Pilosebaceous unit occlusion and secondary inflammatory perifollicular lympho-histiocytic infiltration seem to be the underlying etiopathogenic mechanisms giving rise to hidradenitis suppurativa (HS). Increased levels of tumor necrosis factor (TNF)-alpha and other cytokines such as interleukins 12 and 23 (IL12/23) and interleukins 10 and 17 have been observed in HS lesional skin. Biological drugs have been reported to be effective for HS, but the level and duration of the response are quite variable. Among anti-TNF drugs, adalimumab and infliximab seem to obtain better results in HS. Adalimumab is the only registered systemic agent for HS and results from multicenter clinical trials demonstrate that 58.9% of patients may achieve clinical response without significant adverse events. Continuous treatment seems to maintain the therapeutic response, but discontinuation of the treatment usually results in a rapid relapse of the disease. Infliximab may also obtain a good response profile with 50% improvement of HS lesions. Treatment with ustekinumab for HS resulted in variable results showing a moderate-to-marked improvement in 82% of patients. Anakinra, a recombinant IL-1 receptor antagonist, has been also been postulated as a potential systemic treatment for HS. A reduction in the disease activity in 67% of patients has been reported. Biological drugs seem to represent an effective therapeutic option for HS, but complete and persistent resolution of the disease is rarely achieved. Flares of the disease usually develop regardless the prescribed treatment. Combined treatments including antibiotics and retinoids seem to be a potential additional therapeutic approach. In chronic and severe cases, a surgical approach is mandatory in order to remove persistent scarring tissue. New drugs are currently being evaluated as new insights in the pathogenesis of the disease are elucidated. Several clinical trials with apremilast, anti-IL17 drugs and anti-interleukin-1 alpha are currently ongoing.