Re: Lyrica side effects versus pain relief///

[Guest guest]

Darlene,

The one that almost did me in was chloramphenicol, and it kills oxalobacter

formigenes. Oxalates getting into the bone marrow can produce exactly the

damage that was found in my bone marrow.

Here is information on which antibiotics kill back this indispensible

anaerobic bacteria.

============================

>Date: Fri, 20 May 2005 10:54:09 -0500

>

>Subject: Which antibiotics kill oxalobacter

>

>Listmates,

>

>There are some antibiotics which kill the bacteria that break down

>oxalates. To quote Emedicine's article on hyperoxaluria: " Oxalobacter is

>relatively resistant to penicillin and sulfa but sensitive to macrolides,

>fluoroquinolones, and tetracyclines. "

>

>Here are some names of antibiotics in those classes:

>

>Macrolides

>

> Azithromycin

> Clarithromycin

> Clindamycin

> Erythromycin

> Lincomycin

>

>FLUOROQUINOLONES

> Ciprofloxacin

> Enoxacin

> Grepafloxacin

> Levofloxacin

> Lomefloxacin

> Norfloxacin

> Ofloxacin

> Sparfloxacin

> Trovafloxacin

>

>Tetracyclines

>

> Demeclocycline

> Doxycycline

> Minocycline

> Oxytetracycline

> Tetracycline

>

>If you have taken a generic, and suspect it could have killed off

>oxalabacter, your pharmacist can tell you for which brand name the generic

>was providing substitution.

>

>

Listmates,

Someone mentioned today using flagyl, so I wanted to give you some

information about something good that may be killed back by flagyl and some

other antibiotics, and I'd like to share what you might be able to do to

make sure this temporary situation doesn't cause later problems.

Today I read a study which examined the ability of different antibiotics to

kill the most talented anaerobic degrader of oxalates. Lack of this

bacteria in the stool and GI tract has been noted in many oxalate-related

diseases. This bacteria called oxalobacter formigenes lives by eating

oxalate, and it turns oxalate into something else that isn't harmful. We

have been learning about a lot of negatives that oxalate may have been

producing in children with autism or related disorders when it is absorbed

through a leaky gut.

This is the article:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=124017

It says that oxalobacter formigenes is killed back by:

chloramphenicol (chloromycetin)

nalidixic acid (no longer used in US)

erythromycin

clarithromycin (Biaxin)

co-amoxiclav (Augmentin)

metronidazole (flagyl)

and doxycycline (the only tetracycline they studied).

At the concentration used in these experiments, the two strains they tested

were not killed back by amoxicillin or ampicillin. This may be very good

news since these last two penicillin-related antibiotics may be able to

treat strep, which seems to be an issue in some of the kids on LOD. (Strep

and other bacteria may be encapsulated by calcium oxalate, but not killed,

so they can rear their heads again later and end up reinfecting their host

rather than coming from the outside world.)

This study's findings should tell us about the importance of having the

strategy of staying off high oxalate foods whenever someone takes

antibiotics that might target anaerobes such as these. What can happen

when someone stays HIGH oxalate after such an antibiotic?

I may have mentioned this before. Years ago, I took two rounds of

chloramphenicol (which is on this list). It kills oxalobacter formigenes.

Back in the last 1960's there was a huge stink and they severely restricted

the use of this antibiotic (after it damaged me) because so many people

died from bone marrow failure. Many of these victims had had two rounds of

this drug like I did. The bone marrow issues only occurred in a fraction

of a percentage of patients, but they occurred after a delay of many

months....long after the drug could have had any direct toxicity. Nobody

ever figured out what distinguished the patients who succumbed.

I remembered that some time following taking this drug I began to crave

spinach and developed a daily habit of eating a whole box of frozen spinach

all by myself. Within about four or five months of taking the antibiotic,

I developed bone marrow failure....and this was the very length of delay

they saw in many others. I survived after a splenectomy, but many who had

this delayed onset of " toxicity " did not survive and I don't think anyone

was asking who was eating spinach!

After I began the research on oxalates three years ago, I learned that

oxalate (when it gets in bone marrow) is known to produce EXACTLY the same

damage as the doctors found in my bone marrow, and oxalate can produce the

same damage that also occurred in my retina and caused blindness in one eye

at the same time. Of course, I don't know what predispositions will lead

oxalate to collect in the bone marrow or in the retina in some people but

not in others, but wherever this toxic chemical goes in high amounts, it

isn't pretty!

I'd also like to point out that this may be an important place where the

work on lyme and LOD meet. Maybe a lot of the long sequelae of lyme

disease (all the pain in joints and elsewhere) is imposed by the

appropriate use of antibiotics which unfortunately may kill back

oxalobacter formigenes. This could be similar to what happens in cystic

fibrosis, where liberal use of antibiotics is rather routine. We have had

some very successful LODers with cystic fibrosis on our listserve with VERY

interesting things to report about changes in their sputum..

I'm putting below articles on the connection between lack of oxalobacter

formigenes and the presence of excess oxalate.

I hope this can help spare some people using flagyl an unpleasant

consequence that might not show up for months because it involves a slow

buildup of something toxic.

Does anyone have any stories that make sense in the light of these findings?

By the way, a probiotic made of oxalobacter formigenes is being developed

as a drug and is going through phase III trials. It will probably be out

in about a year to treat kidney disease and will require a prescription. I

know the scientists developing this product and they are eager to do an

autism study after their product is approved!

2: Am J Kidney Dis. 2005 Sep;46(3):440-5.

Absorptive hyperoxaluria leads to an increased risk for urolithiasis or

nephrocalcinosis in cystic fibrosis.

Hoppe B, von Unruh GE, Blank G, Rietschel E, Sidhu H, Laube N, Hesse A.

University Children's Hospital Cologne, Germany, USA. bernd.hoppe@...

BACKGROUND: Hyperoxaluria has been incriminated to account for the increased

incidence of urolithiasis or nephrocalcinosis in patients with cystic fibrosis

(CF). Hyperoxaluria presumably is caused by fat malabsorption and the

absence of

such intestinal oxalate-degrading bacteria as Oxalobacter formigenes. To better

elucidate its pathophysiological characteristics, we prospectively studied

patients with CF by determining these parameters and performing renal

ultrasonography twice yearly. METHODS: In addition to routine tests in urine

(lithogenic and stone-inhibitory substances), the presence of O formigenes was

tested in stool, plasma oxalate was measured, and a [13C2]oxalate

absorption test

was performed in 37 patients with CF aged 5 to 37 years (15 females, 22 males)

who were constantly hyperoxaluric before the study. RESULTS: Hyperoxaluria

(oxalate, 46 to 141 mg/1.73 m2/24 h [0.51 to 1.57 mmol/1.73 m2/24 h]; normal, <

45 mg/1.73 m2/24 h [< 0.5 mmol/1.73 m2/24 h]) was now found in 24 patients

(64.8%). Plasma oxalate levels were elevated in 6 patients (7.92 to 19.5

micromol/L; normal, 6.3 +/- 1.1 micromol/L). Oxalobacter species were

detected in

only 1 patient. Intestinal oxalate absorption was elevated (11.4% to 28.5%;

normal, < 10%) in 23 patients. Hypocitraturia was present in 17 patients

(citrate, 0.35 to 2.8 g/1.73 m2/24 h [0.2 to 1.1 mmol/1.73 m2/24 h]; normal

female, > 2.8 mg/1.73 m2/24 h [> 1.6 mmol/1.73 m2/24 h]; male, > 3.3 mg/1.73

m2/24 h [> 1.9 mmol/1.73 m2/24 h]). Urine calcium oxalate saturation was

elevated

in 17 patients (5.62 to 28.9 relative units; normal female, < 5.5 relative

units;

male, < 6.3 relative units). In 16% of patients, urolithiasis (n = 2) or

nephrocalcinosis (n = 4) was diagnosed ultrasonographically. CONCLUSION:

Absorptive hyperoxaluria and hypocitraturia are the main culprits for the

increased incidence of urolithiasis and nephrocalcinosis in patients with

CF. We

advocate high fluid intake, low-oxalate/high-calcium diet, and alkali citrate

medication, if necessary. Additional studies are necessary to determine the

influence of Oxalobacter species or other oxalate-degrading bacteria on oxalate

handling in patients with CF.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 16129205 [PubMed - indexed for MEDLINE]

3: J Endourol. 2005 Jan-Feb;19(1):102-6.

Effect of antibiotics on Oxalobacter formigenes colonization of human

gastrointestinal tract.

Mittal RD, Kumar R, Bid HK, Mittal B.

Department of Urology, Sanjay Gandhi Postgraduate Institute of Medical

Sciences,

Lucknow, India. ramamittal@...

BACKGROUND AND PURPOSE: Oxalobacter formigenes is a bacterium residing in the

human gastrointestinal tract that degrades oxalate and reduces its availability

for absorption. This bacterium is assumed to be antibiotic sensitive, and

repeated antibiotic therapies could eradicate it. The aim of the present study

was to determine the differences in the colonization by O. formigenes of

individuals who had been on antibiotics for at least 5 days at the time of

sample

collection and individuals who had not taken antibiotics for at least 3 months.

PATIENTS AND METHODS: Stool samples were collected from 80 individuals without

stone disease (35 with and 45 without antibiotic consumption) and 100 patients

with stone disease (20 with and 80 without antibiotic consumption). Oxalobacter

formigenes was detected by a polymerase chain reaction-based method, and the

presence/absence of O. formigenes was correlated with urinary oxalate

concentrations. RESULTS: Lower percentages of individuals without stone disease

and with stone disease who were consuming antibiotics had O. formigenes

colonization than individuals without antibiotic consumption. Urinary oxalate

concentrations were higher in the individuals without O. formigenes than in

colonized individuals. CONCLUSION: Our observations confirm a direct

association

between antibiotic consumption and absence of O. formigenes. Absence of

intestinal O. formigenes could represent a pathogenic factor in calcium oxalate

urolithiasis when antibiotics are prescribed generously.

Publication Types:

Comparative Study

PMID: 15735393 [PubMed - indexed for MEDLINE]

4: J Gastroenterol Hepatol. 2004 Dec;19(12):1403-9.

Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel

disease: possible role in renal stone formation.

Kumar R, Ghoshal UC, Singh G, Mittal RD.

Department of Urology, Sanjay Gandhi Post Graduate Institute of Medical

Sciences,

Lucknow, India.

BACKGROUND AND AIM: Calcium oxalate renal stones (RS) and hyperoxaluria are

common in patients with inflammatory bowel disease (IBD). The absence of

intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause

hyperoxaluria in IBD. The aim of the present study was to examine: (i) the

colonization of O. formigenes in patients with IBD and controls and to

correlate

its presence with urinary oxalate excretion; and (ii) urinary analytes

contributing to RS in IBD. METHODS: Stool samples were studied for O.

formigenes

using polymerase chain reaction and Southern blotting in patients with IBD (n =

48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy

subjects that were used as controls (n = 48). Levels of urinary oxalate,

citrate,

calcium, magnesium, creatinine and uric acid were estimated

spectrophotometrically in each patient and in 13 controls for 24 h.

RESULTS: Five

of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients

with

IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized

with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD).

Patients without O. formigenes had higher urinary oxalate than those with it

(IBD, median 0.48 [range 0.11-2.09]vs 0.43 [range 0.16-1.10] mmol/24 h, P = NS;

RS, median 0.59 mmol/24 h, range 0.14-1.90 vs 0.44 mmol/24 h, range

0.23-0.97; P

= 0.008, Mann-Whitney U-test). Median excretion of oxalate was higher in

IBD and

RS than in controls (0.47 [0.11-2.09], 0.56 [0.14-1.9] and 0.41 [0.21-0.62]

mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD

and RS

than in controls (6.50 [1.38-21.00], 6.78 [1.55-20.30] and 4.99 [1.47-9.60]

mmol/24 h; P < 0.05, Kruskal-Wallis H-test), respectively. Median urinary

magnesium was higher in IBD than in RS and controls (4.57 [1.50-12.30], 3.60

[0.90-6.35] and 2.49 [0.74-4.80]; P < 0.001, Kruskal-Wallis H-test),

respectively. Urinary citrate excretion was comparable in IBD, RS and controls.

CONCLUSIONS: Patients with IBD and RS rarely have O. formigenes in their stools

as compared with controls; this may contribute to hyperoxaluria in IBD.

Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD.

Hypermagnesuria in patients with IBD may protect them from RS.

PMID: 15610315 [PubMed - indexed for MEDLINE]

6: Hinyokika Kiyo. 2003 Jul;49(7):371-6.

[Detection of Oxalobacter formigenes in human feces and study of related

genes in

a new oxalate-degrading bacterium]

[Article in Japanese]

Kodama T, Mikami K, Akakura K, Takei K, Naya Y, Ueda T, Ito H.

Department of Urology, Graduate School of Medicine, Chiba University.

The first objective of the present study was to examine the presence of

Oxalobacter formigenes (an oxalate-degrading bacterium in the human intestine)

according to sex in a large number of Japanese. The second objective was to

study

the presence of three related genes in Bifidobacterium breve, which is

considered

to be a new oxalate-degrading bacterim. Fecal samples were collected from

55 male

and 37 female healthy volunteers. O. formigenes was detected by a polymerase

chain reaction (PCR) and a culture-based method. DNA was amplified by the PCR

method including the site of important base sequences of each gene in order to

detect oxc, frc, and OxlT. O. formigenes was present in 80% of 54 male and

62% of

34 female subjects in the PCR-based assay, while it was present in 62% of

40 male

and 50% of 24 female subjects in the culture-based assay. The partial base

sequences of the three related genes in B. breve were determined. The RNA

polymerase-binding site in promoters and the rho-independent termination

sequence

were preserved in oxc and frc. In conclusion, the rate of the presence of O.

formigenes was the same as in previous reports. Female subjects showed a 15%

lower rate than males. B. breve is considered to be an oxalate-degrading

bacterium since it was found to have oxalic acid-degrading ability and three

genes involved in oxalate degradation.

Publication Types:

English Abstract

PMID: 12968475 [PubMed - indexed for MEDLINE]

7: J Endourol. 2003 May;17(4):239-43.

Molecular epidemiology of fecal Oxalobacter formigenes in healthy adults living

in Seoul, Korea.

Kwak C, Jeong BC, Kim HK, Kim EC, Chox MS, Kim HH.

Department of Urology, Seoul National University College of Medicine and

Clinical

Research Institute, Seoul National University Hospital, Seoul, Korea.

BACKGROUND AND PURPOSE: Oxalobacter formigenes is a member of the intestinal

flora that degrades oxalate. This bacterium maintains an important symbiotic

relation with its hosts by regulating oxalic acid absorption in the

intestine as

well as oxalic acid concentrations in plasma. We tried to define the prevalence

of fecal O. formigenes positivity in healthy adults. MATERIALS AND METHODS:

Whole-bacterial DNA was isolated directly from fresh stool samples obtained

from

233 healthy adults known to be free of urolithiasis. Genus-specific

oligonucleotide sequences corresponding to homologous regions residing in

the oxc

gene that encodes oxalyl-coenzyme A decarboxylase were designed. A PCR-based

assay was done on the stool samples. RESULTS: A PCR product of 416 bp encoding

the oxc gene was detected in 197 of the 233 stool samples (76.8%). Adjusted to

the Seoul population census 1995, the calibrated fecal O. formigenes-positive

rate was estimated to be 76.7%: 79.2% in men and 74.2% in women, with no

significance difference according to age or sex. CONCLUSION: These results

suggest that O. formigenes inhabits the intestine of three fourths of the

normal

Korean populations. These data provide a base for further studies to

uncover the

relation between O. formigenes and urolithiasis.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 12816588 [PubMed - indexed for MEDLINE]

At 11:02 AM 3/4/2008, you wrote:

>,

>What antibiotic? I ended up being deathly allergic to something

>called Trovan; I believe they ended up taking it off the market

>because folks had strokes and died and all kinds of horrid things!

>

>Darlene

>

> > (who had an extremely rare reaction to an antibiotic (1 in

>20,000

> > people) but eventually, they greatly restricted the use of the

>product

> > because there were others like me who began to have bone marrow

>failiure

> > some months after taking the drug. Many of them died, but I

>didn't, obviously)

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