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Editorial
December 2014

Hidradenitis Suppurativa: Current Progress and Future Questions

Author Affiliations
  • 1Department of Dermatology, Massachusetts General Hospital, Boston
  • 2Johns Hopkins University School of Medicine, Baltimore, Maryland
  • 3Department of Dermatology, Harvard Medical School, Boston, Massachusetts
JAMA Dermatol. 2014;150(12):1263-1264. doi:10.1001/jamadermatol.2014.1871

Hidradenitis suppurativa (HS) is a chronic, destructive, debilitating inflammatory skin disease characterized by recurrent, painful, deep-seated nodules and/or abscesses in intertriginous areas.1 It is also relatively common, with a reported prevalence as high as 1% to 4%.2,3 Nevertheless, HS has historically been an orphan disease, unclaimed by any specialty, owing, perhaps largely, to the treatment challenges it poses for physicians and the resulting nonadherence on the part of patients.

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    The Role of Obesity in Hidradenitis Suppurativa
    Iben Marie Miller, Gregor B. Jemec | Roskilde Hospital, Department of Dermatology


    LETTER IN REPLY/COMMENT Iben M. Miller1 & Gregor B.E. Jemec11Department of Dermatology, Roskilde Hospital, Køgevej 7-13, 4000 Roskilde, Denmark Corresponding author: Iben M. Miller, Department of Dermatology, Roskilde Hospital, Køgevej 7-13, 4000 Roskilde, Denmark, miller@dadlnet.dk Word count: 400

    In the recent editorial “Hidradenitis Suppurativa: Current Progress and Future Questions” Pascoe and Kimball have kindly commented our paper on the association of the metabolic syndrome (MetS) and Hidradentis suppurativa (HS)1. They raise the relevant question of the role of the MetS-component obesity in HS: Is obesity a primary rather than a secondary event? Does obesity add to the inflammation of the skin disease? While we wait for the elucidation of the pathophysiological role of obesity in HS, we would like to remind the readers of some additional observations, which may further qualify the discussion: 1. HS patients may also have low BMI (2) indicating that obesity may be a secondary rather than a primary event. Alternatively, the low BMI patients may represent a specific HS subtype. 2. A positive correlation has been described between HS severity and BMI (1,3) suggesting a possible dose-response relationship, which may reflect causality. This observation still does not answer the questions of what is the primary and secondary event. Additionally, no correlation between HS severity and MetS has been found so far (1). 3. Lowering BMI appears to reduce HS symptoms; several cases describe the amelioration of HS following bariatric surgery (4). Furthermore, in a long-term follow-up study of HS patients, lower BMI was associated with a higher likelihood of remission (4). Additionally, lower BMI appears associated with a lower risk of recurrence following CO2 laser evaporation (5). These findings may reflect obesity as a triggering primary event of HS. Alternatively, the findings may indicate that increase of BMI beyond a certain threshold may trigger a genetically latent HS i.e. obesity is not the cause, but a trigger of HS and had a latent HS patient remained at a low BMI, the HS would not have been expressed clinically. 4. An association between HS and high waist circumference has been suggested (1) implying the fat distribution in HS patients to be abdominal i.e. visceral obesity. Visceral fat is known as “active fat” as it functions as and affects endocrine cells and subsequently the immune system (e.g. TNF-alpha). Thus, the distribution of fat may be important when investigating the role of obesity in HS. While waiting for the outcome of prospective studies and investigations into the underlying pathophysiology, the argument for suggesting and aiding weight loss in HS patients is steadily growing, not just for the sake of reducing the risk of co-morbidities but also to improve the disease itself. Iben M Miller, MD, PhD Gregor BE Jemec, Professor, DMScReferences1 Miller IM, Ellervik C, Vinding GR et al. Association of Metabolic Syndrome and Hidradenitis Suppurativa. JAMA dermatology 2014.2 Jemec G. Body Weight in Hidradenitis Suppurativa; Acne and related disorders. London: Martin Dunitz. 1989.3 Sartorius K, Emtestam L, Jemec GB et al. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. The British journal of dermatology 2009; 161: 831-9.4 Kromann CB, Deckers IE, Esmann S et al. Risk-factors, clinical course and long-term prognosis in hidradenitis suppurativa: a cross-sectional study. The British journal of dermatology 2014.5 Riis Mikkelsen P., Dufour ND., Zarchi K. et al. Recurrence rate and patient satisfaction of Co2-laser evaporation of lesions in patients with Hidradenitis Suppurativa, a retrospective study. Dermatologic Surgery 2014; In Press.

    CONFLICT OF INTEREST: Conflict of interest Disclosures: Dr Jemec has received consulting fees from Abbott laboratories, Astra Zeneca, MSD, Novartis, Pfizer, and Dumex-Alpharma; lecture fees from Abbott Laboratories, Galderma, Pfizer, and Roche; grant support from Abbott Laboratories, Pfizer, Photocure, and LEO Pharma; equipment on loan from Michelson Diagnostics; end reimbursement for travel expenses from Abbott Laboratories, Galderma, and Photocure. Dr. Millers PhD Comorbidities in Inflammatory Dermatological Diseases; was funded by a grants from the Danish Agency of Science, Technology, and Innovation and LEO Pharma.
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