Background: Proinflammatory activation and autoimmune processes underlie the pathophysiology of hidradenitis suppurativa (HS). Iron deficiency (ID) is frequently present in inflammation-mediated chronic diseases, irrespective of anemia. Objectives: We aimed to characterize iron status in patients with HS. Methods: Serum concentrations of ferritin, transferrin saturation (Tsat), soluble transferrin receptor and hepcidin were assessed as the biomarkers of iron status in 74 patients with HS and 44 healthy subjects. ID was defined as ferritin <100 µg/L or ferritin 100–299 µg/L with Tsat <20% (following the definition used in the other studies in chronic disease). Results: Compared with controls, patients with HS demonstrated a deranged iron status as evidenced by decreased levels of ferritin (91 ± 87 vs. 157 ± 99 µg/L), Tsat (21.5 ± 10.8 vs. 42.2 ± 11.7%) and hepcidin (31.3 ± 25.9 vs. 44.2 ± 22.0 ng/mL) (all p < 0.05 vs. controls). There was also a trend toward higher values of soluble transferrin receptor (1.23 ± 0.35 vs. 1.12 ± 0.19 mg/L) (p = 0.09 vs. controls). Disease severity (assessed with the Hidradenitis Suppurativa Severity Index and the 3-degree Hurley scale) did not differentiate iron status biomarkers. ID was present in 75% of HS patients, and its prevalence was not related with disease severity (Hurley I/II/III – 82 vs. 73 vs. 67%). In HS, none of the iron status biomarkers correlated with the levels of interleukin-6 (a marker of proinflammatory activation). Conclusions: The majority of HS patients demonstrate derangements in iron status typical of ID. These abnormalities are neither related to proinflammatory activation nor associated with disease severity. Whether it may have a therapeutic impact needs to be further studied.

Psoriasis is a chronic inflammatory skin disease characterized by well-demarcated erythematous plaques with silvery scales that affects 2–3% of the global population. Beyond its dermatological manifestations, psoriasis has recently been recognised as a significant cardiovascular risk factor, patients with psoriasis have an approximately 50% increased relative risk of major cardiovascular events compared with the general population. This review examines the complex relationship between psoriasis and cardiovascular disease, exploring the epidemiological evidence, underlying pathophysiological mechanisms, clinical implications and therapeutic considerations. The inflammatory milieu characteristic of psoriasis, involving T cell activation, cytokine dysregulation and systemic inflammation, creates a pro-atherogenic environment that accelerates cardiovascular disease development. Understanding the mechanisms of cardiovascular risk is crucial for clinicians managing psoriatic patients, as it necessitates comprehensive risk assessment and preventive strategies beyond traditional dermatological care.

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Iron is an essential microelement in the human body due to its role in hematopoiesis, involvement in energetic processes, synthesis and decomposition of lipids, proteins and nuclear acids. Iron deficiency (ID) is common in healthy populations and also frequently coincides with natural course of chronic diseases. The former is typically present when the overall iron body storages are exhausted (absolute ID), most often due to insufficient iron supply, malabsorption or increased blood loss and coincides with anemia. The latter is a result of defected iron metabolism and reflects a condition, when despite adequate iron stores in the body, iron itself is trapped in the reticuloendothelial system, becoming unavailable for the metabolic processes. It typically occurs in the presence proinflammtory activation in chronic conditions such as chronic kidney disease, inflammatory bowel disorders, malignancies and heart failure. To date there are very few publications concerning the potential role of ID in chronic dermatological disorders. We have recently found that patients with psoriasis demonstrate pattern of ID which can be characterized by negative tissue iron balance with depleted iron stores in the body. Interestingly, presence of ID was not related to the severity of psoriasis, but rather determined by patients low body mass index. We are currently investigating the hypothesis that derangements in iron metabolism resulting in ID can be also present in hidradenitis suppurativa – the other chronic dermatologic disease associated with inflammatory and autoimmune activation.

Introduction: Hidradenitis suppurativa (HS) is a chronic, inflammatory, debilitating disease of a relapsing nature involving nodules, abscesses and suppurating lesions of intertriginous areas of the skin. Within recent years there has been a progress in terms of the treatment of hidradenitis suppurativa, nevertheless its therapy still remains limited with very few effective options. Areas covered: This article provides a review of current systemic treatment strategies used in patients with hidradenitis suppurativa – from well-established, traditional methods to new therapeutic alternatives with special focus on biological agents. Expert opinion: The etiology of hidradenitis suppurativa is still not clearly explained, but several factors seem to play a role such as genetics, smoking and obesity. Recent findings have specified that HS is a disease of the hair follicles with bacterial infection and apocrine glands involvement as secondary events. In HS treatment all known pathomechanisms underlying and responsible for development of skin lesions should be taken into account, including hyperkeratinization and occlusion of pilosebaceous unit, bacterial superinfection and extensive, chronic inflammatory response. Thus, retinoids, systemic antibiotics and biologics should be agents of special interest. Summarizing, pharmacological therapies are promising option for HS sufferers, especially in non-advanced cases.