Facial vitiligo affects a substantial proportion of patients with vitiligo and is associated with significant psychosocial burden due to its visibility. Facial vitiligo is primarily classified into nonsegmental and segmental subtypes, each with distinct distribution patterns and prognostic features. Nonsegmental vitiligo is further divided into 3 morphological patterns-centrofacial, panfacial, and hairline-each with unique clinical characteristics and treatment responses. The pathogenesis is multifactorial, involving genetic susceptibility, oxidative stress, and autoimmune destruction of melanocytes. Diagnosis is primarily clinical, supported by Wood lamp examination, dermoscopy, and advanced imaging techniques. First-line treatment includes topical calcineurin inhibitors and ruxolitinib, often combined with phototherapy to maximize repigmentation. The 308-nm excimer laser offers targeted delivery of ultraviolet (UV) radiation, minimizing photodamage to uninvolved skin. For progressive disease, systemic corticosteroids are commonly used for stabilization, with methotrexate, cyclosporine, or azathioprine as alternatives. Surgical interventions, particularly micropunch grafting, are effective options for stable, treatment-refractory cases. Emerging therapies, including oral Janus kinase inhibitors and biologics targeting tissue-resident memory T cells, are under investigation with encouraging preliminary results. Lifestyle modifications, including avoidance of mechanical friction, UV protection, and antioxidant-rich dietary patterns, may serve as supportive adjuncts to medical therapy. Recognizing the clinical heterogeneity of facial vitiligo, this review highlights the necessity of individualized treatment strategies based on clinical phenotypes to optimize therapeutic outcomes and improve quality of life.

We report a woman in her 50s who presented with jaundice and severe hepatocellular injury, concurrently found to have newly diagnosed advanced HIV infection (CD4 count 17, viral load 195 600 copies/mL). In this context, infectious hepatitis or opportunistic infections were the important initial consideration, but viral serology, imaging and liver biopsy excluded opportunistic and viral causes. Markedly raised immunoglobulin G, positive anti-nuclear and smooth muscle antibodies, typical histology and rapid response to corticosteroids confirmed acute autoimmune hepatitis (AIH). She improved on prednisolone, transitioned to azathioprine and commenced antiretroviral therapy with subsequent normalisation of liver function and undetectable HIV viral load. De novo AIH presenting concurrently with advanced HIV and profound immunosuppression is exceptionally rare, with few reported cases in the literature. It highlights that, even in this paradoxical setting, diligent investigation can uncover rare but treatable causes of liver dysfunction.

Myocarditis can closely mimic acute myocardial infarction (AMI), particularly in young patients without atherosclerotic risk factors. We report a 27-year-old man with recurrent severe chest pai7n, transient ST-segment elevations, and markedly elevated high-sensitivity troponin-T, in whom coronary angiography was repeatedly normal. Serial cardiac magnetic resonance and 18F-fluorodeoxyglucose positron-emission tomography revealed a migratory pattern of myocardial inflammation, with new lesions emerging as earlier ones resolved, fulfilling criteria for recurrent myocarditis. Recurrent oral ulcers, folliculitis, arthralgias, and pathergy-like skin reactions raised suspicion for Behçet's disease. Treatment with vasodilators, colchicine, corticosteroids, and azathioprine produced sustained clinical and biochemical remission. This case highlights the importance of considering myocarditis in young patients with recurrent angina-like symptoms and normal coronaries, the value of serial multimodal imaging in detecting migratory inflammation, and the recognition of Behçet's disease as a rare underlying cause of recurrent myocarditis.

An information technology worker of South Asian heritage in his 30s presented with haematemesis and central chest pain. Initial evaluation, including oesophagogastroduodenoscopy, was unremarkable. Subsequent imaging revealed multiple pulmonary artery aneurysms. Blood tests showed a negative autoimmune profile and raised inflammatory markers. Infectious, thromboembolic and connective-tissue differentials were excluded. A history of oral ulcers with genital ulceration, together with vascular involvement, fulfilled International Criteria for Behçet's Disease (ICBD). Given the life-threatening risk, we initiated intravenous methylprednisolone followed by cyclophosphamide, later transitioning to azathioprine with a structured steroid taper. Haemoptysis ceased promptly, and follow-up imaging showed aneurysm resolution. This case illustrates how haemoptysis can masquerade as gastrointestinal bleeding and emphasises the need to consider pulmonary artery aneurysms in young patients with compatible systemic features, where early imaging and rapid immunosuppression may be lifesaving.

Chronic lung allograft dysfunction (CLAD) is the primary cause of late graft loss after lung transplantation, affecting up to half of lung transplant recipients within 5 years and presenting with heterogeneous phenotypes, most commonly bronchiolitis obliterans syndrome (BOS) and restrictive allograft syndrome. Prevention and treatment of CLAD are challenging. This European Society for Organ Transplantation (ESOT) clinical practice guideline was developed by a multidisciplinary Task Force, including patient and allied healthcare representation, using systematic reviews and GRADE methodology. Eight key PICO questions addressing prevention and treatment of CLAD were evaluated. In terms of prevention, recommendations are in favor of using tacrolimus over cyclosporine, either mycophenolate or azathioprine, and azithromycin to reduce the risk of CLAD. Regarding treatment, montelukast could be considered in early-stage BOS. Current data are inconclusive in demonstrating benefits of anti-thymocyte globulin, alemtuzumab or extracorporeal photopheresis compared with standard of care, and do not support the use of antifibrotics in BOS. The Task Force emphasizes the urgent need for high-quality clinical trials and standardized care pathways in CLAD management.

Pyoderma gangrenosum (PG) is a rare, chronic neutrophilic dermatosis characterized by rapidly progressive, painful ulcers. It is frequently associated with systemic inflammatory conditions such as inflammatory bowel disease. The pathogenesis remains incompletely understood, and treatment of refractory cases poses a significant challenge. We present a 26-year-old woman diagnosed with PG, initially managed with systemic corticosteroids and ciclosporin. During follow-up, she developed gastrointestinal symptoms and was subsequently diagnosed with Crohn disease (CD). Despite treatment with azathioprine, infliximab and, later, ustekinumab, the patient experienced repeated flares of both PG and CD. Upon recurrence of PG lesions and CD exacerbation under ustekinumab therapy, systemic corticosteroids were reintroduced, and subcutaneous guselkumab, an interleukin (IL)-23 p19 inhibitor, was initiated. A rapid and sustained clinical response was observed following the second dose of guselkumab, with complete ulcer healing and tapering off corticosteroids. The patient has remained in complete remission from both PG and CD for over 2 years under guselkumab monotherapy. This case adds to the growing body of evidence supporting the use of IL-23 inhibitors, particularly guselkumab, in recalcitrant PG associated with systemic inflammatory comorbidities. Guselkumab may offer a promising therapeutic alternative in the management of treatment-resistant PG, especially in patients with coexisting CD.

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by rapidly progressive painful ulcers, and increasing evidence supports a role for the interleukin-36 pathway in its pathogenesis. We report the case of a 59-year-old woman with idiopathic refractory PG that evolved over 8 years. The patient had an insufficient response to prolonged systemic corticosteroids and azathioprine, with persistent steroid dependency. Spesolimab was initiated as a single 900-mg intravenous infusion in combination with low-dose prednisone (10 mg daily). This led to pain reduction, re-epithelialization and progressive ulcer healing, estimated at 30% after 3 months, 50% after 6 months and 80% after 8 months. No major adverse events were observed, apart from an erysipelas-like reaction around the ulcers 3 months later. Our review of published cases suggests that spesolimab may induce rapid and sustained improvement in refractory PG, although responses appear more heterogeneous in patients with underlying myeloid disorders. Overall, spesolimab appears to be a promising and well-tolerated therapeutic option for refractory PG, but further controlled studies are needed to better define its efficacy and safety, and place in the treatment algorithm.

Background Acute severe ulcerative colitis (ASUC) affects up to 25% of patients with ulcerative colitis. Despite intravenous (IV) corticosteroids as first-line therapy, 30-40% require rescue treatment and up to 40% undergo colectomy within one year. Upadacitinib (UPA) has shown ability to induce rapid response in moderate-severe UC, but real-world data in ASUC remain limited. We aimed to describe outcomes of UPA initiation for ASUC across Mayo Clinic sites. Methods We conducted a descriptive study of 23 adults hospitalized with ASUC between 2022-2025 at Mayo Clinic. Patients with their first ASUC admission who were started on UPA were included. All patients received IV methylprednisolone (40-60 mg/day) within 24-48 hours of admission, followed by UPA initiation (inpatient or shortly after discharge). Clinical, laboratory, and treatment data were extracted from electronic medical records. Outcomes included colectomy during admission and colectomy within one year. Descriptive statistics were done using Microsoft Excel. Results Twenty-three patients received UPA (median age 35 years; 88% pancolitis; 4% PSC). Out of the 23, 18 were started on UPA during the ASUC admission. Before admission, 10 patients (43%) were receiving corticosteroids, three (13%) were on mesalamine, one (4%) on azathioprine, and 12 (52%) were on biologic therapy; four patients (17%) were already on lower dose UPA maintenance. The median number of prior advanced therapies was two (range 1-4). Admission labs showed a mean CRP of 56.3 mg/L (SD 44.9) and fecal calprotectin of 2521.9 µg/g (SD 783.9). Patients received IV corticosteroids for a mean of 3.7 days (SD 1.1), and UPA was initiated at a median of hospital day 3 (IQR 4). 2/18 patients (11.1%), who were started on UPA inpatient, required colectomy during admission. Of the 23 patients who received UPA during hospitalization or shortly after discharge, one year colectomy rate was 4/23 (17%). Conclusions In this cohort, initiation of UPA during hospitalization or shortly after discharge for ASUC was feasible and was associated with lower colectomy rates compared with published outcomes for patients treated with infliximab or cyclosporine, both during hospitalization (11.1% vs. 21% vs. 25%) and at one year (17% vs. 35% vs. 45%). These findings suggest that UPA may serve as an effective rescue option for hospitalized ASUC patients, particularly when rapid control of inflammation is needed. Larger prospective studies are warranted to confirm these observations and to define optimal timing, patient selection, and long-term safety in the ASUC setting.

ObjectiveTo characterize the burden of herpes zoster (HZ) in systemic lupus erythematosus (SLE) and to examine clinical correlates of HZ and patients' attitudes toward the recombinant zoster vaccine (RZV).MethodsWe conducted a single-center retrospective cohort study combined with a cross-sectional survey among consecutive adult outpatients with SLE between December 2024 and June 2025. HZ episodes after SLE diagnosis were ascertained via structured interviews. Incidence rates were calculated as the number of HZ episodes per 1000 person-years from SLE diagnosis to enrollment. Participants were classified into three groups according to the number of HZ episodes: HZ[0], HZ[1], and HZ[≥2] groups. Factors associated with HZ development were assessed using multivariable logistic regression. Patients were asked about willingness to receive RZV ("yes", "no", or "not sure") and reasons for the response.ResultsAmong 170 patients with SLE, 73 (43%) reported at least one HZ episode after SLE diagnosis, and 29 (40% of those with HZ) reported recurrent HZ. During 3138 person-years of follow-up, at least 102 HZ episodes were reported, yielding a minimum incidence of 32.5 per 1000 person-years. In multivariable analysis, ever use of azathioprine (OR 2.74, 95% CI 1.03-7.29) and renal dysfunction (OR 2.59, 95% CI 1.04-6.48) were associated with HZ development. Attitude data were available for 159 patients: 31 (20%) were willing to receive RZV, 47 (30%) were unwilling, and 81 (50%) were unsure.ConclusionsHZ was common and frequently recurrent in this Japanese SLE cohort. Ever use of azathioprine and renal dysfunction were associated with HZ development, while willingness to receive RZV was low. Risk-stratified clinician counselling and shared decision-making may improve acceptance of HZ prevention strategies in high-risk patients with SLE.

Pemphigus vulgaris is a severe autoimmune blistering disease that occasionally develops lesions refractory to conventional systemic immunosuppressive therapy. We report the first documented case of successful treatment of therapy-resistant pemphigus vulgaris using cold atmospheric plasma. A 34-year-old woman presented with extensive oral and genital erosions that dramatically improved after initiating therapy with pulse corticosteroids in combination with cyclophosphamide. In the following weeks, she developed treatment-resistant facial erosions that persisted for 6 months despite aggressive systemic therapy consisting of intravenous immunoglobulin, azathioprine, and plasmapheresis. After 3 weekly cold atmospheric plasma treatments at 33 to 37 °C with a 2 cm torch gap for 3 min per treatment zone, the patient had remarkable clinical improvement, with an estimated > 80% epithelialization of facial erosions within 4 weeks, progressing to complete epithelialization by week 6. Disease activity assessment using the Pemphigus Disease Activity Index confirmed rapid improvement from a baseline of 14 to 0 within 6 weeks. Indirect immunofluorescence was negative throughout treatment. Sustained disease remission was achieved for 24 months. This novel application of cold atmospheric plasma is a promising therapeutic approach for recalcitrant lesions of pemphigus vulgaris.