Acne Rosacea is usually preceded by degenerative changes of the perivascular, and possibly vascular, collagen and elastic tissues in inherently susceptible individuals exposed to climatic factors. These dermal changes are believed to lead to small vessel dilatation resulting in flushing, apparent vessels under the skin surface, and redness. Eventually, the dilated vessels become incompetent with perivascular leakage of potentially inflammatory substances.
Different mediators, including the neurotransmitter peptide substance P, histamine, serotonin, and prostaglandins, have been proposed to be involved in the erythematous response. It is also possible that none of these is responsible but that the reaction is triggered by another, still unknown mechanism.
The presence of microorganisms has also been examined as a potential contributing factor to Acne Rosacea, but results have been inconclusive. Demodex folliculorum mites are merely commensals and do not, in contrast to former belief, play a significant part in the development of Acne Rosacea, although an inflammatory reaction to the mites may be important in this condition. This is different from Demodex folliculorum folliculitis (demodicosis, demodicidosis). Some reports suggest that patients with Acne Rosacea have an increased prevalence of Helicobacter pylori infection, although other reports fail to confirm this association. Eradication of H. pylori has been occasionally associated with an improvement of Acne Rosacea symptoms. Study results are inconsistent, but it has been suggested that H. pylori synthesizes gastrin, which may stimulate flushing.
Acne Rosacea is considered by some authors as a seborrheic disease. Many patients with Acne Rosacea, however, do not show signs of excessive sebaceous activity although others do. One report says that there is no significant association between Acne Rosacea and seborrhea. It is not a primary disease of sebaceous follicles in contrast to acne vulgaris. Comedones are absent and the initial findings are not related to follicles, though papulopustules are follicular bound.
No acceptable evidence of genetic predisposition has been reported so far, although more than one case in a family is often encountered.
what is Rosacea
Rosacea is a common chronic inflammatory disorder of the hair follicles, sebaceous glands and vasculature of the face. The role of Demodex mite in the pathogenesis of Rosacea is controversial.
Rosacea sufferers have recurrent flushing, exacerbated by heat (shower, hot drinks), spicy foods, sunlight, cold, alcohol, and stress. They have sensitive skin, and may complain of dry and gritty eyes.
The peak incidence of Rosacea is 30—50 yr; Females being more affected than Males.
Rosacea sufferers may develop erythema, telangiectases, papules, and pustules of central face; there are no comedones in contrast to acne. Sebaceous hyperplasia, seborrheic dermatitis and facial lymphedema are also more common.
There are 4 Major Subtypes of Rosacea:
Erythematotelangiectatic, papulopustular, ocular, and phymatous.
Chronic inflammation may progress to rhinophyma (enlarged nose; in males). Ocular involvement is also common (e.g., gritty, conjunctival injection, styes, photophobia).
Investigations include clinical diagnosis; uncommonly, skin biopsy is indicated to rule out lupus or sarcoidosis.
Similar conditions that needs to be differentiated from Rosacea are: Acne, lupus erythematosus, perioral dermatitis, sarcoidosis, seborrheic dermatitis.
Treatment of Rosacea is based on severity and subtype.
Lifestyle modification:
Avoid triggers; sun protection and avoidance; facial massage for lymphedema.
Topical antibiotics:
Metronidazole 0.75% gel or 1% cream bid.
Sodium sulfacetamide lotion 10% bid.
Oral antibiotics (moderate to severe cases with inflammatory papulopustular component):
Tetracycline 500 mg po bid
Minocycline 100 mg po od—bid.
Doxycycline 20 mg po bid (subantimicrobial dose therapy) or 100 mg po qd–bid.
Isotretinoin (low dose); less commonly, topical retinoids may be used.
Laser therapy (e.g., PDL, IPL) for telangiectases and ablative laser (e.g., CO2) for rhinophyma.
Camouflage makeup (e.g., Dermablend, Covermark) for erythema.
Ophthalmologist to assess for ocular Rosacea (blepharitis, conjunctivitis, episcleritis).
