ME/CFS for 18 years, recently diagnosed with D-Lactic acidosis as cause of symptoms and illness.

[Aidan Walsh]

Avenger, I had a Cancer scare last January they removed a Cancer tumor in my terminal ileum I lost some of my right side bowel l am told I am Cancer free now. I wonder how could this area play a role in D-lactate Acidosis testing?

My symptoms have not changed at all before or after the Surgery with ME/CFS the Tumor was found in an early stage, I am worried about the fact my Father died from bowel Cancer he had it twice

 

[Aidan Walsh]

Not eating anything with fructose, so not sure. Unless other sugars can create fructose?

They also do not consume any sugar as well & countless products, I saw one woman it took 28 years to be finally diagnosed with HFI

 

[Aidan Walsh]

Hi Jim,
Yes, I read about that also, sprinkle glucose powder over fructose foods to break them down.

But I question if it’s even a factor for someone like myself, eating an extremely limited diet already.

And would the sibo breath test be considered a test for fructose malabsorption as well?

The breath test is very dangerous if you are not diagnosed with HFI hereditary fructose intolerance & if you have it there is a good UK Group on Facebook the UK one...The majority of fruits, lots of Vegs & ingredients should never be consumed with HFI. They buy a safe vitamin from Germany for HFI

 

[Aidan Walsh]

Hi, yes I had extremes of post exertional malaise (this could vary from mild to extreme at different times). The symptoms also felt at times like infections or Flu at times. Jennifer Brea also describes her symptoms as infections, which resolve temporarily with antibiotics (Times interview).

I was bed ridden and also very unwell at times. Often repeated activity would lead to prolonged periods of bed rest. I could not recover from normal activity as I had before becoming unwell. I had very bad symptoms and was expecting to either die or to have to commit suicide because Doctors could not recognize the symptoms (I made my will expecting to die from the symptoms on a number of occasions).

I also had systemic pain (I now have to remember, as receiving treatment and much of this is only a bad memory). I had pin prick sensations during the worst illness when I would become confused or have difficulty thinking and was only diagnosed with D-La when I realized that my symptoms abated after using Antibiotics.

Sometimes I would have tacharrhymias or fast heartbeats after activity, at worst after pushing things with chest pain. Because I was told that there was nothing wrong with me I would repeatedly push things until I became very unwell. My memory was also badly affected and long term acidosis can lead to cellular damage especially to the brain where cells cannot be replaced and it is likely that this may lead to early dementia.

D-La and Bacterial Overgrowth needs urgent research. Bacterial Overgrowth alone can cause malabsorbtion of vitamins and autoimmune disease causing the immune system to attack its host cells. This is a complex problem.

Paul.

@Avenger could a rise in D-Lactate acidosis be involved in any types of porphyria? The reason I ask is certain types of porphyria are in high carbs diets daily

 

[Avenger]

Cannot find anything on this “Julia flora” either. I have been researching d lactic reducing probiotic and found this product I’m going to try,
View attachment 43523

D-lactic Acidosis: Successful Suppression of D-lactate–Producing Lactobacillus by Probiotics;

Hi Eddie B and sb4,
Sorry for not getting back sooner, I have recently found out that 'Chronic Fatigue Syndrome' has been replaced in my records and D-Lactic acidosis removed for the past two years. My Doctor has told me that it must be a mistake and does not know who has done this. It has made it impossible to have the D-Lactic assay performed that will allow me to have a Faecal Transplant. There is far more happening, but I cannot talk about this at present. I am beginning to think that someone doe not want this condition to be recognised! On top of this my beloved Dog Millie died a week ago (she has sat with me on my bed through the worst episodes and not left my side when ill and I am heartbroken).

I have found what I consider an important report (below) concerning Probiotics! They give a list of the Non-D-Lactic producing Probiotics with CFU's used to suppress D-Lacic acidosis. I have had success with using some of these in combinations, but the Probiotic has to be prescribed in Australia? This could be the answer to FMT which is expensive and hard to obtain safely.

''Pro4-50 D-Lactate Free Multistrain Probiotic capsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment''. How did you get on with the Probiotics above and what is the composition it sounds interesing? I would very much like to use the Spectrumceuticals Probiotic but it has to be ordered on prescription! If this works the NHS could use this as a cheap treatment, but my experience so far is that those in charge want to suppress rather than explore on behalf of ME/CFS.

If someone could manufacture this in the UK they could potentially make a fortune. My belief is that at least a Subset of ME/CFS have this Bacterial problem and many may be subclinical. Just because D-Lactic acidosis has only been found in Short Bowel Syndrome would not preclude the rest of the population from D-Lactic overgrowth that can have many causes including Motility which is influenced by the production of Methane and Hydrogen acting to stimulate or reduce motility. For me this has always been about levels of fermented D-Lactate; my own status varies from abnormal fatigue to more severe Flu like with encephalopahy, weakness and breathing difficulty due to acidosis.

Lack of energy in ME would correspond with D-instead of L lactate being produced and converted to Glucose in the Pyruvate/Dehydrogenase chain. D-Lactic overgrowth suppressing L-Lactic producing Bacteria or secondary mechanisms caused by the Neurotoxin D-Lactate affecting all cells and organs including Mitochondria.

This is probably one of the best Non-D-Lacic producing Probiotic formula; but I have also had success with Rhasmosus and now Saccaromyces Boulardii; but this combination has proven success and the result is achieved by crowding out predatory D-Lactic producing bacteria that overgrow under conditions of Dysbiosis or low Bacterial balance; and may correct other underlying causes of Bacterial Overgrowth, but I have found that the results stop within days of stopping Probiotics so this would mean continuing for life. But better than antibiotics which will eventually lead to resistance (although antibiotics have been 'Hobson's choice' for me when I first became ill. I would still choose antibiotics over no quality of life or suicide. Response to antibiotics is also a diagnostic for Bacterial Overgrowth).




Case Report

D-lactic Acidosis: Successful Suppression of D-lactate–Producing Lactobacillus by Probiotics

''Stool composition of the patient was sequenced regularly over that period. His microbiota profile changed completely in species richness, and a clustering of species according to probiotic usage was seen. Importantly, D-lactate–producing Lactobacillus strains disappeared within a few weeks after probiotic introduction and were no longer detected in the subsequent follow-up specimens.''

https://pediatrics.aappublications.org/content/142/3/e20180337.

In his stool, the D-lactate–producing strains Lactobacillus (L) johnsonii and L plantarum were detected. Therefore, a probiotic cocktail with non-D-lactate–producing bacteria (Pro4-50 D-Lactate Free Multistrain Probiotic capsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment. Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year.
After initiation of a cyclic antibiotic treatment and during treatment with probiotics without any antibiotic treatment, stool samples were regularly collected and deeply profiled for stool microbiota composition. We employed 16S-based sequencing, which is used to detect highly conserved and hypervariable regions among bacterial ribosomal RNA and allows identification of bacteria, using Ion Personal Genome Machine System (Thermo Fisher Scientific, Waltham, MA).4 The raw sequences were processed in Quantitative Insights Into Microbial Ecology 1.9.1 pipeline as described,5 and microbiota composition including sample diversity and taxonomy profile (relative abundance: >0.1%) were plotted in R (https://www.r-project.org) by using the phyloseq library.6
To identify any changes in the stool microbiota, we collected 20 stool samples over 160 days before treating the patient with probiotics and 34 stool samples over 348 days during probiotic treatment. We determined α diversity, which is used to identify the number and the proportion of each species represented in a single stool sample.


Pediatrics

. 2018 Sep;142(3):e20180337.
doi: 10.1542/peds.2018-0337. Epub 2018 Aug 8.
D-lactic Acidosis: Successful Suppression of D-lactate-Producing Lactobacillus by Probiotics
Bahtiyar Yilmaz 1, Susanne Schibli 2, Andrew J Macpherson 1, Christiane Sokollik 3
Affiliations expand

• PMID: 30089656
• DOI: 10.1542/peds.2018-0337

Free article
Abstract
Intestinal microbiota composition in children with short bowel syndrome (SBS) is an important factor influencing the clinical outcome. An increase of D-lactate-producing bacteria can lead to D-lactic acidosis, also referred to as D-lactate encephalopathy, with severe neurologic impairment. Antibiotic treatments for D-lactic acidosis in children with SBS offer often only short-term relief. Here, we present the case of a boy with SBS who developed recurrent episodes of D-lactic acidosis even under continuous cycling antibiotic treatment. Microbiological analyses were used to detect the presence of D-lactate-producing Lactobacillus species in the stool samples. A probiotic cocktail was introduced to alter the intestinal microbiota. During follow-up under treatment with probiotics, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year. Stool composition of the patient was sequenced regularly over that period. His microbiota profile changed completely in species richness, and a clustering of species according to probiotic usage was seen. Importantly, D-lactate-producing Lactobacillus strains disappeared within a few weeks after probiotic introduction and were no longer detected in the subsequent follow-up specimens.
Copyright © 2018 by the American Academy of Pediatrics.

 

[Aidan Walsh]

D-lactic Acidosis: Successful Suppression of D-lactate–Producing Lactobacillus by Probiotics;

Hi Eddie B and sb4,
Sorry for not getting back sooner, I have recently found out that 'Chronic Fatigue Syndrome' has been replaced in my records and D-Lactic acidosis removed for the past two years. My Doctor has told me that it must be a mistake and does not know who has done this. It has made it impossible to have the D-Lactic assay performed that will allow me to have a Faecal Transplant. There is far more happening, but I cannot talk about this at present. I am beginning to think that someone doe not want this condition to be recognised! On top of this my beloved Dog Millie died a week ago (she has sat with me on my bed through the worst episodes and not left my side when ill and I am heartbroken).

I have found what I consider an important report (below) concerning Probiotics! They give a list of the Non-D-Lactic producing Probiotics with CFU's used to suppress D-Lacic acidosis. I have had success with using some of these in combinations, but the Probiotic has to be prescribed in Australia? This could be the answer to FMT which is expensive and hard to obtain safely.

''Pro4-50 D-Lactate Free Multistrain Probiotic capsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment''. How did you get on with the Probiotics above and what is the composition it sounds interesing? I would very much like to use the Spectrumceuticals Probiotic but it has to be ordered on prescription! If this works the NHS could use this as a cheap treatment, but my experience so far is that those in charge want to suppress rather than explore on behalf of ME/CFS.

If someone could manufacture this in the UK they could potentially make a fortune. My belief is that at least a Subset of ME/CFS have this Bacterial problem and many may be subclinical. Just because D-Lactic acidosis has only been found in Short Bowel Syndrome would not preclude the rest of the population from D-Lactic overgrowth that can have many causes including Motility which is influenced by the production of Methane and Hydrogen acting to stimulate or reduce motility. For me this has always been about levels of fermented D-Lactate; my own status varies from abnormal fatigue to more severe Flu like with encephalopahy, weakness and breathing difficulty due to acidosis.

Lack of energy in ME would correspond with D-instead of L lactate being produced and converted to Glucose in the Pyruvate/Dehydrogenase chain. D-Lactic overgrowth suppressing L-Lactic producing Bacteria or secondary mechanisms caused by the Neurotoxin D-Lactate affecting all cells and organs including Mitochondria.

This is probably one of the best Non-D-Lacic producing Probiotic formula; but I have also had success with Rhasmosus and now Saccaromyces Boulardii; but this combination has proven success and the result is achieved by crowding out predatory D-Lactic producing bacteria that overgrow under conditions of Dysbiosis or low Bacterial balance; and may correct other underlying causes of Bacterial Overgrowth, but I have found that the results stop within days of stopping Probiotics so this would mean continuing for life. But better than antibiotics which will eventually lead to resistance (although antibiotics have been 'Hobson's choice' for me when I first became ill. I would still choose antibiotics over no quality of life or suicide. Response to antibiotics is also a diagnostic for Bacterial Overgrowth).



Case Report

D-lactic Acidosis: Successful Suppression of D-lactate–Producing Lactobacillus by Probiotics

''Stool composition of the patient was sequenced regularly over that period. His microbiota profile changed completely in species richness, and a clustering of species according to probiotic usage was seen. Importantly, D-lactate–producing Lactobacillus strains disappeared within a few weeks after probiotic introduction and were no longer detected in the subsequent follow-up specimens.''

https://pediatrics.aappublications.org/content/142/3/e20180337.

In his stool, the D-lactate–producing strains Lactobacillus (L) johnsonii and L plantarum were detected. Therefore, a probiotic cocktail with non-D-lactate–producing bacteria (Pro4-50 D-Lactate Free Multistrain Probiotic capsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment. Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year.
After initiation of a cyclic antibiotic treatment and during treatment with probiotics without any antibiotic treatment, stool samples were regularly collected and deeply profiled for stool microbiota composition. We employed 16S-based sequencing, which is used to detect highly conserved and hypervariable regions among bacterial ribosomal RNA and allows identification of bacteria, using Ion Personal Genome Machine System (Thermo Fisher Scientific, Waltham, MA).4 The raw sequences were processed in Quantitative Insights Into Microbial Ecology 1.9.1 pipeline as described,5 and microbiota composition including sample diversity and taxonomy profile (relative abundance: >0.1%) were plotted in R (https://www.r-project.org) by using the phyloseq library.6
To identify any changes in the stool microbiota, we collected 20 stool samples over 160 days before treating the patient with probiotics and 34 stool samples over 348 days during probiotic treatment. We determined α diversity, which is used to identify the number and the proportion of each species represented in a single stool sample.


Pediatrics

. 2018 Sep;142(3):e20180337.
doi: 10.1542/peds.2018-0337. Epub 2018 Aug 8.
D-lactic Acidosis: Successful Suppression of D-lactate-Producing Lactobacillus by Probiotics
Bahtiyar Yilmaz 1, Susanne Schibli 2, Andrew J Macpherson 1, Christiane Sokollik 3
Affiliations expand

• PMID: 30089656
• DOI: 10.1542/peds.2018-0337

Free article
Abstract
Intestinal microbiota composition in children with short bowel syndrome (SBS) is an important factor influencing the clinical outcome. An increase of D-lactate-producing bacteria can lead to D-lactic acidosis, also referred to as D-lactate encephalopathy, with severe neurologic impairment. Antibiotic treatments for D-lactic acidosis in children with SBS offer often only short-term relief. Here, we present the case of a boy with SBS who developed recurrent episodes of D-lactic acidosis even under continuous cycling antibiotic treatment. Microbiological analyses were used to detect the presence of D-lactate-producing Lactobacillus species in the stool samples. A probiotic cocktail was introduced to alter the intestinal microbiota. During follow-up under treatment with probiotics, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year. Stool composition of the patient was sequenced regularly over that period. His microbiota profile changed completely in species richness, and a clustering of species according to probiotic usage was seen. Importantly, D-lactate-producing Lactobacillus strains disappeared within a few weeks after probiotic introduction and were no longer detected in the subsequent follow-up specimens.
Copyright © 2018 by the American Academy of Pediatrics.

Interesting, so complex, any ideas of cost of the product from Australia? Getting a script would be a challenge in the UK

 

[Avenger]

Cannot find anything on this “Julia flora” either. I have been researching d lactic reducing probiotic and found this product I’m going to try,
View attachment 43523
Hi, EddieB,
this looks like a really good alternative Probiotic if it is as high quality as described; It may act similarly to the Australian version. But expensive at 95$ plus 31.87$ shipping on Amazon when this illness impoverishes us; and I am not sure how long it would last as given in teaspoons.

I was prescribed Probiotics to be used with Cyclical Antibiotics in 2016, but this was stopped in 2017 due to NHS policy after a public consultation when they were ''deemed to have low clinical effectiveness'' and a high cost to the NHS. In order to be prescribed Probiotics, it will be necessary to demonstrate to the CCG that there are ''Circumstances where the prescriber believes that in their clinical judgement exceptional circumstances exist that warrant deviation from the recommendation to self care''.

My illness has worsened since 2017 but the CCG would not accept that it was necessary for me to have Probiotics despite frequent cyclical antibiotics and my prescriber stating that this was necessary. The NHS feel that you can supply these yourself, but do not have a clue that we need both quality and quantity for them to work properly. When purchasing Probiotics you cannot guarantee quality as supplied by the NHS who could investigate and supply Non-D-Lactic producing species for ME/CFS with Bacterial Overgrowth. But the cost of high quality Probiotics to those of us who are unable to work due to illness is prohibitive.

The CCG will still not allow me to have Probiotics that are used as treatment for D-Lactic acidosis, even though I have already gained resistance to several antibiotics and Probiotics would stop the necessity to continue using antibiotics; recent studies show that antibiotic resistance can be found in genetic material even in Parks! So antibiotic reistance can be transferred or picked up without using antibiotics; and using Probiotics as an alternative would stop the shedding of resistant genes, which has not been taken into consideration by the NHS.

''UCLA researchers find antibiotic-resistant genes in parks in four California cities. UCLA researchers found that soil in all 24 California parks surveyed, including MacArthur Park in Los Angeles, contained high levels of a gene that resists the antibiotic sulphadimidine. ''


Histamine & D Lactate Free Probiotics Powder 240 Billion CFU 30 Gram | Digestive & Immune Support | High Potency | by Foods for Gut

IngredientsB. Longum, B. Lactis, B. Bifidum, L. Gasseri, L. Salivarius, L. Rhamnosus.Unit Count1.0582 Ounce
About this item

• Ingredients: B. Longum, B. Lactis, B. Bifidum, L. Gasseri, L. Salivarius, L. Rhamnosus.
• Promotes digestive and immune health.Helps maintain regularity and promotes a healthy gut.Anti-candida properties.Reduces duration of diarrhea and bloating.

 

[Avenger]

Interesting, so complex, any ideas of cost of the product from Australia? Getting a script would be a challenge in the UK

Hi Aidan,
sorry I missed your message. We really need this investigating and high quality Probiotics supplied by the NHS; if this works, it should work for different forms of Bacterial Overgrowth including D-Lactic acidosis, but Bacterial Overgrowth is barely recognised by the NHS and most Doctors remain untrained;

Wheras you could probably find more usefull information from Vets treating Bacterial Overgrowth in Dogs!

My belief is that at least a Subset may have D-Lactic acidosis or other forms of Bacterial Overgrowth producing neurotoxins; and modern science has produced this illness as an environmental issue because of the use of chemicals and antibiotics that have damaged millions of years of evolving symbiosis in the Gut. I believe that the use of Antibiotics, Fluoride and Chlorine and many other chemicals are devolving the human Gut. If genetic shedding of resistant material and additional low levels of multiple antibiotics and phosphates continue to leach into our ecosystems this can only worsen............................

I see ME/CFS as an early warning sign that has been dismissed by vacant minds.

 

[Aidan Walsh]

Hi Aidan,
sorry I missed your message. We really need this investigating and high quality Probiotics supplied by the NHS; if this works, it should work for different forms of Bacterial Overgrowth including D-Lactic acidosis, but Bacterial Overgrowth is barely recognised by the NHS and most Doctors remain untrained;

Wheras you could probably find more usefull information from Vets treating Bacterial Overgrowth in Dogs!

My belief is that at least a Subset may have D-Lactic acidosis or other forms of Bacterial Overgrowth producing neurotoxins; and modern science has produced this illness as an environmental issue because of the use of chemicals and antibiotics that have damaged millions of years of evolving symbiosis in the Gut. I believe that the use of Antibiotics, Fluoride and Chlorine and many other chemicals are devolving the human Gut. If genetic shedding of resistant material and additional low levels of multiple antibiotics and phosphates continue to leach into our ecosystems this can only worsen............................

I see ME/CFS as an early warning sign that has been dismissed by vacant minds.

I also wonder if it is possible we all were born with some kind of small bowel disorder? Sorry about the loss of your Dog. I recently had a CT Scan with a Contrast of my neck styloid on both sides one was 24mm the other side was 31 mm for possible Eagle Syndrome, do not know if my Jugular vein was compressed they did

the test lying flat instead or turning left to right. I know someone who was operated on last week a Surgeon in London removed both at the same Surgery an ENT skull-based Neurosurgeon she flew home the next day to Jersey Island & recovering now she said she never felt better but healing will take time hers were thick &

one was 5mm the other 6 mm, mine is thick & pointy. I have seen really good progress on increasing my carbs adding Sugar as well, I did a few samples of urine when I was having bad right side pains the urine was clear, hydrated it turned dark in the Sun which happens in porphyria so maybe it is this or ES above still not sure, I

am waiting on a Surgeon to read my scans if he says ES I will go for the Surgery...I asked my GP about D Lactate Acidosis so she wrote this idea down. I only see my stomach Surgeon end of October I will mention D Lactate Acidosis to him he is open to ideas...The Surgeon the Woman saw is Dr. Ruper Obholzer at Guy

Hospital she is on the Facebook Group on Eagle Syndrome. Nothing touched my right side pain but all gone now with carbs/Sucrose increase I eat a lot of cereals, toast, etc I see a difference. The last few days bad pains in my left thigh like stabbing have really been bad I had to take some Codeine I wonder if compression could

be the pain like blood flow, I noticed a patch of thigh left outside goes Numb & becomes itchy...I hope you get the Medical File back to D Lactate that was very odd what was done. Do you think you will get the fecal transplants? My ES styloid was first found with a Panoramic Dental x-ray on the NHS then Dentist said also I

have TMJ in the right Jaw as well he did the test on my Jaw just looking it was he that sent me to first ENT who did the CT Scan. I wish I could test for D Lactate or porphyria all I did thus far was VP Variegate & Coproporphyria on fecal test both Negative...What an F'n illness CFS or whatever this is called LOL ...I found

out that Blue Horizon does the urine blood & fecal for all Porphyrias types it has to be done on the spot in London at Drs. Laboratory & sent to the lab right away it is about under £400.00...Invitae in San Francisco does the Genetic full panel for about $325.00 has to be signed by a Doctor from here a DNA Swab or Saliva

is sent takes about 14 working days for results back. Forms can be downloaded online. If we have compressions of the Jugular vein maybe it is also disrupting our bowels as well I have seen full recoveries with ES Surgeriesso anything is plausible it even causes autonomic dysfunction & points to Genetics as well

in families I saw one Woman she & her young child both have ES, the little girl is now monitored for growth with scans the Mom had hers removed already...All the best keep in touch Avenger

 

[Aidan Walsh]

I forgot to mention some say anything over 24.58mm is Eagle Syndrome, some others say over 30mm is Eagle Syndrome I have seen smaller than 24mm having Surgery, my Dentist said his concern was mine was too close

to major arteries & thick, pointy I know when I turn my head I get issues especially out walking or crossing the street I also have clear liquid at times comes out of my left nostril so maybe a spinal leak combined & am always congested

 

[kangaSue]

I have had success with using some of these in combinations, but the Probiotic has to be prescribed in Australia?

I think it's more a case here of 'creative marketing' which really just serves the purpose of keeping the price to the consumer high. It's often the case with this marketing model that you just need to chat to an "approved consultant" at one of the supply outlets to purchase the product, and that consultant can just be a pharmacy store employee.

 

[helen1]

@Avenger
Custom Probiotics offers a non D lactate blend, or can customize with any blend of species you request. They ship all over the world. I use them, I think they’re a good company. (That sounds like a commercial for them but I have no involvement lol)

https://www.customprobiotics.com/

 

[Avenger]

Dietary management of D-lactic acidosis in short bowel syndrome; Probiotics used at Birmingham Children's Hospital for D-Lactic acidosis;

Hi Helen,
Custom Probiotics sounds very interesting. Where are they based and are the Probiotics regulated and checked?

The most important thing concerning Probiotics is quality, quantity and reliability; and I have found from experimenting quantity is most important and have had to increase the quantity for some probiotics to work. I have had complete success with some combinations, being able to return to all Carbohydrates and Sugars, although the effects stop within days of stopping use of them. But the NHS have stoopped me having them on the grounds that Probiotics are innefective and I have not been able to afford them continuously; when Probiotics have been used for children at Birmingham Children's Hospital as treatment for D-La.

I also found that it was good to use a supplement to feed the Probiotic Bacteria and I used Inulin powder, 100% Fructo-Oligosaccaride 'FOS' Pre-Biotic which was taken with the Probiotics.

I have petitioned the NHS CCG stating that Probiotics would stop me needing more expensive Antibiotics and would save me from Antibiotic resistance, but have been denied despite often dangerous symptoms that under NHS policy should be take as exceptional circumstances. This is a crazy situation to be in. It seems that they want to deny my diagnosis and ignore my care needs and I will eventually develop C.Diff or total resistance at which point I could not tolerate the severity of the symptoms and would have only one option left (caring NHS!). I can see only one motivation for their actions and they scare me!

The way that Probiotics are delivered to the Gut is also important. I am looking for a regular supplier so that I can use the Probiotics long term, but have run up debt. as many of us must have.

I have found this report from Birmingham Children's Hospital who have used Probiotics to treat D-Lactic acidosis in Children with short Bowel Syndrome; I still believe that we are not precluded from D-Lactic overgrowth, just because we do not have short bowel syndrome; The strangest part of haveing D-Lactic acidosis as an adult male is that I am precluded from the expertise at Birmingham Children's Hospital who are, one of two Hospitals in the world (so I am told) capable of processing a D-Lactic assay;


Dietary management of D-lactic acidosis in short bowel syndrome

A J Mayne, D J Handy, M A Preece, R H George, I W Booth Institute of Child Health, University of Birmingham and The Children's Hospital, Birmingham A J Mayne D J Handy M A Preece R H George I W Booth Correspondence to: Dr I W Booth, Institute of Child Health, Francis Road, Birmingham B16 8ET.

Accepted 26 October 1989
Abstract Manipulation of carbohydrate intake was used to treat severe, recurrent D-lactic acidosis in a patient with short bowel syndrome. Dietary carbohydrate composition was determined after assessment of D-lactic acid production from various carbohydrate substrates by faecal flora in vitro. This approach may be preferable to repeated courses of antibiotics. D-lactic acidosis is a well recognised, but rare, complication of short bowel syndrome and intestinal bypass surgery.' 2 To date, seven children have been reported in whom this disorder occurred as a complication of short bowel syndrome. Non-absorbed carbohydrate is fermented by colonic organisms, but lactobacilli when present, unlike most other bacteria, produce D-lactic acid, which cannot be metabolised by D-lactate dehydrogenase. Absorption leads to a severe metabolic acidosis. Treatment has been directed at altering the colonic flora with antibiotics,2 3 or by administering a standard bacterial flora orally. After prolonged parenteral nutrition she was discharged nine months later on a normal diet together with energy supplements given as sip feed

 

[helen1]

@Avenger
They’re in California:
https://www.customprobiotics.com/

 

[EddieB]

Hi Avenger,
Sorry for all your hardships of late.
I tried that probiotic product, did did not do well. It seems any probiotic causes me to have increases in gas/bloating which drives up the reflux. I’ve also been trying Miyarisan butyrate probiotic, but having the same troubles.

I am in contact with a functional nutritionist that has me testing out two things. One is a binder to grab toxins, and the other is an IgG (non dairy) supplement. Too soon to tell, but her intent is to reduce the LPS and other organic acids.

I avoid posting on these open forums, please PM me if you would like to discuss further.

 

[Avenger]

Hi Avenger,
Sorry for all your hardships of late.
I tried that probiotic product, did did not do well. It seems any probiotic causes me to have increases in gas/bloating which drives up the reflux. I’ve also been trying Miyarisan butyrate probiotic, but having the same troubles.

I am in contact with a functional nutritionist that has me testing out two things. One is a binder to grab toxins, and the other is an IgG (non dairy) supplement. Too soon to tell, but her intent is to reduce the LPS and other organic acids.

I avoid posting on these open forums, please PM me if you would like to discuss further.

Hi Eddie, Kanga Sue, Aidan and Helen1,
sorry has been a while. This is very quick; I need some advice; can you pass this to anyone who may help including Ron Davis. I am awaiting Spinal Surgery on the 30th September. The last month has been particularly bad and the NHS Chief Executive have stated that 'Chronic Fatigue Syndrome' is to remain in my records! and that they cannot put D-Lactic acidosis in my records! (Attachments below).

CFS was not only placed in my discharge summary, but in my A&E and Significant Medical History; Someone has been in my records and changed them, when I am still supported by the Consultant Gastroenterologist who diagnosed D-Lactic acidosis and receiving antibiotics and awaiting FMT which can only be done after I have a D-Lactic assay as prerequisite for licensing.

They are putting me at risk especially during Covid-19; I believe that my human rights are being abused.

But I am not being allowed the D-Lactic assay even after multiple promises from A&E and Microbiology;

Blood Gasses were requested by 4 Doctors from 2002, after falling ill in 1999 and frequent abdominal pain, breathing difficulty, confusion, Seizure, weakness and memory difficulty when most ill; but never performed in 20 years. They preferred to believe that my symptoms were Somatic, when I responded to antibiotics.

I was refused a Doctor Call Out because the Doctor in 2002, who stated that I was drunk; and no Blood Gas test has ever been done since requested. The letter from the Chief Executive avoids my statement that I have never had arterial Blood Gas investigations or D-Lactic acidosis tests since 1st requested in 2017. I have other request letters sent to A&E, but they are all being ignored and CFS has been placed in my records, which my Doctor has attempted to remove. Whoever is doing this may reinstate it.

The only reason that I can give for this behavior is that the Chief Executive do not want to accept my diagnosis and would rather real me in as Psychological or Somatic; I have no idea how to deal with this (the letter is from the Chief Executive).

I am not being allowed the D-Lactic assay requested by at least 6 Doctors and Consultants and I most certainly have not had arterial Blood Gasses performed in 20 years. I have Gastroenterology Consultants and assurances of D-Lactic investigations, but I am having to travel to Birmingham during dangerous fluctuating transient symptoms to have the investigations because I am not being allowed at my own hospital.

I have had to come off antibiotics and become very unwell to have the investigations, but can only get them performed in Birmingham and bloods sent to the Birmingham Children's Hospital (where the expertise is, but I am excluded).

I am publishing part of the letter sent to me; I really need some help with this; my consultant is still backing my diagnosis but the NHS Chief Executive in my area will not allow me to verify my diagnosis through a D-Lactic Assay; I have no chance of FMT without a D-Lactic assay and will have to remain on failing antibiotics as I gain further resistance. I have not been allowed the probiotics used for D-Lactic patients in UK, USA and Europe. I am being deliberately sabotaged and acted against. I am at my wits end and close to a breakdown and surgery tomorrow!

D-lactic Acidosis: Successful Suppression of D-lactate–Producing Lactobacillus by Probiotics Bahtiyar Yilmaz, PhD,a Susanne Schibli, MD,b Andrew J. Macpherson, MD, PhD,a Christiane Sokollik, MDb

Intestinal microbiota composition in children with short bowel syndrome (SBS) is an important factor influencing the clinical outcome. An increase of D-lactate–producing bacteria can lead to D-lactic acidosis, also referred to as D-lactate encephalopathy, with severe neurologic impairment. Antibiotic treatments for D-lactic acidosis in children with SBS offer often only short term relief. Here, we present the case of a boy with SBS who developed recurrent episodes of D-lactic acidosis even under continuous cycling antibiotic treatment. Microbiological analyses were used to detect the presence of D-lactate–producing Lactobacillus species in the stool samples. A probiotic cocktail was introduced to alter the intestinal microbiota. During follow-up under treatment with probiotics, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year. Stool composition of the patient was sequenced regularly over that period. His microbiota profile changed completely in species richness, and a clustering of species according to probiotic usage was seen. Importantly, D-lactate–producing Lactobacillus strains disappeared within a few weeks after probiotic introduction and were no longer detected in the subsequent

Paul.

 

[kangaSue]

@Avenger You said earlier on in this thread that you were taking Multiflor (reply #234), was that a miss-spelling and you actually meant you were taking Mutaflor?
I'm prompted to ask that from reading the following blog article saying that beneficial ecoli is also lacking in ME/CFS patients;
https://www.fxmedicine.com.au/blog-...ng-probiotic-strains-chronic-fatigue-syndrome

 

[Avenger]

@Avenger You said earlier on in this thread that you were taking Multiflor (reply #234), was that a miss-spelling and you actually meant you were taking Mutaflor?
I'm prompted to ask that from reading the following blog article saying that beneficial ecoli is also lacking in ME/CFS patients;
https://www.fxmedicine.com.au/blog-...ng-probiotic-strains-chronic-fatigue-syndrome

Hi KangaSue,
I came out of spinal surgery a few days ago. I am sendingo this of my phone andi feel pretty weak.
Yes i used Ecoli in one of many Probiotic experiments
Rhasmosus is one of my favirites. But i will put up a beter list when i am out. Will try of out tomorrow.

 

[Jwarrior77]

Had anyone noticed that their stool is pale of of strange consistency? I've been taking ox bile and it's helped a little bit especially with the symptoms but not everything. I don't know if I need to take more. Bile helps regulate and even kill microbial growth so I think that's why it's helping. I also realized when I develop irritable bowel I don't get the d-lactate symptoms. However when I was healthy I would get irritable bowel all the time. Now I hardly get it which is very strange.

 

[Avenger]

This may be one of the most important Reports that I have placed online;

Plasma D (-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion;
Ischema of the Gastrointestinal Tract.

I am writing 14 days after Spinal Surgery, so please forgive any errors; I am still in pain and badly fatigued.

This is of direct relevance to how I developed D-Lactic/Bacterial Overgrowth Symptoms; There are many ways to develop Bacterial Overgrowth. But this is of direct relevance to myself and possibly many others; I developed Sepsis due to intestinal injury and was then given repeat antibiotics. This is the first time that I have fully understood the implications of the report below and I believe that it may be relevant to a number of us. I believe that Non-Steroidal Anti-Inflammatories are capable of causing such Gastrointestinal injury and Ischema. I have only realised now that I was given nothing to protect my Gut (just over 20 years ago) while taking prescribed NSAID's at high dosage to stop pain from two shoulder tears and pars defect with collapsed disc, that was all misdiagnosed as Chronic Fatigue Syndrome or Somatization disorder.

NSAID's stop the healing process by inhibiting Cox1, Cox2 enzymes, Proteoglycan and Prostaglandin Synthesis to over 90% which is the cause for damage to the mucosal lining. COX-1 produces prostaglandins that activate platelets and protect the stomach and intestinal lining. NSAIDs block the COX enzymes and reduce production of prostaglandins;''NSAIDs inhibit prostaglandin synthesis, which normally potentiates the pain caused by other inflammatory mediators (such as histamine and bradykinin). NSAIDs work by reversibly inhibiting cyclo-oxygenase (COX) enzymes — the two main types of COX enzyme are COX-1 and COX-2, which have different physiological functions.''

It took from my falling ill in 1999 untill 2003 when Sepsis was first diagnosed; but the infection was never fully eradicated and Sepsis returned and I was given repeat Antibiotics; But the Somatization disorder diagnosis was never rescinded, because I remained ill from undiagnosed D-Lactic acidosis, with repeat bouts of breathing difficulty and abdominal pain and multiple neurological symptoms deemed Somatic. When illness started in 1999, I had such bad abdominal pain that I was frequently in hospital and then a blockage (extreme constipation) and was taken into hospital on holiday when breathing difficulty began.


Prior to falling ill in 1999, I was given high doses of NSAID's (Non-Steroidal Anti-Inflammatory) Drugs for several years at high dosage before becoming unwell, when I developed repeated extreme abdominal pain, pounding abdomen, and illness including breathing difficulty that was just dismissed; when my illness was passed off as 'Chronic Fatigue Syndrome', ME, Anxiety and finally diagnosed as Somatization disorder by a Clinician who only saw me on one short occasion (Doctors are simply not trained to understand Bacterial Overgrowth and the symptoms, including abdominal pain are used to make a psychological diagnosis of Somatization; If you have abdominal pain with seeming no explanation, then you will be blamed as Somatizing, because no one was trained to recognise such a condition that can lead to Bacterial Overgroth or D-Lactic illness; and Doctors have still not been trained to do so). If you develop hyperventilation due to acidosis it will be misunderstood as anxiety, overbreathing or hyperventilation syndrome (when hyperventilation is a natural process to eliminate acidosis and CO2). 4 Doctors requested Arterial Blood Gasses from 2002, which were never performed to date; so my symptoms reamained undiagnosed because normal blood tests were often unremarcable as found for many D-Lactic patients even during exacerbation of symptoms (Oxygen levels can remain normal, but you cannot utilise the Oxygen due to increased CO2 and acidity when Mitochondrial Dysfunction occurs). The only signature for this form of acidosis is a Blood Gas, D-Lactic or Faecal assay (to show specific bacteria in overgrowth). Breathing difficulty feels like being suffocated and you naurally breath faster.

The investigations necessary to make such a diagnosis were never performed for myself. The Doctor who diagnosed Somatization disorder in 1999, wrote to other Doctors urging them not to perform further investigations. The Non-Steroidals were later blamed by two Gastroenterologists as the cause of the Infection that led to Sepsis, Bacterial Overgrowth and D-Lactic symptoms.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806238/

World J Gastroenterol. 1997 Dec 15; 3(4): 225–227.

Published online 1997 Dec 15. doi: 10.3748/wjg.v3.i4.225
PMCID: PMC4806238
PMID: 27053870
Plasma D (-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion
Yong-Ming Yao, Yan Yu, Ye Wu, Lian-Rong Lu, and Zhi-Yong Sheng
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Go to:
Abstract
AIM: To observe the kinetics of D (-)-lactate alteration in both portal and systemic circulation systems, and its relationship with intestinal injury in rats subjected to acute intestinal ischemia-reperfusion.
METHODS: Anesthetized rats underwent a 75-min superior mesenteric artery occlusion followed by a 6-h reperfusion. Plasma D (-)-lactate levels were measured by an enzymatic spectrophotometric assay.
RESULTS: Intestinal ischemia for 75 min resulted in a significant elevation of D (-)-lactate levels in the portal vein, as compared with the baseline values (P < 0.05). Plasma D (-)-lactate levels had a tendency to further increase after reperfusion, up to 6 h. Similar alterations in D (-)-lactate were also found in systemic circulation, and there were no significant differences between the portal and systemic circulations at any time point. Moreover, the macropathological evaluation scores were significantly correlated to the portal D (-)-lactate levels in animals at various time points (r = 0.415, P < 0.01). In addition, there was a remarkable rise of endotoxin concentration within the portal vein at the end of the 75-min ischemic period (P < 0.05), reaching a peak at 2 h post-reperfusion.
CONCLUSION: Acute intestinal ischemia is associated with failure of the mucosal barrier resulting in increased plasma D (-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might further increase D (-)-lactate levels, which are correlated to the macropathological alterations. Plasma D (-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.
Keywords: D (-)lactate, Endotoxin, Intestinal injury, Reperfusion injury
Go to:
INTRODUCTION
Major trauma and shock may initiate a cascade of events leading to sepsis with subsequent multiple organ failure. Gut mucosal barrier dysfunction is assumed to play an important role in causing the septic process[1]. From our and other studies, it has been suggested that enteric organisms and/or their toxins might translocate across the intestinal mucosa, entering the systemic circulation via the lymphatic or portal systems and resulting in the development of remote organ damage in animals and patients with shock following hemorrhage, trauma, or burns[1-3].
The intestine is one of the most sensitive tissues to ischemia-reperfusion injury. Reperfusion of the intestine is often associated with increased mucosal permeability and ulceration. Mucosal injury has been assessed either morphologically or by measuring the permeability of the mucosal barrier to small or large solutes; however, there exists no reliable serum marker for the early diagnosis of acute intestinal insult in clinical practice.
D (-)-lactate is produced by indigenous bacteria found in the gastrointestinal tract, and mammals do not possess the enzyme systems to rapidly metabolize it[4]. Therefore, an increase in D (-)-lactate might reflect an efflux of bacteria and/or their products into circulation as a result of mucosal injury. Recently, a report was published showing that serum D (-)-lactate was increased in animal models of acute intestinal ischemia and simple obstruction[5]; yet, it remains unclear whether this process is associated with a significant dysfunction in mucosal barrier following reperfusion.
The present study was designed to determine the kinetics of plasma D (-)-lactate changes, and to examine whether D (-)-lactate levels are correlated to intestinal damage in rats caused by acute intestinal ischemia-reperfusion injury.

RESULTS
As shown in Figure Figure1,1, intestinal ischemia for 75 min resulted in a significant elevation in D (-)-lactate levels in portal vein as compared with the baseline values (P < 0.05). Plasma D (-)-lactate levels had a tendency to further increase after reperfusion, up to 6 h. Similar alterations in D (-)-lactate were also found in systemic circulation (Figure (Figure1),1), there were no significant differences between the portal and systemic circulations at any time point.

Figure 1
Kinetics of plasma D (-)-lactate alteration in portal and systemic circulation systems. Six to nine animals were assessed for each time point. Data are expressed as x ± sx-. aP < 0.05 and bP < 0.01 vs baseline values.
The animals were found to have no abnormal changes in bowel functions before the induction of intestinal ischemia. SMA occlusion for 75 min caused marked intestinal damage, which was much worse upon reperfusion. The macropathological evaluation scores were 2.0 ± 0.2, 2.2 ± 0.2 and 2.7 ± 0.1 at 0.5, 2, and 6 h after reperfusion. The macropathological evaluation scores of intestine were significantly correlated to portal D (-)-lactate levels in animals at various time points (r = 0.415, P < 0.01; Figure Figure22).

Figure 2
Correlation between the macropathological evaluation scores of intestine and the portal D (-)-lactate levels in animals subjected to intestinal ischemia-reperfusion injury.
The endotoxin concentration within portal vein rose remarkably in the control animals, being 9.5-fold over the baseline values at the end of 75-min ischemia (P < 0.05). It reached a maximum at 2 h after clamp release, and decreased gradually up to the end of the observation period (Figure (Figure33).

Figure 3
Changes in plasma endotoxin concentration in portal vein following acute intestinal ischemia-reperfusion injury. Six to nine animals were assessed for each time point. Data are expressed as x ± sx-. aP < 0.05 and bP < 0.01 vs baseline values.
Go to:
DISCUSSION
In the present experiment, we observed that ischemia-reperfusion of the small bowel resulted in a significant elevation in D (-)-lactate levels in both portal and systemic blood. This was potentially associated with failure of the intestinal mucosal barrier leading to the subsequent escape of indigenous endotoxin/bacteria to the circulation systems. Our data also suggested that an early and sustained rise in systemic D (-)-lactate might occur during mesenteric ischemia, even without further reperfusion injury[5].
The normal gut epithelium provides an anatomical and physiological barrier to the toxic intestinal contents. Conditions which lead to mesenteric hypoperfusion, such as those seen in hemorrhage and other shock states, have been shown to cause breakdown of the intestinal mucosal barrier[1-3,9]. In this study, the status of the mucosal barrier was assessed quantitatively using a plasma marker, namely D (-)-lactate. D (-)-lactate is strictly a product of bacterial fermentation, and it is known to be produced by many species of bacteria found in the gut flora[4,5], while mammalian tissue does not produce D-lactic acid, which may not or only slowly be metabolized. D-lactic acid accumulating in the blood can generally be considered as a result of active bacterial metabolism due to systemic infections or some gastrointestinal disorders. In fact, D-lactate acidosis has been described in humans with short bowel syndrome, as well as bacterial infections[10]. More recently, in a clinical study, Murray et al[11]demonstrated that patients found to have mesenteric ischemia at laparotomy had significantly elevated D (-)-lactate levels in peripheral blood as compared with the patients with other acute or normal abdominal conditions. Thus, circulating D (-)-lactate could aid in diagnosing acute mesenteric ischemia[5]. From the current experiment, it is clearly revealed that marked elevation in plasma D (-)-lactate occurred during the occlusive episode, which had a tendency to further increase after release of the clamp and was correlated with a progressive disintegration in the histology of the small bowel in response to reperfusion injury. Therefore, plasma D (-)-lactate appears to be a useful marker reflecting gut barrier damage in the setting of acute ischemia-reperfusion insult.

The mechanisms by which intestinal ischemia-reperfusion leads to a sustained elevation in plasma D (-)-lactate are not entirely understood from this experiment; although, it is possible that acute intestinal insult might cause substantial mucosal injury and increase permeability, thereby inducing an efflux of bacteria and their metabolic products into the portal circulation. In this study, the pathological examination showed marked intestinal lesions during ischemia, which became worse upon reperfusion. Another possible explanation would be that an increased gut permeability might attribute to release of inflammatory mediators, particularly tumor necrosis factor, which is considered to be induced by gut-derived endotoxin/bacteria, as well as hypoxia. These mediators may directly damage the mucosal barrier function[6]. In addition, it has been reported that ischemia-reperfusion injury to the intestine is associated with overgrowth of the residing microbial flora, and normally low plasma D (-)-lactate levels could be elevated markedly as a result of increased release of D-lactate by bacterial proliferation concomitant to increased mucosal permeability. Our previous observation that the overgrowth of Gram-negative bacteria in the intestinal tract was associated with an increase in intraluminal bacterial products, such as endotoxin following hemorrhage and resuscitation[3], gives further support to this opinion. Finally, since D-lactate is not metabolized in the liver; persistent elevation of D-lactate level in both portal and systemic circulation systems following intestinal ischemia-reperfusion injury resulted in similar D (-)-lactate concentration in the peripheral and portal vein throughout the observation period. Therefore, our data might be of potential importance, serving as the experimental basis for the favorable clinical use of D (-)-lactate in the diagnosis of acute intestinal disorders related to ischemia-reperfusion injury.
In summary, these data suggest that acute intestinal ischemia is associated with failure of the mucosal barrier resulting in increased plasma D (-)-lactate levels in both portal and systemic blood, and it is also remarkably enhanced by the subsequent reperfusion. Plasma D (-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insult.
Go to:
ACKNOWLEDGMENTS
The authors express their gratitude to all colleagues who have been of considerable help in the realization of this study, in particular to Dr. Zhou Bao-Tong, Dr. S Bahrami, and Dr. G Schlag.
Go to:
Footnotes

S- Editor: A L- Editor: Filipodia E- Editor: Li RF

Go to:
References
1. Swank GM, Deitch EA. Role of the gut in multiple organ failure: bacterial translocation and permeability changes. World J Surg. 1996;20:411–417. [PubMed] [Google Scholar]
2. Yao YM, Bahrami S, Leichtfried G, Redl H, Schlag G. Pathogenesis of hemorrhage-induced bacteria/endotoxin translocation in rats. Effects of recombinant bactericidal/permeability-increasing protein. Ann Surg. 1995;221:398–405. [PMC free article] [PubMed] [Google Scholar]
3. Yao YM, Sheng ZY, Tian HM, Wang YP, Yu Y, Fu XB, Lu LR, Wang DW, Ma YY. Gut-derived endotoxemia and multiple system organ failure following gunshot wounds combined with hemorrhagic shock: an experimental study in the dog. J Trauma. 1995;38:742–746. [PubMed] [Google Scholar]
4. Smith SM, Eng RH, Buccini F. Use of D-lactic acid measurements in the diagnosis of bacterial infections. J Infect Dis. 1986;154:658–664. [PubMed] [Google Scholar]
5. Murray MJ, Barbose JJ, Cobb CF. Serum D(-)-lactate levels as a predictor of acute intestinal ischemia in a rat model. J Surg Res. 1993;54:507–509. [PubMed] [Google Scholar]
6. Yao YM, Bahrami S, Redl H, Schlag G. Monoclonal antibody to tumor necrosis factor-alpha attenuates hemodynamic dysfunction secondary to intestinal ischemia/reperfusion in rats. Crit Care Med. 1996;24:1547–1553. [PubMed] [Google Scholar]
7. Brandt RB, Siegel SA, Waters MG, Bloch MH. Spectrophotometric assay for D-(-)-lactate in plasma. Anal Biochem. 1980;102:39–46. [PubMed] [Google Scholar]
8. Schlag G, Redl H, van Vuuren CJ, Davies J. Hyperdynamic sepsis in baboons: II. Relation of organ damage to severity of sepsis evaluated by a newly developed morphological scoring system. Circ Shock. 1992;38:253–263. [PubMed] [Google Scholar]
9. Haglund U. Gut ischaemia. Gut. 1994;35:S73–S76. [PMC free article] [PubMed] [Google Scholar]
10. Marcos MA, Vila J, Gratacos J, Brancos MA, Jimenez de Anta MT. Determination of D-lactate concentration for rapid diagnosis of bacterial infections of body fluids. Eur J Clin Microbiol Infect Dis. 1991;10:966–969. [PubMed] [Google Scholar]
11. Murray MJ, Gonze MD, Nowak LR, Cobb CF. Serum D(-)-lactate levels as an aid to diagnosing acute intestinal ischemia. Am J Surg. 1994;167:575–578. [PubMed] [Google Scholar]