INTRODUCTION
Hidradenitis suppurativa (HS) is a chronic inflammatory disease that causes painful, foul-smelling, and movement-restricting lesions in intertriginous regions. One of the primary therapies for HS and one of the two FDA-approved treatments for severe HS is adalimumab (Humira), a tumor necrosis factor (TNF-alpha) antagonist,1,2 TNF-alpha plays a role in the inflammatory cascade, which can lead to a cytokine storm, excessive or uncontrollable release of proinflammatory cytokines.3,4 Due to their high mortality rate, cytokine storms have garnered significant attention, as seen in events such as the avian influenza outbreak of 2005 and the COVID-19 pandemic.4
Both autoimmune disorders and pathogen-induced triggers can induce cytokine storms and HS can be considered an intersection of both.2,3,5 HS, while not caused by a specific infection, is propagated by the presence of bacteria in and on the skin, agitating the immune system. The linkage between HS and autoimmune diseases, such as systemic lupus erythematosus and inflammatory bowel disease, has been observed.5,6 Identification of cytokine storm patterns in HS will lead to a better understanding of the disease.
Both autoimmune disorders and pathogen-induced triggers can induce cytokine storms and HS can be considered an intersection of both.2,3,5 HS, while not caused by a specific infection, is propagated by the presence of bacteria in and on the skin, agitating the immune system. The linkage between HS and autoimmune diseases, such as systemic lupus erythematosus and inflammatory bowel disease, has been observed.5,6 Identification of cytokine storm patterns in HS will lead to a better understanding of the disease.
CASE
A 55-year-old male Caucasian man visited the clinic for HS treatment. The patient had Hurley stage 3, with the presence of dermal tunnels. The patient reported having no history of smoking, but was obese with a BMI of 39.5, noted as smoking and obesity are factors linked to HS severity.5 The patient was not taking any pain medication and his HS was stable at the time of serum collection.
Serum cytokine levels for the patient and 3 HS-free healthy controls were measured in quadruplicate using a QAH-NEU cytokine array (RayBiotech).
Serum cytokine levels for the patient and 3 HS-free healthy controls were measured in quadruplicate using a QAH-NEU cytokine array (RayBiotech).
DISCUSSION
Multiple cytokines were heavily upregulated in the serum of the HS patient (Table 1). Notable HS treatment target TNF-alpha was found to be upregulated in the patient compared to the healthy controls 7.47-fold. Also, among these were several proinflammatory cytokines. Interleukin 1beta (IL-1beta) was the most upregulated with over 400-fold expression and is associated with inflammasome activity. It can amplify the cascade and induce the activation of other cytokines such as IL-6, IL-8, and MCP-1, which were upregulated in the patient 25-fold, 21.6-fold, and 2.54-fold, respectively.4 Elevated IL-1beta and IL-6 are known to be correlated with more severe inflammation and worse disease outcomes.6 IL-6 is also associated with restricting the development of T-regs, immune cells responsible for suppressing immune response and maintaining self-tolerance.7 Both IL-6 and IL-8 play a major role in the attraction of neutrophils to inflammation sites.1
