Acne

Update on the pathophysiology of acne

Brigitte Dréno (France)

Acne is a chronic inflammatory disease of the pilosebaceous unit. Its pathophysiology includes hyperseborrhoea, abnormal follicular keratinization and dysbiosis of the microbiome, where 2 bacteria play a crucial role, namely Cutibacterium acnes and Staphylococcus epidermidis.
Recent research has shed some new light on the involvement of the sebaceous gland, as well as on the pro-inflammatory activity of the cutaneous microbiome.
During puberty, alteration of the sebaceous lipid profile, called dysseborrhoea, stress, irritation, cosmetics and potential dietary factors lead to inflammation and formation of different types of acne lesions. Dysbiosis, the process leading to a disturbed skin barrier and disequilibrium of the cutaneous microbiome, leads to a loss of diversity of C. acnes phylotypes. This loss of diversity then activates the innate immunity via the expression of protease activated receptors (PARs), tumour necrosis factor (TNF) α and toll-like receptors (TLRs), and the production of interferon (INF) γ, interleukins IL-8, IL-1, IL17A) and matrix metalloproteinases (MMPs) by keratinocytes and monocytes around the follicle, resulting in the inflammation and partial destruction of pilosebaceous unit.

The future of treatment is firstly based on probiotics, prebiotics, antimicrobial peptides and phages. Rebalancing the natural microbiome of the skin by restoring the natural skin barrier is also crucial. In severe acne, the field of biologics is still to be explored. Finally, regulating quantity and quality of sebum is also a challenge.
The aim of this talk will be to provide an update on the involvement of the sebaceous gland, the innate immunity and the cutaneous microbiome in acne and how all of these new data can help in the development of future treatments.

Low dose versus standard doses of isotretinoin in moderate-to-severe acne: Low doses

Jo-Ann See (Australia)

Despite our experience using oral isotretinoin for moderate to severe acne since the 1980s there is still uncertainty as to the “best” dosage regimes. This concerns not only the daily dose but also the duration of treatment and relevance of a cumulative dose.

Several health agencies such as the European Medicines Agency (EMA) have recommended standard doses of isotretinoin for fixed periods of time. The rationale may be to provide therapeutic guidance to a prescriber but also to limit the duration of exposure to women of child bearing age who may become pregnant.

Yet, many doctors and patients prefer lower dosage (0.1-0.5mg/kg/day) as this can still be effective and possibly more importantly, to limit side effects which are usually dose related and enhance adherence. Lower doses may also be used with concurrent physical therapy modalities such as light chemical peel, IPL and fractionated laser. The initiation of treatment with a lower dose may also minimise the risk of an acute acne flare up. Using lower dosages gives the prescriber flexibility to individualise dosage as side effects can be balanced with response to the medication.

Acneiform drug eruptions

Alberto Mota (Portugal)

As the name implies, acneiform eruption resembles acne vulgaris due to its predominant papulopustular nature and locations involved, but in contrast with the latter it lacks primary comedogenesis. Other differential clinical features are sudden onset at any age, a more monomorphic morphology and itching nature, inconsistent results with the conventional treatments for acne and the possibility to develop in hospitalized patients. Sometimes it resembles other common inflammatory eruptions like rosacea, in particular if Demodex is involved.

Eruptions like acne have been reported in association with infections, hormonal and metabolic disorders, genetic or congenital abnormalities, exposure to chemicals and in drug-induced scenarios. The use of facial mask during the recent covid19 pandemic resulted in the exacerbation of pre-existing facial acneiform eruptions.
One of the most common manifestations of drug-induced acneiform eruption is the steroid acne, with drugs like anticonvulsants, antidepressants, antituberculosis, antibiotics and chemotherapy compounds being the most common culprits. The withdrawal of the drug implied is not always possible and treatment attempts with conventional anti-acne drugs provide variable results.

Systemic drugs used in the treatment and sometimes prevention of acneiform eruptions are tetracyclines, systemic retinoids and dapsone. Topical modalities with dapsone, corticosteroids, benzoyl peroxide (with or without clindamycin), EGFR, vitamin K1 and ivermectin have also been reported.

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