D-lactic acidosis

Chan NN, Darko D, O Shea D. Lactic acidosis with therapeutic metformin blood level in a low-risk diabetic patient. Diabetes Care 1999 22(1) 178. 

Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Medicine (Baltimore) 1998 77 73-82. 

A limited quantity of D-lactate is converted to pyruvate by a mitochondrial flavoprotein enzyme D-2-hydroxy acid dehydrogenase. Thus, the development of D-lactate acidosis requires excessive production of D-lactate and an impairment in its metabolism. The clinical manifestations of D-lactic acidosis are characterized by episodes of encephalopathy after ingestion of foods containing carbohydrates. 

The diagnosis of D-lactic acidosis is suspected in patients with disorders of the small intestine causing malabsorption and when the serum anion gap (Chapter 39) is elevated in the presence of normal serum levels of L-lactate and other organic acids. Measurement of serum D-lactate requires special enzymatic procedures utilizing D-lactate dehydrogenase and NADH. As D-lactate is converted to pyruvate, NADH is oxidized to NAD+ which is detected spectrophotometrically (Chapter 8). 

The treatment of D-lactic acidosis consists of oral administration of antibiotics, limitations of oral carbohydrate intake, and recolonization of the colon by bacterial flora which do not produce D-lactate. 

Lactic acidosis can occur in patients with SBS and may result in symptoms of ataxia and dehrium. D-Lactic acid is produced by the fermentation of malabsorbed carbohydrates by colonic bacteria, and increased concentrations are associated with small bowel bacterial overgrowth. " The diagnosis of D-lactic acidosis should be considered in patients with a functional colon who have an unexplained metabolic acidosis and an elevated anion gap. ... 

Convincing data in lactic acidosis is lacking D Manage underlying etiology... 

Answer D. Fasted MCAD patients typically present with nonketotic hypoglycemia, lactic acidosis, and plasma dicarbosylates. 

Graham DL, Laman D, Theodore J, Robin ED Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema. Arch Intern Med 137 1051-1055, 1977... 

Caution [B (D if near term), M] Contra Sulfonamide or salicylate sensitivity, porphyria, GI/GU obst avoid in hepatic impair Disp Tabs SE GI upset discolors urine dizziness, HA, photosens, oligospermia, anemias, Stevens-Johnson synd Interactions T Effects OF oral anticoagulants, oral hypoglycemics, MTX, pheny-toin, zidovudine X effects W/ antibiotics X effects OF digoxin, folic acid, Fe, procaine, proparacaine, sulfonylureas, tetracaine EMS T Effects of anticoagulants monitor EGG and BP for signs of hypovolemia and electrolyte disturbances d/t D skin urine may become yellow-orange may stain contact lenses T risk of photosensitivity Rxns OD May cause NA, drowsiness, HA, abd pain, skin Rxns, lactic acidosis, and jaundice symptomatic and supportive... 

Park, Y, Savarese, B., Kleiner, D. et al. (1995) Hepatic failure and lactic acidosis due to fialuridine (FIAU), an investigational nucleoside analogue for chronic hepatitis B. New England Journal of Medicine, 333, 1099-1105. 

Moyle, G.J., Dutta, D., Mandalia, S., Morlese, )., Asboe, D. and Gazzard, B.G. (2002) Hyperlactataemia and lactic acidosis during antiretroviral therapy relevance, reproducibility and possible risk factors. AIDS, 16 (10), 1341-1349. 

Adefovir dipivoxil is well tolerated. A dose-dependent nephrotoxicity has been observed in clinical trials, manifested by increased serum creatinine with decreased serum phosphorous and more common in patients with baseline renal insufficiency and those receiving high doses (60 mg/d). Other potential adverse effects are headache, diarrhea, asthenia, and abdominal pain. As with other NRTI agents, lactic acidosis and hepatic steatosis are considered a risk owing to mitochondrial dysfunction. No clinically important drug-drug interactions have been recognized to date. Pivalic acid, a by-product of adefovir dipivoxil metabolism, can esterify free carnitine and result in decreased carnitine levels. However, it is not felt necessary to administer carnitine supplementation with the low doses used to treat patients with HBV (10 mg/d). 

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