In this two-part article, Richard Parker, cosmetic chemist and Director of Rationale Skincare explains rosacea, a common and often misdiagnosed condition.
There is no doubt that rosacea still carries many negative social judgments. And it can be not just embarrassing but downright debilitating for patients. Compounding all this, rosacea is still commonly misdiagnosed. Treatment remains convoluted and complicated and is more about lifetime management than cure, so an incorrect diagnosis only leads to treatments that don't work and prolonged suffering for the rosacea patient.
So its vital that we study the latest information on rosacea, in order to make the correct diagnois and recommend treatments that are going to alleviate the condition and put the patient in the driver's seat in terms of managing this condition. Today, we're going to look at how common a problem rosacea really is, then examine the course of the disease over a lifetime. Next, we'll evaluate the way rosacea presents clinically, and identify some of its common variants of the disorder. I'm going to take you through a microscopic look at rosacea, studying the microbial and cellular aspects of the condition. And most importantly, we'll learn how to differentiate rosacea from so many other conditions that present as inflamed red lumps and bumps. Having learned to recongnise rosacea for what it is, we'll conclude by learning the latest treatment modalities to bring patients relief and management strategies.
Occurrence
It's often called "The Curse of the Celts" due to its revalence in fair skinned populations, and it's estimated that rosacea will affect approximately 5% of caucasians. So of the hundred people most of us know in life, roughly 5 of those will be rosacea sufferers. So its quite high.
Later on we're going to learn about the various stages of rosacea as the disease progresses, and the early stage of rosacea, stage 1, characterised by pronounced flushing and blushing, affects approximately three times more women than men.
On the other hand, men are far more likely to develop the hyperplasiac aspects of the disease, characteristed by bulky tissue in the centrofacial area and the pronounced rhinophyma often incorrectly associated with alcoholism.
And as we've discussed earlier, for men and women, the psychological impact of rosacea can be extremely distressing.
In the early stages of rosacea, there are recurrent episodes of blushing which will eventually become permanently red, and this is usually evident before the age of 20. Rosacea is most common, however, in the third and fourth decades of life and peaks between the ages of 40 and 50 years.
Pathogenesis
Although we still don't know the exact cause of rosacea, several factors have presented themselves consistently over our study of the disease to be suspected as at least contributory factors. It must be said, however, that these factors have yet to be definitely confirmed. So here are some interesting facts....
Firstly, we know that rosacea patients are constitutionally predisposed to flushing and blushing, and if you've known a rosacea sufferer from childhood, you will know that this tendency appears very early in life.
Also of enormous interest, and I believe great significance is the fact that migraine headaches have been shown to be two to three times more common in rosacea patients. Interesting huh? Taken together, these factors suggest the possibility of a more vascular pathogenesis for rosacea.
So a reasonable explanation of the basic abnormality of rosacea would be, to quote two of the world authorities on rosacea, the German dermatologists Jansen & Plewig, "a microcirculatory disturbance of the function of the facial angular veins directly involved in the brain-cooling vascular mechanism. "
Quite a big difference to the old beliefs about rosacea being an offshoot of acne, or a sign of alcoholism.
One hypothesis holds that rosacea is always preceded by degenerative changes of the perivascular, and possibly vascular, collagen and elastin tissues in inherently susceptible individuals exposed to climatic factors. These dermal changes are believed to lead to small vessel dilation resulting in flushing, telangiectasias and erythema.
Eventually, the dilated vessels become incompetent with perivascular leakage of potentially inflammatory substances into surrounding tissues., which is what we see here.
It appears that different mediators, including the neurotransmitter peptide substance P, histamine, serotonin and prostoglandins, have been proposed to be involved in the erythema responses seen in rosacea. And of course it is possible that other, yet unidentified mediators could also be involved. This is histamine.
And of course for many years now the presence of microorganisms has also been examined as a potential contributing factor to rosacea, but despite exhaustive research, the results remain inconclusive. It used to be believed that this guy, the mite Demodex Folliculorum that lives on everyone's skin, was a causal factor in rosacea. Now we know that it is commensal, rather than causal, that is, that it exists almost alongside the condition, although it may well be that Demodex Folliculaorum may play a part in the inflammatory nature of the condition.
Some reports suggest that patients with rosacea have en elevated prevalence of Heliobacter Pylori infection, although other reports have failed to confirm this association. We have been able to bring about imrovements in patients where we have been able to eradicate H.pylori, although these results too remain inconsistent.
It has been suggested that H.pylori synthesises the hormone gastrin, (which stimulates the secretion of gastric acid), which may in turn stimulate flushing.
Some reports suggest that patients with rosacea have en elevated prevalence of this bacterium, Helicobacter Pylori, although other reports have failed to confirm this association. We have been able to bring about imrovements in patients where we have been able to eradicate H.pylori, although these results too remain inconsistent.
It has been suggested that H.pylori synthesises the hormone gastrin, (which stimulates the secretion of gastric acid), which may in turn stimulate flushing.
It has also been suggested that H.pylori synthesises the hormone gastrin, and here is the molecular model for gastrin.Now gastrin stimulates the secretion of gastric acid, and it may be thought that this hormone may be directly or indirectly responsible for the phenomena of facial flushing. But we still don't know for sure.
Some dermatologists believe rosacea to be a seborrheic disease. The problem with this theory, however, is that while some patients show signs of excessive sebaceous activity, many others do not.
Most agree that there is no significant association between rosacea and seborrhea. Rosacea is not a primary disease of individual sebaceous follicles in the way that acne vulgaris is.
Indeed a very significant feature of rosacea is that comedones are completely absent and the initial signs of rosacea are not related to follicles, although in the later stages of the disease, papulopustules are follicular bound.
I mean, look at this lady's skin, she doesn't look oily at all, does she?
Regarding the role of heredity in this disease, we've found no acceptable evidence at this time that there is a genetic predisposition to rosacea, although more than one case in a family is often reported.
Clinical Findings
Rosacea is classified as a centrofacial disease. Its primarily localised on the nose, cheeks, chin, forehead and glabella. A condition known as extrafacial roseacea does exist, where can appear on the chest, neck, back, balded scalp or even the limbs. But this is rare and often overlooked.
The hallmarks of rosacea are livid red erythema and telangiectases, preceded by episodes of flushing, papules and pustules. And as we've mentioned previously, comedones are notably absent. If comedones are present, they are always con-comitant, such as solar comedones, acne vulgaris or acne cosmetica.
In severe cases, papules are numerous enough ot be confluent. Granulomatous changes can emerge in the later stages, sometimes receiving special designations such as lupoid rosacea.
And as previously mentioned, rhinophymas and other phymas can be the ultimate tissue reaction with the disease, particularly in men.
For didactic as well as for therapeutic reasons, we classify rosacea into stages, which may develop successively. In some patients, however, there is a clear-cut progression through these stages, but in others, this successions does not necessarily occur.
Rosacea patients characteristically react with erythema on the central areas of the face, less often the nexk and v-shaped area of the chest. These individuals are constitutionally predisposed to flushing and blushing
Blushing is a temporary phenomena, which always occurs in response to emotional stimuli such as embarrasement. Look at the difference in colour between this girl's hands and her face. Also check out her body language. She's clearly mortified about something, and it shows!
Flushing is different. It's more intense, and it lasts longer. Although it can be brought on by strong emotions, flushing is more usually a response to numerous non-specific stimuli such as ultraviolet radiation, heat, cold or chemical irritation. Or more commonly known, by alcoholic beverages, hot drinks and spices.
So let's take a closer look at the various stages of rosacea.
In Stage 1, the erythema persists for hours and days, and this conidtion used to be called erythema congestivum.Telangiectases become progressively more prominent, forming sprays on the nose, nasolabial folds, cheeks and glabella.
Most of these patients complain of sensitive skin that stings and burns after application of cosmetics, fragrances and almost all organic sunscreens. Which, out of interest, is one reason why zinc oxide is so good for rosacea patients.
Trauma from abrasives and peeling agents readily induces long-lasting erythema. So microdermabrasion is contraindicated for these patients, although mild peeling with low doses of ascorbic acid and/or TCA can improve the conidtion. Topical niacinamide has also been found helpful.
At Stage 2, dome-shaped inflammatory papules less than 0.5-1.0mm in size, with or without pustules, crop up and persist for weeks.
The lesions are always follicular in orgin vellus and sebaceous follicles are involved.
Although patients with concomitant acne may exhibit comedones, comedones should be considered part of the acne process. Always remember that they are unrelated to rosacea.
The deeper inflammatory lesions may heal with scarring, but rosacea scars tend to be small and shallow. Like acne, a sign of rosacea is that facial pores become more prominent.
If there has been solar exposure for decades, the stigmata of photodamaged skin become superimposed with those of rosacea, namely elastosis, solar comedones and heliodermatosis.
Toward the end of Stage 2, papulopustular attacks become increasingly frequent, with the condition finally extending over the enture face and also the scalp. Indeed itchy follicular pustules of the scalp are typical, with these containing either the normal bacterial flora or they may be sterile.
A small proportion of rosacea patients will go on to develop Stage 3, the worst expression of the disease. Stage 3 is characterised by lare inflammatory nodules, furunculoid infiltrations and tissue hyperplasia. These lesions appear particularly on the cheeks and nose, less often on the chin, forehead or ears. The facial contours of these patients become coarse, thickened and irregular.
Finally, the patient shows inflamed and thickened edamatous skin with large pores,the so-called peau d'orange or orange peel skin.
These features are caused by inflammatory infiltration, connective tissue hypertrophy with masses of collagen deposition, diffuse sebaceous gland hyperplasia, and overgrowth of individual sebaceous glands. The ultimate deformities are the phymas, such as rhinophyma.
Bella Beauty Magazine #16
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