Luis Garza, M.D., Ph.D., on what hidradenitis suppurativa is not

Hidradenitis suppurativa is not a classic infection, nor is it a classic autoimmune disease, according to Luis Garza, M.D., Ph.D., a professor of dermatology at Johns Hopkins University School of Medicine. Instead, he places it in the same family as psoriasis.

“It’s more like in the family [of] psoriasis, which is … what we call an auto-inflammatory disease more than an autoimmune disease,” Garza said in a recent interview with Managed Healthcare Executive (MHE).

Garza is an expert on hidradenitis suppurativa, a skin condition that is becoming more common. He says that at any given time he is taking care of 150 hidradenitis suppurativa patinets.

Unlike lupus or autoimmune thyroiditis, hidradenitis suppurativa does not appear to be driven by the T cells and B cells of the adaptive immune system, in Garza’s view. He said he believes the inflammation stems from an early part of the immune system that senses problems before adaptive immunity is turned on. In his view, many current therapies treat the downstream effects of hidradenitis suppurativa while missing what happens early in its pathogenesis.

As for causation, Garza describes a model that combines genetics and environment. Many patients report affected relatives, and mutations involving gamma-secretase are known to predispose people to hidradenitis suppurativa. “We have a model where we think there’s probably both a combination of … a genetic kind of predilection and then an exposure that brings people over the top,” Garza said. That formulation is why among the many people who eat processed foods, only a few develop the disease, he told MHE.

Smoking is a known risk factor, and hidradenitis suppurativa improves considerably when people stop smoking, according to Garza. Metabolic syndrome is also a risk factor. Garza said that elevated insulin levels related to metabolic disease may trigger the disease. He describes a “witch’s brew” in which environmental exposures incite the earliest inflammation and smoking and metabolic disease “add fuel to the fire.”

Bacteria are involved, too, which is why patients respond to antibiotics. Garza described people as normally existing in a “state of truce” with their microbiome, but that equilibrium breaks down in hidradenitis suppurativa. As the disease progresses and tunnels form under the skin, bacteria that do not normally grow in the skin begin to thrive there.

“Although they didn’t start the party, they’re staying for the party,” Garza said.

Those tunnels in the skin are a signature feature of hidradenitis suppurativa. Normally skin grows outward, Garza explains, which is part of how the body defends itself. In hidradenitis suppurativa. That growth turns inward, forming tunnels so that pressing on one end releases pus from another. Garza said he sees analogies to cancer biology worth studying, although hidradenitis suppurativa is not a cancer.

Garza also discussed the roles of apocrine glands and hair follicles with MHE. Apocrine glands are concentrated in the underarms and groin, which initially generated excitement about a link to hidradenitis suppurativa. Garza said that the nodules and other manifestations of the disease also appear in skin folds elsewhere, so apocrine glands are probably not solo players in the disease. Hair follicles may be related to tunnel formation, he said.