Facial dermatoses/rashes

This section includes acne vulgaris and rosacea. Lupus erythematosus and photodermatoses which also cause facial rashes are discussed on p. 1021 and 1036.

Acne vulgaris

This chronic condition is associated with the blockage of the pilosebaceous duct and appears on areas of the skin, such as the face, chest and back, where sebaceous glands are most numerous and active. Superficial blocking of the pilosebaceous orifice at the surface of the skin is manifest commonly as a comedo or ‘blackhead’; this may be associated with or followed by a variety of inflammatory changes.


The incidence of acne vulgaris appears to be the same for both sexes; lesions are evident at a younger age in girls and occur with their earlier sexual maturation. The disease is usually more extensive and serious in males. The majority of patients are clear of acne lesions by their early twenties but about 6% of patients will have disease continuing between the ages of 25 and 40 years.


There is no unifying concept with which to explain the pathogenesis of the most common patterns of this disease.

Alteration of the sebaceous glands

The principal age of onset is at puberty when, under the influence of androgenic hormones, sebaceous glands undergo hypertrophy and increase the production of sebum. A greasy skin and scalp usually accompany the polymorphic lesions, which are distributed on the face, chest and back. The secretion of sebum may, however, remain the same or even be increased in the twenties when the acne has cleared.


Propionibacterium acnes, an anaerobic diphtheroid, is present within the pilosebaceous duct, and has lipolytic enzymes capable of altering the local lipid constituents. The products of this organism’s enzyme activity, principally fatty acids, have been obtained from within the duct; however, they have little inflammatory property when  applied to the skin in the majority of acne subjects. P. acnes has been shown to alter the cell-mediated immune response and to stimulate the classical and alternative complement pathways. The local accumulation of complement found in and around the duct may thus be due to the presence of P. acnes. Proinflammatory mediators, also induced by the organism, are chemoattractants and are capable of producing some of the clinical features seen with active disease.

The sebaceous gland becomes decreased in size and in activity when isotretinoin (l3-cis-retinoic acid) is used in the treatment of acne, and the numbers of P. acnes diminish in parallel.
There is no convincing evidence, however, that the numbers of this organism are altered effectively by any of the oral antibiotics that are used in the treatment of the disease.


The superficial portion of the follicular duct undergoes keratinization and an early finding in acne is an increase in the amount of keratin material at this site. It is probable that one of the several effects of isotretinoin, which can so dramatically improve serious acne, is that it alters this abnormal production of keratin.


The effect of androgens on the disease is clearly seen in a number of young women in whom the disease continues beyond the teens. Up to 50% of such patients may show evidence of increased circulatory androgen levels, with raised total and free testosterone and/or lowered sex hormone- binding globulin. The alteration of these abnormal findings with treatment may lead to the clinical improvement
of seemingly intractable disease.


The ‘blackhead’ or comedo is the common first-stage lesion, the pigmentation being provided by melanin from the hair. In the absence of such lesions, the diagnosis of acne vulgaris is less likely. Closed comedones or ‘whiteheads’ are flesh-coloured lesions that are most commonly seen on the cheeks or chin, especially with incidentallight or when the skin is slightly stretched. Such lesions  represent very firmly obstructed follicles and are often the forerunners of more actively inflamed papules and pustules. Alteration of the water content of the keratin plugs may occur with hormonal changes during the menstrual cycle or with the application of moisturizing creams, e.g. in ‘cosmetic acne’, when whitehead lesions become predominant. The development of inflammatory papules and pustules will follow the release into the skin of the contents of a blocked follicle and the diffusion of chemoattractant materials across the wall. The pustules are sterile and
produce no growth of organisms on routine culture. More marked inflammatory changes may lead to large cysts, scarring and keloid formation. Increased local trauma may cause exacerbation of the disease; this may occur with head-gear, the pressure of strapping across the shoulders or trunk, or on special sites, e.g. beneath the chin in professional violin players (fiddler’s neck’).
When unusual sites are involved, such as the forearms and thighs, there is a folliculitis which can be produced by substances such as cutting oils in industry. Oils applied to the scalp may affect forehead skin (‘pomade acne’). Acne conglobata may be seen in association with hidradenitis suppurativa. It may lead to profound facial scar ring. It is familial. Severe acute-onset pustulo nodular disease (pyoderma faciale) in females may also lead to very severe scarring. Acne fulminans in young men may produce severe systemic upset.



Scientific studies show no relationship between food and acne. If, however, any individual experiences a worsening of their disease, after eating chocolate for example, this should be removed from their diet.
• Local applications
A VARIETY OF ABRASIVES, ASTRINGENTS OR EXFOLIATIVES are useful particularly in comedonal disease. Most of these agents contain benzoyl peroxide in concentrations of between 2.5 and 10%, presented as
lotions, creams or gels, alone or in combination with sulphur. Treatment should initially be with low concentrations (usually applied at night), with the concentration being increased with time and as tolerance develops. Erythema, dryness and scaling or peeling of the skin are often seen in the first weeks of treatment and diminish with time.
WASHING WITH POVIDONE-IODINE SURGICAL SCRUB, which contains a surfactant, may ‘freshen’ the skin and give short-term relief from greasiness.
SUNSHINE OR UV LIGHT from artificial sources also helps the comedonal stage of the disease. TOPICAL ANTIBIOTICS available for use are clindamycin phosphate, tetracycline hydrochloride and erythromycin 2% in alcoholic solution.
TOPICAL RETINOIC ACID (tretinoin) in concentrations of 0.01–0.025% in a lotion or a gel or 0.025–0.05% as a cream is helpful for the comedonal stage.

Systemic therapy

ANTIBIOTICS. Pustular and inflammatory disease will respond to oral antibiotics such as tetracycline, oxytetracycline, erythromycin and co-trimoxazole. Treatment with tetracycline 250 mg two or three times daily is often not effective until the drug has been taken for 2 weeks and courses should extend over months. Iron and calcium will markedly diminish the absorption of oxytetracycline or tetracycline, which should therefore be given at least 30 min before food. The absorption of minocycline (100 mg daily) is less affected by food but the drug is more expensive. Drug resistance of P. acnes seen with tetracycline is unusual with minocycline. HORMONES. The alteration of abnormal hormone levels in women may often improve acne. The use of a suitableoral contraceptive pill in which the progestogen component does not produce androgenic effects in the skin may help over the course of 6-8 months or more Cyproterone acetate, an antiandrogen, has been combinedat a low dosage (2 mg) with ethinyloestradiol  (35 J.Lg)to produce an oral contraceptive; this needs to be prescribed for periods of up to 1 year in order to gain full benefit for the skin.

Severe cystic acne that is unresponsive to the treatments outlined above is the current indication for theuse of isotretinoin. Four months of therapy in doses of 1.0 mg kg” per day by mouth will produce a remission
of the disease in more than 90% of patients for periods of up to 8 years. The side-effects are as for acitretin.


This chronic inflammatory facial eruption consists of erythema, often accompanied by papules, sterile pustules and telangiectasia.


Those most commonly affected are fair-skinned, middleaged females who often give a history of a ready flushing tendency which is triggered by a warm atmosphere, emotional upset, hot drinks, spicy food or alcohol. Males often have more severe disease but black Africans are rarely affected with rosacea.


There is no cohesive view that can explain the combination of clinical findings and pathological changes. Histological sections frequently show changes that are interpreted as folliculitis, but a more constant feature is
hyperplasia of the connective tissue around dilated blood vessels of the superficial dermis. This suggests that actinic (i.e. sunlight-induced) damage to the skin is an important component of the disease. The possibility that affected persons might be unduly sensitive to the effect of vasoactive mediators, such as sympathomimetic amines, histamine and acetylcholine, has not been substantiated, though endogenous opiates may playa role.


Patients demonstrating the most florid aspects of the disease will have an intense erythema of the skin overlying the flush areas of the face, i.e. the cheeks, nose and chin. The presence of papules and pustules distinguishes rosacea from the facial eruptions of SLE. The lesions are intermittent initially, but with chronic disease the erythema is persistent and marked telangiectasia appears. Other less-common features include lymphoedema of the cheeks or lower eyelids and rhinophyma. In the latter condition there is irregular thickening of the skin of the nose and the follicular orifices are enlarged. The skin ofthe nose is bright or purplish red. In severe cases there is  marked thickening of the skin on the surrounding cheeks. Rhinophyma can occasionally be the only manifestation of rosacea.
Approximately one-half of the patients with rosacea have a variety of ocular lesions. Blepharitis and conjunctivitis are the most common findings, but episcleritis, iritis and keratitis also occur, the latter being a potentially serious complication.



TETRACYCLINE in doses of 250 mg two or three times daily for periods of at least 12 weeks will improve the inflammatory aspect of the eruption in most patients.
METRONIDAZOLE may be of help when tetracycline is not effective, but care must be taken with the use of this drug over prolonged periods. Two months’ treatment at doses of 200 mg three times daily is often adequate.
HYDROCORTISONE combined with 0.5-1% sulphur as a cream may bring some relief of facial discomfort. ISOTRETINOIN (l3-cis-retinoic acid) at doses of 0.5- 1 mg kg:” for a period of 4 months has been shown to help resistant disease.
Rhinophyma is improved by shaving hypertrophic tissues from the nose, although regrowth of tissue frequently occurs.

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