Glynis Steele
Senior Member
- Messages
- 404
- Location
- Newcastle upon Tyne UK
D-lactic acid
Hi,
I found this which states that anion gap might be normal, in some cases of acidosis. I have also read that in short bowel patients, their lactate level appeared normal.
Clinical presentation, the plasma anion gap
There are two major ways acidosis is defined from routine
laboratory data. First, organic acids may be added to the body so
quickly that both the H and the anion are retained; this results
in metabolic acidosis and an elevated value for the plasma anion
gap [6466] (upper right portion of Fig. 6). Second, metabolic
acidosis may be present without a rise in the plasma anion gap. In
this latter setting, either the D-lactate anion was retained in the
lumen of the GI tract (with the H being absorbed or titrated by
bicarbonate in the lumen of the GI tract), or it was excreted in the
urine, but in either case, the cation lost with it was Na and/or K
ion [671 (not a H or NH4 ion, lower right portion of Fig. 6).
This latter type of metabolic acidosis is akin to the over-production
of hippuric acid in glue sniffers [68]. Since D-lactate anions
are reabsorbed by the kidney much less readily than is L-lactate
[54, 69, 70], as time progresses, the anion gap may decline without
resulting in a rise in the plasma bicarbonate concentration-that is,
D-Iactate is excreted as its Na or K salt (Fig. 6). Hence there
are a number of mechanisms that may contribute to the presentation
whereby the rise in the plasma anion gap might not match
the fall in the plasma bicarbonate concentration. Not only might
this lead to a diagnostic problem, it has implications for therapy
because, once the organic anions are excreted as their Na or
salts, these anions are no longer available for metabolism to
regenerate bicarbonate, and the patient might have developed a
deficit of Na and/or K4.
I feel that because of CFS patients having a complete bowel, perhaps the mechanisms of developing d-lactic are different. Maybe a small bowel overgrowth. Another part of this article states:
When there is bacterial overgrowth in the small intestine, the concentration of brushborder
enzymes may decrease [27]. Thus ingested disaccharides
and complex carbohydrates may not be hydrolyzed at an adequate
rate because of low luminal disaccharidase activity. These sugars
may then be fermented by bacteria which have colonized the small
intestine or may be delivered to the colon where they can undergo
anaerobic fermentation by colonic bacteria.
I also have another paper, which I cannot now seem to access called "Lactobacilli and Acidosis in Childnren with Short Small Bowel" which states that "lactobacilli can be divided into two major groups: homolactic and heterolactic. The homolactic oned produce lactic acids only from fermentable sugars (not lactulose).......because sugar hydrogen breath tests are based on bacterial fermentative production of molecular hydrogen from the sugar, whereas this type of bacteria cannot do so, it is useless to examine overgrowth of lactobacilli or malabsorption of sugars by means of a sugar (lactulose) breath test. We confirmed that molecular hydrgen was not detectable in a breath test."
So a lactobacilli overgrowth in the small bowel would not be picked up in a hydrogen breath test.
I know Paul Gooley, a biochemist, is currently researching dla in CFS patients in Australia, he was part of the De Meirleir paper. I presume he must think it is possible for this to occur in CFS patients.
I do not have CFS, or know of anyone who has it. I have been ooking at dla for some years now, for my daughters uninvestigated symptoms. When I saw the De Meirleir paper, I just thought I would point out what I do know about dla, in the hope that someone here might be interested. In the De Meirleir paper it says that the symptoms of CFS/DLA are strikingly similar, and I guess I just wanted to offer some possible insight.
Best
Glynis
Hi,
I found this which states that anion gap might be normal, in some cases of acidosis. I have also read that in short bowel patients, their lactate level appeared normal.
Clinical presentation, the plasma anion gap
There are two major ways acidosis is defined from routine
laboratory data. First, organic acids may be added to the body so
quickly that both the H and the anion are retained; this results
in metabolic acidosis and an elevated value for the plasma anion
gap [6466] (upper right portion of Fig. 6). Second, metabolic
acidosis may be present without a rise in the plasma anion gap. In
this latter setting, either the D-lactate anion was retained in the
lumen of the GI tract (with the H being absorbed or titrated by
bicarbonate in the lumen of the GI tract), or it was excreted in the
urine, but in either case, the cation lost with it was Na and/or K
ion [671 (not a H or NH4 ion, lower right portion of Fig. 6).
This latter type of metabolic acidosis is akin to the over-production
of hippuric acid in glue sniffers [68]. Since D-lactate anions
are reabsorbed by the kidney much less readily than is L-lactate
[54, 69, 70], as time progresses, the anion gap may decline without
resulting in a rise in the plasma bicarbonate concentration-that is,
D-Iactate is excreted as its Na or K salt (Fig. 6). Hence there
are a number of mechanisms that may contribute to the presentation
whereby the rise in the plasma anion gap might not match
the fall in the plasma bicarbonate concentration. Not only might
this lead to a diagnostic problem, it has implications for therapy
because, once the organic anions are excreted as their Na or
salts, these anions are no longer available for metabolism to
regenerate bicarbonate, and the patient might have developed a
deficit of Na and/or K4.
I feel that because of CFS patients having a complete bowel, perhaps the mechanisms of developing d-lactic are different. Maybe a small bowel overgrowth. Another part of this article states:
When there is bacterial overgrowth in the small intestine, the concentration of brushborder
enzymes may decrease [27]. Thus ingested disaccharides
and complex carbohydrates may not be hydrolyzed at an adequate
rate because of low luminal disaccharidase activity. These sugars
may then be fermented by bacteria which have colonized the small
intestine or may be delivered to the colon where they can undergo
anaerobic fermentation by colonic bacteria.
I also have another paper, which I cannot now seem to access called "Lactobacilli and Acidosis in Childnren with Short Small Bowel" which states that "lactobacilli can be divided into two major groups: homolactic and heterolactic. The homolactic oned produce lactic acids only from fermentable sugars (not lactulose).......because sugar hydrogen breath tests are based on bacterial fermentative production of molecular hydrogen from the sugar, whereas this type of bacteria cannot do so, it is useless to examine overgrowth of lactobacilli or malabsorption of sugars by means of a sugar (lactulose) breath test. We confirmed that molecular hydrgen was not detectable in a breath test."
So a lactobacilli overgrowth in the small bowel would not be picked up in a hydrogen breath test.
I know Paul Gooley, a biochemist, is currently researching dla in CFS patients in Australia, he was part of the De Meirleir paper. I presume he must think it is possible for this to occur in CFS patients.
I do not have CFS, or know of anyone who has it. I have been ooking at dla for some years now, for my daughters uninvestigated symptoms. When I saw the De Meirleir paper, I just thought I would point out what I do know about dla, in the hope that someone here might be interested. In the De Meirleir paper it says that the symptoms of CFS/DLA are strikingly similar, and I guess I just wanted to offer some possible insight.
Best
Glynis