Re: now acetominphen/paracetamol/Tylenol and glutathion Why loss of appetite?

[Guest guest]

Here are some messages I sent to the DSTNI listserv a couple of years

ago when we were discussing this there”

I found a couple of other articles and will post them separately.

KathyR

******************************************************************

Normally, Tylenol is metabolized by several different systems in

the liver(in

stages). One of the intermediate metabolites of Tylenol is

very  toxic,and

can kill liver cells,unless the metabolite is changed to a

 harmless

" final " metabolite by glutathione.(for example, an

overdose of  Tylenol

by a person who had normal glutathione levels before

taking the Tylenol

can cause liver failure/death because the liver is

overwhelmed and

can't detoxify the Tylenol ..and if enough liver cells are

 damaged,the

liver fails,causing death)

 

 Now,the

problem with Ds is that Glutathione is decreased due to

 overproduction

of SOD,so people with Ds are even more susceptible

to the effects

of Tylenol than someone who has normal glutathione

 levels..Ok,,,now

here is the long answer/explanations part:

 

 Caroline

Skalsky posted that Dr. Jill mentioned(during the

panel  discussion

at the New Orleans Conference) that Tylenol should not be

 used for

people with Ds because it 'blocks glutathione, which is

 essential

for the brain. "

 

 Then Kathy

Lee posted this:

 

 http://www.lef.org/protocols/prtcl-001.shtml

 

  " When

a person takes acetaminophen, it is metabolized by a number of

 metabolic

systems in the liver, including one called the P450

system.

 This

results in an intermediate by-product, or metabolite, that is

very  reactive

and can kill liver cells. This intermediate metabolite is

 normally

converted to a harmless final metabolite by an antioxidant

in  the

liver called glutathione (Uhlig et al. 1990; Deleve et al. 1991;

 Richie et

al. 1992). A large dose of acetaminophen reduces the

 glutathione

supply, resulting in progressive necrosis of the liver,

 sometimes

evidenced in as little as 5 days. Alcoholics and those on

 certain

medications that stimulate the P450 system are at particular

 risk

because, with increased P450 activity, more toxic intermediate

is created

than there is glutathione available to further metabolize

it to  something

harmless. Although not fatal, chronic acetaminophen use

 decreases

the functional capacity of the liver. "

 

 Now,,here

is something that I just found,which explains about

 glutathione

in Ds:

 http://www.edelsoncenter.com/Diseases_Treatment/down_upd.htm

  " Down's

Syndrome Update

 

 In

reviewing the literature on Down Syndrome

it is safe to say that

 there is

general agreement as to the causes and many of the effects

of  Down Syndrome. This simple statement will prove to

be vital by the

end of this

monologue. It is not all that frequent for there to be such

 general

agreement as to the true causes of any illness.

 

 All of the

symptoms and problems associated with Down Syndrome

are

 secondary

to a genetic defect concerning chromosome 21. This

chromosome  has

an extra copy of itself (and so Trisomy 21) and therefore has an

 overabundance

of specific genetic material which ultimately leads

to the physical

and mental problems associated with Down Syndrome.

 Specifically

what happens is as follows:

 

 The defect

causes the overproduction of the enzyme Superoxide

Dismutase

 (SOD). SOD

then directly converts the free radical Superoxide into

 Hydrogen

Peroxide (H2O2)

 

*****The amount of hydrogen peroxide produced is in excess

of

" normal "  amounts and quickly uses up the enzymes, glutathione

peroxidase*****

and

catalase, which are intended to deal with the peroxide. The

body  cannot

deal with the buildup of hydrogen peroxide. This excess

causes  cell

damage and apoptosis (cell death). The elevated hydrogen

peroxide  also

combines with iron to increase the production of the extremely

 damaging

hydroxyl (OH-)

radical (Yankner) (Odetti, et al).

According to

 Badwey, the

hydroxyl radical is the most noxious of the free radical

 species.

Damage to biologically important macromolecules (proteins,

DNA,  RNA,

cell membranes) results due to the body's inability to prevent

 these

oxidative interactions. This pathology can and does effect

other  chromosomes.

Allowed to continue this will lead to Alzheimer-like

 dementia by

the third or fourth decade of life (deHaar).

 

 ***The

glutathione deficiency from the overproduction of peroxide

and the

overabundance of cystathionine beta synthase (another enzyme),

 caused by

another Trisomy 21 gene, causes a serine deficiency and a

 homocysteine

increase which lead to vascular damage and DNA and RNA

 damage.***

Homocysteine causes the production of additional free

 radicals

which then damage the endothelial linings of the vascular

 system. " " "

 

 End quote

 

 This is an

article about the problems that Tylenol can cause in

people with

HIV/AIDS because they,too,have low glutathione...I thought it

was  interesting...

 

 http://www.aegis.com/pubs/catie/1997/CATE7906.html

Concerns about Tylenol

 

 TreatmentUpdate79

- Vol. 7, No. 9; July 1997

  Hosein

 

 

 <snip>

 Results

 

 By

analysing urine samples, researchers found that people with AIDS

 were, on

average, less able to detoxify Tylenol compared to other

 subjects.

***This difference was statistically significant; that

is, not likely

due to luck or chance.****

 

 *******The

likely reason for the reduced ability of people with

AIDS to  detoxify

Tylenol is that their livers don't contain enough GSH

 (glutathione).

Liver and other cells use GSH to protect themselves

from  harmful

chemical reactions.****** <snip>

 

 How to get

more GSH

 

 *****The

body makes GSH using the amino acid cysteine, *****which is

 found in

eggs, dairy products and supplements such as Immunocal<.

 Another

more direct way of obtaining cysteine is to take

supplements

of

 NAC

(N-acetyl-cysteine), which is licensed in North America

for the

 treatment

of Tylenol poisoning and is available from some buyers

clubs  and

health food stores. Nutritional guidelines for PHAs produced by

Lark  Lands and Chester Myers and

others, are available from CATIE.

 

 REFERENCES:

 

 1. Esteban

A. -Mateo M, Boix V, et al. Abnormalities in the

 metabolism

of acetaminophen in patients infected Human

Immunodeficiency

 Virus

(HIV). Methods and Findings in Experimental and Clinical

 Pharmacology

1997;19(2):129-132.

 

 2.

Herzenberg LA, De SC, Dubs JG, et al. Glutathione

deficiency

is

 associated

with impaired survival in HIV disease. Proceedings of the

 National Academy of Sciences USA 1997;94(5):1967-1972.

 

 3. Blair

PJ, Boise LH, Perfetto SP, et al. Impaired induction of the

 apoptosis-protective

protein Bcl-xl in activated PBMC from

asymptomatic

 HIV-infected

individuals. Journal of Clinical Immunology

 1997;17(3):234-246.

 

 4.

WG, Rotstein OD, Jimenez M, et al. Augmented intracellular

 glutathione

inhibits Fas-triggered apoptosis of activated human

 neutrophils.

Blood 1997;89(11):4175-4181.

 

 

ALSO<

)))))))))))))))))))))))))))))))))))))))))))))))))))))))

 

 Check

out the conclusion on this abstract:

(note..'febrile' means 'fever' and 'afebrile' means 'without fever'

.... " Hepatotoxicity " (hepat=liver)is the official term for liver

damage

caused by medications and other chemicals " )

This study was done on kids who do not have Ds....since people with Ds

already have reduced glutathione,it stands to reason that they would be

even more at risk for having problems with this medicine.

http://www.blackwell-synergy.com/openurl?genre=article & sid=nlm:pubmed & issn=0306-5251 & date=2003 & volume=55 & issue=3 & spage=234

Abstract

British Journal of Clinical Pharmacology

Volume 55 Issue 3 Page 234 - March 2003

doi:10.1046/j.1365-2125.2003.01723.x

Glutathione, glutathione-dependent enzymes and antioxidant status in

erythrocytes from children treated with high-dose paracetamol

Eran Kozer, 1, ph Barr, Revital Greenberg2, Ingrid

Soriano2, Mordechai Bulkowstein2, Irena Petrov3, Zehava Chen-Levi1,

Bernard Barzilay3, & Matitiahu Berkovitch2

Aim To investigate glutathione and antioxidant status changes in

erythrocytes from febrile children receiving repeated supratherapeutic

paracetamol doses.

Methods Fifty-one children aged 2 months to 10 years participated in the

study. Three groups were studied: group 1 (n = 24) included afebrile

children who did not receive paracetamol; and groups 2 (n = 13) and 3 (n

= 14) included children who had fever above 38.5°C for more than 72 h.

Patients in group 2 received paracetamol at a dose of 50 ± 15 (30-75) mg

kg1 day1 and those in group 3 received paracetamol above the recommended

therapeutic dose, ie 107 ± 28 (80-180) mg kg1 day1. A blood sample was

taken for the measurement of liver transaminases, gammaglutamil

transferase (GGT), reduced glutathione (GSH), glutathione reductase

(GR), glutathione peroxidase (GPX), glutathione S-transferase (GST),

superoxide dismutase (SOD) and antioxidant status.

Results Aspartate aminotransferase activity in group 3 was higher than

in the other groups (P = 0.027). GSH, SOD and antioxidant status were

significantly lower in group 3 compared with groups 1 and 2 (mean

differences: for GSH 3.41 µmol gHb1, 95% confidence interval (CI)

2.10-4.72, and 2.15 µmol gHb1, 95% CI 0.65-3.65, respectively; for SOD

856 U min1 gHb1, 95% CI 397-1316, and 556 U min1 gHb1, 95% CI 30-1082,

respectively; and for antioxidant status 0.83 mmol l1 plasma, 95% CI

0.30-1.36, and 0.63 mmol l1 plasma, 95% CI 0.02-1.24, respectively). GR

activity was significantly lower in groups 3 and 2 in comparison with

group 1 (mean differences 3.44 U min1 gHb1, 95% CI 0.63-6.25, and 5.64 U

min1 gHb1, 95% CI 2.90-8.38, respectively). Using multiple regression

analysis, paracetamol dose was found to be the only independent variable

affecting GR, GST and SOD activities (P = 0.007, 0.003 and 0.008,

respectively).

Conclusions In febrile children, treatment with repeated

supratherapeutic doses of paracetamol is associated with reduced

antioxidant status and erythrocyte glutathione concentrations. These

significant changes may indicate an increased risk for hepatotoxicity

and liver damage.

One more:

Acetominophen is the generic,and is in several different medicines...

Acetominophin is the ingredient that is metabolized by glutathione in

the liver. So use of *any* medicine that has acetominophin as an ingredient

should be avoided when possible.

Tylenol is just a brand name for one product that contains

acetominophen.

Lots of cold/sinus remedies(for example) have acetominophen in

them:

http://www4.dr-rath-foundation.org/THE_FOUNDATION/News/2003/pharmaceutical_business/2003-02-14-3.htm

From: Down Syndrome Treatment [mailto:Down Syndrome Treatment ] On Behalf Of Müller

Sent: Saturday, July 15, 2006

10:44 AM

Down Syndrome Treatment

Subject: Re:

Why loss of appetite?

Thanks for the hint, Kathy. Had never heard of that before!

What else could we give him then as pain relief/fever drug?

Why loss of appetite?

(19Mo/9kg) eats about 700-800g of pureed food per day and hardly drinks

anything (a little water, but he refuses more). Since last March he has been gaining

weight nicely this way. Since the start of July and

since it got very hot here (and still is), his temperature went up to 37,5

deg. Centigrade (98,6F), sometimes up to 38,1 (100,4F) or even 38,4 (101,12F),

without any infection symptoms.

At the same time he started eating less. At first about 200g less per day, but

since last Monday, 10th of July, when he got 2 vaccinations

(dipht./catal./pert. + the 2nd dose of measels/rub/mumps) his appetite went

down even more, down to about 350 - bis 450g/day. His nappies have been more or

less dry since yesterday, maybe a little wet in the morning. Our paed.

thought the elevated temp. and loss of appetite might

be caused by the heat. But we're worried, because has already lost

300g in only 6 days, without there being any change in sight. We just phoned

the paed. on weekend duty and he suggested we give him something (paracetamole)

to bring his temp. down a bit in order to normalize his appetite.

Is there

anything else we should do or will the situation just resolve by itself?

Is it only

the heat or the vaccinations?

Thanks,

/Switzerland

[Guest guest]

Kathy,

Man...is this timely for me. I had no idea. Question remains, what

do you give for pain relief/fever reduction for our kids? My son

has surgery scheduled at the end of July, and tylenol w/codeine was

mentioned as a take home for pain -- or just tylenol. What on earth

would I use instead??

Sharon

>

> Here are some messages I sent to the DSTNI listserv a couple of

years ago

> when we were discussing this there "

>

> I found a couple of other articles and will post them separately.

>

> KathyR

>

> ******************************************************************

>

> Normally, Tylenol is metabolized by several different systems in

> the liver(in stages). One of the intermediate metabolites of

Tylenol is

> very toxic,and can kill liver cells,unless the metabolite is

changed to a

> harmless " final " metabolite by glutathione.(for example, an

> overdose of Tylenol by a person who had normal glutathione

levels before

> taking the Tylenol can cause liver failure/death because the liver

is

> overwhelmed and can't detoxify the Tylenol ..and if enough liver

cells are

> damaged,the liver fails,causing death)

>

> Now,the problem with Ds is that Glutathione is decreased due to

> overproduction of SOD,so people with Ds are even more susceptible

> to the effects of Tylenol than someone who has normal glutathione

> levels..Ok,,,now here is the long answer/explanations part:

>

> Caroline Skalsky posted that Dr. Jill mentioned(during the

> panel discussion at the New Orleans Conference) that Tylenol

should not be

> used for people with Ds because it 'blocks glutathione, which is

> essential for the brain. "

>

> Then Kathy Lee posted this:

>

> http://www.lef.org/protocols/prtcl-001.shtml

>

>

> " When a person takes acetaminophen, it is metabolized by a number

of

> metabolic systems in the liver, including one called the P450

> system.

> This results in an intermediate by-product, or metabolite, that

is

> very reactive and can kill liver cells. This intermediate

metabolite is

> normally converted to a harmless final metabolite by an

antioxidant

> in the liver called glutathione (Uhlig et al. 1990; Deleve et al.

1991;

> Richie et al. 1992). A large dose of acetaminophen reduces the

> glutathione supply, resulting in progressive necrosis of the

liver,

> sometimes evidenced in as little as 5 days. Alcoholics and those

on

> certain medications that stimulate the P450 system are at

particular

> risk because, with increased P450 activity, more toxic

intermediate

> is created than there is glutathione available to further

metabolize

> it to something harmless. Although not fatal, chronic

acetaminophen use

> decreases the functional capacity of the liver. "

>

> Now,,here is something that I just found,which explains about

> glutathione in Ds:

> http://www.edelsoncenter.com/Diseases_Treatment/down_upd.htm

> " Down's Syndrome Update

>

> In reviewing the literature on Down Syndrome it is safe to say

that

> there is general agreement as to the causes and many of the

effects

> of Down Syndrome. This simple statement will prove to be vital by

the

> end of this monologue. It is not all that frequent for there to be

such

> general agreement as to the true causes of any illness.

>

> All of the symptoms and problems associated with Down Syndrome are

> secondary to a genetic defect concerning chromosome 21. This

> chromosome has an extra copy of itself (and so Trisomy 21) and

therefore

> has an

> overabundance of specific genetic material which ultimately leads

> to the physical and mental problems associated with Down Syndrome.

>

> Specifically what happens is as follows:

>

> The defect causes the overproduction of the enzyme Superoxide

> Dismutase

> (SOD). SOD then directly converts the free radical Superoxide into

> Hydrogen Peroxide (H2O2)

>

> *****The amount of hydrogen peroxide produced is in excess

> of " normal " amounts and quickly uses up the enzymes, glutathione

> peroxidase*****

> and catalase, which are intended to deal with the peroxide. The

> body cannot deal with the buildup of hydrogen peroxide. This

excess

> causes cell damage and apoptosis (cell death). The elevated

hydrogen

> peroxide also combines with iron to increase the production of the

> extremely

> damaging hydroxyl (OH-) radical (Yankner) (Odetti, et al).

> According to

> Badwey, the hydroxyl radical is the most noxious of the free

radical

> species. Damage to biologically important macromolecules

(proteins,

> DNA, RNA, cell membranes) results due to the body's inability to

prevent

> these oxidative interactions. This pathology can and does effect

> other chromosomes. Allowed to continue this will lead to

Alzheimer-like

> dementia by the third or fourth decade of life (deHaar).

>

> ***The glutathione deficiency from the overproduction of peroxide

> and the overabundance of cystathionine beta synthase (another

enzyme),

> caused by another Trisomy 21 gene, causes a serine deficiency and

a

> homocysteine increase which lead to vascular damage and DNA and

RNA

> damage.*** Homocysteine causes the production of additional free

> radicals which then damage the endothelial linings of the vascular

> system. " " "

>

> End quote

>

> This is an article about the problems that Tylenol can cause in

> people with HIV/AIDS because they,too,have low glutathione...I

thought it

> was interesting...

>

> http://www.aegis.com/pubs/catie/1997/CATE7906.html

>

> Concerns about Tylenol

>

> TreatmentUpdate79 - Vol. 7, No. 9; July 1997

> Hosein

>

>

> <snip>

> Results

>

> By analysing urine samples, researchers found that people with

AIDS

> were, on average, less able to detoxify Tylenol compared to other

> subjects. ***This difference was statistically significant; that

> is, not likely due to luck or chance.****

>

> *******The likely reason for the reduced ability of people with

> AIDS to detoxify Tylenol is that their livers don't contain

enough GSH

> (glutathione). Liver and other cells use GSH to protect

themselves

> from harmful chemical reactions.****** <snip>

>

> How to get more GSH

>

> *****The body makes GSH using the amino acid cysteine, *****which

is

> found in eggs, dairy products and supplements such as Immunocal<.

> Another more direct way of obtaining cysteine is to take

> supplements of

> NAC (N-acetyl-cysteine), which is licensed in North America for

the

> treatment of Tylenol poisoning and is available from some buyers

> clubs and health food stores. Nutritional guidelines for PHAs

produced by

> Lark Lands and Chester Myers and others, are available from

CATIE.

>

> REFERENCES:

>

> 1. Esteban A. -Mateo M, Boix V, et al. Abnormalities in the

> metabolism of acetaminophen in patients infected Human

> Immunodeficiency

> Virus (HIV). Methods and Findings in Experimental and Clinical

> Pharmacology 1997;19(2):129-132.

>

> 2. Herzenberg LA, De SC, Dubs JG, et al. Glutathione

> deficiency is

> associated with impaired survival in HIV disease. Proceedings of

the

> National Academy of Sciences USA 1997;94(5):1967-1972.

>

> 3. Blair PJ, Boise LH, Perfetto SP, et al. Impaired induction of

the

> apoptosis-protective protein Bcl-xl in activated PBMC from

> asymptomatic

> HIV-infected individuals. Journal of Clinical Immunology

> 1997;17(3):234-246.

>

> 4. WG, Rotstein OD, Jimenez M, et al. Augmented

intracellular

> glutathione inhibits Fas-triggered apoptosis of activated human

> neutrophils. Blood 1997;89(11):4175-4181.

>

>

> ALSO<

> )))))))))))))))))))))))))))))))))))))))))))))))))))))))

>

> Check out the conclusion on this abstract:

> (note..'febrile' means 'fever' and 'afebrile' means 'without fever'

> ... " Hepatotoxicity " (hepat=liver)is the official term for liver

damage

> caused by medications and other chemicals " )

>

> This study was done on kids who do not have Ds....since people

with Ds

> already have reduced glutathione,it stands to reason that they

would be

> even more at risk for having problems with this medicine.

>

> http://www.blackwell-synergy.com/openurl?genre=article

> <http://www.blackwell-synergy.com/openurl?

genre=article & sid=nlm:pubmed & issn=

> 0306-5251 & date=2003 & volume=55 & issue=3 & spage=234>

> & sid=nlm:pubmed & issn=0306-

5251 & date=2003 & volume=55 & issue=3 & spage=234

>

>

>

> Abstract

>

>

> British Journal of Clinical Pharmacology

> Volume 55 Issue 3 Page 234 - March 2003

> doi:10.1046/j.1365-2125.2003.01723.x

>

>

> Glutathione, glutathione-dependent enzymes and antioxidant status

in

> erythrocytes from children treated with high-dose paracetamol

> Eran Kozer, 1, ph Barr, Revital Greenberg2, Ingrid

> Soriano2, Mordechai Bulkowstein2, Irena Petrov3, Zehava Chen-Levi1,

> Bernard Barzilay3, & Matitiahu Berkovitch2

>

> Aim To investigate glutathione and antioxidant status changes in

> erythrocytes from febrile children receiving repeated

supratherapeutic

> paracetamol doses.

>

> Methods Fifty-one children aged 2 months to 10 years participated

in the

> study. Three groups were studied: group 1 (n = 24) included

afebrile

> children who did not receive paracetamol; and groups 2 (n = 13)

and 3 (n

> = 14) included children who had fever above 38.5°C for more than

72 h.

> Patients in group 2 received paracetamol at a dose of 50 ± 15 (30-

75) mg

> kg1 day1 and those in group 3 received paracetamol above the

recommended

> therapeutic dose, ie 107 ± 28 (80-180) mg kg1 day1. A blood sample

was

> taken for the measurement of liver transaminases, gammaglutamil

> transferase (GGT), reduced glutathione (GSH), glutathione reductase

> (GR), glutathione peroxidase (GPX), glutathione S-transferase

(GST),

> superoxide dismutase (SOD) and antioxidant status.

>

> Results Aspartate aminotransferase activity in group 3 was higher

than

> in the other groups (P = 0.027). GSH, SOD and antioxidant status

were

> significantly lower in group 3 compared with groups 1 and 2 (mean

> differences: for GSH 3.41 µmol gHb1, 95% confidence interval (CI)

> 2.10-4.72, and 2.15 µmol gHb1, 95% CI 0.65-3.65, respectively; for

SOD

> 856 U min1 gHb1, 95% CI 397-1316, and 556 U min1 gHb1, 95% CI 30-

1082,

> respectively; and for antioxidant status 0.83 mmol l1 plasma, 95%

CI

> 0.30-1.36, and 0.63 mmol l1 plasma, 95% CI 0.02-1.24,

respectively). GR

> activity was significantly lower in groups 3 and 2 in comparison

with

> group 1 (mean differences 3.44 U min1 gHb1, 95% CI 0.63-6.25, and

5.64 U

> min1 gHb1, 95% CI 2.90-8.38, respectively). Using multiple

regression

> analysis, paracetamol dose was found to be the only independent

variable

> affecting GR, GST and SOD activities (P = 0.007, 0.003 and 0.008,

> respectively).

>

> Conclusions In febrile children, treatment with repeated

> supratherapeutic doses of paracetamol is associated with reduced

> antioxidant status and erythrocyte glutathione concentrations.

These

> significant changes may indicate an increased risk for

hepatotoxicity

> and liver damage.

>

>

>

> One more:

>

> Acetominophen is the generic,and is in several different

medicines...

>

>

>

> Acetominophin is the ingredient that is metabolized by glutathione

in the

> liver. So use of *any* medicine that has acetominophin as an

ingredient

> should be avoided when possible.

>

>

>

> Tylenol is just a brand name for one product that contains

acetominophen.

>

>

>

> Lots of cold/sinus remedies(for example) have acetominophen in

them:

>

>

>

> http://www4.dr-rath-

foundation.org/THE_FOUNDATION/News/2003/pharmaceutical_b

> usiness/2003-02-14-3.htm

>

>

>

>

>

>

>

>

>

>

>

>

> _____

>

> From: Down Syndrome Treatment

> [mailto:Down Syndrome Treatment ] On Behalf Of

> Müller

> Sent: Saturday, July 15, 2006 10:44 AM

> Down Syndrome Treatment

> Subject: Re: Why loss of appetite?

>

>

>

> Thanks for the hint, Kathy. Had never heard of that before!

>

> What else could we give him then as pain relief/fever drug?

>

>

>

> Why loss of appetite?

>

> (19Mo/9kg) eats about 700-800g of pureed food per day and

hardly

> drinks anything (a little water, but he refuses more). Since last

March he

> has been gaining weight nicely this way. Since the start of July

and since

> it got very hot here (and still is), his temperature went up to

37,5 deg.

> Centigrade (98,6F), sometimes up to 38,1 (100,4F) or even 38,4

(101,12F),

> without any infection symptoms.

> At the same time he started eating less. At first about 200g less

per day,

> but since last Monday, 10th of July, when he got 2 vaccinations

> (dipht./catal./pert. + the 2nd dose of measels/rub/mumps) his

appetite went

> down even more, down to about 350 - bis 450g/day. His nappies have

been more

> or less dry since yesterday, maybe a little wet in the morning.

Our paed.

> thought the elevated temp. and loss of appetite might be caused by

the heat.

> But we're worried, because has already lost 300g in only 6

days,

> without there being any change in sight. We just phoned the paed.

on weekend

> duty and he suggested we give him something (paracetamole) to

bring his

> temp. down a bit in order to normalize his appetite.

>

> Is there anything else we should do or will the situation just

resolve by

> itself?

>

> Is it only the heat or the vaccinations?

>

>

> Thanks,

> /Switzerland

>

[Guest guest]

In a message dated 7/15/06 11:17:45 PM, sharondcaswell@... writes:

tylenol w/codeine was

mentioned as a take home for pain -- or just tylenol. What on earth

would I use instead??

Sharon

Motrin.

Our Olivia had a horrible reaction to Tylenol with Codeine after her tonsillectomy.

Joan

[Guest guest]

We use Motrin and is more willing to take it and it seems to work more

effectively.

Fort Wayne - mom to , 8 Ds and Hannah, 7 (currently annoying me!)

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

From: sharondcaswell <sharondcaswell@...>

Date: 2006/07/15 Sat PM 11:17:29 CDT

Down Syndrome Treatment

Subject: Re: now acetominphen/paracetamol/Tylenol and glutathion

Why loss of appetite?

Kathy,

Man...is this timely for me. I had no idea. Question remains, what

do you give for pain relief/fever reduction for our kids? My son

has surgery scheduled at the end of July, and tylenol w/codeine was

mentioned as a take home for pain -- or just tylenol. What on earth

would I use instead??

Sharon

>

> Here are some messages I sent to the DSTNI listserv a couple of

years ago

> when we were discussing this there "

>

> I found a couple of other articles and will post them separately.

>

> KathyR

>

> ******************************************************************

>

> Normally, Tylenol is metabolized by several different systems in

> the liver(in stages). One of the intermediate metabolites of

Tylenol is

> very toxic,and can kill liver cells,unless the metabolite is

changed to a

> harmless " final " metabolite by glutathione.(for example, an

> overdose of Tylenol by a person who had normal glutathione

levels before

> taking the Tylenol can cause liver failure/death because the liver

is

> overwhelmed and can't detoxify the Tylenol ..and if enough liver

cells are

> damaged,the liver fails,causing death)

>

> Now,the problem with Ds is that Glutathione is decreased due to

> overproduction of SOD,so people with Ds are even more susceptible

> to the effects of Tylenol than someone who has normal glutathione

> levels..Ok,,,now here is the long answer/explanations part:

>

> Caroline Skalsky posted that Dr. Jill mentioned(during the

> panel discussion at the New Orleans Conference) that Tylenol

should not be

> used for people with Ds because it 'blocks glutathione, which is

> essential for the brain. "

>

> Then Kathy Lee posted this:

>

> http://www.lef.org/protocols/prtcl-001.shtml

>

>

> " When a person takes acetaminophen, it is metabolized by a number

of

> metabolic systems in the liver, including one called the P450

> system.

> This results in an intermediate by-product, or metabolite, that

is

> very reactive and can kill liver cells. This intermediate

metabolite is

> normally converted to a harmless final metabolite by an

antioxidant

> in the liver called glutathione (Uhlig et al. 1990; Deleve et al.

1991;

> Richie et al. 1992). A large dose of acetaminophen reduces the

> glutathione supply, resulting in progressive necrosis of the

liver,

> sometimes evidenced in as little as 5 days. Alcoholics and those

on

> certain medications that stimulate the P450 system are at

particular

> risk because, with increased P450 activity, more toxic

intermediate

> is created than there is glutathione available to further

metabolize

> it to something harmless. Although not fatal, chronic

acetaminophen use

> decreases the functional capacity of the liver. "

>

> Now,,here is something that I just found,which explains about

> glutathione in Ds:

> http://www.edelsoncenter.com/Diseases_Treatment/down_upd.htm

> " Down's Syndrome Update

>

> In reviewing the literature on Down Syndrome it is safe to say

that

> there is general agreement as to the causes and many of the

effects

> of Down Syndrome. This simple statement will prove to be vital by

the

> end of this monologue. It is not all that frequent for there to be

such

> general agreement as to the true causes of any illness.

>

> All of the symptoms and problems associated with Down Syndrome are

> secondary to a genetic defect concerning chromosome 21. This

> chromosome has an extra copy of itself (and so Trisomy 21) and

therefore

> has an

> overabundance of specific genetic material which ultimately leads

> to the physical and mental problems associated with Down Syndrome.

>

> Specifically what happens is as follows:

>

> The defect causes the overproduction of the enzyme Superoxide

> Dismutase

> (SOD). SOD then directly converts the free radical Superoxide into

> Hydrogen Peroxide (H2O2)

>

> *****The amount of hydrogen peroxide produced is in excess

> of " normal " amounts and quickly uses up the enzymes, glutathione

> peroxidase*****

> and catalase, which are intended to deal with the peroxide. The

> body cannot deal with the buildup of hydrogen peroxide. This

excess

> causes cell damage and apoptosis (cell death). The elevated

hydrogen

> peroxide also combines with iron to increase the production of the

> extremely

> damaging hydroxyl (OH-) radical (Yankner) (Odetti, et al).

> According to

> Badwey, the hydroxyl radical is the most noxious of the free

radical

> species. Damage to biologically important macromolecules

(proteins,

> DNA, RNA, cell membranes) results due to the body's inability to

prevent

> these oxidative interactions. This pathology can and does effect

> other chromosomes. Allowed to continue this will lead to

Alzheimer-like

> dementia by the third or fourth decade of life (deHaar).

>

> ***The glutathione deficiency from the overproduction of peroxide

> and the overabundance of cystathionine beta synthase (another

enzyme),

> caused by another Trisomy 21 gene, causes a serine deficiency and

a

> homocysteine increase which lead to vascular damage and DNA and

RNA

> damage.*** Homocysteine causes the production of additional free

> radicals which then damage the endothelial linings of the vascular

> system. " " "

>

> End quote

>

> This is an article about the problems that Tylenol can cause in

> people with HIV/AIDS because they,too,have low glutathione...I

thought it

> was interesting...

>

> http://www.aegis.com/pubs/catie/1997/CATE7906.html

>

> Concerns about Tylenol

>

> TreatmentUpdate79 - Vol. 7, No. 9; July 1997

> Hosein

>

>

> <snip>

> Results

>

> By analysing urine samples, researchers found that people with

AIDS

> were, on average, less able to detoxify Tylenol compared to other

> subjects. ***This difference was statistically significant; that

> is, not likely due to luck or chance.****

>

> *******The likely reason for the reduced ability of people with

> AIDS to detoxify Tylenol is that their livers don't contain

enough GSH

> (glutathione). Liver and other cells use GSH to protect

themselves

> from harmful chemical reactions.****** <snip>

>

> How to get more GSH

>

> *****The body makes GSH using the amino acid cysteine, *****which

is

> found in eggs, dairy products and supplements such as Immunocal<.

> Another more direct way of obtaining cysteine is to take

> supplements of

> NAC (N-acetyl-cysteine), which is licensed in North America for

the

> treatment of Tylenol poisoning and is available from some buyers

> clubs and health food stores. Nutritional guidelines for PHAs

produced by

> Lark Lands and Chester Myers and others, are available from

CATIE.

>

> REFERENCES:

>

> 1. Esteban A. -Mateo M, Boix V, et al. Abnormalities in the

> metabolism of acetaminophen in patients infected Human

> Immunodeficiency

> Virus (HIV). Methods and Findings in Experimental and Clinical

> Pharmacology 1997;19(2):129-132.

>

> 2. Herzenberg LA, De SC, Dubs JG, et al. Glutathione

> deficiency is

> associated with impaired survival in HIV disease. Proceedings of

the

> National Academy of Sciences USA 1997;94(5):1967-1972.

>

> 3. Blair PJ, Boise LH, Perfetto SP, et al. Impaired induction of

the

> apoptosis-protective protein Bcl-xl in activated PBMC from

> asymptomatic

> HIV-infected individuals. Journal of Clinical Immunology

> 1997;17(3):234-246.

>

> 4. WG, Rotstein OD, Jimenez M, et al. Augmented

intracellular

> glutathione inhibits Fas-triggered apoptosis of activated human

> neutrophils. Blood 1997;89(11):4175-4181.

>

>

> ALSO<

> )))))))))))))))))))))))))))))))))))))))))))))))))))))))

>

> Check out the conclusion on this abstract:

> (note..'febrile' means 'fever' and 'afebrile' means 'without fever'

> ... " Hepatotoxicity " (hepat=liver)is the official term for liver

damage

> caused by medications and other chemicals " )

>

> This study was done on kids who do not have Ds....since people

with Ds

> already have reduced glutathione,it stands to reason that they

would be

> even more at risk for having problems with this medicine.

>

> http://www.blackwell-synergy.com/openurl?genre=article

> <http://www.blackwell-synergy.com/openurl?

genre=article & sid=nlm:pubmed & issn=

> 0306-5251 & date=2003 & volume=55 & issue=3 & spage=234>

> & sid=nlm:pubmed & issn=0306-

5251 & date=2003 & volume=55 & issue=3 & spage=234

>

>

>

> Abstract

>

>

> British Journal of Clinical Pharmacology

> Volume 55 Issue 3 Page 234 - March 2003

> doi:10.1046/j.1365-2125.2003.01723.x

>

>

> Glutathione, glutathione-dependent enzymes and antioxidant status

in

> erythrocytes from children treated with high-dose paracetamol

> Eran Kozer, 1, ph Barr, Revital Greenberg2, Ingrid

> Soriano2, Mordechai Bulkowstein2, Irena Petrov3, Zehava Chen-Levi1,

> Bernard Barzilay3, & Matitiahu Berkovitch2

>

> Aim To investigate glutathione and antioxidant status changes in

> erythrocytes from febrile children receiving repeated

supratherapeutic

> paracetamol doses.

>

> Methods Fifty-one children aged 2 months to 10 years participated

in the

> study. Three groups were studied: group 1 (n = 24) included

afebrile

> children who did not receive paracetamol; and groups 2 (n = 13)

and 3 (n

> = 14) included children who had fever above 38.5°C for more than

72 h.

> Patients in group 2 received paracetamol at a dose of 50 ± 15 (30-

75) mg

> kg1 day1 and those in group 3 received paracetamol above the

recommended

> therapeutic dose, ie 107 ± 28 (80-180) mg kg1 day1. A blood sample

was

> taken for the measurement of liver transaminases, gammaglutamil

> transferase (GGT), reduced glutathione (GSH), glutathione reductase

> (GR), glutathione peroxidase (GPX), glutathione S-transferase

(GST),

> superoxide dismutase (SOD) and antioxidant status.

>

> Results Aspartate aminotransferase activity in group 3 was higher

than

> in the other groups (P = 0.027). GSH, SOD and antioxidant status

were

> significantly lower in group 3 compared with groups 1 and 2 (mean

> differences: for GSH 3.41 µmol gHb1, 95% confidence interval (CI)

> 2.10-4.72, and 2.15 µmol gHb1, 95% CI 0.65-3.65, respectively; for

SOD

> 856 U min1 gHb1, 95% CI 397-1316, and 556 U min1 gHb1, 95% CI 30-

1082,

> respectively; and for antioxidant status 0.83 mmol l1 plasma, 95%

CI

> 0.30-1.36, and 0.63 mmol l1 plasma, 95% CI 0.02-1.24,

respectively). GR

> activity was significantly lower in groups 3 and 2 in comparison

with

> group 1 (mean differences 3.44 U min1 gHb1, 95% CI 0.63-6.25, and

5.64 U

> min1 gHb1, 95% CI 2.90-8.38, respectively). Using multiple

regression

> analysis, paracetamol dose was found to be the only independent

variable

> affecting GR, GST and SOD activities (P = 0.007, 0.003 and 0.008,

> respectively).

>

> Conclusions In febrile children, treatment with repeated

> supratherapeutic doses of paracetamol is associated with reduced

> antioxidant status and erythrocyte glutathione concentrations.

These

> significant changes may indicate an increased risk for

hepatotoxicity

> and liver damage.

>

>

>

> One more:

>

> Acetominophen is the generic,and is in several different

medicines...

>

>

>

> Acetominophin is the ingredient that is metabolized by glutathione

in the

> liver. So use of *any* medicine that has acetominophin as an

ingredient

> should be avoided when possible.

>

>

>

> Tylenol is just a brand name for one product that contains

acetominophen.

>

>

>

> Lots of cold/sinus remedies(for example) have acetominophen in

them:

>

>

>

> http://www4.dr-rath-

foundation.org/THE_FOUNDATION/News/2003/pharmaceutical_b

> usiness/2003-02-14-3.htm

>

>

>

>

>

>

>

>

>

>

>

>

> _____

>

> From: Down Syndrome Treatment

> [mailto:Down Syndrome Treatment ] On Behalf Of

> Müller

> Sent: Saturday, July 15, 2006 10:44 AM

> Down Syndrome Treatment

> Subject: Re: Why loss of appetite?

>

>

>

> Thanks for the hint, Kathy. Had never heard of that before!

>

> What else could we give him then as pain relief/fever drug?

>

>

>

> Why loss of appetite?

>

> (19Mo/9kg) eats about 700-800g of pureed food per day and

hardly

> drinks anything (a little water, but he refuses more). Since last

March he

> has been gaining weight nicely this way. Since the start of July

and since

> it got very hot here (and still is), his temperature went up to

37,5 deg.

> Centigrade (98,6F), sometimes up to 38,1 (100,4F) or even 38,4

(101,12F),

> without any infection symptoms.

> At the same time he started eating less. At first about 200g less

per day,

> but since last Monday, 10th of July, when he got 2 vaccinations

> (dipht./catal./pert. + the 2nd dose of measels/rub/mumps) his

appetite went

> down even more, down to about 350 - bis 450g/day. His nappies have

been more

> or less dry since yesterday, maybe a little wet in the morning.

Our paed.

> thought the elevated temp. and loss of appetite might be caused by

the heat.

> But we're worried, because has already lost 300g in only 6

days,

> without there being any change in sight. We just phoned the paed.

on weekend

> duty and he suggested we give him something (paracetamole) to

bring his

> temp. down a bit in order to normalize his appetite.

>

> Is there anything else we should do or will the situation just

resolve by

> itself?

>

> Is it only the heat or the vaccinations?

>

>

> Thanks,

> /Switzerland

>

[Guest guest]

For some surgeries you will not have a choice --they won't let you

give motrin --blood thinner or something like that is the reason and

you can't risk bleeding obviously. The thing is to just be aware of

the problems and give as little as possible. I know when Evan had

mastoid surgery, I had no choice but he only got the one dose or so

at the hospital --I simply didn't give it at home and he didn't seem

to need it anyway --Dr. L also said you may have to give it for

surgeries since there is nothing else safe.

Priscilla K

--- sharondcaswell <sharondcaswell@...> wrote:

> Kathy,

>

> Man...is this timely for me. I had no idea. Question remains,

> what

> do you give for pain relief/fever reduction for our kids? My son

> has surgery scheduled at the end of July, and tylenol w/codeine was

>

> mentioned as a take home for pain -- or just tylenol. What on

> earth

> would I use instead??

>

> Sharon

>

>

> >

> > Here are some messages I sent to the DSTNI listserv a couple of

> years ago

> > when we were discussing this there "

> >

> > I found a couple of other articles and will post them separately.

> >

> > KathyR

> >

> >

> ******************************************************************

> >

> > Normally, Tylenol is metabolized by several different systems in

> > the liver(in stages). One of the intermediate metabolites of

> Tylenol is

> > very toxic,and can kill liver cells,unless the metabolite is

> changed to a

> > harmless " final " metabolite by glutathione.(for example, an

> > overdose of Tylenol by a person who had normal glutathione

> levels before

> > taking the Tylenol can cause liver failure/death because the

> liver

> is

> > overwhelmed and can't detoxify the Tylenol ..and if enough liver

> cells are

> > damaged,the liver fails,causing death)

> >

> > Now,the problem with Ds is that Glutathione is decreased due to

> > overproduction of SOD,so people with Ds are even more

> susceptible

> > to the effects of Tylenol than someone who has normal glutathione

> > levels..Ok,,,now here is the long answer/explanations part:

> >

> > Caroline Skalsky posted that Dr. Jill mentioned(during the

>

> > panel discussion at the New Orleans Conference) that Tylenol

> should not be

> > used for people with Ds because it 'blocks glutathione, which is

> > essential for the brain. "

> >

> > Then Kathy Lee posted this:

> >

> > http://www.lef.org/protocols/prtcl-001.shtml

> >

> >

> > " When a person takes acetaminophen, it is metabolized by a

> number

> of

> > metabolic systems in the liver, including one called the P450

> > system.

> > This results in an intermediate by-product, or metabolite, that

> is

> > very reactive and can kill liver cells. This intermediate

> metabolite is

> > normally converted to a harmless final metabolite by an

> antioxidant

> > in the liver called glutathione (Uhlig et al. 1990; Deleve et

> al.

> 1991;

> > Richie et al. 1992). A large dose of acetaminophen reduces the

> > glutathione supply, resulting in progressive necrosis of the

> liver,

> > sometimes evidenced in as little as 5 days. Alcoholics and those

>

> on

> > certain medications that stimulate the P450 system are at

> particular

> > risk because, with increased P450 activity, more toxic

> intermediate

> > is created than there is glutathione available to further

> metabolize

> > it to something harmless. Although not fatal, chronic

> acetaminophen use

> > decreases the functional capacity of the liver. "

> >

> > Now,,here is something that I just found,which explains about

> > glutathione in Ds:

> > http://www.edelsoncenter.com/Diseases_Treatment/down_upd.htm

> > " Down's Syndrome Update

> >

> > In reviewing the literature on Down Syndrome it is safe to say

> that

> > there is general agreement as to the causes and many of the

> effects

> > of Down Syndrome. This simple statement will prove to be vital

> by

> the

> > end of this monologue. It is not all that frequent for there to

> be

> such

> > general agreement as to the true causes of any illness.

> >

> > All of the symptoms and problems associated with Down Syndrome

> are

> > secondary to a genetic defect concerning chromosome 21. This

> > chromosome has an extra copy of itself (and so Trisomy 21) and

> therefore

> > has an

> > overabundance of specific genetic material which ultimately

> leads

> > to the physical and mental problems associated with Down

> Syndrome.

> >

> > Specifically what happens is as follows:

> >

> > The defect causes the overproduction of the enzyme Superoxide

> > Dismutase

> > (SOD). SOD then directly converts the free radical Superoxide

> into

> > Hydrogen Peroxide (H2O2)

> >

> > *****The amount of hydrogen peroxide produced is in excess

> > of " normal " amounts and quickly uses up the enzymes, glutathione

> > peroxidase*****

> > and catalase, which are intended to deal with the peroxide. The

> > body cannot deal with the buildup of hydrogen peroxide. This

> excess

> > causes cell damage and apoptosis (cell death). The elevated

> hydrogen

> > peroxide also combines with iron to increase the production of

> the

> > extremely

> > damaging hydroxyl (OH-) radical (Yankner) (Odetti, et al).

> > According to

> > Badwey, the hydroxyl radical is the most noxious of the free

> radical

> > species. Damage to biologically important macromolecules

> (proteins,

> > DNA, RNA, cell membranes) results due to the body's inability to

>

> prevent

> > these oxidative interactions. This pathology can and does effect

>

> > other chromosomes. Allowed to continue this will lead to

> Alzheimer-like

> > dementia by the third or fourth decade of life (deHaar).

> >

> > ***The glutathione deficiency from the overproduction of

> peroxide

> > and the overabundance of cystathionine beta synthase (another

> enzyme),

> > caused by another Trisomy 21 gene, causes a serine deficiency

> and

> a

> > homocysteine increase which lead to vascular damage and DNA and

> RNA

> > damage.*** Homocysteine causes the production of additional free

> > radicals which then damage the endothelial linings of the

> vascular

> > system. " " "

> >

> > End quote

> >

> > This is an article about the problems that Tylenol can cause in

> > people with HIV/AIDS because they,too,have low glutathione...I

> thought it

> > was interesting...

> >

> > http://www.aegis.com/pubs/catie/1997/CATE7906.html

> >

> > Concerns about Tylenol

> >

> > TreatmentUpdate79 - Vol. 7, No. 9; July 1997

> > Hosein

> >

> >

> > <snip>

> > Results

> >

> > By analysing urine samples, researchers found that people with

> AIDS

> > were, on average, less able to detoxify Tylenol compared to

> other

> > subjects. ***This difference was statistically significant; that

>

> > is, not likely due to luck or chance.****

> >

> > *******The likely reason for the reduced ability of people with

> > AIDS to detoxify Tylenol is that their livers don't contain

> enough GSH

> > (glutathione). Liver and other cells use GSH to protect

> themselves

> > from harmful chemical reactions.****** <snip>

> >

> > How to get more GSH

> >

> > *****The body makes GSH using the amino acid cysteine,

> *****which

> is

> > found in eggs, dairy products and supplements such as

> Immunocal<.

> > Another more direct way of obtaining cysteine is to take

> > supplements of

> > NAC (N-acetyl-cysteine), which is licensed in North America for

> the

> > treatment of Tylenol poisoning and is available from some buyers

>

> > clubs and health food stores. Nutritional guidelines for PHAs

> produced by

> > Lark Lands and Chester Myers and others, are available from

> CATIE.

> >

> > REFERENCES:

> >

> > 1. Esteban A. -Mateo M, Boix V, et al. Abnormalities in the

> > metabolism of acetaminophen in patients infected Human

> > Immunodeficiency

> > Virus (HIV). Methods and Findings in Experimental and Clinical

> > Pharmacology 1997;19(2):129-132.

> >

> > 2. Herzenberg LA, De SC, Dubs JG, et al. Glutathione

> > deficiency is

> > associated with impaired survival in HIV disease. Proceedings of

>

> the

> > National Academy of Sciences USA 1997;94(5):1967-1972.

> >

> > 3. Blair PJ, Boise LH, Perfetto SP, et al. Impaired induction of

>

> the

> > apoptosis-protective protein Bcl-xl in activated PBMC from

> > asymptomatic

> > HIV-infected individuals. Journal of Clinical Immunology

> > 1997;17(3):234-246.

> >

> > 4. WG, Rotstein OD, Jimenez M, et al. Augmented

> intracellular

> > glutathione inhibits Fas-triggered apoptosis of activated human

> > neutrophils. Blood 1997;89(11):4175-4181.

> >

> >

> > ALSO<

> > )))))))))))))))))))))))))))))))))))))))))))))))))))))))

> >

> > Check out the conclusion on this abstract:

> > (note..'febrile' means 'fever' and 'afebrile' means 'without

> fever'

> > ... " Hepatotoxicity " (hepat=liver)is the official term for liver

> damage

> > caused by medications and other chemicals " )

> >

> > This study was done on kids who do not have Ds....since people

> with Ds

> > already have reduced glutathione,it stands to reason that they

> would be

> > even more at risk for having problems with this medicine.

> >

> > http://www.blackwell-synergy.com/openurl?genre=article

> > <http://www.blackwell-synergy.com/openurl?

> genre=article & sid=nlm:pubmed & issn=

> > 0306-5251 & date=2003 & volume=55 & issue=3 & spage=234>

> > & sid=nlm:pubmed & issn=0306-

> 5251 & date=2003 & volume=55 & issue=3 & spage=234

> >

> >

> >

> > Abstract

> >

> >

> > British Journal of Clinical Pharmacology

> > Volume 55 Issue 3 Page 234 - March 2003

> > doi:10.1046/j.1365-2125.2003.01723.x

> >

> >

> > Glutathione, glutathione-dependent enzymes and antioxidant status

>

> in

> > erythrocytes from children treated with high-dose paracetamol

> > Eran Kozer, 1, ph Barr, Revital Greenberg2,

> Ingrid

> > Soriano2, Mordechai Bulkowstein2, Irena Petrov3, Zehava

> Chen-Levi1,

> > Bernard Barzilay3, & Matitiahu Berkovitch2

> >

> > Aim To investigate glutathione and antioxidant status changes in

> > erythrocytes from febrile children receiving repeated

> supratherapeutic

> > paracetamol doses.

> >

> > Methods Fifty-one children aged 2 months to 10 years participated

>

> in the

> > study. Three groups were studied: group 1 (n = 24) included

> afebrile

> > children who did not receive paracetamol; and groups 2 (n = 13)

> and 3 (n

> > = 14) included children who had fever above 38.5°C for more than

> 72 h.

> > Patients in group 2 received paracetamol at a dose of 50 ± 15

> (30-

> 75) mg

> > kg1 day1 and those in group 3 received paracetamol above the

> recommended

> > therapeutic dose, ie 107 ± 28 (80-180) mg kg1 day1. A blood

> sample

> was

> > taken for the measurement of liver transaminases, gammaglutamil

> > transferase (GGT), reduced glutathione (GSH), glutathione

> reductase

> > (GR), glutathione peroxidase (GPX), glutathione S-transferase

> (GST),

> > superoxide dismutase (SOD) and antioxidant status.

> >

> > Results Aspartate aminotransferase activity in group 3 was higher

>

> than

> > in the other groups (P = 0.027). GSH, SOD and antioxidant status

> were

> > significantly lower in group 3 compared with groups 1 and 2 (mean

> > differences: for GSH 3.41 µmol gHb1, 95% confidence interval (CI)

> > 2.10-4.72, and 2.15 µmol gHb1, 95% CI 0.65-3.65, respectively;

> for

> SOD

> > 856 U min1 gHb1, 95% CI 397-1316, and 556 U min1 gHb1, 95% CI 30-

> 1082,

> > respectively; and for antioxidant status 0.83 mmol l1 plasma, 95%

>

> CI

> > 0.30-1.36, and 0.63 mmol l1 plasma, 95% CI 0.02-1.24,

> respectively). GR

> > activity was significantly lower in groups 3 and 2 in comparison

> with

> > group 1 (mean differences 3.44 U min1 gHb1, 95% CI 0.63-6.25, and

>

> 5.64 U

> > min1 gHb1, 95% CI 2.90-8.38, respectively). Using multiple

> regression

> > analysis, paracetamol dose was found to be the only independent

> variable

> > affecting GR, GST and SOD activities (P = 0.007, 0.003 and 0.008,

> > respectively).

> >

> > Conclusions In febrile children, treatment with repeated

> > supratherapeutic doses of paracetamol is associated with reduced

> > antioxidant status and erythrocyte glutathione concentrations.

> These

> > significant changes may indicate an increased risk for

> hepatotoxicity

> > and liver damage.

> >

> >

> >

> > One more:

> >

> > Acetominophen is the generic,and is in several different

> medicines...

> >

> >

> >

> > Acetominophin is the ingredient that is metabolized by

> glutathione

> in the

> > liver. So use of *any* medicine that has acetominophin as an

> ingredient

> > should be avoided when possible.

> >

> >

> >

> > Tylenol is just a brand name for one product that contains

> acetominophen.

> >

> >

> >

> > Lots of cold/sinus remedies(for example) have acetominophen in

> them:

> >

> >

> >

> > http://www4.dr-rath-

> foundation.org/THE_FOUNDATION/News/2003/pharmaceutical_b

> > usiness/2003-02-14-3.htm

> >

> >

> >

> >

> >

> >

> >

> >

> >

> >

> >

> >

> > _____

> >

> > From: Down Syndrome Treatment

> > [mailto:Down Syndrome Treatment ] On Behalf Of

>

> > Müller

> > Sent: Saturday, July 15, 2006 10:44 AM

> > Down Syndrome Treatment

> > Subject: Re: Why loss of appetite?

> >

> >

> >

> > Thanks for the hint, Kathy. Had never heard of that before!

> >

> > What else could we give him then as pain relief/fever drug?

> >

> >

> >

> > Why loss of appetite?

> >

> > (19Mo/9kg) eats about 700-800g of pureed food per day and

> hardly

> > drinks anything (a little water, but he refuses more). Since last

>

> March he

> > has been gaining weight nicely this way. Since the start of July

> and since

> > it got very hot here (and still is), his temperature went up to

> 37,5 deg.

> > Centigrade (98,6F), sometimes up to 38,1 (100,4F) or even 38,4

> (101,12F),

> > without any infection symptoms.

> > At the same time he started eating less. At first about 200g less

>

> per day,

> > but since last Monday, 10th of July, when he got 2 vaccinations

> > (dipht./catal./pert. + the 2nd dose of measels/rub/mumps) his

> appetite went

> > down even more, down to about 350 - bis 450g/day. His nappies

> have

> been more

> > or less dry since yesterday, maybe a little wet in the morning.

> Our paed.

> > thought the elevated temp. and loss of appetite might be caused

> by

> the heat.

> > But we're worried, because has already lost 300g in only 6

> days,

> > without there being any change in sight. We just phoned the paed.

>

> on weekend

> > duty and he suggested we give him something (paracetamole) to

> bring his

> > temp. down a bit in order to normalize his appetite.

> >

> > Is there anything else we should do or will the situation just

> resolve by

> > itself?

> >

> > Is it only the heat or the vaccinations?

> >

> >

> > Thanks,

> > /Switzerland

> >

>

>

>

>

>

>

Priscilla Kendrick, married 28 years to Darrel and parents of 9 kids including

Evan, 10, born with Down Syndrome and Spina Bifida

" My strength is made perfect in weakness. "

" My grace is sufficient. " II Corinthians 12:9 KJV

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