Vessel regrowth and lasers (was Re: need help with ansers from laser doc.)..

[Guest guest]

> This evidence, albeit anecdotal, reminds me a little of

> the laser abstract you recently posted where the doctors were

> pleased with improvement, but patients weren't.

, I recall 's laser abstract where physicians and patients

disagreed on the severity of the condition, but in that study both

groups agreed on improvement and all other measured factors. I just

discussed that study with Rick. Am I forgetting about a second

abstract?

> Anything that causes an insult to the skin has the potential to

cause

> angiogenesis (e.g. blistering, bruising, swelling). This is why

the

> newer lasers, and Photoderm in particular, are of theoretical

benefit

> because they are more selective for the blood vessel. Dr. Nase has

> *always* cautioned against casuing deep bruising or blistering of

the

> skin, because it will likely cause angiogenesis -- i.e. more

redness

> and flushing. In fact, Nase also cautioned against only having 2

or

> 3 treatments because of the potential for angiogenesis.

I recognize your source of info on the above is Dr. Nase, but maybe

you know the answers to these questions: In the absence of outward

manifestation of vessel injury such as blistering and bruising, what

evidence is there that angiogenesis won't take place? What evidence

is there that angiogenesis is not induced after several treatments?

> <questions about aretries and veins snipped - pass!>

Don't we all wish we could pull that " snipped-pass " routine in real

life? <g>

> Dr. Ormerod's study on psoriasis followed the topical treatment of

> psoriasis patients with an NO inhibitor (L-NAME). I believe it was

> double-blind placebo controlled but don't have access to the full

> text any more. Dr. Ormerod used laser-doppler to measure blood

flow

> through the cheeks where topical L-NAME was applied. He found a

40%

> reduction in blood flow using laser-doppler. He also meausured the

> production of VEGF and found a significant decrease (can't remember

> the exact figures).

Let's accept that all as valid. Still, research on psoriasis may or

may not be relevant to rosacean. That's the study that needs to be

done -- that NO inhibition and/or decreased VEGF correlates to

clinical improvement in rosacea. I could well be wrong, but in

discussions with other members online it sounds like most researchers

and/or newer studies are having difficulty confirming topical NOI

results.

> The reasons why it's hypothesised that NO inhibition could reduce

> flushing is that NO is involved in many forms of skin flushing and

> redness, including to heat, irritation, etc. (Nase's book has a lot

> of references on this). In addition, simply blocking endothelial NO

> production which occurs continuously from vessel walls leads to

> reduction in blood-flow through those vessels (this is what the

> Ormerod paper documented).

But how do we know that the flushing in rosacea is dependent on NO?

Nitric oxide is only one of the many peptides that cause

vasodilation. It was hot research when Dr. Nase was writing in the

late 90s, at least partly due to the Nobel Prize award to its

discoverer. But I honestly don't know if it's still hot stuff in

rosacea research, in comparison to other peptides and in

consideration of this entire area of research.

> This obviously has potential to reduce

> residual redness and discomfort. I have had discussions with

doctors

> (other than Ethan Lerner) who have run preliminary trials with NO

> inhibitors on rosacea with no visible benefit (I don't know whether

> they used laser-doppler). This raises more questions than it

> answers. Was there still the reduction in blood flow as measured

on

> Psoriasis patients? Why did this not reduce redness? Was the NO

> inhibitor getting to the larger feed vessels where it was needed?

> Was the cream base optimised? Was the NO inhibitor the lasest and

> most potent? etc. etc.

All good questions and points. I guess we'll have to wait for

reproducible studies by independent researchers that include clinical

correlations -- in other words, that the changes in small peptide

levels follow not just physiologic events like blood flow (important

to document in its own right) but also clinical improvement and

worsening. Are you aware of any lab or researcher even close to

working on this yet?

Marjorie

Marjorie Lazoff, MD

[Guest guest]

> This evidence, albeit anecdotal, reminds me a little of

> the laser abstract you recently posted where the doctors were

> pleased with improvement, but patients weren't.

, I recall 's laser abstract where physicians and patients

disagreed on the severity of the condition, but in that study both

groups agreed on improvement and all other measured factors. I just

discussed that study with Rick. Am I forgetting about a second

abstract?

> Anything that causes an insult to the skin has the potential to

cause

> angiogenesis (e.g. blistering, bruising, swelling). This is why

the

> newer lasers, and Photoderm in particular, are of theoretical

benefit

> because they are more selective for the blood vessel. Dr. Nase has

> *always* cautioned against casuing deep bruising or blistering of

the

> skin, because it will likely cause angiogenesis -- i.e. more

redness

> and flushing. In fact, Nase also cautioned against only having 2

or

> 3 treatments because of the potential for angiogenesis.

I recognize your source of info on the above is Dr. Nase, but maybe

you know the answers to these questions: In the absence of outward

manifestation of vessel injury such as blistering and bruising, what

evidence is there that angiogenesis won't take place? What evidence

is there that angiogenesis is not induced after several treatments?

> <questions about aretries and veins snipped - pass!>

Don't we all wish we could pull that " snipped-pass " routine in real

life? <g>

> Dr. Ormerod's study on psoriasis followed the topical treatment of

> psoriasis patients with an NO inhibitor (L-NAME). I believe it was

> double-blind placebo controlled but don't have access to the full

> text any more. Dr. Ormerod used laser-doppler to measure blood

flow

> through the cheeks where topical L-NAME was applied. He found a

40%

> reduction in blood flow using laser-doppler. He also meausured the

> production of VEGF and found a significant decrease (can't remember

> the exact figures).

Let's accept that all as valid. Still, research on psoriasis may or

may not be relevant to rosacean. That's the study that needs to be

done -- that NO inhibition and/or decreased VEGF correlates to

clinical improvement in rosacea. I could well be wrong, but in

discussions with other members online it sounds like most researchers

and/or newer studies are having difficulty confirming topical NOI

results.

> The reasons why it's hypothesised that NO inhibition could reduce

> flushing is that NO is involved in many forms of skin flushing and

> redness, including to heat, irritation, etc. (Nase's book has a lot

> of references on this). In addition, simply blocking endothelial NO

> production which occurs continuously from vessel walls leads to

> reduction in blood-flow through those vessels (this is what the

> Ormerod paper documented).

But how do we know that the flushing in rosacea is dependent on NO?

Nitric oxide is only one of the many peptides that cause

vasodilation. It was hot research when Dr. Nase was writing in the

late 90s, at least partly due to the Nobel Prize award to its

discoverer. But I honestly don't know if it's still hot stuff in

rosacea research, in comparison to other peptides and in

consideration of this entire area of research.

> This obviously has potential to reduce

> residual redness and discomfort. I have had discussions with

doctors

> (other than Ethan Lerner) who have run preliminary trials with NO

> inhibitors on rosacea with no visible benefit (I don't know whether

> they used laser-doppler). This raises more questions than it

> answers. Was there still the reduction in blood flow as measured

on

> Psoriasis patients? Why did this not reduce redness? Was the NO

> inhibitor getting to the larger feed vessels where it was needed?

> Was the cream base optimised? Was the NO inhibitor the lasest and

> most potent? etc. etc.

All good questions and points. I guess we'll have to wait for

reproducible studies by independent researchers that include clinical

correlations -- in other words, that the changes in small peptide

levels follow not just physiologic events like blood flow (important

to document in its own right) but also clinical improvement and

worsening. Are you aware of any lab or researcher even close to

working on this yet?

Marjorie

Marjorie Lazoff, MD