Acne vulgaris is a highly prevalent chronic inflammatory disorder of the pilosebaceous unit that affects the majority of adolescents and young adults. Its pathogenesis is multifactorial and is driven largely by hormonal dysregulation, which promotes excess sebum production and follicular hyperkeratinisation, resulting in pore occlusion and the characteristic inflammatory lesions accompanied by swelling and erythema. Acne is caused by Cutibacterium acnes, which colonizes and activates acquired and innate immune responses. Acne is also produced owing to stimulation of the IGF-1 factor, disturbance of the omega-3 and omega-6 cycles, suppression of FoxO1, and activation of mTORC1, which assists in boosting sebum production. Proven treatments target these mechanisms by utilizing systemic and topical drug-delivery systems. Topical retinoids, which have antiinflammatory and anti-acne properties, such as azelaic acid, benzoyl peroxide, salicylic acid, dapsone, and topical or oral antibiotics, are used to treat acne. However, these formulations have limitations, including the need for prolonged treatment, persistent skin irritation, and the development of antibiotic resistance. To overcome these limitations, novel approaches have been utilized, including AI, nano-based formulations, nanoemulsions, semi-synthetic formulations, and herbal formulations. Recent improvements in acne therapy have focused on enhancing effectiveness and safety. The goal of recent developments in acne therapy is to improve treatment efficacy and safety. New drug delivery systems incorporating nanotechnology improve targeting of damaged areas and reduce side effects.

Leprosy, also known as Hansen´s disease, remains a public health concern, with around 200 000 new cases reported worldwide each year. Recent strategies to reduce transmission include post-exposure prophylaxis (PEP) with single-dose rifampicin, which has shown moderate protective efficacy and is being increasingly implemented on scale. However, widespread rifampicin use outside combination therapy raises concerns regarding the potential emergence of antimicrobial resistance (AMR) in Mycobacterium leprae and Mycobacterium tuberculosis. Although AMR in leprosy is less common than that in tuberculosis, resistance to rifampicin, dapsone, and fluoroquinolones highlights the need for systematic surveillance. However, AMR surveillance remains inconsistently implemented, with inadequate laboratory capacity, insufficient political prioritisation, and fragmented global coordination posing major barriers. In this Personal View, we argue that AMR surveillance should be an integral component of leprosy control and PEP programmes. We outline key challenges and propose pragmatic policy recommendations, including strengthening laboratory capacity, integrating surveillance into national programmes, and leveraging existing tuberculosis diagnostic networks. Embedding AMR surveillance within PEP strategies supports the long-term effectiveness of treatment and prevention efforts while minimising unintended consequences for global health.

Anti-p200 pemphigoid is a rare autoimmune subepidermal blistering disease with limited evidence guiding its management. We report a 49-year-old woman with refractory anti-p200 pemphigoid who failed treatment with high-dose prednisone and dapsone and developed significant corticosteroid-related toxicity, including hypertension, hypertrichosis, steroid-induced myopathy, and psychological distress. Given her history of complicated diverticulitis requiring bowel resection, dupilumab was initiated as a steroid-sparing therapeutic option. Pruritus improved within two weeks, near-complete remission was achieved after two months, and sustained disease control was maintained for six months, allowing substantial corticosteroid tapering without treatment-related adverse events.

Classical sulfonamides share a formal SO2NH motif, yet their molecular environments impose distinct frontier-orbital responses. We examined thirteen classical sulfonamides and dapsone using a staged, quality-controlled workflow that separated exploratory GFN2-xTB/Composite-SEPI (the study-specific exploratory electronic-prioritization score) screening from full-panel B3LYP-D3BJ/def2-SVP optimization/frequency analysis, canonical PBE0-D4/def2-TZVP refinement with the conductor-like polarizable continuum model for water (CPCM(water)), and an orthogonal ωB97X-D4 sensitivity layer. Revision-stage robustness tests additionally challenged geometry, additive D4 dispersion, population partitioning, and the basis-set dependence of charged-state Fukui descriptors. Corrected B3LYP and fixed-geometry PBE0 gaps preserved the same lower-gap regime (Pearson r = 0.935; Spearman ρ = 0.934). Full-panel PBE0 reoptimization showed modest but measurable gap sensitivity (mean absolute error (MAE) = 0.0595 eV; root-mean-square error (RMSE) = 0.0696 eV; 7/14 with |Δgap| ≥ 0.050 eV) while preserving the lower-gap top-three identity. PBE0 and ωB97X-D4 retained the relative gap landscape (r = 0.959; ρ = 0.978), and Mulliken-Löwdin cross-checks preserved the dominant HOMO and LUMO fragments for 14/14 molecules. In sulfadiazine, sulfamerazine, and sulfamethazine, the occupied and virtual frontier orbitals remained spatially separated between the aryl/aniline and diazine-containing regions. Diffuse-basis def2-TZVPD tests yielded negative vertical electron affinities and positive anion α-spin singly occupied molecular orbital (SOMO) energies for 14/14 molecules, making f+ and the dual descriptor basis-sensitive while f- remained comparatively robust. Formal SO2NH identity therefore masks reproducible electronic heterogeneity, but the reported quantities remain method-dependent isolated-molecule descriptors and do not establish charge-transfer states or biological activity predictions.

Antimicrobial agents, originally developed for infectious diseases, have become attractive candidates for repurposing in neurodegenerative and neuroinflammatory diseases owing to their anti-inflammatory, antioxidant, immunomodulatory, and neuroprotective activities. In this review, we critically examine the therapeutic potential of selected antimicrobial classes, including tetracyclines (e.g., minocycline), macrolides (e.g., azithromycin), antimalarial agents (e.g., chloroquine/hydroxychloroquine), sulfones (e.g., dapsone), and antiparasitic agents (e.g., ivermectin), in non-infectious neurological diseases. We performed a narrative review of pre-clinical and clinical studies to investigate the effects of these agents on the main neuropathological mechanisms, such as neuroinflammation, oxidative stress, mitochondrial dysfunction, impaired autophagy, and gut-brain axis dysregulation. The available evidence suggests that many of the antimicrobial agents have beneficial effects in a number of neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, stroke, and traumatic brain injury. These agents have been shown to modulate microglia activation, to inhibit production of pro-inflammatory cytokines, and to alter intracellular signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells. Furthermore, by reshaping the gut microbiota, antimicrobials modulate immune signaling, alter neurotransmitter levels, and compromise blood-brain barrier integrity-thereby positioning the gut-brain axis as central to their mechanism of action. Repurposing antimicrobial agents is a pragmatic and novel approach to treat complex neurological disorders with available approved drugs. Despite the encouraging evidence, we must carefully manage challenges such as antimicrobial resistance, off-target effects, and regulatory considerations. Further well-designed clinical trials are essential to validate their long-term safety and efficacy in neurodegenerative and neuroinflammatory diseases.

We report the case of an 88-year-old female patient presenting with progressive, severely pruritic skin lesions and scattered blisters on the trunk and extremities. Histological examination revealed subepidermal blister formation with a neutrophil-rich infiltrate. Differentiation from other autoimmune blistering diseases was initially challenging. The diagnosis was ultimately guided by the linear IgA deposition pattern along the dermoepidermal junction on direct immunofluorescence. This case highlights the diagnostic difficulties of this rare condition and the rapid clinical improvement following appropriate therapy.

Lupus miliaris disseminatus faciei (LMDF) is a rare inflammatory granulomatous dermatosis of unknown etiology, primarily affecting young adults. It presents as a symmetric papular eruption, predominantly on the mid-facial region, often leading to unsightly depressed scars. We report the case of a 28-year-old woman with persistent facial papules evolving into atrophic scars. Dermoscopy showed orange-brown globules, fine linear vessels, and scarred areas. Histology revealed epithelioid granulomas with fibrinoid necrosis and a lymphocytic infiltrate. The patient was treated with isotretinoin (20 mg/day for nine months) with partial improvement. Management of LMDF remains challenging due to the absence of standardized treatments. Therapeutic options include dapsone, oral corticosteroids, isotretinoin, biologic agents, and laser therapy. This case highlights the importance of early diagnosis and individualized treatment to minimize scarring and psychological impact.