Summary:
Seven cases illustrate a variety of other bacterial marker abnormalities when D-lactate is high. The patterns instruct about etiologies and intervention strategies.

dizziness
nervous shudder
nervous tick
peripheral neuropathy
spastic gait
tremors
weakness

K91 Urine Organix Profile

37

F

12/1/2003

History Case 1. 37 y/o F - 90 days before the specimen was taken, the patient had completed a 90-day sequence of Cipro, then Bactrum, then Augmentin for interstitial cystitis. Case 2. 4 y/o M Autistic Case 3. 2 y/o M Case 4. 63 y/o F Case 5. 55 y/o F Case 6. 65 y/o F Case 7.This profile is from a 4 y/o child who had never taken oral antibiotics, but who was given 10-14 billion L. acidophilus daily from 2 mo to 1.5 yr old. She recently has been displaying increasing severity of nervous shuddering, ticks, and OCD tendencies with greatly increased amounts of flatulence. Description of Results Case 1. D-lactate = 0.5 ug/mg creatinine (5th quintile cutoff = 1.9). All intestinal bacterial product concentrations are wwell below their fifth quintile cutoff values and phenylpropionate is below detection limit. Case 2. D-lactate = 4.1. General bacterial overgrowth is indicated by this pattern of elevation for every bacteria-specific marker. Extreme elevation is seen for p-hydroxyphenylacetate, indican, and tricarballylate, as well as for D-Lactate. Case 3. D-lactate = 4.3. This case shows a mixed or transitional pattern with significant elevation of D-lactate along with high phenylacetate, indican, and tricarballylate. Case 4. D-lactate = 2.2. The elevated D-lactate with very low levels of three markers and elevations of two others presents a strong indication of transition to L. acidophilus predominance. Case 5. D-lactate = 3.2. Here we see D-lactate higher than in Case 4 with only one other marker high, further indicating that the predominant overgrowth is that of L. acidophilus. Case 6. D-lactate = 3.3. This pattern is very similar to that in Case 5. Note the generally lower levels of other products. Case 7. D-lactate = 3.2. No products of specific bacterial origin are present other than D-Lactate. The benzoate and hippurate elevations are likely due to difficulty with meeting hepatic glycine conjugation demands rather than increased intestinal bacterial benzoate production. Recommendations Based on the laboratory data relevant to urinary markers of intestinal dysbiosis, the following interventions should be considered. Case 1. Use multiple species probiotics to assure re inoculation of a sparsely populated gut. Case 2. Consider courses of antibiotics and probiotics to bring general overgrowth under control. Case 3. Since there may be a transitioning to L. acidophilus dominance, care should be used in the dosing of that organism. Otherwise, various upper bowel microflora balancing interventions may be employed. Case 4. Even more care should be exercised with L. acidophilus in this case where more sever suppression of other organisms is indicated. Stop any use of that type of probiotic. Use carbohydrate restriction, including starch as the major maltose-releasing dietary source (specific carbohydrate diet). Case 5. Similar recommendations to Case 4, except the D-lactate is higher, so, if L. acidophilus overgrowth is the origin, then the situation is more likely to worsen if that probiotic is used. Case 6. Similar to Case 5. Note the very high level of p-hydroxyphenyllactate, indicating cell regulatory distress that may relate to toxic effects of D-lactate. Case 7. When L. acidophilus overgrowth is strongly indicated, stopping any supplementation with that organism and starting the carbohydrate restrictions discussed above constitute the first line of intervention. Since antibiotics have never been used by this patient, we can eliminate their overuse as a cause of the imbalanced flora. A short course of luminally active broad spectrum antibacterial such as Augmentin may be considered, followed by introduction of favorable organisms other than L. acidophilus. Other Comments Profound D-lactic acidemia resulting from iatrogenic carbohydrate malabsorption has been reported associated with small intestine resection. Many species of bacteria produce D-lactic acid. As luminal pH drops, however, L. acidophilus uniquely survives to proliferate and to become the source of toxic amounts of D-lactate due to overwhelming of hepatic clearance. The presence of elevated D-lactate alone does not necessarily implicate L acidophilus, but as other markers of bacterial growth fall and D-lactate persists, then the evidence of specific L. acidophilus overgrowth becomes heavier. There is still the question of whether the use of L. acidophilus supplements can be the cause of the overgrowth. There are multiple reports of beneficial effects from daily use of several billion organisms taken orally. However, the following individuals should be considered risks for excessive supplementation of the organism. Young children Immunocompromised patients Nutritionally deficient patients Patients with carbohydrate malabsorption, including maltase-deficient genetic variants. Case 7 is very likely to demonstrate simple over-use of L. acidophilus in a child resulting in D-lactic aciduria with neurologic symptoms.

Lab Data Figure . D-Lactate Study 1-2.gif Figure . D-Lactate Study 2-2.gif Figure . D-Lactate Study 3-2.gif Figure . D-Lactate Study 4-2.gif Figure . D-Lactate Study 5-2.gif Figure . D-Lactate Study 6-2.gif Figure . D-Lactate Study 7-1.gif