Acne and post-inflammatory hyperpigmentation – Dr. I. Bodokh

Post-inflammatory hyperpigmentation can appear following any type of inflammatory lesion - acne lesions, eczema, insect bites, lichen, psoriasis, wounds, etc. It mainly affects people with brown or black skin (phototypes IV to VI) but can also affect others. The pathophysiology has yet to be fully explained.

In acne pigmentation can sometimes be seen very quickly after inflammatory lesions. These hyperpigmented maculae follow on from very inflammatory, peeling or irritated acne (following rubbing or accidental touching of the acne lesions). They also appear after exposure to the sun or to light. These pigmentations are unusual in that they spread around acne lesions. This mainly affects women with so-called hormonal acne predominantly in the areas of the perimandibular, the chin and the neck.

These hyperpigmented maculae around acne lesions are mainly seen in female patients with hyperandrogenism - marked facial hair, an androgenic hairline and irregular menstrual cycles.
This hyperpigmentation can also come after acne lesions in patients who have used an irritant anti-acne treatment, such as an over-use of topical retinoids applied on to wet skin and with rubbing of the lesions.

This would increase the inflammation and the irritation and would cause the treatment to the stopped.
This is why such acne must be treated using low, progressive doses of topicals and why the patients must be informed of the action of the retinoids on both the receptors and the inflammation and that they don’t need to use large amounts of this to make it work.

This inflammatory hyperpigmentation must be distinguished from non-inflammatory hyperpigmentation which is sometimes associated with so-called hormonal acne in female adults with hyperandrogenism, or with melasma.

Scarring, erythematous lesions can sometimes be seen, above all after treatment with isotretinoin, retinoids or adapalene.
These appear after several months of treatment and aren’t limited to the acne area. They subside once the treatment has been stopped, but the pigmented post-inflammation maculae appear in the first few weeks. In the majority of cases the patient has lesions of different evolutive ages and has a mix of inflammatory lesions, blackheads, scarring erythematous maculae, inflammatory and pigmented lesions and also scarring pigmented maculae.

If the treatment is well managed then the acne lesions will disappear and will be replaced with pigmented maculae and/or erythematous maculae. Erythematous maculae disappear quickly and spontaneously after 2-3 months, whilst hyperpigmented maculae can remain for up to 2 years.

Treating the inflammation first

In patients with pigmented acne the treatment should first of all target the inflammation. The treatment combines: systemic antibiotic therapy (cyclins), proper protection from the sun and a local therapy (a combination of antibiotics + vitamin A acid/benzoyl peroxyde + adapalene). This treatment should be applied in small amounts on clean, dry skin and just once every two days to begin with in order to avoid inflammation and irritation. The patient must refrain from rubbing or touching the acne lesions (and refrain from sleeping face-down in cases of acne with blackheads on the chin). We could also consider adding an azelaic acid-based topical with a depigmenting effect, this would again be applied in small quantities and just once every two days to begin with.

The use of high factor sun screen is essential.

If the inflammation continues to make the pigmentation worse after a month then we must not hesitate to prescribe a local corticosteroid therapy in the form of the Kligman depigmenting trio or the Kligman depigmenting duo without retinoid acid. The impact will be more linked to the action of the dermo-corticoid rather than that of the hydroquinone. This short-term corticosteroid therapy restricts the inflammation and thus restricts the pigmentation, but we must also bear in mind that this could create favourable conditions for the emergence of steroid acne.

In practice local treatment should be used firstly with antibiotics. Once the inflammation has disappeared the local treatment can be increased, whilst being careful to not irritate the skin. Post-inflammatory hyperpigmentation is indeed more frequent in cases of exposure to the sun but it can also happen even when there hasn’t been such exposure.

The pigmented scars are more visible on non-tanned skin so some patients may expose themselves to the sun in order to hide these marks. This is not advised as exposure to the sun may in fact worsen the pigmentation of the lesions, this is why the use of a high-factor sun screen is recommended.

The role of other treatments

Isotretinoin should be considered after failure with a correctly attempted treatment with systemic antibiotics and local therapies (antibiotics, benzoyl peroxyde, adapalene, azelaic acid, niacinamide) or if the improvement with these is slow. The treatment should be started at a low dose (0.2mg/kg up to a maximum of 30mg per day) and should be combined with a short systemic corticosteroid therapy in order to avoid inflammation early on in the treatment.

In the summer months zinc can be used in the treatment of inflammatory acne in young women.

Propionibacteria acnes is capable of producing porphyrins in anaerobic environments. The synthesis of porphyrins is even more significant than the spread of C. acnes, in particular in cases of hyperseborrhoea. When exposed to the light the porphyrins activate and contribute to the follicular inflammation and then with the formation of singlet oxygen the amount of C. acnes is reduced, leading to a secondary improvement of the acne.

Therefore, LED treatment could act on C. acnes but it would not have a direct impact on post-inflammatory acne pigmentation. LED treatment could have a positive impact but, on the other hand, it could cause keratinisation of the epidermis and, like with exposure to the sun, it could result in inflammation when the treatment is stopped.

Epilating lasers, in particular in cases of peri-pilofollicular pigmentations, can be effective when using low fluences and the pigmentation is progressively reduced in these areas.

Peelings, notably with kojic acid, can be useful in terms of treating residual pigmented scarring, although these can sometimes disappear spontaneously. However, peelings should only be used once the inflammatory lesions have disappeared.

Cosmetic products often and most importantly enable the treatments to be better tolerated, using these in association with depigmenting topical steroids in vitro (kojic acid, arbutin, glycyrrhizic acid, glabridin, etc) can be offered despite the fact that the proven clinical impact is debatable. This option can be used after failure with the Kligman depigmenting trio. The concentration of this should also be adjusted. And that is where the true science of our profession lies…

This article has been written by Dr. I. Bodokh, dermatologist at Centre hospitalier de Cannes (France)