Rosacea and Chlamydia pneumoniae

[Guest]

Last year, in doing some research for myself and in putting

together the Rosacea Support Resource Pages:

http://rosacea-research.org/wiki/index.php/Main_Page

I ran across a study which seems to create a strong link

between rosacea and infection with the gram-negative bacteria,

Chlamydia pneumoniae. Since then, I've done quite a bit more

research on this link and I've put together some of this research in a

pdf that I have forwarded along to be attached to this thread.

Would you please take a look at it, and give me your opinions?

I've been undergoing the full antibiotic + N-acetyl

cysteine (NAC) treatment for Cpn since the beginning

of this year and have made quite a recovery, with many

of my symptoms all but disappearing. But through

some private e-mails with Dr Wheldon (described in the

forwarded pdf) I'm now becoming increasingly convinced

that NAC may be the key to treatment, and I believe

that since it is a commonly used supplement, it alone

might might allow for a winnowing down of Cpn loads

over time and potentially provide actual remission for

many rosaceans.

As you know too, I'm a strong believer in co-pathogen

involvement in rosacea. I believe demodex mites,

fungal infections, and potentially h.pylori and s.

aureus play a role in many of the symptoms we

experience as rosaceans, but I believe also that a

persistent gram-negative bacteria like Cpn may be the

key to providing the type of environment that these

other pathogens thrive in and then contribute to.

I wanted to run this by you as I'm sort of at a loss

as to where in the medical community to go with this.

I've run this by a few researchers, but don't seem

to be getting any responses back from them.

I'd also like to keep this very quiet and off the public boards

for the time being if you don't mind. I am concerned with

people being able to kill off a gram negative bacteria and

thus releasing a load of endotoxins with a readily available

OTC supplement like NAC without a basic knowledge of the

harm these endotoxins can do to the body. I believe NAC

with its antioxidant (and potential endotoxin moderating effects)

might be the answer to a slow, safe method for decreasing Cpn loads

over time, potentially even eliminating them with the help of

a strengthened immune system, but I certainly don't have

the medical background to make this call. Also, while Drs

Stratton and Wheldon have proven that NAC + antibiotics does

decrease Cpn loads in the body (potentially eliminating them)

and appears to relieve the symptoms of several inflammatory

diseases, using NAC alone to do this is still just a theory that I

(and Dr Wheldon) think may well work.

I am hoping to get one of you kind doctors to take an interest

in this research and discuss this information further with Dr Stratton

at Vanderbilt University and Dr Wheldon in the UK. Both have

built up a tremendous amount of knowledge about Cpn.

Thanks again in advance for any help you may be able

to provide.

Dan Fries

You may download a pdf of the report by going to this url >

http://irosacea.org/pdf/cpn.pdf

[Guide]

I have received the following MAC MEMBERS replies:

Dr. Cordain wrote:

From my perspective, Dan's paper indeed has merit and converges upon a common link by which diet may also promote AR. The key here is VEGF which is a potent vasodilator and angiogenic agent suspected in the etiology of AR. EGF-R signaling induces VEGF expression and angiogenesis (1, 2). Pharmaceuticals which block EGF-R elicit an acne like rash on the face and upper body with a histology closer to infectious folliculitis (3) because no comedones are present (4). It is likely that pharmaceutical blockers of the EGF-R actually upregulate the EGF-R in keratinocytes (5). Hence, environmental agents which have the capacity to increase flux through the EGF-R/VEGF axis may be crucial in the development of AR.

Three points as they relate to diet and flux through this pathway are 1) hyperinsulinemia 2) milk, and 3) wheat. Hyperinsulinemia chronicaly elevates non esterified free fatty acids in plasma (6) which in turn causes overexpression of the EGF-R (7). Bovine milk contains physiologic concentrations of EGF which are not destroyed by pasteurization and which survive gut proteolytic degradation. The EGF-R is one of the few hormonal receptors to be expressed luminally in the gut, hence the consumption of bovine milk almost certainly must increase flux through the EGF-R/VEGF axis and be a contributor to AR in genetically susceptible individuals. Finally, whole wheat contains the lectin wheat germ agglutinin (WGA) which survives digestion intact in the human gut and enters circulation by binding the luminally expressed EGF-R (8). Once in circulation WGA is not overcome by either liver or an IgG response, hence it has the capacity to bind all cells expressing the EGF-R. In vitro, WGA activates the EGF-R to a greater extent than its endogenous ligand (9) and also displaces endogenous ligand binding by 50% (10), which in theory would represent a double whammy by upregulating the receptor while simultaneously increasing tyrosine kinase flux. A starting point for a clinical dietary trial in AR patients then would be diets free of wheat and dairy and which also minimize the insulin response. There is evidence to show that peanut lectin (PNA) also rapidly enters circulation following ingestion (11) and likely binds the EGF-R because the EGF-R contains sugars specific to WGA, PNA and other dietary lectins.

References:

1. Zhong H, Chiles K, Feldser D, Laughner E, Hanrahan C, Georgescu MM, Simons JW, Semenza GL. Modulation of hypoxia-inducible factor 1alpha expression by the epidermal growth factor/phosphatidylinositol 3-kinase/PTEN/AKT/FRAP pathway in human prostate cancer cells: implications for tumor angiogenesis and therapeutics. Cancer Res. 2000 Mar 15;60(6):1541-5.

2. Jiang BH, Jiang G, Zheng JZ, Lu Z, Hunter T, Vogt PK. Phosphatidylinositol 3-kinase signaling controls levels of hypoxia-inducible factor. Cell Growth Differ. 2001 Jul;12(7):363-9.

3, Lenz HJ. Anti-EGFR mechanism of action: antitumor effect and underlying cause of adverse events. Oncology (Williston Park). 2006 Apr;20(5 Suppl 2):5-13.

4. Molinari E, De Quatrebarbes J, Andre T, Aractingi S. Cetuximab-induced acne. Dermatology. 2005;211(4):330-3.

5. Hannoud S, Rixe O, Bloch J, Le Pelletier F, Lebrun-Vignes B, Doarika A, Khayat D, Chosidow O. Skin signs associated with epidermal growth factor inhibitors. Ann Dermatol Venereol. 2006 Mar;133(3):239-42.

6. Boden G, Shulman GI. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest. 2002 Jun;32 Suppl 3:14-23.

7. Vacaresse N, Lajoie-Mazenc I, Auge N, Suc I, Frisach MF, Salvayre R, Negre-Salvayre A. Activation of epithelial growth factor receptor pathway by unsaturated fatty acids.Circ Res. 1999 Nov 12;85(10):892-9

8. Gabor F, Bogner E, Weissenboeck A, Wirth M. The lectin-cell interaction and its implications to intestinal lectin-mediated drug delivery. Adv Drug Deliv Rev. 2004 Mar 3;56(4):459-80.

9. Franco R, Lezama R, Ordaz B, Pasantes-Morales H. Epidermal growth factor receptor is activated by hyposmolarity and is an early signal modulating osmolyte efflux pathways in Swiss 3T3 fibroblasts. Pflugers Arch. 2004 Mar;447(6):830-9. Epub 2004 Jan 16.

10. Vale RD, Shooter EM.Epidermal growth factor receptors on PC12 cells: alteration of binding properties by lectins. Cell Biochem. 1983;22(2):99-109.

11. Wang Q, Yu LG, Campbell BJ, Milton JD, Rhodes JM. Identification of intact peanut lectin in peripheral venous blood.Lancet. 1998 Dec 5;352(9143):1831-2.

Loren Cordain, Ph.D., Professor

Department of Health and Exercise Science

Colorado State University

_________________________________________________

Dr. Wedrychowski wrote:

Brady,

In my opinion, the paper has merit and should be posted. Too little for a long time was/is known about rosacea i.e. there will be no treatment or cure in the near future.

That is why incomplete, fragmentary data should not be ignored as long as it is legitimate. The opposite of the above is propagating, for instance, that "people with AIDS have rosacea even though rosacea does not cause AIDS" etc.

Key words in this presentation are:

1. Chronic inflammatory diseases

2.Pathogen infection which include chlamydia pneumoniae

3. Lipopolysaccharides induce inflammatory responses

Take care

Andrzej

_____________________________________

Dr. Latkany wrote:

Interesting but I do not believe that chlamydia

is a cause so I cannot support this research.

I would rather our time is spent looking at a better

way of diagnosing the more subtle cases and making a link

from there.

--

Robert Latkany, M.D.

Founder/Director Dry Eye Clinic NY Eye & Ear Infirmary

Center for Ocular Tear Film Disorders at Laser & Corneal Surgery

________________________________________

Dr. Jones wrote:

Hi,

Certainly a plausible hypothesis, but testing would be a fairly high risk venture. These things rarely pan out and there’s currently relatively data to support the hypothesis. However, the potential payoff is very big in terms of increased understanding of pathophysiology and treatment options. If you like high risk/high gain projects, I’d say this is a reasonably good one.

-Dave

David A. Jones, MD, PhD

Department of Dermatology

Brigham and Women's Hospital

______________________________________________

Dr Tseng wrote:

This is an exciting direction worth further exploration. My curiosity is how Cpn gets into the rosacea skin epithelium? Could this be mediated via molecular mimickry?

Scheffer C. G. Tseng, M.D., Ph.D.

Director, Ocular Surface Center

Medical Director, Ocular Surface Research & Education Foundation

Director, R & D Department, TissueTech, Inc.

______________________________________

Dr. Clark wrote:

Hello. This piece needs quite a bit od work. It is an interesting idea that CP may contribute to rosacea but there is at the present time little if any peer reviewed literature supporting this. Specifically, the study on CP and acne rosacea (the abstract is included) showed CP in biosies of people with rosacea but did not do normal controls which is just bad science. If this piece is to be acceptable, it needs to be presented as an interesting hypothesis for which, right now, there is little evidence. Also it is poorly written; cathelicidin needs to be introduced in detail as to what it is. Hyperbole such as “numbers in this study are amazing” needs to be removed.

Also, the fact that rosacea gets better with azithro DOES NOT in itself support a bacterial etiology for this disorder. Azithro and other abx (TCNS) have potent anti-inflammatory activities and at least in acne, it has been shown that does too small to kill bacteria improve patients via the anti-inflammatory effects of the medication.

Regards,

Rachael A. Clark, M.D., Ph.D.

Harvard Skin Disease Resarch Center

___________________________________

Dr. Sun wrote:

Dear Mr. Barrows,

I email this to you again because there is an error in sending the message. Please let me know if you receive it.

Thanks for fowarding the paper to me.

There are a few things I am not very clear:

1. I had a tough time knowing the purpose of the paper until the last paragraph - need a better study for the relationship of Cpn and Rosacea; or how Cpn facilitate other pathogens to exacerbate Rosacea?

2. What is the focus of the study: is it the causal relationship; the mechanism of how Cpn cause Rosacea; on what level of the mechanism that one wish to address this causal relationship (molecular, cellular, populational, etc)

3. For any type of study, one would always have to fulfill the Kosh's hypothesis

- there is an association between A and disease B

- one would isolate A from sample/population with disease B

- when one treats A, disease B disappear

- when transfer A to popuation/person C, person C gets disease B

4. it is easier to pick one small aspect of a question to discuss

- why this aspect is important;

- how much work has alread be done on this aspect of the question

- what needs to be done to completely understand the question of interest on this particular aspect

- only put in information that addresses your argument directly; for example, if one is interested in populational/associational studies, molecules LL37 may not help clarify the point even though it is a favor molecule of the grant write;

I hope this is not too harsh and not too general. Thanks, Jenny

____________________________________

Dr. Brodell wrote:

Chlamydia may well be involved in Rosacea....but, this is a difficult

thing to prove. There are others who believe rosacea is an

inflammatory process or caused by mites, pityrosporon, etc. Z-Pak can

work in rosacea, but not more so than other antibiotics in my

experience. Look forward to reading more on this subject in the

future.

Dr. BOB

_____________________________________

[Guest]

Hello Dr Cordain.

Very interesting, thank you for this additional

information. I'll need to do some additional reading

to understand all of this.

As some additional information you may find

interesting, infection with a pathogen like Cpn has

some dietary implications. I certainly don't have

your level of expertise, and you may already know much

of this, but here are a couple of key points from what

I understand:

First, per Dr Wheldon (Microbiologist and FCRPath) in a

review of the book "The potbelly syndrome: how common

germs cause obesity, diabetes and heart disease":

"non-resolving intracellular infections can, over

long periods of time, subvert the body's defences by

causing chronic elevation of cortisol while provoking

chronic activation of pro-inflammatory cytokines;

this has serious repercussions, including type II

diabetes, atheroma and heart disease."

I believe he is referencing the ability of chronically

raised cortisol levels to increase insulin resistance

and increase blood glucose levels from what little I

have read about this:

http://en.wikipedia.org/wiki/Cortisol

Also Dr Wheldon states "Infections activate a set of

protein messengers called pro-inflammatory cytokines.

One of these, Tumour Necrosis Factor-alpha, is

produced in response to bacterial endotoxin. Cortisol,

as one of its many functions, acts as a damper on the

pro-inflammatory cytokines, preventing them getting

out of hand. This is a two edged sword: in chronic

infections you get raised cortisol levels and raised

proinflammatory cytokines together. This is seen in

many chronic inflammtory processes. It is found in

diseases as diverse as Multiple Sclerosis (during

relapses and as the disease becomes progressive) and

coronary artery disease; it is found in Alzheimer's

disease."

One of my favorite quotes from Dr Wheldon is this from

the same article: "Symptoms of raised cortisol levels

and raised proinflammatory cytokines should warn you:

look for an infection. And if the CRP is raised, look

hard for an infection."

His full review of the book can be found on the

cpnhelp.org website at the following link:

http://www.cpnhelp.org/?q=book_review

Second, Cpn is an iron using organism, and while

as we know excess iron may lead to increase pathogen

burdens, many people suffering from Cpn infection

seem to be suffereing from iron deficiency. In

addition, Dr Stratton and his collegues have

discovered that Cpn

seems to interfere with heme production, causing what

he calls a "secondary porphyria", with resulting skin

symptoms that I believe may explain some of the

symptoms many of us rosaceans have - thinned, fragile

skin, blistering, itching, swelling, and sensitivity

to the sun and potentially other forms of light among

others. I'm wondering if even potentially

temporarily high levels of porphyrins might help

explain why some rosaceans have such a violently

negative reaction to IPL and laser treatment since

many foods, beverages and medicines are also known to

increase porphyrin levels. More info on Dr

Stratton's theories of secondary porphyria can be

found on the cpnhelp.org website here:

http://www.cpnhelp.org/?q=secondaryporphyria

and here:

http://www.cpnhelp.org/?q=HostCellInteractionpdf

Dan

[Guest]

Hi Dr Latkany.

Thanks so much for taking the time to review this. I

completely understand your reservations, but still I

was hoping to maybe pique your interest with some

additional information on Cpn since there seems to

actually be many more studies relating to Cpn causing

ocular inflammatory reactions and increased

vascularization through stimulating increased VEGF

production than there are studies of Cpn in

dermatological diseases:

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Identification of Chlamydia pneumoniae within human

choroidal neovascular membranes secondary to

age-related macular degeneration

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

The Relationship between chlamydia trachomatis and

chlamydia pneumoniae as the cause of neonatal

conjunctivitis (ophthalmia neonatorum)

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Surfactant proteins A and D enhance the phagocytosis

of Chlamydia into THP-1 cells

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Chlamydia pneumoniae--the etiologic agent of

follicular conjunctivitis followed by

keratoconjunctivitis sicca in adult patients

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Chlamydia in anterior ischemic optic neuropathy

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_DocSum

Chlamydia pneumoniae seropositivity and the risk of

nonarteritic ischemic optic neuropathy

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_DocSum

Chlamydial antibodies in patients with previous acute

anterior uveitis

There are of course studies which seem to refute these

findings, but from what I understand the problem with

many of these studies is that current tests for Cpn

are notoriously inaccurate, producing a large number

of false negatives.

Tests can be inaccurate for the following, and other,

reasons:

* The test may not be sensitive enough. Antigen

tests for Cpn are said to be relatively inaccurate.

PCR tests are the most sensitive, but dependent on the

particular primers used, whether the dna used by the

test matches the particular strain of Cpn one has,

whether the test used accounts for the type of sample

well (blood, sputum, cerebrospinal fluid, etc), the

accuracy of the technician (PCR is particularly

trickey in a technical sense), and so on.

* If the infection is predominantly in cryptic

phase, there is no serology evident.

* If the patient's immunei system is significantly

depleted, they will not show positive antigens for the

organism infecting them (they are immuno-incompetant).

More info on this can be found on the cpnhelp.org site

here:

http://www.cpnhelp.org/?q=diagnosis_issues

Most interestingly, I think though, is that one study

seems to suggest that oral supplementation with NAC

seems to help improve symptoms of chronic blepharitis

(something many of us rosaceans also share - I was

first diagnosed with blepharitis when I was @ 10):

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

N-acetylcysteine in chronic blepharitis

Thanks again for your time and efforts in reviewing this information.

Dan

[Guest]

Thank you Dr Jones.

I definitely agree with you that this could be a risky

venture. In my extremely uneducated opionion, one

way to help minimize the risk would be to

solicit assistance from Dr Stratton and his

colleagues at Vanderbilt University, potentially

funding a study through them or some group that works

closely with them.

Cpn has been implicated in many inflammatory diseases

over a period of 10+ years, yet far too many recent

studies have used inaccurate testing techniques to

test for the presence of Cpn and/or have tried a

couple of weeks of macrolide antibiotics to resolve

symptoms. When the studies fail on either account,

they conclude Cpn does not play a role in whatever

disease process they are studying.

IMHO, Dr Stratton has already explained through his

studies why these techniques do not work, that all but

the most specific testing for Cpn can produce large

numbers of false negatives and that Cpn exists as a

persistant intra and extra-cellular pathogen with

multiple forms that need to be addressed.

Macrolides like Azithromycin (often used as the sole

antibiotic in current studies) seem to force the RB

form of Cpn to go cryptic and may have some activity

against the RB form itself, however they don't appear

to address the infectious EB form. So once the

short term dose of macrolide is removed, the

infectious EBs just start the process of creating new

RB forms again and the cycle continues.

Why waste precious resources reinventing the wheel

like so many studies seem to doing both in the past

and now. It seems to me it would be better to pick up right

from where Dr Stratton and his colleagues have left

off.

Just my pesonal opinion, but I thought it might be

helpful to explain some of this history in order to

help make sure any new study would potentially be

successful.

Thanks again for your efforts.

Dan

[Guest]

Thank you Dr Tseng.

Again, I really don't have a medical background, but

from what I understand, Cpn can ride around in the

vascular system via infected monocytes. When they

"leak out" of the vascular system to say some site of

injury (in a normal inflammatory response), they can

then infect and persist in local tissue cells.

Perhaps a severe sunburn or some other mechanism and

the resulting inflammation is what might first allow

Cpn to set up "house" in rosacean facial epithelial

cells and show up in biopsies as the Fernandez-Obregon

and Patton study seems to suggest.

In fact, there are several interesting studies in

diabetic ulcers showing localized Cpn involvement.

Here's once such study:

http://archderm.ama-assn.org/cgi/content/e...tract/137/5/671

I believe Dr Stratton at Vanderbilt has also done some

work in this particular area.

Finally here is some research from the Pasteur

Institute which seems to answer some of the questions

of how chemically Cpn enters epithelial cells. I

thought you might find this interesting as well:

http://www.pasteur.fr/recherche/RAR/RAR200...05/Ubic-en.html

Thanks again for your interest...

Dan

[Guest]

Doctors & All,

JimK, the founder of cpnhelp.org posts an approved summary of a recent interview (Aug 2006) he had with Dr Stratton of Vanderbilt University relating to some of Dr Stratton's observations of current Cpn research. It is a very interesting read and can be found from the following link:

http://www.cpnhelp.org/?q=recentobservations

Dan

[Steve95301]

That is an interesting article. I find the hypothesis to be elegant, dissolving as it does the distinctions between varying conditions and proposing a bigger picture.

Just the other day at rosaceagroup.org I posted: "I miss the science." Let me just say that this thread is like a breath of fresh air. Please, keep this discussion going- I only wish I were knowledgeable enough to contribute (some day...)

Doctors & All,

JimK, the founder of cpnhelp.org posts an approved summary of a recent interview (Aug 2006) he had with Dr Stratton of Vanderbilt University relating to some of Dr Stratton's observations of current Cpn research. It is a very interesting read and can be found from the following link:

http://www.cpnhelp.org/?q=recentobservations

Dan

[dfries2003]

Thanks Steve.

All,

I've found some studies which also seem to suggest that in addition to being antichlamydial, N-acetyl cysteine seems to have antiangiogenic properties:

http://ajp.amjpathol.org/cgi/content/full/164/5/1683

N-Acetyl-Cysteine Promotes Angiostatin Production and Vascular Collapse in an Orthotopic Model of Breast Cancer

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum The induction of vascular endothelial growth factor by ultrafine carbon black contributes to the increase of alveolar-capillary permeability

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum Inhibition of angiogenesis-driven Kaposi's sarcoma tumor growth in nude mice by oral N-acetylcysteine

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_DocSum Vascular endothelial growth factor (VEGF) and melanoma. N-acetylcysteine downregulates VEGF production in vitro

And studies seem to suggest that NAC can reduce upgregulated inducible nitric oxide (iNOS) production:

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum N-acetylcysteine prevents nitrosative stress-associated depression of blood pressure and heart rate in streptozotocin diabetic rats

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum Protective effects of N-acetylcysteine treatment post acute paraquat intoxication in rats and in human lung epithelial cells

[dfries2003]

Hi All,

And welcome Dr Stratton. Its good to see you on board. I personally cannot thank you enough for all your efforts in studying Cpn and its potential involvements in inflammatory diseases.

Although I still have a ways to go in treatment, my rosacea is now pretty much gone except on occasion. And although I started treatment with great hopes that the link between rosacea and Cpn was a strong possibility and have seen same wonderful results in treatment so far myself, I was greatly encouraged recently when I made contact with one patient on an early Vanderbilt anti-Cpn protocol who reported that her rosacea disappeared completely in 2004 with Cpn treatment and has not returned since (I use the nic "Red" when posting on cpnhelp):

http://www.cpnhelp.org/?q=no_herx_ing_no_metronidaz

She (Astrodiana) wrote:

"My rosacea began at about age 40 and disappeared the

last year I was on the cPn protocol, age 54. it began

with flushing and burning, usually when I was active,

but there was no predicting when it might happen. It

was mainly on my face, but sometimes down my neck,

and after a couple of years of this, it progressed to

a few broken blood vessels and occasional breakouts

around my mouth and chin usually. I would describe it

as cycstic acne...and my skin had always been very

clear. I used to love the sun and tan well, but after

the rosacea began, I would just break capillairies

when I would be out in the sun. Went to the

dermatologist, and began taking minocycline 100mgs

daily and using topical metrogel on my face day and

night - this was age 43. I was told to avoid hot

showers and baths and hot drinks, alcohol, and spicey

foods...I don't drink but I had one sip of wine a

couple of times on holidays and went into a full flare

up of the skin. The dermatologist also told me that

sinus problems go hand in hand with rosacea, and i

sure had those. Her treatments seemed to do little or

nothing for my rosacea, but when I mentioned to my

holistic MD that I had been dx'd with rheumatoid

arthritis at age 26, he talked about The Road Back

Foundation having found that many cases of RA could be

treated with minocycline for at least 48 weeks and see

at least some imrpovement, all the way up to remission

(back then, they did not realize it was MYCOPLASMS

they were attacking the the minocin)...since I had

already been on the minocin for about 5 months at that

time, my MD suggested that I stay on it, add DHEA and

see what it could do for my rosacea. I stayed on the

Minocin @ 100mgs daily for one year. At the end of

that time, my RA was gone! Sed rate normal, RA factor

GONE, and seemingly complete healing. I have had no

signs of RA since then.

But the rosacea stayed with me...and was only slightly

less likely to flare with the use of metrogel day and

night. I found that an injection of Medrol for

allergies given by my internist works well to calm

down and clear the skin of rosacea symptoms...and for

a few years I got those shots as often as he would

give them to me...every two months. It now seems to

have disappeared completely, and that happened

sometime in 2004, a few months after I finished my

protocol. 2004 was the first year i could go without

the shot of medrol and not have the rosacea flaring

up. The last two years, I have only gotten one shot a

year, during tree pollen season in Spring. I just

looked in the mirror...the broken capillaries are gone

from my face and around my nose, and there are only a

few very faint traces of broken blood vessles left on

my nose. I flush still, probably once every few

months, but it goes away and leaves no other skin

problems behind.

Not sure what ocular rosacea is, but i imagine if it

is bloodshot eyes, YES - I had that as often as it

would flare. My eyes would get dry and itch a lot

too. All gone now

"

And further wrote:

" haven't thought about it until you asked...which is

GOOD, I guess - but I actually CAN use just about

anything on my face now - and usually just use the

safeguard soap in the shower to wash my face or a

light facial cleanser... before, could never even use

makeup, a moisturizer, any product made for senstive

skin. If I tried to make my face up, I would be so

broken out by the time I got to wherever I was going,

I looked worse than with no make up. Rosacea and

vanity cannot coexist. the best I could hope for was

clean.

The fact that my skin is clear now is a bonus I never

expected or dared to consider. I am also very

surprised that the broken capillaries are gone...that

is something NOBODY told me could happen. I can now

wear make-up or look good without it. I can travel

without a lot of junk in my cosmetic bag that won't

help anyway. yes....YES!!! I go like "normal people"

now!"

Oh to be able to throw away all the special cleansers and moisturizers and just wash my face in the shower, with safeguard soap no less...

FYI, in order to prevent issues of versioning, I've moved the pdf doc above linking Cpn with Rosacea to the RSRP pages. I've also updated the doc to include some additional information to try to strengthen the link according to some of the comments above. The RSRP page on Cpn can be found at this link:

http://rosacea-research.org/wiki/index.php...ydia_pneumoniae

I've also blogged a chronicle of my treatment for Cpn and Rosacea on the cpnhelp website in hopes that it may help other rosaceans in the future:. I'll continue to update this chronicle as I continue treatment:

http://www.cpnhelp.org/?q=cpn_treatment_for_rosacea

Dan

[Charles Stratton, MD]

Hi All,

And welcome Dr Stratton. Its good to see you on board. I personally cannot thank you enough for all your efforts in studying Cpn and its potential involvements in inflammatory diseases.

Although I still have a ways to go in treatment, my rosacea is now pretty much gone except on occasion. And although I started treatment with great hopes that the link between rosacea and Cpn was a strong possibility and have seen same wonderful results in treatment so far myself, I was greatly encouraged recently when I made contact with one patient on an early Vanderbilt anti-Cpn protocol who reported that her rosacea disappeared completely in 2004 with Cpn treatment and has not returned since (I use the nic "Red" when posting on cpnhelp):

http://www.cpnhelp.org/?q=no_herx_ing_no_metronidaz

She (Astrodiana) wrote:

"My rosacea began at about age 40 and disappeared the

last year I was on the cPn protocol, age 54. it began

with flushing and burning, usually when I was active,

but there was no predicting when it might happen. It

was mainly on my face, but sometimes down my neck,

and after a couple of years of this, it progressed to

a few broken blood vessels and occasional breakouts

around my mouth and chin usually. I would describe it

as cycstic acne...and my skin had always been very

clear. I used to love the sun and tan well, but after

the rosacea began, I would just break capillairies

when I would be out in the sun. Went to the

dermatologist, and began taking minocycline 100mgs

daily and using topical metrogel on my face day and

night - this was age 43. I was told to avoid hot

showers and baths and hot drinks, alcohol, and spicey

foods...I don't drink but I had one sip of wine a

couple of times on holidays and went into a full flare

up of the skin. The dermatologist also told me that

sinus problems go hand in hand with rosacea, and i

sure had those. Her treatments seemed to do little or

nothing for my rosacea, but when I mentioned to my

holistic MD that I had been dx'd with rheumatoid

arthritis at age 26, he talked about The Road Back

Foundation having found that many cases of RA could be

treated with minocycline for at least 48 weeks and see

at least some imrpovement, all the way up to remission

(back then, they did not realize it was MYCOPLASMS

they were attacking the the minocin)...since I had

already been on the minocin for about 5 months at that

time, my MD suggested that I stay on it, add DHEA and

see what it could do for my rosacea. I stayed on the

Minocin @ 100mgs daily for one year. At the end of

that time, my RA was gone! Sed rate normal, RA factor

GONE, and seemingly complete healing. I have had no

signs of RA since then.

But the rosacea stayed with me...and was only slightly

less likely to flare with the use of metrogel day and

night. I found that an injection of Medrol for

allergies given by my internist works well to calm

down and clear the skin of rosacea symptoms...and for

a few years I got those shots as often as he would

give them to me...every two months. It now seems to

have disappeared completely, and that happened

sometime in 2004, a few months after I finished my

protocol. 2004 was the first year i could go without

the shot of medrol and not have the rosacea flaring

up. The last two years, I have only gotten one shot a

year, during tree pollen season in Spring. I just

looked in the mirror...the broken capillaries are gone

from my face and around my nose, and there are only a

few very faint traces of broken blood vessles left on

my nose. I flush still, probably once every few

months, but it goes away and leaves no other skin

problems behind.

Not sure what ocular rosacea is, but i imagine if it

is bloodshot eyes, YES - I had that as often as it

would flare. My eyes would get dry and itch a lot

too. All gone now

"

And further wrote:

" haven't thought about it until you asked...which is

GOOD, I guess - but I actually CAN use just about

anything on my face now - and usually just use the

safeguard soap in the shower to wash my face or a

light facial cleanser... before, could never even use

makeup, a moisturizer, any product made for senstive

skin. If I tried to make my face up, I would be so

broken out by the time I got to wherever I was going,

I looked worse than with no make up. Rosacea and

vanity cannot coexist. the best I could hope for was

clean.

The fact that my skin is clear now is a bonus I never

expected or dared to consider. I am also very

surprised that the broken capillaries are gone...that

is something NOBODY told me could happen. I can now

wear make-up or look good without it. I can travel

without a lot of junk in my cosmetic bag that won't

help anyway. yes....YES!!! I go like "normal people"

now!"

Oh to be able to throw away all the special cleansers and moisturizers and just wash my face in the shower, with safeguard soap no less...

FYI, in order to prevent issues of versioning, I've moved the pdf doc above linking Cpn with Rosacea to the RSRP pages. I've also updated the doc to include some additional information to try to strengthen the link according to some of the comments above. The RSRP page on Cpn can be found at this link:

http://rosacea-research.org/wiki/index.php...ydia_pneumoniae

I've also blogged a chronicle of my treatment for Cpn and Rosacea on the cpnhelp website in hopes that it may help other rosaceans in the future:. I'll continue to update this chronicle as I continue treatment:

http://www.cpnhelp.org/?q=cpn_treatment_for_rosacea

Dan

The use of NAC in the therapy of chronic C. pneumoniae infections is explained below. Alone, I do not think it would eradicate this pathogen. We recommend it be used in combination with other antibiotics. Take care.

ELIMINATION OF EXTRACELLULAR ELEMENTARY BODIES.

Elementary bodies are the only infectious forms of Chlamydia. During the unique life cycle of Chlamydia, extracellular elementary bodies are produced, and it is these elementary bodies that infect new host cells. Extracellular elementary bodies in healthy humans are more common than appreciated. For example, during the winter respiratory tract infection season, 33% of healthy blood donors had positive cultures for C. pneumoniae from buffy coat samples of their blood (1). Clearly these infectious elementary bodies in the systemic circulation or in any other extracellular fluids should be eliminated before they are able to infect a new host cell. Fortunately, there are unique physiochemical agents that are specifically able to eliminate these extracellular chlamydial elementary bodies. Unless these extracellular elementary bodies are eliminated in the host, antichlamydial therapy for chronic chlamydial infections must be prolonged until all of these extracellular elementary bodies have infected host cells and thus can be eliminated during their metabolically active stages. This clearly is undesirable as it prolongs the therapy of chronic chlamydial infections as well as increases the chance for resistance.

Infectious chlamydial elementary bodies can be made less infectious by the use of thiol-containing compounds. Specific thiol-containing compounds that may be effective include meso-2,3-dimercaptosuccinic acid (meso-DMSA), an oral chelating agent currently used to treat lead poisoning (2). Meso-DMSA is a weak acid with four ionizable hydrogens. Moreover, meso-DMSA has two highly charged carboxyl groups, which prevent its passage through human cell membranes. Meso-DMSA thus remains in the extracellular fluid where it readily can encounter extracellular chlamydial elementary bodies. The two thiol (sulfhydryl) groups on the succimer molecule are able to dissolve the disulfide bonds in outer membranes of extracellular chlamydial elementary bodies. For Chlamydiae, the dissolution of the outer membrane thereby initiates the transition of the elementary body form to the reticulate body form. Because this occurs in the extracellular milieu where there is no available energy source for the chlamydiae, the nascent reticulate body perishes.

Another thiol-containing compound that inhibits the infectivity of chlamydial elementary bodies is penicillamine (3). Penicillamine, D L-ß, ß-dimethlcysteine, is a sulfhydryl amino acid that was first isolated from the urine of patients with chronic liver disease who were receiving parenteral penicillin. Its use against chlamydial elementary bodies, however, may be somewhat curtailed by a variety of undesirable side effects (4), which do not appear to be problems with meso-DMSA.

In addition, there is an alternative method of providing a controlled release of penicillamine under physiologic conditions that provides greater safety. This simply is the use of oral penicillins as these undergo, in part, acid hydrolysis to penicillamine in the human host. Thus, oral penicillins such as amoxicillin can be used as a low-cost alternative to meso-DMSA and/or penicillamine. The in-vivo production of penicillamine from the degradation of penicillins undoubtedly accounts, in part, for the well-known in-vitro ability of penicillins to prevent the development of infectious chlamydial elementary bodies in cell cultures (5-8).

Finally, N-acetyl cysteine is another thiol-containing compound that has been safely used in humans for many years (9, 10) and also breaks down the disulfide bonds in the elementary body.

1. Cirino F, Webley WC, Croteau NL, Andrzejewski C Jr, Stuart ES. Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescent microscopy and flow cytometry techniques. BMC Infectious Diseases 2006; 6:23

2. Aposhian HV, Aposhian MM. Meso-2,3-dimercaptosuccinic acid: chemical, pharmacological and toxicological properties of an orally effective metal chelating agent. Annual Review of Pharmacology and toxicology 1990; 30: 279 - 306.

3. Perrett D. The metabolosm and pharmacology of D-penicillamine in man. Journal of Rheumatology 1981; 8(Suppl 7): 51 - 55.

4. Scheinberg IH. Toxicity of penicillamine. Postgraduate Medical Journal 1974; 44(Suppl): 11 - 13.

5. Tamura A, Manire GP. Effect of penicillin on the multiplcation of meningopneumonitis organisms (Chlamydia psittici). Journal of Bacteriology 1968; 96: 875 - 880.

6. Kramer MJ, Gordon FB. Ultrastructural analysis of the effects of penicillin and chlortetracycline on the development of a genital tract Chlamydia. Infection and Immunity 1971; 3: 333 - 341.

7. Kuo C-C, Grayston JT. In vitro susceptibility testing of Chlamydia sp. TWAR. Antimicrobial Agents and Chemotherapy 1988; 32: 257 - 258.

8. Shiao LC, Wang S-P, Grayston JT. Sensitivity and resistance of TRIC agents to penicillin, tetracycline, and sulfa drugs. American Journal of Ophthalmology 1967; 63: 1558 - 1568.

9. Dekhuijzen PN. Antioxidant properties of N-acetylcycteine: their relevance in relation to chronic obstructive pulmonary disease. European Respiratory Journal 2004; 23:629-36.

10. Atmaca G. Antioxidant effects of sulfur-containing amino acids. Yonsei Medical Journal 2004; 45:776-88.

[dfries2003]

Thank you again Dr Stratton. Since discusions about NAC alone therapy were really just speculations mostly on my part, I've removed this discussion from the document I put together linking Cpn and Rosacea:

http://rosacea-research.org/wiki/index.php...ydia_pneumoniae

Thanks again so much for your input.

All, I (as Red) had an interesting exchange with Dr Wheldon (as DW) on cpnhelp over the weekend relating to the underlying pathology in many of the chronic disorders that have been linked with Chlamydia pneumoniae, namely a pathology of small blood vessel disease or vasculitis, localized tissue destruction, and nerve involvement. Evidently this pathology can be found in inflammatory disorders such as multiple sclerosis, Crohn's disease and interstitial cystitis as well as rosacea:

http://www.cpnhelp.org/?q=multiple_sclerosis_damage

Dan

[Guest]

So more information on this subject can be found here >

http://members.irosacea.org/index.php?showtopic=102

[dfries2003]

Hi All,

I just noticed the Fernandez-Obregon / Patton study I orignally referenced which implicated C. pneumoniae with rosacea has now been included in the current issue (Feb 2007) of Cutis (Cutaneous Medicine for the Practicioner):

http://www.cutis.com/asp/archive/article.a...mp;FileType=abs

The abstract on Cutis now also states: "These preliminary data suggest the need for further investigation with clinical trials to study long-term tolerability and efficacy and also strongly implicate C pneumoniae in the pathogenesis of acne rosacea.".

Strongly implicated! Alright. Of course as Dr Stratton's research indicates, single antibiotic therapy is very unlikely to eradicate a persistent C. pneumoniae infection. Still, hopefully this article will help generate some research interest.

BTW, although it was also pointed out in the linkout above, I've recently created a page pointing out the potential link between C. pneumoniae and rosacea for cpnhelp.org, and I believe this page better explains the potential link than my original attempt:

http://www.cpnhelp.org/chlamydia_pneumoniae_an_0

Dan