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Dermatitis herpetiformis (DH) is an inflammatory disease of the skin, considered the specific cutaneous manifestation of celiac disease (CD). Both DH and CD occur in gluten-sensitive individuals, share the same Human Leukocyte Antigen (HLA) haplotypes (DQ2 and DQ8), and improve following the administration of a gluten-free diet. Moreover, almost all DH patients show typical CD alterations at the small bowel biopsy, ranging from villous atrophy to augmented presence of intraepithelial lymphocytes, as well as the generation of circulating autoantibodies against tissue transglutaminase (tTG). Clinically, DH presents with polymorphic lesions, including papules, vesicles, and small blisters, symmetrically distributed in typical anatomical sites including the extensor aspects of the limbs, the elbows, the sacral regions, and the buttocks. Intense pruritus is almost the rule. However, many atypical presentations of DH have also been reported. Moreover, recent evidence suggested that DH is changing. Firstly, some studies reported a reduced incidence of DH, probably due to early recognition of CD, so that there is not enough time for DH to develop. Moreover, data from Japanese literature highlighted the absence of intestinal involvement as well as of the typical serological markers of CD (i.e., anti-tTG antibodies) in Japanese patients with DH. Similar cases may also occur in Caucasian patients, complicating DH diagnosis. The latter relies on the combination of clinical, histopathologic, and immunopathologic findings. Detecting granular IgA deposits at the dermal-epidermal junction by direct immunofluorescence (DIF) from perilesional skin represents the most specific diagnostic tool. Further, assessing serum titers of autoantibodies against epidermal transglutaminase (eTG), the supposed autoantigen of DH, may also serve as a clue for the diagnosis. However, a study from our group has recently demonstrated that granular IgA deposits may also occur in celiac patients with non-DH inflammatory skin diseases, raising questions about the effective role of eTG IgA autoantibodies in DH and suggesting the need of revising diagnostic criteria, conceivably emphasizing clinical aspects of the disease along with DIF. DH usually responds to the gluten-free diet. Topical clobetasol ointment or dapsone may be also applied to favor rapid disease control. Our review will focus on novel pathogenic insights, controversies, and management aspects of DH.

Psoriasis is a chronic immune-mediated inflammatory cutaneous disease characterized by elevated levels of inflammatory cytokines and adipokine Lipocalin-2 (LCN-2). Recently, natural plant-based products have been studied as new antipsoriatic compounds. We investigate the ability of a leaf extract of the marine plant Posidonia oceanica (POE) to inhibit psoriatic dermatitis in C57BL/6 mice treated with Imiquimod (IMQ). One group of mice was topically treated with IMQ (IMQ mice) for 5 days, and a second group received POE orally before each topical IMQ treatment (IMQ-POE mice). Psoriasis Area Severity Index (PASI) score, thickness, and temperature of the skin area treated with IMQ were measured in both groups. Upon sacrifice, the organs were weighed, and skin biopsies and blood samples were collected. Plasma and lesional skin protein expression of IL-17, IL-23, IFN-γ, IL-2, and TNF-α and plasma LCN-2 concentration were evaluated by ELISA. PASI score, thickness, and temperature of lesional skin were reduced in IMQ-POE mice, as were histological features of psoriatic dermatitis and expression of inflammatory cytokines and LCN-2 levels. This preliminary study aims to propose P. oceanica as a promising naturopathic anti-inflammatory treatment that could be introduced in Complementary Medicine for psoriasis.

Bullous pemphigoid (BP) and pemphigus vulgaris (PV) represent the most prevalent conditions among autoimmune bullous skin diseases, considered a major cause of severe morbidity and, in certain cases, mortality. The hallmark of the two diseases is the presence of autoantibodies directed against proteins located in the basement membrane of the skin, which determines the formation of blisters. In recent years, interest in the role of microbiota in relation to health-disease status has progressively increased. In particular, based on the gut–skin axis, accumulating evidence has emerged on the potential association between the composition and diversity of microbial communities in the gut, skin, and even in the oral cavity and the risk of developing BP and PV. Dysbiosis, characterized by a generally higher relative abundance of Firmicutes and a depletion of probiotics/beneficial species, might contribute to the pathogenesis of both diseases. Despite the still limited number of studies and the need for further large-scale multicenter studies, the knowledge gathered so far is suggestive of a novel modifiable risk factor representing a potential target for adjuvant treatments of these disabling and life-threatening conditions.

Background: A current popular aesthetic problem, especially among younger women, is striae distensae (SD), also referred to as “stretch marks.”. Aim: The potential use of the 675 nm laser has been investigated in the treatment of SD. Methods: Patients underwent three sessions of the 675 nm laser with a 1-month interval between sessions. A total of three sessions were performed. The Manchester Scar Scale was used to assess stretch mark changes, and the mean scores related to each parameter at baseline and 6M FU after the last treatment session were measured. A clinical photographic evaluation was performed to show the aesthetic improvement of SD. Results: The patients’ treated areas were the abdomen, thighs, buttocks, and breasts. Mean scores related to each Manchester Scar Scale parameter, with their relative percentage change, at baseline and 6M FU after the last treatment session were significantly improved. The total mean Manchester Scar Scale score significantly diminished from 14.16 (±1.30) to 10.06 (±1.32) at 6M FU (p < 0.01). The clinical photographs showed promising aesthetic SD improvement. Conclusions: 675 nm laser therapy demonstrated a good tolerance for the treatment of stretch marks applied to various body areas preventing any discomfort for the patient and with a significant improvement in skin texture.

It is well known that viral infections play a relevant role in inducing or protecting from autoimmune diseases, thus representing a major environmental factor in the disruption of the immune system in genetically susceptible individuals. Since the beginning of the Covid-19 pandemic a great number of clinical and epidemiological studies have demonstrated that SARS-CoV-2 infection is no exception to the rule by interfering on many different levels in the normal functioning of our immune system. Even though a growing number of case series and case reports has been cited in the literature linking the infection to the new onset of autoimmune diseases, to date very little has been reported concerning a possible correlation between the virus and the clinical resolution of any kind of autoimmune pathology. Here we describe an interesting case of abrupt and unexpected resolution of Lichen planus pemphigoides mucocutaneous lesions in a fully vaccinated patient after a mildly symptomatic SARS-CoV-2 respiratory infection and we speculate on the possible underlying mechanisms correlating the two events.

Pemphigus encompasses a group of muco-cutaneous autoimmune bullous diseases characterized by the loss of adhesion between keratinocytes. The disease is associated with increased morbidity and mortality. We characterized clinical patterns, survival, comorbidities, and drug prescriptions in patients with pemphigus referred to the Section of Dermatology of the University of Florence from January 2010 to December 2021. A total of 149 patients were identified (female/male sex ratio = 2.0). Median age at diagnosis was 57.7 ± 17.2 years; 108 patients were diagnosed with pemphigus vulgaris (PV) (72.5%) and 35 (23.5%) with pemphigus foliaceus (PF). Paraneoplastic pemphigus (PNP) and IgA-pemphigus accounted for three patients each. The overall survival rate was 86.9%. Accordingly, 14 (9%) patients died during the study period. The average age at death was 77.8 ± 9.3. Age at diagnosis was a risk factor for death in patients with pemphigus. Average concentration of Dsg3-IgG and Dsg1-IgG was 85.6 ± 68.8 and 75.9 ± 68.4, respectively. The most serious comorbid diseases included cerebro- and cardiovascular accidents and malignancies. Regarding the treatment regimen, we found a substantially stable use of systemic steroids in the 2010-2018 period; the prevalence of use of mycophenolic acid increased, whereas that of azathioprine decreased. The use of rituximab showed the highest increase in the 2013-2018 period. Proton-pump inhibitors and antibiotics were the most frequently prescribed non-immunomodulating drugs. In this large series of the patients, patients with pemphigus showed a high incidence of serious comorbid diseases, highlighting the importance of a multidisciplinary approach for a proper management of the patients. Rituximab was the immunomodulating drug showing the highest increase in use over time, reflecting the growing evidence of its efficacy as a first-line treatment in pemphigus.

Management of cutaneous lupus erythematosus (CLE) involves a combination of preventive measures, topical and systemic drugs, fairly similar for the different subtypes. Although guidelines exist, to date, no specific drugs have been specifically licensed for CLE. Antimalarials remain the first-line systemic treatment, but many patients do not respond, making refractory lupus a challenge for clinicians. The choice of alternative medication should be based on effectiveness, safety and cost. Most of the available drugs for CLE have been adapted from systemic lupus erythematosus (SLE) treatment but the existing literature is limited to small studies and evidence often lacks. As knowledge of pathogenesis of both CLE and SLE is improving, promising new therapies are emerging. In this review, we discuss the available medications, focusing on the novelties under development for CLE.

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.

Bullous Pemphigoid (BP) is a common autoimmune blistering disorder with unknown aetiology. During the last decades, its association with various common comorbidities, including cardiovascular, metabolic, neuropsychiatric, and neoplastic disorders, has been established. However, in recent years an increasing number of BP cases have also been reported in association with rarer diseases, including Acquired Reactive Perforating Collagenosis (ARPC). Patients with coexisting BP and ARPC have been reported to share common clinical features including metabolic comorbidities e.g., Diabetes Mellitus (DM). As the evolution from ARPC cutaneous involvement to classic BP lesions has been more frequently described, it has been suggested that it may represent a new clinical variant of BP with a specific pathogenetic background. Here is reported a challenging case in which a typical onset of BP was later followed by the eruption of atypical ARPC lesions in a patient with multiple non-compensated metabolic and cardiovascular comorbidities.