**4. Etiology**

Although the etiology of HS has not been fully elucidated, there is a genetic predisposition, as up to 40% of patients with HS have a positive family history. Some *Hidradenitis Suppurativa Perineal and Perianal DOI: http://dx.doi.org/10.5772/intechopen.105632*

other factors not so well described may also be associated, such as hormonal changes and hyperandrogenic states, use of oral contraceptives, lithium, chemical irritants such as antiperspirants and deodorants, metabolic syndrome, inflammatory bowel disease, diabetes, and spondyloarthropathy that can lead to an increase in morbidity and mortality [15, 16].

Smoking and obesity are possible secondary causes of the disease and factors of worse prognosis. Some studies suggest that nicotine acts by stimulating and leading to dysfunctional glandular secretion, further altering neutrophil chemotaxis, leading to more severe diseases [13, 14]. Some studies have proven the association between smoking and perianal HS in 70% of patients; thus, one of the pillars of treatment is discouraging smoking [14–16].

Obesity can aggravate HS by retaining sweat and breaking the follicular and glandular ostia [15].

Bacterial colonization in HS is uncertain, being more associated as a secondary cause of the pathology. It can exacerbate the disease, but it is not a primary etiologic factor; there is no bacterial growth in more than half of the initial cases [15]. Bacterial infection occurs secondary to follicular occlusion. The most common bacteria are *Staphylococcus aureus* and *Staphylococcus epidermidis*. *Chlamydia trachomatis* and some anaerobes such as *Peptostreptococcus, Bacteroides,* and *Fusobacterium* can also be found. *Escherichia coli*, *Klebsiella*, and *Proteus* are more common in perineal HS [15, 16].
