Lactic acid is a byproduct of mitochondrial energy production that is normally eliminated from the body. When the mitochondria have been damaged, lactic acid builds up in our cells and blood stream resulting in Lactic Acidosis.
Symptoms of lactic acidosis include: diarrhea; fast, shallow breathing; muscle pain or cramping; unusual sleepiness; unusual tiredness or weakness.
Lactate is a product of anaerobic glucose metabolism
Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Ninety percent of metformin is excreted unchanged by the kidneys and lactic acidosis typically occurs in patients with renal insufficiency.
Lactic acidosis appears to result from biguanide interference causing an increase in production and decrease in clearance of lactate leading to higher cellular lactate levels. Intracellular redox potential then shifts from aerobic to anaerobic metabolism. A decrease in pyruvate carboxylase activity, the rate limiting enzyme in the formation of glucose from lactate, can also decrease hepatic metabolism of lactate.
A metformin dosage of 850mg twice a day, or 500mg three times a day, usually gives good diabetic control. Caution is needed when increasing the daily dosage beyond 1.7g, especially in the elderly and those with mild renal disease.
Lactic acidosis may also result from anti-HIV drug therapy, which damages mitochondria Mitochondria need an enzyme called polymerase gamma to reproduce. Almost all nucleoside analogue drugs (NRTIs) such as Epivir (lamivudine, 3TC), HIVID (zalcitabine, ddC), Retrovir (zidovudine, AZT), Videx (didanosine, ddI), Zerit (stavudine, d4T), and Ziagen (abacavir) interfere with polymerase gamma to some degree. As a result, the NRTI class of drugs can block the production of new mitochondria, which then results in lower numbers of mitochondria and interference with their ability to function normally.
Lactic acidosis type B1 is be associated underlying diseases, including: diabetes mellitus, bowel ischemia, severe iron-deficiency anemia, liver disease, alcoholic ketoacidosis, pancreatitis, malignancy (leukemia, lymphoma, lung cancer), infection, renal failure, seizures, heat stroke, pheochromocytoma, thiamine deficiency, short gut syndrome, and other carbohydrate malabsorption syndromes.
Lactic acidosis type B2 is associated with medicinal and toxic causes, including: acetaminophen, alcohols and glycols (ethanol, ethylene glycol, methanol, propylene glycol), antiretroviral nucleoside analogs (zidovudine, didanosine, lamivudine), beta-adrenergic agents (epinephrine, ritodrine, terbutaline), biguanides (phenformin, metformin), cocaine, cyanogenic compounds (cyanide, aliphatic nitriles, nitroprusside), diethyl ether, 5-fluorouracil, halothane, iron, isoniazid, propofol, sugars and sugar alcohols (fructose, sorbitol, and xylitol), salicylates, strychnine, sulfasalazine, and valproic acid.
Lactic acidosis type B3 may result in those with inborn errors of metabolism. These include glucose-6-phosphatase deficiency (von Gierke disease), fructose-1,6-diphosphatase deficiency, pyruvate carboxylase deficiency, pyruvate dehydrogenase deficiency, oxidative phosphorylation deficiency, and methylmalonic aciduria.
Anion gap (AG): Calculation from serum electrolytes (AG = sodium - [CO2 + chloride]).
Arterial blood gas (ABG): The base deficit, derived from blood gas analysis, gives an approximation of tissue acidosis, an indirect evaluation tissue perfusion. However, several studies have been conducted finding poor correlation between serum lactate and base deficit levels.
Serum lactate: The normal serum lactate level is approximately 1 mmol/L with a range up to 2 mmol/L.
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