# Understanding the Intricate Pathophysiology of Psoriasis and Related Skin Disorders
## 4 Sporiasis and Associated Dermatologic Disorders
On the other hand, the pathogenesis of HS remains incompletely understood, although immune dysregulation is thought to play a crucial role in its etiology. A key event in the development of HS lesions is the occlusion of hair follicles, triggered by hyperkeratosis and hyperplasia of the follicular epithelium, which ultimately leads to cyst formation. Recent studies have identified elevated levels of the cytokines IL-1, IL-23, and IL-17 in HS lesions, suggesting a significant role for Th17 cells in disease pathogenesis. The initial trigger in the pathogenesis involves the recognition of bacteria and cellular debris as pathogen- and damage-associated molecular patterns (PAMPs and DAMPs) by Toll-like receptors (TLRs) or NOD-like receptors (NLRs) in the dermis, leading to the activation of innate immunity [12]. PAMPs and DAMPs stimulate the inflammasome response, activating the NOD-like receptor protein 3 (NLRP3) in macrophages and neutrophils, which, in turn, leads to the production of caspase-1 and proinflammatory cytokines such as TNF-\(\alpha\) and IL-18. IL-18 induces the release of chemokines, from fibroblasts, which primarily attract neutrophils. TNF-\(\alpha\), produced by macrophages and dendritic cells, upregulates TLRs and stimulates keratinocytes to release various chemokines, including CXCL8, CXCL11, and CCL2, which recruit lymphocytes, neutrophils, and monocytes into the dermis. Additionally, IL-23 and IL-12, produced by activated dendritic cells, promote the polarization of CD4+ T lymphocytes into Th17 and Th1 cells. IL-17, produced by Th17 cells, further enhances macrophage production of IL-18 and TNF-\(\alpha\), amplifying the immune response [12]. In their case series, [PERSON] and colleagues documented a 3.8% prevalence of psoriasis in patients with HS. All of their patients presented with psoriasis before the onset of HS, suggesting that the flares of psoriasis with hyperkeratosis could induce follicular occlusion, which is considered the primary event in HS [13]. The link between psoriasis and HS is influenced by genetic factors. Both conditions are categorized as autoimmunity keratinization disorders, characterized by excessive activation of the innate immune system. This activation is influenced by genetic predispositions, including variations in genes such as IL-36 RN and CARD14, as well as components of the IL-1 pathway, like IL1 RN, TNF receptor 1, and TNFAIP3. The rare genetic disorder known as PsAPASH syndrome, encompassing \"Psoriatic Arthritis, Pyoderma Gangreno-sum, Acne, and Suppurative Hidradenitis\" is believed to stem from mutations in the PSTPIP1 gene. This provides additional support for the theory that genetic factors may underline the association between psoriasis and HS. The disruption of the skin microbiome, especially the growth of certain bacterial species, such as _Staphylococcus aureus_, may play a crucial role in both HS and psoriasis. Remarkably, the risk of developing HS in patients with more severe or well-established psoriasis may be greater. A hazard ratio (HR) of 2.867 was observed in patients with more than two inpatient visits for psoriasis. Additionally, psoriasis patients with more than two visit records who received a topical corticosteroid prescription had a roughly two-fold increased risk of developing HS. While topical corticosteroids are used to treat posoriasis, prolonged use may damage the follicular structure, which partially explains the predisposition to developing HS. It is a paradox that a 5.914 HR was noted for psoriasis patients with more than two visit records who received a vitamin D prescription. Vitamin D reported benefits for both psoriasis and HS. It was concluded that the prescription of vitamin D analogs indicates a more severe psoriasis, which, in turn, elevates the risk of HS [14]. Due to shared pathogenic mechanisms, biological therapies like adalimumab are effective for both HS and psoriasis.