About 1 percent to 2 percent of people in the United States have hidradenitis suppurativa, and it most commonly affects women who are African American or biracial.Hidradenitis suppurativa, also known as HS, is a chronic skin condition that causes painful bumps or boils to form under the skin that can sometimes rupture. It commonly affects the underarm and groin areas. About 1 percent to 2 percent of people in the United States have HS, according to the HS Foundation, and it most commonly affects women who are African American or biracial.
While experts are still not completely sure what causes HS, it typically starts around puberty, suggesting that hormones may play a role. Experts believe genetics likely play a role in HS, because it can be seen in family members of those affected. Research also suggests that HS is caused by an over-active immune response.
What are the symptoms of HS?
HS typically begins in an area with thick, coarse hair within the armpits or groin. Those who have HS may notice breakouts that look like pimples or boils. These breakouts may clear after a while, but they may continue to develop later again in the same area.
“If these bumps keep coming back, especially in the same location, it may be HS,” said Tiffany Mayo, M.D., associate professor in the UAB Department of Dermatology. “If you suspect you have HS, I recommend seeking help from a medical professional. Tell them what you are experiencing and ask them if this could be HS.”
One of the first signs of HS is that tender, deep nodules that look like pimples, cysts or boils may appear. Before the nodule appears, individuals who have HS may notice some discomfort in that area. As HS progresses, the nodules may grow and join together forming tunnels underneath the skin. When this happens, the nodules can fill with pus and become painful, leading to what is known as an abscess. The abscesses can break open leading to blood and pus spilling out. This repetitive cycle of inflammation and healing can lead to tunnels and scarring. Some people see small black bumps in areas of HS flares that look like blackheads.
“HS sometimes can look similar to an infection, so people may assume it is contagious or due to poor hygiene; however, that is not the case,” Mayo said. “HS is an inflammatory medical condition. It is not an infection. It is not contagious. And it is not an indication of poor personal hygiene.”
How is HS diagnosed?
While HS can look like other skin conditions, UAB dermatologists are trained to spot the differences between HS and other conditions. While assessing a patient, a dermatologist may ask the patient if they have noticed any symptoms of HS. They will examine some of the bumps or nodules that have developed and talk to the patient to gather some additional information that can help them provide a diagnosis.
How is HS treated?
While HS cannot be cured, dermatologists can develop a treatment plan to lessen some of the symptoms of this condition, including reducing flare-ups, healing wounds, relieving pain and preventing HS from worsening.
“Dermatologists are knowledgeable about HS and can help you determine the best treatment option for you,” Mayo said.
Treatment plans may include skin care plans, including the use of certain products that can reduce inflammation from HS, or medications, including antibiotics, retinoids, hormonal medication or biologics that can help stop pus and inflammation. Dermatologists may turn to in-office procedures including corticosteroid injection, laser hair removal, laser surgery, removing HS lesions or deroofing, which includes removing the skin that covers the top of an abscess, so it can heal sealing off the tunnel or nodule. Dermatologists may prioritize wound care or pain control. If HS has caused the patient to develop depression or anxiety, dermatologists may also recommend counseling or support groups to help the patient feel supported as they navigate this condition. Clinical trials continue to offer new improved therapies for HS.
To make an appointment, schedule a consultation or refer a patient to UAB Dermatology, please call 205-996-7546.
UAB researchers develop a model for targeted intervention
There is evidence that suggests HS is a complex inflammatory skin disease involving the interplay of epithelial-immune crosstalk. Last year, researchers at UAB identified a model for targeted intervention for HS. The study, published in the Proceedings of the National Academy of Sciences, suggests that combining biological therapies with certain medications can block the chromatin landscape of the inflammatory gene that plays a role in HS.
For this study, UAB researchers analyzed HS epithelial cells and demonstrated that basal cells located at the bottom of the epidermis — the outermost layer of the skin — can control their lineage and increase the number of keratinocytes, the cells primarily focused on protecting and repairing the skin.
In this study, Mohammad Athar, Ph.D., professor and vice chair of Research in the UAB Department of Dermatology, states that HS initiation and progression are likely caused by a dysregulated immune response, altered keratinocyte function and changes in the microbiome of the skin. However, to further explore the underlying cause of this condition, Athar and his team, including Lin Jin, Ph.D., and Chander Raman, Ph.D., research faculty members at the UAB Department of Dermatology, investigated the HS skin cells and found that basal progenitor cells that serve as repair cells for the skin dysregulate their lineage restriction and increase pathogenic keratinocyte clones, leading to an augmented growth of skin cells and HS inflammation.
The research team outlined the reprogrammed transcriptional profiles in HS basal stem/progenitor cells and identified two keratinocyte populations that amplify immune responses in people with HS. These populations are marked by genes, S100A7/8/9 and KRT6 triggering IL1 and IL10 and drive the immune and inflammatory responses to an infection. These signals, along with HS-specific cytokines and chemokines, recruit specific populations of immune cells and promote the progression of the disease.
In the study, the researchers presented a database uncovering distinct chromatin accessibility patterns in healthy skin and skin with HS. Chromatin accessibility refers to how easily other molecules in the body can interact with one’s DNA. Researchers found numerous activated enhancers, which significantly and specifically turn on the expression of inflammatory genes in HS. This study allowed researchers to identify a pattern for the targeted intervention in HS by combining biological therapies with novel pharmacological agents to block the chromatin landscape of genes that lead to inflammation in individuals with HS.
“HS is a debilitating skin disease, which impacts quality of life among the young patient populations, particularly Black women,” Athar said. “Understanding cause of racial diversity and gender bias is the focus of investigation in our laboratory. Dr. Lin Jin is developing novel epigenetic approaches to ultimately discover personalized treatment for this disease. The diagnosis of disease in individual patients will be based on the identification of unique cell populations with unique gene signatures as the major driver of HS. Our approach is highly innovative and may be successful in the near future to find a highly effective treatment for these patients.”