Evidence regarding golimumab, a monoclonal anti-TNF-alpha antibody, is scarce; only two case reports exist in the literature. The first described use of golimumab in a patient with severe HS and psoriatic arthritis who failed adalimumab and anakinra previously. With golimumab, her HS worsened despite improvement in her psoriatic arthritis. She was therefore considered to have failed golimumab. The second report detailed a 42-year-old female with UC, HS, and pyostomatitis vegetans treated with golimumab (200 mg followed by 100 mg every 4 weeks). This patient had remission of her dermatologic symptoms and UC within 2 months of starting therapy. Little can be inferred from these case reports regarding the effectiveness of golimumab in the treatment of HS.
Certolizumab-pegol is another biologic targeting TNF-alpha, and is the only anti-TNF-alpha agent that does not cross the placenta. The inability of certolizumab to cross the placenta may relate to the absence of an Fc region, a factor implicated in placental transfer, due to pegylation. There is a report of certolizumab utilized in a pregnant HS patient as an alternative to adalimumab. With only one mention in the literature, no assessment of certolizumab's efficacy in HS can be ascertained.
There are several safety concerns to consider when treating patients with TNF-alpha inhibitors. Data regarding the prevalence of these events in HS patients is scarce given the small number of HS patients treated with TNF-alpha inhibitors to date and few RCTs in the literature. These factors restrict the ability of researchers to perform meta-analyses: further limiting the study of adverse events in this population. Therefore, safety information is largely borrowed from the psoriasis, rheumatology, and gastroenterology literature.
TNF-alpha is heavily implicated in mediating immune response to pathogens. Immunosuppression resulting from anti-TNF-alpha therapy increases susceptibility to infections, especially concerning is the potential reactivation of latent TB through diminished granuloma integrity. In a meta-analysis of 29 RCTs accounting for 11,879 patients, TB reactivation risk was significantly elevated in patients treated with anti-TNF-alpha medications. Consequently, patients initiating anti-TNF-alpha therapy should be screened for latent TB and annually thereafter.
Another consideration with anti-TNF-alpha medications is increased risk of malignancy. One meta-analysis of the RA literature found an increased risk of all-site malignancy associated with anti-TNF-alpha medications, with an odds ratio (OR) of 3.29 (95% CI: 1.19-9.08). However, in subsequent meta-analyses of RA patients, these results were not replicated. Concomitant therapies are also likely important in development of these adverse events. A meta-analysis of the IBD literature also failed to find a significantly increased cancer risk in patients receiving anti-TNF-alpha therapy, although the authors cited concern that limited follow-up times could lead to less detection and cancer event reporting. Importantly, increased risk of nonmelanoma skin cancers (NMSC) associated with anti-TNF-alpha therapy has been reported. One study reported a relative risk (RR) of 2.02 (95% CI 1.11-3.95), and another demonstrated a RR of 1.45 (95% CI 1.15-1.76). Lymphoma risk is also increased in patients treated with anti-TNF-alpha therapy compared with the general population; but not when compared with RA patients treated with classic disease-modifying anti-rheumatic drugs. Diseases requiring anti-TNF-alpha therapy inherently involve chronic inflammatory states, which may lead to the development of lymphoma. It is difficult to say whether exposure to anti-TNF-alpha medications or the chronic inflammatory load experienced by these patients are to blame for the observed increase in lymphoma.
Neuropathy has been reported in HS patients taking anti-TNF-alpha medications. The prevalence of anti-TNF-alpha related neuropathies is estimated at 0.60% and largely resolve upon withdrawal of anti-TNF-alpha therapy.