily by pyruvate concentration and to a lesser extend by the redox state. Increased lactate production may result from tissue hypoxia, alkalosis, catecholamine and alanine transamination to pyruvate. Hyperlactatemia is observed in many pathological conditions. Current diagnostic criteria for lactic acidosis are a pH less than 7.35 and lactate concentration greater than 5 to 6 mmol/l. In our study series, malignancy was the most common underlying disease accompanied by lactic acidosis. Organ failure, cardiovascular disease and diabetes mellitus were also common. The prognosis of patients with these diseases were grave. In cases of lactic acidosis associated with diabetes mellitus, alcoholic liver disease, rhabdomyolysis and diabetic comas were noticeable as complications. Alcohol abuse was the most common cause of lactic acidosis associated with diabetes mellitus. In these cases, laboratory data showed prominent hyperlactatemia, hyperglycemia and acidemia and elevated anion gap. The mortality rate in these cases was 36% and higher in cases with organ failure. Treatment of lactic acidosis consists of alkalization by sodium bicarbonate with carbicarb, insulin-glucose-infusion, dichloroacetate therapy, tham administration, bicarbonate-buffered peritoneal dialysis and high bicarbonate-containing dialysis.