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Thanks - I'll forward your message to Dr. Drucker.

Chris.

On Thu, 23 Dec 1999, Petraglia wrote:

> Chris:

> I have scleroderma and underwent about 60 hyperbaric chamber treatments

> last year. Ulcers on my knuckles which defied any type of medical

> treatment including ointments, plastic surgery, and even Chinese

> medicine left me with the prospect of loosing some fingers.

> Immediately, the hyperbaric treatments improved the wounds at a rapid

> pace and eventually, all traces of bloody and oozing knuckles was gone.

> One year later with the return of the cold weather, some minor ulcers

> have appeared and I anticipate returning for a few treatments. The

> recent reoccurrence is very minor and could be ignored if I choose.

>

> The very first treatment had a profound impact on my wounds. My wounds

> actually hurt halfway thru the first treatment, which was a sign of

> increased blood flow and healing. As far as helping the sclorderma

> itself, although my condition has improved greatly, my opinion is that

> the hyperbaric treatment was not responsible, although doctors claim

> that my antibiotic treatment may actually be helped by oxygen.

>

> The only drawback is blurred vision for up to months after treatments

> have ceased. Not a bad trade in all though, 10 fingers for reading

> glasses.

> P

>

> Adlard wrote:

> >

> > From: Adlard <cadlard@...>

> >

> > We heard from Dr. Drucker in California who is using antibiotics and other

> > supportive therapies. He would like to hear from any of the group who have

> > used oxygen therapy, especially hyperbaric oxygen, and if it helped. I'll

> > pass on any messages.

> >

> > Thanks, Chris.

> > _____________________________________________________________________

> >

> > Currently, I am looking into hyperbaric O2 therapy as a method of helping by

> > its anti-microbial effects. Do you know of anyone who has incorporated

> > hyperbaric oxygen as a treatment? I know it is very helpful for patients

> > with chronic fatigue.

> >

> > Thanks again, Dr. Drucker

>

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I know of two people who have tried hyperbaric oxygen. One had CFS with

mycoplasma infection. The other had Lyme disease. Both felt better after

one month of treatment but were unable to afford continued treatment due to

the expense. I believe Dr. Nicolson has suggested that any way of

increasing oxygen will fight mycoplasma infections as they grow better with

little or no oxygen. How many of you have tried the hydrogen peroxide and

epsom salts baths? I believe the hypothesis behind them working is the

same - get more oxygen to the tissues.

a Carnes

paulajeanne@...

> From: Petraglia <johnp@...>

>

> Chris:

> I have scleroderma and underwent about 60 hyperbaric chamber treatments

> last year. Ulcers on my knuckles which defied any type of medical

> treatment including ointments, plastic surgery, and even Chinese

> medicine left me with the prospect of loosing some fingers.

> Immediately, the hyperbaric treatments improved the wounds at a rapid

> pace and eventually, all traces of bloody and oozing knuckles was gone.

> One year later with the return of the cold weather, some minor ulcers

> have appeared and I anticipate returning for a few treatments. The

> recent reoccurrence is very minor and could be ignored if I choose.

>

> The very first treatment had a profound impact on my wounds. My wounds

> actually hurt halfway thru the first treatment, which was a sign of

> increased blood flow and healing. As far as helping the sclorderma

> itself, although my condition has improved greatly, my opinion is that

> the hyperbaric treatment was not responsible, although doctors claim

> that my antibiotic treatment may actually be helped by oxygen.

>

> The only drawback is blurred vision for up to months after treatments

> have ceased. Not a bad trade in all though, 10 fingers for reading

> glasses.

> P

>

> Adlard wrote:

> >

> > From: Adlard <cadlard@...>

> >

> > We heard from Dr. Drucker in California who is using antibiotics and

other

> > supportive therapies. He would like to hear from any of the group who

have

> > used oxygen therapy, especially hyperbaric oxygen, and if it helped.

I'll

> > pass on any messages.

> >

> > Thanks, Chris.

> > _____________________________________________________________________

> >

> > Currently, I am looking into hyperbaric O2 therapy as a method of

helping by

> > its anti-microbial effects. Do you know of anyone who has incorporated

> > hyperbaric oxygen as a treatment? I know it is very helpful for

patients

> > with chronic fatigue.

> >

> > Thanks again, Dr. Drucker

>

>

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Why would you get blurred vision from oxygen treatments. How do these

treatments work? I mean how do you do it and how often? Can you do it

at home, and does it help the inflammation of RA?

Thank you,

Gloria

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Thankyou to all the people who sent in their experiences with oxygen

therapy for Dr. Drucker. He sent this thankyou message:

______________________________________________________________________

Thanks for the info. regarding hyperbaric O2. I will continue to

investigate. Currently , I am looking for a chamber, preferably used, to

incorporate into my treatment. Overall, I believe it to be very helpful.

Happy New Year, Mark

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  • 3 years later...

HBO exposure transiently suppresses stimulus-induced proinflammatory

cytokine

Risks include barometric otitis media-CP

2 suffered significant morbidity-CP children

Central nervous system oxygen toxicity

oxidative stress can disrupt brain stem function

oxygen-induced convulsions

cataract formation due to toxic effect of oxygen on lenses?

--------------------------------------------------------------------------

Clin Exp Immunol. 2003 Oct;134(1):57-62.

Hyperbaric oxygen inhibits stimulus-induced proinflammatory cytokine

synthesis by human blood-derived monocyte-macrophages.

Benson RM, Minter LM, Osborne BA, Granowitz EV.

Baystate Medical Center, Tufts University School of Medicine, Springfield,

MA 01199, USA.

Hyperbaric oxygen (HBO) is 100% oxygen administered at elevated atmospheric

pressure to patients with inflammatory diseases. We developed an in vitro

model to investigate the effects of HBO on stimulus-induced proinflammatory

cytokine transcription and translation.

Human blood-derived monocyte-macrophages were stimulated before being

transferred to an HBO chamber where they were incubated at 97.9% O2, 2.1%

CO2, 2.4 atmospheres absolute, 37 degrees C. Controls were maintained in the

same warm room at normoxia at sea level, hyperoxia or increased pressure

alone.

A 90-min HBO exposure inhibited IL-1beta synthesized in response to

lipopolysaccharide by 23%, lipid A by 45%, phytohaemagglutinin A (PHA) by

68%, and tumour necrosis factor (TNF)-alpha by 27%. HBO suppressed

lipopolysaccharide-, lipid A- and PHA-induced TNF-alpha by 29%, 31% and 62%,

respectively. HBO transiently reduced PHA-induced steady state IL-1beta mRNA

levels. Hyperoxia alone and pressure alone did not affect cytokine

production.

The immunosuppressive effect of HBO was no longer evident in

monocyte-macrophages exposed to HBO for more than 3 h. Interestingly, cells

exposed to HBO for 12 h synthesized more IL-1beta than cells cultured under

control conditions.

In summary, HBO exposure transiently suppresses stimulus-induced

proinflammatory cytokine production and steady state RNA levels.

PMID: 12974755 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------\

-----------------------------------------

Rev Neurol. 2003 Aug 16-31;37(4):359-64.

[Hyperbaric oxygen treatment for children with cerebral palsy]

[Article in Spanish]

Papazian O, Alfonso I.

Departamento de Neurologia, Centro de Espasticidad y Movimientos

Involuntarios, Miami Children's Hospital, Florida 33155, USA.

oscar.papazian@...

AIMS: Demand from parents has made hyperbaric oxygenation (HO) inhalation

the most popular and rapid growing therapy for children with cerebral palsy

(CP). To review peer reviewed articles of HO in children with CP to

determine its efficacy and risks, literature was searched on-line using

PubMed indexed for MEDLINE (1996-2003) for articles under CP and HO

headings.

METHOD: We found 16 references: 5 articles (1 uncontrolled pilot study, 2

from a single controlled study, 1 case report of complications and 1

revision) and 11 letters to the editor. The control study showed significant

improvements in the middle, at the end and 3 months after 40 treatments with

OH (O2=100%/1.75 AA) and placebo (O2=21%/1.3 AA) in the gross motor function

measure, (2.9% vs 3%), self-control, auditory attention and visual working

memory. There were no significant differences between the groups. Side

effects included barometric otitis media (48.2% and 22.2% in the OH and

placebo groups).

The authors and the Advisory Scientific Committee of the American Academy of

Cerebral Palsy and Developmental Medicine agreed that the positive results

in both groups were due to a participation effect. The Southern Africa

Undersea and Hyperbaric Association discouraged the ongoing, widespread, and

informal use of HO for children with CP in South Africa based on the results

of this randomized controlled study.

CONCLUSION: There are no scientific evidences for the use of HO in children

with CP. Risks include barometric otitis media.

PMID: 14533113 [PubMed - in process]

--------------------------------------------------------------------------------\

----------

Pediatrics. 2000 Dec;106(6):E80. Related Articles, Links

Hyperbaric oxygen therapy for cerebral palsy: two complications of

treatment.

Nuthall G, Seear M, Lepawsky M, Wensley D, Skippen P, Hukin J.

Intensive Care Unit, Children's and Women's Hospital, Vancouver, Canada.

There is growing interest in the use of hyperbaric oxygen therapy (HBO(2))

for children with cerebral palsy. Although there is no rigorous evidence to

support this management, private hyperbaric centers have been established

throughout the United States and Canada.

There is likely to be increasing pressure on pediatricians and other health

professionals to prescribe HBO(2). We describe 2 children with cerebral

palsy who suffered significant morbidity immediately after treatment with

hyperbaric oxygen.

Both the temporal association and pathologic findings suggest that the

hyperbaric treatment is likely to have been responsible for the resulting

complications. As with any new therapy, we suggest waiting for the results

of a randomized, controlled trial before recommending this treatment.

Publication Types:

Case Reports

PMID: 11099623 [PubMed - indexed for MEDLINE]

-------------------------------------------------------------

Essex C.

Hyperbaric oxygen and cerebral palsy: no proven benefit and potentially

harmful.

Dev Med Child Neurol. 2003 Mar;45(3):213-5. No abstract available.

PMID: 12613780 [PubMed - indexed for MEDLINE]

: Clin Exp Immunol. 2003 Oct;134(1):57-62.

--------------------------------------------------------------------------------\

-------------

Undersea Hyperb Med. 2003 Summer;30(2):147-53.

Central nervous system oxygen toxicity during routine hyperbaric oxygen

therapy.

Hampson N, Atik D.

Center for Hyperbaric Medicine, Virginia Mason Medical Center, Seattle,

Washington, USA.

Hyperbaric oxygen therapy is associated with a recognized risk for

clinically apparent central nervous system (CNS) toxicity. The risk for

oxygen-induced convulsions during routine hyperbaric treatment of most

routine conditions is extremely low. However, reports from the 1980's

describing the incidence of CNS oxygen toxicity differ significantly from

more recent reports since 1996.

This retrospective study was conducted to determine the incidence of

hyperbaric oxygen-induced seizures among patients treated at our facility

for routine, non-emergent indications. In addition, the period studied was

selected to examine the incidence of CNS oxygen toxicity between two brands

of oxygen delivery hoods.

We reviewed our treatment experience for approximately 10,000 routine

patient treatments performed prior to and following a change in the brand of

oxygen hoods used. Among 20,328 total patient treatments performed from 1992

to 2001, 6 patients experienced an oxygen-toxic seizure for an overall

incidence of 1 in 3,388 treatments (0.03%). No difference in seizure

incidence was seen between the two brands of oxygen hoods utilized.

We conclude that the incidence of oxygen-toxic seizures in our patient

population is approximately three-fold greater than historical reports and

in agreement with more recent reports. The reason for this apparent increase

in incidence of CNS oxygen toxicity is unknown.

PMID: 12964858 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------\

-------------------------------

Nitric Oxide. 2003 Aug;9(1):18-23.

Relationship between protein nitration and oxidation and development of

hyperoxic seizures.

Chavko M, Auker CR, McCarron RM.

Operational and Undersea Medicine Department, Naval Medical Research Center,

Silver Spring, MD 20910-7500, USA. ChavkoM@...

Recent studies have implicated nitric oxide (NO*) as a mediator of CNS

hyperbaric O2 (HBO2) toxicity. One mechanism by which NO* may contribute to

HBO2-induced brain toxicity involves a neurotoxic, pro-oxidative action of

NO* via the formation of the potent oxidant peroxynitrite (ONOO-).

The present study compares: (a) the formation of protein nitrotyrosine as a

marker of ONOO- accumulation and (B) protein oxidation as an indicator of

reactive oxygen species production during HBO2 exposure. Rats were exposed

to 5 atm 100% O2 to pre-convulsive exposure or until the occurrence of

electroencephalographic (EEG) seizures. After exposures, brains were

analyzed for protein nitrotyrosine (NT) and protein carbonyl measurement by

Western blot and for superoxide dismutase (SOD) activity by NBT assay.

The results show a significant increase in protein NT, exceeding control

level by several fold. There was only a slow and non-significant increase in

the quantity of oxidized proteins during the pre-convulsive phase of HBO2

exposure. Levels of both protein NT and protein carbonyls were significantly

(p<0.05) elevated after seizures. Total SOD activity was not changed during

preconvulsive exposures, but was significantly (p<0.05) elevated

post-seizures.

The specific neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole

(7-NI), significantly reduced the increases in seizure-induced protein NT

and protein carbonyl and at the same time very effectively (p<0.05) delayed

onset of HBO2 seizures. Pre-seizure increases in protein NT might indicate

its role in the mechanism of HBO2-induced brain toxicity. This is supported

by the observed capacity of 7-NI to inhibit tyrosine nitration and increase

time to seizure.

PMID: 14559428 [PubMed - in process]

--------------------------------------------------------------------------------\

------------------------------------

J Appl Physiol. 2003 Sep;95(3):910-21. Epub 2003 Apr 18.

Hyperbaric oxygen and chemical oxidants stimulate CO2/H+-sensitive neurons

in rat brain stem slices.

Mulkey DK, RA 3rd, Putnam RW, Dean JB.

Department of Anatomy and Physiology, State University, Dayton, OH

45435, USA.

Hyperoxia, a model of oxidative stress, can disrupt brain stem function,

presumably by an increase in O2 free radicals. Breathing hyperbaric oxygen

(HBO2) initially causes hyperoxic hyperventilation, whereas extended

exposure to HBO2 disrupts cardiorespiratory control. Presently, it is

unknown how hyperoxia affects brain stem neurons.

We have tested the hypothesis that hyperoxia increases excitability of

neurons of the solitary complex neurons, which is an important region for

cardiorespiratory control and central CO2/H+ chemoreception. Intracellular

recordings were made in rat medullary slices during exposure to 2-3 atm of

HBO2, HBO2 plus antioxidant (Trolox C), and chemical oxidants

(N-chlorosuccinimide, chloramine-T). HBO2 increased input resistance and

stimulated firing rate in 38% of neurons; both effects of HBO2 were blocked

by antioxidant and mimicked by chemical oxidants. Hypercapnia stimulated 32

of 60 (53%) neurons.

Remarkably, these CO2/H+-chemosensitive neurons were preferentially

sensitive to HBO2; 90% of neurons sensitive to HBO2 and/or chemical oxidants

were also CO2/H+ chemosensitive. Conversely, only 19% of HBO2-insensitive

neurons were CO2/H+ chemosensitive. We conclude that hyperoxia decreases

membrane conductance and stimulates firing of putative central

CO2/H+-chemoreceptor neurons by an O2 free radical mechanism. These findings

may explain why hyperoxia, paradoxically, stimulates ventilation.

PMID: 12704094 [PubMed - in process]

--------------------------------------------------------------------------------\

------------------------------------------

Brain Inj. 2003 Mar;17(3):225-36.

A review of the scientific evidence on the treatment of traumatic brain

injuries and strokes with hyperbaric oxygen.

Alternative Therapy Evaluation Committee for the Insurance Corporation of

British Columbia.

OBJECTIVE: This review sought to determine the strength of the scientific

evidence relating to the therapeutic use of hyperbaric oxygen for traumatic

brain injury or stroke. In order to reduce the possibility of omitting

relevant human clinical trials, parallel searches of the Medline, HealthStar

and Embase databases were undertaken, and input was sought from local

experts in hyperbaric medicine as well as from a widely noted proponent of

this therapy.

Papers retrieved were reviewed to ensure that they reported the results of

comparative clinical trials and were then reviewed by a panel of scientists.

Papers were scrutinized for methodological flaws, and the clinical

significance of the results was examined.

OUTCOME: The strongest papers indicated either no effect or harm from

hyperbaric oxygen when used to treat traumatic brain injuries or strokes.

CONCLUSION: The scientific literature up to August 2001 does not support the

use of hyperbaric oxygen for traumatic brain injuries and strokes.

Publication Types:

Review

Review Literature

PMID: 12623499 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------\

---------------------------------------

Invest Ophthalmol Vis Sci. 2003 Aug;44(8):3476-84. Related Articles, Links

Lenticular oxygen toxicity.

Schaal S, Beiran I, Rubinstein I, B, Dovrat A.

Alberto Moscona Department of Ophthalmology, Rambam Medical Center, Haifa,

Israel.

PURPOSE: To investigate the possible toxic effect of oxygen on lenses in an

organ culture. METHODS: Bovine lenses were exposed to four different

combinations of ambient pressure and oxygen concentration in an organ

culture throughout a 7-day period. Lens transparency, histology, enzymatic

activities, and photomicrographs were compared in study and control groups.

RESULTS: No differences were observed between study and control lenses in

all measured parameters in a group subjected to a single exposure of 100%

oxygen under increased (i.e., hyperbaric) ambient conditions and a group

exposed repeatedly to high ambient pressure and normal oxygen partial

pressure.

Decreased lenticular transparency and enzymatic activities along with

structural changes were observed in lenses exposed repeatedly to 100% oxygen

concentration under both normal and increased ambient pressures. The

observed changes were oxygen-load-dependent: the higher the oxygen partial

pressure and the longer the time of exposure, the more severe the changes

observed. Optical and structural changes in the lens occurred in a

centripetal orientation: the greater the oxygen load, the more central the

damage.

CONCLUSIONS: High oxygen load has a toxic effect on bovine lenses in organ

culture. These effects appear to be cumulative: the higher the oxygen

partial pressure and the greater the number of exposures, the more severe

the changes observed in the lenses. Changes marking toxicity follow the

route of oxygen diffusion into the lens, from the periphery to the center.

Cautious interpretation of the results may indicate a role of oxygen (and/or

its derivatives) in human cataract formation.

PMID: 12882797 [PubMed - indexed for MEDLINE]

_________________________________________________________________

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