Admin Control Panel

New Post | Settings | Change Layout | Edit HTML | Edit posts | Sign Out

Scroll down and select country
MEBO TMAU TESTING CURRENTLY SUSPENDED INDEFINITELY

MEBO - UBIOME study 2018

'PRESS RELEASE'

NCT03582826
ClinicalTrials.gov

MEBO Gut Microbiome Study
"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"
Funded by uBiome Research Grant

"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"

Dynamics of the Gut Microbiota in
Idiopathic Malodor Production
& PATM

Started May 2018 - Ongoing

Current people sent kits : 100/100
3 kits per person

NO LONGER RECRUITING

Participation info : LINK English

MEBO Map Testing & Meetups


Full details : https://goo.gl/TMw8xu
want listed ? contact info@meboresearch.org

MEBO Private Facebook Group
to join : go to
or contact
Ubiome Gut EXPLORER
10% OFF

Update : discount is suspended
Join/Watch the weekly
BO Sufferers Podcasts

MEBO TMAU Videos

Petitions

TMAU Petition world
TMAU UK end total:262
TMAU UK ends 23/01/20
TMAU Petition USA end total 204
USA : Moveon open
TMAU (Dominican)
Metabolomic Profiling Study
NCT02683876

Start : Aug 2016
Stage 1 : 27 Canadian volunteers to test
Latest click here (26 oct) :
17 samples returned


Note : Stage 1 is Canada only.
Return cut-off date : passed
Analysis can take 6/8 weeks
Analysis start in/before Nov
MEBO Research is a
EURORDIS and
NORD Member Organization
See RareConnect

Popular Posts (last 30 days)

Upcoming get-togethers


Let us know if you want a meetup listed

Subscribe to Blog

Enter your email address:

Delivered by FeedBurner

You will be sent a verification email

Subscribe in a reader

Blog Archive

London TMAU meeting with Prof Liz Shephard
19th Oct 11am - 1pm
St Mary's Hospital
Praed St, Paddington
London W2 1NY
click to read more

MEBO Research Clinical Trials

Click here to read details of the MEBO Clinical Trials
NCT03582826 - Ongoing not recruiting
Microbial Basis of Systemic Malodor and PATM Conditions (PATM)
United States 2018 - ongoing

NCT02683876 - Completed
Exploratory Study of Relationships Between Malodor and Urine Metabolomics
Canada and United States 2016 - ongoing

NCT03451994 - Completed
Exploratory Study of Volatile Organic Compounds in Alveolar Breath
United Kingdom and United States 2013 - ongoing

NCT02692495 - Completed
Evaluation of Potential Screening Tools for Metabolic Body Odor and Halitosis
United Kingdom 2009 - 2012

Sunday, November 29, 2009

Bad drug reactions in people with systemic body odor

Systemic body odor/halitosis : Do you have bad reactions to drugs/medicines ?

People with systemic body odor and/or halitosis often mention they have bad reactions to drugs. This isn't surprising, since drugs and odorous compounds are probably often dealt with by the phase1/phase2 biotransformation enzyme group of enzymes, of which FMO3 is one. In general, we have 2 'layers' of these enzymes, phase1 and phase2 (in truth there are many exceptions to the 'rules'). FMO3 is one of the phase1 enzymes, along with the CYP450 family of enzymes, which is regarded as the 'main player' in Phase1 (perhaps because greater understanding of FMO3 is needed). These enzymes are often involved in oxidation reactions (such as FMO3 oxidizing trimethylamine to trimethylamine-n-oxide).

FMO3 is very commonly involved in many oxidation reactions (probably thousands of substrates). Often, a substrate can take an alternative slower route if for some reason the preferred enzyme is saturated (though not trimethylamine, apparently).

In this paper, the researchers looked at the 'clearance' from the blood (detoxification) of the drug Voriconazole. They say that most of the detoxification of voriconazole in humans is done by CYP3A4, CYP2C19, and flavin-containing monooxygenase 3 (FMO3). Apparently in children the clearance rate is faster because they don't use CYP3A4 so much.

body odorAlthough researchers learn more about these enzymes, each paper must be taken with some trepidation, in that often on the journey to agreement about facts, they contradict each other. However as time goes by, a picture emerges.

Whilst having no FMO3 enzyme does not seem to result in death or visual illness, and those with reduced FMO3 function are expected to live a normal lifespan, the enzyme seems to be involved in thousands of substrate oxidation reactions. So it is likely that most FMO3 research is more likely going to be a consequence to bad reactions to drugs (or uselessness of drugs that these enzymes activate, as well as detoxicate) rather than for trimethylaminuria, which the medical community probably has no interest in. Not unless we can promote or petition for research ourselves.
In Vitro Hepatic Metabolism Explains Higher Clearance of Voriconazole in Children versus Adults: Role of CYP2C19 and FMO3.
Yanni SB, Annaert PP, Augustijns P, Ibrahim JG, Benjamin DK, Thakker DR.
1 The University of North Carolina at Chapel Hill;

Voriconazole is a broad spectrum antifungal agent for treating life threatening fungal infections. Its clearance is approximately three-fold higher in children compared to adults. Voriconazole is cleared predominantly via hepatic metabolism in adults, mainly by CYP3A4, CYP2C19, and flavin-containing monooxygenase 3 (FMO3). In vitro metabolism of voriconazole by liver microsomes prepared from pediatric and adult tissues (n=6/group) mirrored the in vivo clearance differences in children versus adults, and showed that the oxidative metabolism was significantly faster in children compared to adults as indicated by the in vitro half-life (T (1/2)) of 33.8 +/- 15.3 versus 72.6 +/- 23.7 min, respectively. The K(m) for voriconazole metabolism to N-oxide, the major metabolite formed in humans, by liver microsomes from children and adults was similar (11.0 +/- 5.2 muM versus 9.3 +/- 3.6 muM, respectively). In contrast, apparent V(max) was approximately 3-fold higher in children compared to adults (120.5 +/- 99.9 versus 40.0 +/- 13.9 pmol/min/mg). The calculated in vivo clearance from in vitro data was found to be approximately 80% of the observed plasma clearance values in both populations. Metabolism studies in which CYP3A4, CYP2C19, or FMO was selectively inhibited provided evidence that contribution of CYP2C19 and FMO toward voriconazole N-oxidation was much greater in children than in adults, whereas CYP3A4 played a larger role in adults. While expression of CYP2C19 and FMO3 is not significantly different in children versus adults, these enzymes appear to contribute to higher metabolic clearance of voriconazole in children versus adults.

http://www.ncbi.nlm.nih.gov/pubmed/19841059

0 comments:

Post a Comment