Lactic acidosis fructose

Benign Not evident while sole nutrition is breast milk Severe hypoglycemia and lactic acidosis after fructose ingestion Vomiting, apathy, diarrhea Liver damage and jaundice Proximal renal tubule disorder resembling Fanconi syndrome Treatment eliminate sources of fructose from diet... 

Fructose 1,6-diphosphatase Episodic hypoglycemia and lactic acidosis good prognosis when fasting is avoided... 

Infusions of fructose or sorbitol can cause lactic acidosis (425,426), particularly in combination with ethanol. 

Fructose has been used as an alternative to dextrose in parenteral nutrition, but its use is not recommended by some because of the risk of lactic acidosis. Although popular in many countries, it has therefore been suggested that the use of intravenous infusions containing fructose and sorbitol should be abandoned. ... 

Lactic acidosis can also result from inhibition of lactate utilization in gluconeoge-nesis (e.g., hereditary fructose intolerance, which is due to a defective aldolase gene). If other pathways that use glucose-6-P are blocked, glucose-6-P can be shunted into glycolysis and lactate production (e.g., glucose 6-phosphatase deficiency). 

Intravenous fructose feeding can lead to lactic acidosis caused by which of the following ... 

Glycerol is used as a therapeutic agent to reduce elevated intracranial and intraocular pressure and, until recently, was considered safe for oral and intravenous use. However, children with hepatic fructose-1,6-diphosphatase deficiency may develop lactic acidosis and hypoglycaemia after the use of glycerol. In adults, 20% glycerol in isotonic saline has caused haemolysis, haemoglobinuria and acute renal failure (42). 

It is not clear if this opinion must also be extended to the other biguanides. Less cases of lactic acidosis are reported after buformin or metformin therapy. Czyzyk (81 ), in a study on increases in lactate levels induced by alcohol or fructose after pretreatment with biguanides, found a rise in lactate levels for all types of biguanides. Th re is no indication that buformin or metformin will prove more beneficial if they are compared with phenformin. 

Investigations of liver biopsy material for enzymes involved in lactic acidosis and ketogenesis showed normal activites of pyruvate carboxylase, citrate synthetase, isocitrate dehydrogenase, glutamate-pyruvate transaminase, reduced activity of fructose 1,6-bisphosphatase and notably reduced activity of cytosolic acetoacetyl-CoA thiolase. The latter was found to be due to altered kinetic properties of the enzyme and this was confirmed in cultured skin fibroblasts, the enzyme being much more sensitive to coenzyme A inhibition than the normal enzyme. Activity of succinyl-CoA 3-keto acid-CoA transferase was not reported. 

Some months later, a statement by the Australian Drug Evaluation Committee reflected similar thinking and made closely similar recommendations (52). It was pointed out, inter alia, that the rapid metabolism of fructose and sorbitol can cause rapid accumulation of uric and lactic acids as well as phosphate depletion, especially in states of anoxia, and that acidosis and decreased tissue energy metabolism can occur. Glucose has, among other things, the advantage that it poses no risk to patients with familial laevulose intolerance. 

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