No abstract

No abstract

Most patients respond to oral isotretinoin very well, when it is prescribed appropriately. However, there are some patients who remain refractory to treatment. This presentation will discuss the several reasons for this refractory state. Very uncommonly a mistaken diagnosis such as epidermoid cyst or steatocystoma multiplex may be responsible. Although most patients respond well to a dose of 0.5–1.0 mg/kg for 4–8 months, a small number of patients need either a higher dose or a longer duration of therapy. Very often there is no obvious explanation for this, except that in a small number of patients there may be drug inter‐reactions that somehow interfere with the absorption and metabolism of isotretinoin. Recently we had two patients who had previously responded to oral isotretinoin but who failed to show an improvement in their acne. The mechanism for this is not known. Certain types of acne, especially in those patients with many whiteheads, and in particular many macrocomedones, may also be refractory to treatment or flare badly whilst on roaccutane treatment. Such patients need gentle cautery of the large comedones. Other explanations include patients with significant endocrine disease such as polycystic ovarian syndrome or late onset congenital adrenal hyperplasia. The development of significant side‐effects, be this mucocutaneous, systemic or laboratory events are other explanations for a refractory state, simply because the patient is not able to take the appropriate dose of the drug. Some patients develop significant increased inflammation whilst on oral isotretinoin necessitating the use of oral, topical or intra‐lesional steroids.

For a long time, the mantra of acne pathogenesis debates has been that acne vulgaris lesions develop when (supposedly largely androgen-mediated) increased sebum production, ductal hypercornification, and propionibacteria come together with local inflammatory process in the unlucky affected individual. And yet, the exact sequence, precise interdependence, and choreography of pathogenic events in acne, especially the 'match that lights the fire' have remained surprisingly unclear, despite the venerable tradition of acne research over the past century.However, exciting recent progress in this -conceptually long somewhat stagnant, yet clinically, psychologically, and socioeconomically highly relevant -everyday battlefield of skin pathology encourages one to critically revisit conventional concepts of acne pathogenesis. Also, this provides a good opportunity for defining more sharply key open questions and intriguing acne characteritics whose underlying biological basis has far too long remained uninvestigated, and to emphasize promising new acne research avenues off-the-beaten-track -in the hope of promoting the corresponding development of innovative strategies for acne management.