What is Pathophysiology?
The cause of HS is not fully understood and is likely multifactorial with several factors contributing to the development of the characteristic pain, purulent drainage, sinus tract, and scar formation. Even though our current understanding is incomplete, it is important to understand that you did not cause your HS, the symptoms are not due to poor hygiene, and HS is not contagious. Below we discuss several of the currently accepted views.
HS was originally thought to be caused by a defect of the sweat gland, but this view has changed and it is now widely accepted to be a problem with the hair follicle. Build-up of keratin (a type of protein) within the hair follicle eventually plugs the hair follicle, causing further build up, and eventually the hair follicle ruptures and releases this material into the surrounding skin resulting in an intense inflammatory response.1
Sometimes bacteria can be isolated from HS lesions, while other times cultures from HS lesions are sterile (no bacteria found).2 Those affected by HS frequently experience the characteristic symptoms of an infection, such as pain, tenderness, warmth, and purulent drainage. It may be reasonable to assume that since symptoms tend to improve after antibiotics, that HS is caused primarily by bacteria, however this is not the case.
Recently, HS has been described as a biofilm disease. When numerous bacteria secrete a sticky material known as a polysaccharide matrix and bind to a surface they now exist in what is known as a biofilm. When bacteria exist in a biofilm they become highly resistant to antibiotics. A recent study looking at biopsy samples (pieces of skin) from patients with HS, demonstrated that biofilms were associated with chronic HS.3 Although, biofilms likely don’t form primarily, this may be the reason that HS become very resistant to medical management as it becomes more severe.
Several markers of inflammation exist in the blood and skin and can be used to assess the inflammatory state of the body. Abnormal levels of these markers have been implicated in the development of several diseases and similarly found to be abnormal in HS. Additional research is needed to determine the implications of these abnormal levels, but these findings have led to the use of biologic medications, such as adalimumab and infliximab for the treatment of hidradenitis suppurativa.
Nutrition is an understudied and notoriously difficult topic to research in medicine. The majority of evidence is based on individual experience with few published articles in the literature, but the impact of diet on HS infiltrates through social media and online message boards with reports of improvement that ranges from minimal or no effect to complete resolution. In one survey study involving 47 patients who followed dairy free diets, no patients experienced disease progression and 83% improved to various degrees.4 In another study, 12 subjects underwent surgical excision followed by diet modification with no wheat or brewers yeast consumption with immediate disease stabilization during a 12 month period of follow up.5
Additional research is needed in order to allow for comprehensive diet counseling. Some patients have reported improvement after exclusion of nightshades, simple carbohydrates, and dairy, but the impact of diet modification appears to be highly individual and should be discussed with your physician or nutritionist. Dieticians can provide individualized meal plans to make sure that you are getting all of the required nutrients.
Several other factors have been implicated in the development of HS. Smoking is more common among people with HS than among the general population, and the components of smoke are known to promote hyperkeratosis (causing follicular occlusion) and also increases inflammation potentially worsening HS.6 Mechanical factors caused by skin to skin contact and obesity may also contribute to the overall inflammatory state of HS and the development or progression of HS.
Lastly, hormones are potentially implicated in HS. It is known that more women are affected by HS than men and therefore a hormonal component has been hypothesized. Androgens, a type of hormone, can increase proliferation of the keratinocytes (skin cells), however the hormonal profile of patients with HS is usually found to be normal.6
With numerous factors implicated in the development of HS, it is clear that additional research is needed and the trigger for one patient may not be consistent across the entire population.
- Jemec GB, Hansen U. Histology of hidradenitis suppurativa. J Am Acad Dermatol. 1996;34(6):994-999.
- Ring HC, Riis Mikkelsen P, Miller IM, et al. The bacteriology of hidradenitis suppurativa: a systematic review. Exp Dermatol. 2015;24(10):727-731.
- Ring HC, Bay L, Nilsson M, et al. Bacterial Biofilm in Chronic Lesions of Hidradenitis Suppurativa. Br J Dermatol. 2016.
- Danby FW. Diet in the prevention of hidradenitis suppurativa (acne inversa). J Am Acad Dermatol. 2015;73(5 Suppl 1):S52-54.
- Cannistra C, Finocchi V, Trivisonno A, Tambasco D. New perspectives in the treatment of hidradenitis suppurativa: surgery and brewer’s yeast-exclusion diet. Surgery. 2013;154(5):1126-1130.
- Prens E, Deckers I. Pathophysiology of hidradenitis suppurativa: An update. J Am Acad Dermatol. 2015;73(5 Suppl 1):S8-11.