CORRECT DIAGNOSIS:

Isotretinoin induced acne conglobata

DISCUSSION:

Acne conglobata is an uncommon form of acne exacerbation without systemic involvement.1 This condition affects men more frequently than women ranging from 18-30 years old. It is more commonly seen in individuals who are using anabolic-androgenic steroids for bodybuilding. Acne conglobata usually presents as progressive cystic acne with underling burrowing and interconnecting abscesses formations. Foul-smelling purulent drainage can also be found. As a result, irregular plaque-like, atrophic, keloidal scars developed producing pronounced disfigurement. Treatment options for acne conglobata include cessation of anabolic steroid use if it is the cause, systemic antibiotics or isotretinoin.

Isotretinoin has been used since the 1980s for the treatment of acne.2 Due to multiple side effect profiles and teratogenicity in reproductive female patients, isotretinoin is reserved for nodulocystic acne, that has failed multiple systemic therapies with scarring tendency. Despite the many listed potential cutaneous and systemic side effects and the need for close monitoring while on isotretinoin therapy, this medication remains widely used by dermatologists as “a miracle acne therapy.” It provides good control of nodulocystic acne and prevents further scarring from inflammatory acne. Interestingly it is the treatment of choice for acne conglobate and acne fulminans in combination with oral steroids. Of note, there are multiple case reports describing acne fulminans induced by isotretinoin use.4,5 However, isotretinoin induced acne conglobata has not been reported in the literature.

Our patient is an unfortunate case as a result of istoretinoin use. Instead of improvement, he developed acne conglobata which resulted in atrophic and keloidal scars. The etiology of acne fulminans or conglobate is unknown. The cause of istotretinoin induced may be due to an explosive immunologically mediated type III or type IV hypersensitivity reaction of Propionibacterium acnes antigens. Another cause may be due to a genetically determined change in neutrophil activity with hyperreactivity to chemoattractants, which may result in decreased phagocytosis of P. acnes. Isotretinoin induces fragility of the pilosebaceous duct epithelium allows massive contact of P. acnes antigens or P. acnes chemoattractants with the immune system to occur.6 The pathogenesis has also been speculated to be associated with systemic inflammatory cytokinemia, including tumor necrosis factor-α (TNF-α), as infliximab has shown beneficial results as a treatment.

The literature reports acne fulminans induced by isotretinoin with starting doses ranging from 0.5-1mg/kg/day or 40-80mg/day.6 Recent clinical trials for acne treatment have proposed increasing the starting dose of isotretinoin from the standard 0.5 mg/kg/day to as high as 1.5mg/kg/day with a cumulative dose increase from the standard 120-150 mg/kg to as high as 290 mg/kg.7,8 Our patient was treated with Isotretinoin 20-80mg and developed signs of exacerbation of his acne with keloidal scarring 3 months into treatment. Caution must be taken as our patient demonstrates that a rapid increase in the dose of isotretinoin may induce side effects such as acne conglobate or acne fulminans.

TREATMENT:

The treatment of acne fulminans or conglobata can be challenging with systemic steroids as the drug of choice for 3-5 months to avoid relapse.8 Our patient was started on systemic steroids prior to visiting our clinic. Multiple treatment options have been discussed with the patient and his parents during his initial visit to improve his acne and scarring. The patient was initially given clarithromycin with minimal improvement noted. The antibiotic was then switched to Bactrim which the patient has been tolerating well. He has reduced inflammation of acne lesions on the face and neck. The patient is also receiving monthly intralesional Kenalog injection to the keloidal scars and glycolic acid chemical peels. He is also receiving Fraxel which has demonstrated improvement. The patient has been on this regimen for a few months and has noticed a gradual improvement of both his acne and scars.

REFERENCES:

Strauss, J., & Thiboutot, D. (2006). Acne vulgaris and acneiform eruptions. In Fitzpatrick’s Dermatology in General Medicine (7th ed., pp. 690-703).

Patton, T., Zirwas, M., & Wolverton, S. (2007). Systemic retinoids. In Comprehensive Dermatologic Drug Therapy (2nd ed., pp. 275-300).

Roche Laboratories. (2010). Isotretinoin (Accutane) package insert. Nutley, NJ.

Pereira, M., Roncada, E., Oliveira, C., et al. (2011). [Title]. Anais Brasileiros de Dermatologia, 86(5), 983-985. https://doi.org/10.1590/S0365-05962011000500018

Joly, P., Prost, C., Gaudemar, M., et al. (1991). Acne fulminans triggered by isotretinoin therapy. Annales de Dermatologie et de Vénéréologie, 118(5), 369-372.

Cyrulnik, A. A., Viola, K. V., Gewirtzman, A. J., & Cohen, S. R. (2012). High-dose isotretinoin in acne vulgaris: Improved treatment outcomes and quality of life. International Journal of Dermatology, 51(9), 1123-1130. https://doi.org/10.1111/j.1365-4632.2012.05310.x

Blasiak, R. C. (2013). High-dose isotretinoin treatment and the rate of retrial relapse, and adverse effects in patients with acne vulgaris. JAMA Dermatology, 149(12), 1392-1398. https://doi.org/10.1001/jamadermatol.2013.5083

Zaba, R. (2011). Acne fulminans: Explosive systemic form of acne. Journal of the European Academy of Dermatology and Venereology, 25(5), 501-507. https://doi.org/10.1111/j.1468-3083.2010.03780.x