Intestinal bacteria express either a D- or an L(+)-lactate-specific dehydrogenase, or both . Additionally, some Lactobacillus species have DL-lactate racemase which catalyzes the conversion between D- and L(+)-lactate. Thus, colonic D-lactate may be formed either from pyruvate by bacterial D-lactate dehydrogenase or from L(+)-lactate by racemization. In addition, relative expression levels of L(+)- and D-lactate have been shown in vitro to be affected by bacterial growth conditions (eg, sodium acetate, pH) for some bacterial species. Carbohydrates such as hexoses (eg, glucose, galactose and fructose) that are ingested into the intestinal tract are fermented by bacterial glycolytic pathways to pyruvate and either L(+)- or D-lactate. L(+)- and D-lactate are intermediary products that other colonic bacteria can metabolize to short chain fatty acids (eg, acetate, butyrate and propionate), and are used for energy by mucosal cells of the colon ; lactic acid in itself can affect microbial survival.
D-lactic acidosis is an unusual condition manifested with nonspecific signs and symptoms similar to other causes of metabolic acidosis. There have been no large cohort studies but there have been two reviews of the condition that have detailed many of the case reports in the literature before 1999 ; additional reports in children have been subsequently published. None of the reports included infants younger than one year of age, although a few young children have been diagnosed with this condition. Clinically, most of the patients have presented with nonfocal neurological signs and symptoms such as confusion, ataxia, dysarthric speech, aggressiveness, inappropriate behaviour, stupor and even coma. The younger the patient, the more often episodes of irritability and drowsiness are reported; occasionally, hyperventilation was noted. Discover tons of opportunities to shop with best pharmacy on the internet and get celexa for depression paying a lot less money every time you shop for the drugs you need.