Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but serious cutaneous reactions characterized by epidermal and mucocutaneous detachment, most often drug-induced. SJS and TEN are considered the opposite extremes of the same spectrum of disease, where the percentage of skin involvement is 30% in TEN; the in-between range is called an SJS/TEN overlap. We present the case of a 64-year-old patient who was treated with lamotrigine, an anti-epileptic drug, and developed SJS/TEN. After being hospitalized and recovering for three days due to the worsening of the clinical presentation, he was transferred to a burn center. Making an early diagnosis and identifying the appropriate drug is crucial for setting the correct treatment and reducing mortality. Advanced supportive care is required.

Background/Objectives: Cutaneous lupus erythematosus (CLE) is a complex autoimmune skin disease driven by genetic predisposition, environmental triggers, and immune dysregulation. Environmental factors such as ultraviolet radiation, smoking, and certain drugs can initiate disease onset by inducing keratinocyte apoptosis. The subsequent release of nucleic acids and danger-associated molecular patterns activates pattern recognition receptors (PRRs) on keratinocytes and immune cells, leading to the production of type I and type III interferons (IFNs) and pro-inflammatory cytokines. The objective of this review is to summarize recent advances in understanding the immunopathogenesis of CLE, with particular attention to emerging cellular players and their therapeutic implications. Methods: A narrative review of the recent literature was performed, including experimental, translational, and clinical studies investigating the cellular and molecular mechanisms underlying CLE and novel targeted treatments derived from these findings. Results: Although plasmacytoid dendritic cells (pDCs) have traditionally been considered the major producers of IFN-I, recent data indicate that pDCs in CLE are functionally impaired and are not the primary source. Other cells, such as keratinocytes have emerged as key producers of IFN-I, contributing to a prelesional, IFN-rich microenvironment. This promotes the recruitment and activation of dendritic cells and other inflammatory myeloid subsets, which are now recognized as central players in amplifying local inflammation. Concurrently, T cells infiltrate the skin, where cytotoxic CD8⁺ T cells attack keratinocytes and CD4⁺ T cells further propagate inflammation via cytokine production. B cells and plasma cells produce autoantibodies, forming immune complexes that perpetuate inflammation. Neutrophils release neutrophil extracellular traps (NETs), exposing autoantigens and further stimulating IFN pathways. Macrophages contribute by presenting autoantigens, producing pro-inflammatory mediators, and failing to effectively clear apoptotic cells and immune complexes. Conclusions: The dynamic interplay between the innate and adaptive immune systems sustains the chronic inflammatory state characteristic of CLE. Based on the pathogenetic novelties, new therapeutic agents targeting specific molecules have been developed, which may improve the treatment of this complex disease in the future.

Dermatitis herpetiformis (DH) is the specific cutaneous manifestation of celiac disease (CD), both of which require lifelong management. A comprehensive literature review was conducted to gather evidence on gender-related differences aiming at reducing healthcare inequalities. While women tend to be more symptomatic, the diagnosis is often delayed, leading to a reduced quality of life and an increased risk of long-term complications. This may be partly a consequence of the fact that they are more likely to present with seronegative forms. Moreover, in women, reproductive issues, known to be associated with DH and CD, along with osteopenia/osteoporosis, and anemia are particularly prevalent. It should be also noted that beyond personal diagnosis, DH and CD also affect women indirectly, as they often take on caregiving roles for affected family members. The lifelong adherence to a gluten-free diet, the only effective treatment for DH, imposes a substantial lifestyle and financial burden. Gluten-free diet is frequently perceived as both gendered and class-based, placing a disproportionate strain on women and lower-income households. In this regard, recent recommendations to prioritize naturally gluten-free foods rather than "gluten-free" products, may offer some relief. However, the responsibility for acquiring the skills necessary for such dietary choices often falls predominantly on women.

Bullous pemphigoid (BP) is the most common autoimmune blistering disorder in older patients and is typically managed with long-term immunosuppressive therapy tailored to the patient’s comorbidities and overall health. Patients who are frail with concurrent haematological malignancies represent a particularly vulnerable population due to their impaired immunity and treatment-related immunosuppression. We report the case of an 85-year-old man with mantle cell lymphoma, previously treated with rituximab and ibrutinib, who developed BP confirmed by histology, direct immunofluorescence, indirect immunofluorescence and enzyme-linked immunosorbent assay. Initial disease control was achieved with systemic corticosteroids and methotrexate. Subsequently, he developed a subcutaneous thoracic nodule consistent with panniculitis, followed by cerebral nocardiosis and Pneumocystis jirovecii pneumonia. Despite successful remission of BP, his clinical course was complicated by life-threatening infections requiring prolonged hospitalization. This case highlights the delicate balance between controlling autoimmune disease and preventing severe opportunistic infections in older, frail patients with haematological malignancies. Current BP guidelines should be refined by integrating better frailty assessment, infection prophylaxis and tailored immunosuppressive strategies.