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   Disability cause...
   Acne management
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Year : 1990  |  Volume : 56  |  Issue : 5  |  Page : 349-353

The pathogenesis, dlsability and management of acne

Correspondence Address:
Y Andrew Finlay

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How to cite this article:
Finlay Y A. The pathogenesis, dlsability and management of acne. Indian J Dermatol Venereol Leprol 1990;56:349-53

How to cite this URL:
Finlay Y A. The pathogenesis, dlsability and management of acne. Indian J Dermatol Venereol Leprol [serial online] 1990 [cited 2020 Sep 24];56:349-53. Available from:

The last ten years have seen several exciting advances in our understanding of acne and our ability to treat this condition effectively. The cause of acne is now much better understood, though several controversies persist, and we now have much greater insight into the major impact that acne has on our patient's lives. The introduction of more effective regimens of oral antibiotic therapy and the advent of oral retinoids have transformed the control of this disease.

  Pathogenesis Top

Scientific meetings are always enlivened by controversy, and at the recent international meeting on "Acne and Related Disorders"[1]. there was a classic argument about the role of comedones in the cause of acne. On the one hand Dolitsky and Shalita[2] outlined the widely held view that a change in follicular epithelial differentiation resulted in microcomedo formation. These micro comedones result in the formation of non-inflammatory lesions, which become colonized by bacteria, resulting in inflammatory lesions. Shuster[3] in contrast, argued that the prime cause of acne is the increase in sebum production; following this there is bacterial colonisation and inflammation resulting in histopathological and clinical lesions. According to Shuster there is no good evidence that follicular ducts are indeed 'blocked', and the 'blocked duct' is a myth. It should be noted, however, that both parties agree on the importance of bacterial colonisation in the production of acne lesions.

An increase in circulating androgens at puberty leads to sebaceous glands increasing in size and producing more sebum. Both circulating testosterone and dehydroepiandrosterone are implicated in males and females; the levels of these circulating androgens are usually not abnormally raised in people with acne, but rather it seems likely that there is an end organ hyper response to normal circulating androgens. In affected individuals the clinical severity of acne is proportional to the level of sebum production, not to the level of circulating androgens.

There is therefore little evidence to suggest that acne is fundamentally related to any "hormonal imbalance", even though there may be additional hormonal influences in acne; we know for example that,60% of females experience some worsening of their acne in the week before menstruation. Pregnancy has an unpredictable variable effect on acne, but in a few women the high oestrogen (and hence higher side-effect risk) contraceptive pill may be beneficial.

Comedones are the result of an abnormal accumulation of cornified cells within the hair follicle. Using the rabbit ear model, several components of sebum have been shown to be comedogenic, including some free fatty acids and squalene. A recent interesting theory[4] concerning the accumulation of cornified cells in the follicles centres around the possibility that a localised deficiency of linoleic acid may promote the accumulation of these cells, possibly by increasing corneocyte adhesiveness. Linoleic acid is an essential fatty acid which may move from plasma into sebaceous gland cells and thence into sebum. The large volume of sebum produced in patients with acne may result in a dilution effect and localised ductal deficiency of linoleic acid.

In patients with acne, the skin is colonised with propriono-bacterium acnes and with staphylococcus epidermidis. These are very important in the pathogenesis of inflammation in acne, though not in comedogenesis. Both p. acnes and possibly ductal keratinocytes release chemotactic mediators, and perivascular lymphocytes and polymorphonuclear leucocytes are attracted to the area around the sebaceous gland and hair follicle. Pustules, papules and nodules form: when a follicular duct ruptures, keratin from cornified cells and lipids from the duct penetrate into the dermis, resulting in a further irritant inflammatory reaction. The acne inflammation in a typical lesion lasts up to 14 days, and results in dermal damage and scarring.

There are a number of other factors concerning pathogenesis which are worth mentioning. It is not clear, for instance, why in the vast majority of people acne resolves with age. There is neither a reduction in the number of p. acnes organisms in the skin, nor a reduction of sebum production. Although dietary manipulation is attempted by many patients to try to control their acne, there is no good evidence that there is any true association between diet and acne. On the contrary, in a controlled trial published some years ago[5], there was no difference in disease activity between patients who did and who did not take chocolate.

  Disability caused by acne Top

In daily clinical work, dermatologists see at first hand the major psychological and social effects of skin disease, both on patients and their families. These effects have often been underestimated; methods have recently been developed[6] to measure "acne disability". Measurement of this disability is important for several reasons. It, may improve our effectiveness as clinicians, by stimulating us to match our therapeutic aggressiveness to the extent of the disease impact on the patient and it may provide a way to gain resources for dermatology in competition with specialities dealing with life threatening disease. Finally, measurement of disability provides a research method to allow alternative and relevant methods of assessing new therapies.

In a study of 100 patients with acne[6], we recorded acne disability in a structured manner and created an "Acne Disability Index". This study demonstrated that nearly one half of a group of acne patients, who had been referred to hospital, deliberately avoided social functions or altered the planning of future events, and a third found that their sporting activities were interfered with because of their acne, often because they wished to avoid using public changing rooms. Over a third of the patients said their acne had interfered with their sexual relationships. 26% of the patients said they would have made a different career choice if they had been free of acne; a very important point that parallels a report from Leeds[7] which indicated that the rate of unemployment amongst young adults with severe acne is significantly higher in both males and females than in control groups without acne.

In our study[6] an attempt was made to assess the overall degree of disability and distress caused to each patient by asking hypothetical financial questions. One of these, for example, asked how much each patient would be prepared to pay for a complete cure for their acne, if such a thing existed. A wide range of possible financial options were given; the few patients who responded in the lowest cost range (L25 or less, 22%) were presumably not concerned by their skin condition, whereas those who indicated the upper financial range (L500 or more, 33%), were expressing their deep distress.

Recently, at the 1990 British Association of Dermatologists Annual Meeting, we reported' on the practical use of a much simplified disability index in the routine management of acne. A very short (5 question) questionnaire is completed unaided by the patient in less than a minute; the sum of the scores of the answers provides an overall guide to the patient's current disability. This was used in 6E patients during therapy for their acne. In 22 (33%) of patients treated with oral antibiotics the disability index at the start of the treatment was 5.2, and at follow up (mean of 8 weeks; had been reduced to 1.8. In 16 (24%) o' patients treated with oral retinoids the disability index fell from 8.2 to 3.7 at follow up. This perhaps indicates that although oral retinoids are extremely effective therapeutically, the psychological and social effects of very severe acne do not recover as rapidly as the improvement in the disease activity.

The advantages of using this simple abbreviated questionnaire are that it adds patient orientated dimension to the consultation and that it may identify patients with high disability, who need very active therapy.

  Acne management Top

Successful management of a patient with acne usually involves either topical, systemic or physical treatment modalities, but always involves correct handling of the patient. It is worth stressing the importance of the "handling" of the patient, because the success of most forms of therapy depends on patient compliance. This essential patient co-operation will usually only occur if the patient understands in simple terms both the cause of their condition and a realistic concept of how long treatment must be continued to maximise the likelihood of success.

  Topical therapy Top

The most effective current topical therapies used are benzoyl peroxide, topical antibiotics and topical retinoic acid. Sulphur preparations should however first be mentioned; they have been used in acne for over 100 years. There is some controversy over the relevance to humans of the comedogenic effect of topical sulphur demonstrated in animal models. Although these preparations generally have a poor cosmetic appearance, and are of doubtful efficacy, they are at least inexpensive.

Benzoyl peroxide is used in a variety of strengths from 2.5 to 10%. Although it effect on sebum production, its use does reduce total comedone number, and it may have a direct anti-inflammatory action. The most pronounced action of benzoyl peroxide is its effect in reducing skin surface bacteria.

The topical antibiotics currently used in the United Kingdom (UK) include tetracycline, erythromycin and clindamycin. These all reduce surface and ductal p. acnes, but erythromycin and tetracycline may also reduce surface free fatty acid levels. Topical retinoic acid is available as a . cream or gel; its use reduces comedogenesis and reduces the number of non-inflamed lesions - its prime indication is therefore acne with multiple comedones.

It has recently been suggested[9] that topical azaleic acid may be of value in acne. Azaleic acid is a dicarboxylic acid derived from Pityrosporum ovale. It may have a direct antibacterial activity, or an effect on follicle keratinization. Initial clinical trials[10] suggest it may have an equivalent clinical effectiveness to other topical remedies discussed above.

  Oral therapy Top

Oral therapy for acne consists of either long term oral antibiotics, `hormonal' approaches, or the dramatically effective oral isotretinoin. Oral antibiotics used frequently in the UK in acne include tetracycline and oxytetracycline, minocycline and erythromycin; their mode of action is primarily antibacterial, affecting p. acnes, but they also have a separate anti-inflammatory action.

Tetracycline and oxytetracycline are very widely used and are an effective therapy for mild to moderate acne. They do however have to be taken ideally for a minimum of 3-6 months, and at a dosage of 1 gram daily, to gain the maximum effect. One disadvantage is that the absorption of these drugs may be reduced by food or milk therefore for maximum absorption the drugs should be taken at least an hour before meals. Erythromycin is as effective as tetracycline and has the advantage of not being contraindicated in pregnancy.

Minocycline is said to have some advantages over oxytetracycline, though it is significantly more expensive. In vivo, minocycline has greater antibacterial activity than tetracycline against p. acnes and staphlococci, and results in less staphlococcal resistance than tetracycline[11]. It has also been suggested that there is more rapid resolution of some acne lesions with minocycline therapy[12]. The major clinical advantage of the drug is that it is very well absorbed and so can therefore be taken with food; it is therefore of especial value where absorption or compliance is a problem.

The use of a high oestrogen oral contraceptive pill to help treat resistant acne in females has now fallen from fashion with the advent of much more effective therapy. However, the antiandrogen cyproterone acetate (2mg) may be used ,in conjunction with ethinyloestradiol (30 µg) as a treatment for acne in females in whom treatment with oral antibiotics has failed. The ethinyloestradiol is given for its contraceptive action during the therapy, which should be taken for 6 - 12 months to gain maximum benefit.

The major single recent advance in the therapy of severe acne has been the introduction of oral isotretinoin (13-cis-retinoic­acid). This drug primarily works by suppressing sebum excretion; it is a very effective therapy and the treatment of choice for severe nodulocystic acne. Unfortunately it is expensive and has a variety of potential side effects, the most notable being that it teratogenic.

Amongst other therapies used for acne are ultraviolet B radiation and intralesional triamcinolone. UVB is of relatively little value and so has largely been dropped as a regular form of therapy, but intralesional triamcinolone is very effective in the therapy of isolated large acne cysts. Simple cosmetic procedures such as comedone extraction may be helpful in some patients.

In this brief review of acne pathogenesis, disability and treatment, the following key points have been stressed:

1. Although some aspects of the cause of acne are not fully understood, the association with increased sebum excretion and the important role of p. acnes are clear.

2. Social disability resulting from acne may be profound, and can now be simply measured in the clinic.

3. The mainstay of treatment of moderate acne is the use of long term oral antibiotics, given in high dosage. Severe nodulo-cystic acne responds well to oral isotretinoin.

  Acknowledgements Top

This article is based on a series of lectures given by author in July 1990 in Bombay, Calcutta and New Delhi, organised by Lederle, the pharmaceutical division of Cyanamid India Limited.

  References Top

1.Acne and Related Disorders (1989). Editors R Marks and G Plewig. Martin Dunitz, London..  Back to cited text no. 1    
2.Dolitsky C, Shalita AR. Pathogenesis of inflammatory acne. Chapter 15 in : Acne and Related Disorders (1989). Editors R Marks and G Plewig. Martin Dunitz, London.  Back to cited text no. 2    
3.Shuster S. The blocked duct and the dying mythology of acne. Chapter 16 in : Acne and Related Disorders (1989). Editors R Marks and G Plewig. Martin Dunitz, London.  Back to cited text no. 3    
4.Downing DT, Stewart ME, Wertz PW, et al. Essential fatty acids and acne. Amer Acad Dermatol, 1986; 14: 221-225.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Fulton JE, Plewig G, Kligman AM. Effect of chocolate on acne vulgaris. J Amer Med Asso, 1969; 210: 2071-1074.  Back to cited text no. 5    
6.Motley RJ, Finlay AY. How much disability is caused by acne? Clin and Exper Dermatol, 1989; 14: 194-198.  Back to cited text no. 6    
7.Cunliffe WJ. Acne and unemployment. Brit J Dermatol, 1986; 115: 386.  Back to cited text no. 7    
8.Motley RJ, Finlay AY. Practical use of a disability index in the routine management of acne. Brit J Dermatol, 1990; 123 (Suppl. 37): 21-22.  Back to cited text no. 8    
9.Strauss JS. The pathogenesis of acne: how might azelaic acid act? J Dermatological Treatment, 1989; 1 (Suppl. 1): 3-6.  Back to cited text no. 9    
10.Gollnick H, Graupe K. Azelaic acid for the treatment of acne: comparative trials. J Dermatological Treatment, 1989; 1 (Suppl. 1): 27-30.  Back to cited text no. 10    
11.Eady EA, Cove JH, Holland KT, Cunliffe WJ. Superior antibacterial action and reduced incidence of bacterial resistance in minocycline compared to tetracycline-treated acne patients. Brit J Dermatol, 1990; 122: 233-244.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Hubbell CG, Hobbs ER, Fist MT, White JW. Efficacy of minocycline compared with tetracycline in treatment of acne vulgaris. Arch Dermato, 1982; 118: 989-992.  Back to cited text no. 12    

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