Demodex Mites and Elastotic Degeneration

[Mistica]

Originally Posted by Brady Barrows

Have you considered that IPL may have contributed to this? It is odd to me that photo dynamic therapy (PDT) helps rosacea for a while with several treatments and then comes back later. I think in years to come we will see the long term effects of rosaceans using PDT which hasn't been around long enough to know what they are. Long term clinical studies will eventually be performed what the risks are for treating rosacea with PDT.

Perhaps PDT kills bacteria? The acid being the key factor, with light to activate it.

And yes, as I said, IPL treatments which went wrong are definitely a cause of my damage. It can be seen with the eye, so it has to be within as well. This is aside from damage resulting from the disease process. Based on Dan's results, the latter is able to be repaired. IPL damage can't be. At least, not fully.

[Brady Barrows]

Originally Posted by Michael_V

I am currently reading my second dermatology text (since medical school!) in an attempt to understand what is actually happening to us. The first was Rosacea: Diagnosis and Management by Frank Powell. This slim 140 page book should be issued to every dermatologist upon completing residency. The second is Facial Skin Disorders by Ronald Marks.

While I haven't read Marks book I have read Powell's book and wrote a review at this link. If every rosacean went to the dermatologist armed with this book he would definitely get the attention of his physician.

Yes, Powell shows that the vascular theory is only just that and the pathogenesis of rosacea is still up in the air. He tends to suggest that he feels that light damage is at the core of the beast, but he is careful not to be dogmatic about it and leaves the subject open to debate.

[Mistica]

Originally Posted by Brady Barrows

Aloha Mistica. I am doing fine, mahalo. How about you? I have no idea what my vitamin D levels are. I take 1000 I.U. of Vitamin D3 every day along with 25,000 I.U. of Beta Carotene along with a handful of vitamins and supplements. If I am out in the sun during the day I try to remember to bring a hat. I only use sun screen when I go into the water which is a rare treat. Never considered Rifaximin and not likely will consider it. While we do get sunny days here, obviously, we do get a significant number of days of cloud cover as well. But I sure don't get those red rosey cheeks and nose from the bitter cold days when I lived in New England.

I am happy to hear you are doing well.

I am much better than when we last spoke due to my high dose vitamin D therapy, but the road is rocky and compared to normal people, I am still very debilitated. Two months ago, I was all excited as I really felt I was on a constant uphill ride, but I fell off the happy train soon afterwards due to several reasons. Now I am struggling to get on track again.
I am still much better than I was intially and I try to hang on to that as it is all I have really, but I do wish I knew for certain if this was going to work or not.

Have you been following the vitamin D thread? If so, do you have any thoughts you would like to share?

[Brady Barrows]

Originally Posted by Mistica

If UV light is a causative factor, why don't we have rosacea on our limbs?

I have rarely had exposure to sunlight. In fact, I had so little, I became vitamin D deficient.
Due to my melasma, which occurred years before I developed rosacea, I avoided sun exposure to my face. I used sunblock religiously and never left the house without an umbrella. Darting from the car to a building etc. Never wandered around outside.

I know I am just one example, but my case is interesting as not only have I had little UV exposure, I am one of the worse rosacea cases.

I can't help but feel the connective tissue damage we suffer only shares similarities with excessive UV exposure.

A bit like having a bruise. It can be produced externally through trauma, or it can occur as the result of an internal factor. But by all appearances, it is simply a bruise.

Remember that it just a theory. I tend to be rather skeptical and have to work hard at trying to be open to possibilities. When they say that the sun is our enemy I think they have a point, but as you just pointed out sunlight is needed to absorb Vitamin D which is an essential nutrient. So we need a certain amount of sun exposure. I think to totally avoid the sun and wear sun block all the time may in the long term be damaging to our skin. We need some sun on our skin and it needs to be controlled. I think your body gives a signal to your brain that we have had enough sun if we listen to those signals. But when you are having fun in the sun you ignore the signals. I know that when I was young I received countless sun burns and my skin is the light, fair skinned with red hair when I was a child. Maybe it is true that such sun damage later causes a tendency to get rosacea, being a sort of genetic environmental trigger. Maybe a little PDL would be a good thing? But too much light obviously is not a good idea. Sometimes I have noticed that just leaving the skin alone for a few days, or a week is what is needed. I think we may be irritating our skin with too much treatment. Skin needs to heal on its own sometimes. Just some thoughts.

[Brady Barrows]

Originally Posted by Mistica

I am happy to hear you are doing well....

...Have you been following the vitamin D thread? If so, do you have any thoughts you would like to share?

That one has become such a long thread that I haven't really been keeping up. I do believe that we need more Vitamin D due to the article I read in Reader's Digest a while back. The minimum daily requirement that the government recommends is way too low so that is why i supplement my diet with 1000 I.U. a day. I also believe we need more than just Vit D so that is why I take a handful of vitamins and minerals every day.

[Brady Barrows]

Originally Posted by Michael_V

I am currently reading my second dermatology text (since medical school!) in an attempt to understand what is actually happening to us. The first was Rosacea: Diagnosis and Management by Frank Powell. This slim 140 page book should be issued to every dermatologist upon completing residency...

Anyway, there were some interesting tid bits in the latter that I thought I would share.

Regarding Demodex mites:

"Some have believed that the demodex mite is involved in the pathogenesis of this disease and this idea gains some support from the greatly increased numbers of demodices in rosacea. The evidence for this is slim. Although the follicles may be packed with demodex mites, the follicles are not in fact the focal points of inflammation ... In fact, inflammatory cells are mostly found around the vessels in the mid dermis rather than involving the follices. [Further,] the mite is occasionally seen sitting in the middle of skin tissue without any surrounding inflammation ... [and] few of the successful therapeutic agents for rosacea are directly miticidal. It is possible that the increase in mites could be a result of rosacea rather than the cause. The dilated follicles in rosacea and the dilatation of the superficial capillary vasculature with pooling of the blood might well provide an attractive microclimate for the demodices."

There was a period during the early days of the r-s forum that carried through for about five years or more where demodex was thought to be not a big factor in rosacea due to the influence of certain influential rosacea 'authorities.' Now this is no longer the case and I have been on a crusade of calling demodectic rosacea a variant of rosacea which is as valid a variant as any of the other variants. Powell confirms the role of demodectic rosacea as a factor to consider and encourages testing for demodex with skin grafts under a microscope counting the demodex density. If physicians would test for demodex using Powell's suggestions in his book and we get a million or so such tests recorded over a number of years we will eventually discover the number of rosaceans who have demodectic rosacea vs other rosacea classifications or variants. This is one of the main benefits of Powell's book is that he has clearly explained the demodex factor in rosacea and that physicians over look it and rarely test for it. Demodectic Rosacea will be eventually recognized as a variant of rosacea. The evidence is over whelming. But the medical community is slow to respond to such evidence. Whether the demodex is the culprit or pre-existing rosacea causes the increase in demodex the point is to test for demodex. How many rosaceans in this forum have been tested for demodex density with a skin graft sample under a microscope? The numbers are so few that it is embarassing. Why don't physicians do this test? Ask your physician. But if you asked your physician with Powell's book in your hand and showed your physician page 37 where he clearly says to take a skin scraping and examine it under a microscope and refers the physician to Chapter 5.

[Brady Barrows]

"Another theory of pathogenesis relates to the presence of abundant Demodex folliculorum mites in the facial skin of patients with rosacea. These small worm-like organisms are inhabitants of the sebaceous follicles of normal adult facial skin. They were first described in the 1800s, but their role in the homeostasis of facial skin is unknown. They have been reported to transport bacteria on the skin surface, and the population can increase markedly in certain circumstances. They can be easily extracted from the follicles where they are found, often in groups, head downward, feeding on sebaceous material. They have eight short subby legs with claw-like end processes, which they use to move about the facial skin surface from one follicle to another. This apparently occurs at night (it has been shown that the mites react negatively to light.) These organisms seem to live in a harmnious relationship with their hosts and in normal circumstances do not excite an inflammatory reaction in the skin. It is not known if they perform any useful function in human skin, and it is probably impossible to fully eradicate them as the skin seems to become recolonized rapidly following antimite treatment. In patients with rosacea, these mites are greatly increased in number and are found mainly in the centrofacial convexities--the areas typically affected by the inflammatory papules and pustules. Histologic sections of inflammatory lesions show the pathologic changes to be centered on the follicles and mites or the fragments of disrupted mites are often seen in the follicular canals surrounded by inflammatory cells. Sometimes ruptured follicles are seen with particles of demodex mites extruded into the dermis. In these cases foreign body granuloma formation to the follicular aeration and/or the mite is a feature of the histopatholgic changes. Immunosuppressed patients (with HIV infection or on immunosuppressive therapy or patients having renal dialysis) or those who have applied immune-modulating drugs (topical steroids/cacineurin inhibitors) to the face may also have increased numbers of demodex mites on the skin. This suggests a possible role of local immune mechanisms restricting the demodex population in normal facial skin. Some immunosuppressed patients may also develop a pustular eruption similar to rosacea with multiple mites identified not only on skin biopsies, but also visualized by microscopic examination of the scale obtained by gently scraping the skin surface. In some individuals these eruptions were cleared when antimite treatment was used. Finally, it has been shown that these mites have related bacteria, some of which are susceptible to the antibiotics used to treat the papules and pustules of rosacea. These facts could explain the effectiveness of topical and systemic antibiotics in the management of this disorder." Rosacea Diagnosis and Management by Frank C. Powell, pages 69, 70

Did your physician perform a skin scraping and look under the microscope for demodex density? Why don't physicians perform this simple test? Powell encourages physicians to perform a demodex density test.

[Brady Barrows]

Originally Posted by drums

It seems to me that this would mean my body is not initiating my flush response abnormally (as it seems to be) when I exercise or eat spicy foods or feel angry or embarrassed--those are, in fact, appropriate times to flush--but my facial soft tissues are abnormal and are not supporting and controlling the flush as they should, so the flush is too intense, and the blood stays too long, pools in my unsupported vessels, and then eventually leaks out into my dermis, inciting inflammation, itching, papules, and pustules.

It’s just my opinion but in normal humans shouldn’t a flush terminate by sweating and therefore would flushing not be a vital part of the sweating process.
It seems to me its quite normal to flush during exercise or eating spicy foods or feel angry or embarrassed. I think its more important to find out why the flushing does not terminate by sweating because flushing without sweating to me seems to be more of an abnormality than the flushing itself.
The way I see it is the reason for this is possibly a fault with the hypothalamus as part of its many functions is to signal the neurotransmitters in the skin and initiate sweating.

Maybe perhaps you could have something to say why flushing does not calculate into sweating

drums,
you seem to be in a cosmic entanglement with sweetness and light on another forum. However, as shown in your counterpart's thread, the results discussed in this other thread show little consistency in you theory as are all the theories for rosacea. Some say you are on to something while others say no. What Powell says is true, one of the problems with rosacea is "rosacea’s definition has been vague, that the etiology is unknown." The NRS has tried to classify rosacea and named ONE VARIANT. That has helped and Dr. Powell was instrumental in classifying rosacea since he was on the team that did it. However, this classification system has some controversy, especially how it implies a progression of the disease which the 'expert committee' who did this classification vigorously denies any progression of the disease. Powell goes into great details how one can get Type 3 without going through types one and two. Numbers imply progression. And what about all the other rosacea variants that are proposed by physicians who are not on the 'expert committee' formed by the NRS? These are completely ignored by the classification system. In short, the definition of rosacea is vague. And lack of sweating hasn't been on anyone's rosacea research paper as far as I know. But, maybe someone has studied this subject in a clinical paper and someone in this forum or another one will find such a paper that goes along with your theory.

[Brady Barrows]

Originally Posted by Wistar

Also from the same book:

"Recently, because of a demodicidal action, permethrin has been tried in inflammatory rosacea and found to be quite effective."

It is a bit odd the author would write evidence is slim and then a few pages later refer to evidence that suggests otherwise.

In Chapter 5, on page 75 of Powell's book under the subheading, 'Differential Diagnosis and Investigations,' Powell writes, "These patients have also been shown to have a major increase in the demodex mite count on their facial skin using the cyanoacrylate skin biopsy technique." In discussing Pityriasis folliculorum on pages 81-2 he writes, "The diagnosis of pityriasis folliculorum is facilitated by the use of dermatoscopy, which shows a distinctive picture of the presence of multiple white keratotic material consisting of keratin encrusted demodex mites protruding upwards from the follicular orifices. Scraping the skin surface with the blunt side of a scalpel blade and spreading the scrapings on a glass slide reveals the presence of multiple dead and living D. folliculorum mites. The condition appears to be caused by an overpopulation of mites facilitated by the frequent use of creams and the lack of face washing with soap and water."

He then states on page 82:

"There is no laboratory test or investigation that will confirm the diagnosis of PPR. Specific investigations may be required to rule out similar appearing conditions (many of which will be identified by listening carefully to the patient's medical history and examining the skin lesions). These include skin swabs for bacterial culture, skin scrapings for the presence of demodex mites, scrapings for fungal KOH and fungal culture, skin biopsy for histological examination, (and rarely culture) skin surface biopsy for demodex mite quantification, patch tests, photopatch tests and very rarely systemic workup with appropriate blood tests and radiological examinations."

So I would hardly say that the evidence is slim until it is completely ruled out. And why rule it out if the evidence is so slim. You can see why physicians rarely test for demodex now can't you? However, Powell encourages testing for demodex to rule it out.

[college_senior]

Brady,

Thank you for being our Daniel Boone during our journey through rosacea.

My question is simple. I am going to visit my dermatologist, a very nice lady who prescribed me accutane for my acne back In January. I am acne free, but now developing P&P's around my nose and cheeks since ending the course three months ago.

I have permanent redness on my face, and it is all over like a mask. (Not just the cheeks or nose or forehead, but literally the whole face.)

Could demodex mites have something to do with this permanent redness? Should I have my derm do a skin scrape and check?