Pemphigoid gestationis (PG) is a rare blistering dermatosis usually seen in the second and third trimesters of pregnancy. Treatment of PG is aimed towards the relief of pruritus and prevention of new lesions from developing, often involving high-potency topical corticosteroids, antihistamines, oral corticosteroids and other systemic immune modulators for patients with symptoms of greater severity. Recently, dupilumab, a monoclonal antibody against the alpha subunit of the interleukin-4 receptor, has been used successfully in bullous pemphigoid. We discuss the case of a 34-year-old Asian woman at 32 weeks' gestation who presented with progressive and severely pruritic oedematous urticarial plaques and patches dispersed across the trunk and extremities, with scattered tense bullae. A skin biopsy confirmed the diagnosis of PG. The patient was placed on high-dose oral corticosteroids and concomitant topical steroids, with minimal resolution after attempts to taper oral steroids over the next 4 weeks. Oral prednisone was continued at 17.5 mg for the remainder of her pregnancy given the risks associated with higher dosages. After delivery, the patient's disease worsened, requiring an increase in prednisone. Given that the patient was breastfeeding, dupilumab was initiated as a steroid-sparing agent allowing patient to be tapered off prednisone with significant improvement and control of her disease. The safety of dupilumab for infants who are being breastfed remains under discussion. Herein, we discuss the existing literature and considerations regarding pregnancy and breastfeeding for patients with PG on dupilumab.

Bullous erythema multiforme (BEM) is an acute immune-mediated mucocutaneous disease, with drug induction being one of its common causes. Omalizumab, a recombinant humanized IgG1 monoclonal antibody targeting free IgE, is widely used in chronic spontaneous urticaria and asthma due to its favorable safety profile, while severe cutaneous bullous adverse reactions induced by it are extremely rare. We report a 36-year-old female patient with a history of bronchial asthma, allergic rhinitis, allergic conjunctivitis, and chronic spontaneous urticaria who developed generalized wheals. After the first subcutaneous injection of omalizumab 300 mg, multiple raised, edematous erythematous papules and plaques, vesicles, and bullae appeared on the trunk, limbs, palms, soles, and oral mucosa 17 days later, accompanied by fever, chills, and fatigue. Laboratory examinations showed elevated eosinophil count and IgE level, and skin biopsy from the left upper limb revealed focal epidermal necrotic keratinocytes, intraepidermal and subepidermal blister formation, and massive eosinophilic infiltration. The patient was diagnosed with omalizumab-induced BEM. Initial treatment with methylprednisolone combined with intravenous immunoglobulin (IVIG) was ineffective. The condition was successfully controlled after increasing the dose of methylprednisolone and adding oral upadacitinib. This case suggests that omalizumab may induce BEM, and combination therapy with high-dose glucocorticoids and JAK inhibitors may be an effective strategy for refractory cases. Clinicians should be alert to such rare adverse reactions when using omalizumab.

Autoimmune bullous diseases (AIBDs), including pemphigus vulgaris (PV), pemphigus foliaceus (PF), and bullous pemphigoid (BP), are mediated by autoantibodies against desmogleins (DSG1, DSG3) or hemidesmosomal proteins (BP180, BP230). While enzyme-linked immunosorbent assay (ELISA) is commonly applied for antibody detection, chemiluminescent immunoassay (CLIA) offers advantages such as a broader dynamic range and higher automation. To compare the diagnostic performance of CLIA and ELISA for detecting autoantibodies in patients with AIBDs, we collected 255 serum samples (92 controls, 84 BP, 69 PV, 10 PF) and 85 blister fluid samples (42 controls, 43 BP). Serum was tested for anti-BP180, anti-BP230, anti-DSG1, and anti-DSG3 antibodies using both assays; blister fluid was tested for anti-BP180 and anti-BP230. Using established cut-offs, the assays demonstrated good diagnostic accuracy for anti-BP180, anti-DSG1, and anti-DSG3 in serum, and excellent concordance (>90%). Receiver operating characteristic analysis revealed acceptable to excellent diagnostic value for both sample types, with CLIA generally achieving a higher area under the curve. Spearman's correlation and linear regression analyses confirmed moderate to strong agreement between the two methods. In conclusion, CLIA showed strong concordance with and comparable diagnostic accuracy to ELISA for AIBD serodiagnosis. Furthermore, this is the first study to evaluate CLIA for autoantibody detection in blister fluid from BP patients, demonstrating that blister fluid may serve as a less invasive sample type for diagnosis. Our cut-off analysis in a treated cohort also suggested that manufacturer-recommended thresholds may yield false-negative results, highlighting the need for population-specific reference intervals.

Immune checkpoint inhibitors (ICIs) can precipitate autoimmune bullous diseases, among which bullous pemphigoid (BP) is uncommon but has significant clinical implications. We report a 72-year-old man with poorly differentiated gastric adenocarcinoma and liver metastases who developed generalized pruritic erythema after the 4th cycle of sintilimab, followed by tense blisters after the 8th cycle. Upon admission (January 2025), over 30% of his body surface area (BSA) was affected, accompanied by pruritus that impacted his sleep. Histopathology showed eosinophilic cell infiltration within the epidermis and mild spongiosis. Edema was observed between collagen fibers in the papillary dermis, accompanied by a small number of lymphocytes and histiocytes. Moderate (+++) mixed inflammatory cell infiltration was observed in the superficial dermis, primarily consisting of lymphocytes (approximately 60%) and eosinophils (approximately 30%), with a small number of neutrophils (approximately 10%). Direct immunofluorescence (DIF) revealed IgG and C3 along the basement membrane zone (BMZ). Serum autoantibodies demonstrated significantly elevated BP180 (392.01 RU/mL) and low BP230 (9.29 RU/mL), while desmoglein-1 (8.38 U/mL) and desmoglein-3 (5 U/mL) were negative/low, supporting BP rather than pemphigus. The rash met the CTCAE (Common Terminology Criteria for Adverse Events) v5.0 criteria for Bullous dermatitis, Grade 3, with concomitant Pruritus, Grade 3. Daily intravenous methylprednisolone 60 mg was initiated, leading to cessation of new blister formation within 7 days and improvement in pruritus. Sintilimab was discontinued during treatment and resumed after BP was brought under control (approximately 1 month later); the patient has maintained remission for more than 12 months since resuming Sintilimab treatment, and no recurrence has been observed. The temporal association with PD-1 blockade, objective clinicopathologic confirmation, and lack of strong alternative culprits support a possible causal relationship. Early biopsy, DIF, and targeted serology enable timely CTCAE-guided management and informed decision-making for pausing or rechallenging PD-1 therapy.

Dermatitis herpetiformis (DH) is a chronic autoimmune blistering dermatosis associated with gluten-sensitive enteropathy and characterized by intensely pruritic papulovesicular eruptions, typically distributed symmetrically on extensor surfaces. Although DH classically presents with grouped vesicles and excoriated papules, atypical and exuberant manifestations may represent a substantial diagnostic challenge, frequently mimicking infectious, inflammatory, and autoimmune blistering disorders. We report the case of a 30-year-old woman presenting with a one-year history of progressive, intensely pruritic vesiculobullous and erosive lesions involving the trunk and extremities, accompanied by painful oral ulcerations, hemorrhagic crusts, extensive excoriations, secondary bacterial infection, and diffuse post-inflammatory hyperpigmentation. The patient was initially diagnosed with Behçet disease and subsequently hospitalized for suspected disseminated herpetic infection, receiving systemic corticosteroids and intravenous acyclovir without significant clinical improvement. Dermatological examination revealed widespread erosive and vesiculobullous lesions associated with severe inflammatory activity and oral aphthoid ulcerations. Histopathological examination of active lesions demonstrated intraepidermal blister formation associated with eosinophilic infiltrate and scattered acantholytic cells, findings that initially suggested alternative autoimmune blistering disorders. Direct immunofluorescence (DIF) demonstrated characteristic granular IgA deposition predominantly localized at the tips of dermal papillae, confirming the diagnosis of DH despite atypical histopathological findings. Serological evaluation further revealed positive anti-tissue transglutaminase and anti-endomysial antibodies, corroborating the diagnosis. Treatment with dapsone combined with a strict gluten-free diet resulted in marked clinical improvement. This case highlights the importance of clinicopathological and immunopathological correlation in atypical presentations of autoimmune blistering diseases and underscores the essential role of DIF in establishing the diagnosis of DH.

Pemphigus vulgaris (PV) is a rare, potentially life-threatening autoimmune blistering disorder characterized by intraepidermal acantholysis caused by IgG autoantibodies directed against desmoglein 1 and 3. Although most cases are idiopathic, certain medications, including antibiotics, have been implicated as potential triggers in susceptible individuals. We report the case of a 61-year-old man with a history of nonischemic cardiomyopathy, chronic kidney disease, and substance use disorder who developed widespread flaccid bullae six days after initiation of intravenous ceftriaxone for a suspected urinary tract infection. Histopathologic examination demonstrated suprabasal intraepidermal acantholysis with intraepidermal vesicles containing neutrophils and eosinophils, along with preservation of the basal epidermal layer in a characteristic "row of tombstones" pattern, findings highly suggestive of PV. Ceftriaxone was promptly discontinued, and the patient was treated with high-dose systemic corticosteroids, resulting in marked clinical improvement. Ceftriaxone-induced PV is an exceedingly rare adverse reaction, with few cases reported in the literature. The proposed pathogenesis involves drug-induced neoantigen formation or stimulation of pathogenic autoantibody production in genetically predisposed individuals. Early recognition of drug-induced PV is essential, as continued exposure may result in extensive mucocutaneous involvement, secondary infection, and increased morbidity. Prompt withdrawal of the offending agent and initiation of immunosuppressive therapy are critical for improving clinical outcomes.

Acral vitiligo responds less well to NB-UVB than non-acral disease, but site-specific immunologic changes during therapy are incompletely defined. The objective of this study was to compare NB-UVB-associated changes in T cell subsets and soluble mediators in acral versus non-acral vitiligo. Thirty patients with non-segmental vitiligo were enrolled. Ten underwent paired biopsies (acral and non-acral) before and after 6 months of NB-UVB for flow cytometry (Tregs, CD8+ T cells, CD8+CD45RO+ memory T cells, CD8+CD69+CD103+ TRM). Suction-blister fluid ELISA assessed IFN-γ-axis mediators (CXCR3, CXCL9, CXCL10, IFN-γ, IL-1β) in two separate groups: 10 treatment-naïve patients and 10 patients who had completed 6 months of NB-UVB therapy. Non-parametric tests used Benjamini-Hochberg FDR correction (pFDR). In paired biopsies (n = 10; CD8 n = 9), memory T cells decreased after NB-UVB in acral (4.38 [3.47-5.98] to 1.38 [0.73-2.21]; pFDR = 0.041) and non-acral lesions (5.23 [4.27-6.75] to 1.08 [0.48-2.54]; pFDR = 0.0039). TRM declined in acral (5.95 [3.17-7.41] to 0.65 [0.15-1.15]; pFDR = 0.0039) and non-acral sites (4.12 [2.50-5.57] to 0.69 [0.28-1.19]; pFDR = 0.0039). Tregs showed a site-divergent pattern: acral Tregs decreased (0.56 [0.41-0.75] to 0.08 [0.03-0.23]; pFDR = 0.0067) while non-acral Tregs increased (0.40 [0.24-0.61] to 0.95 [0.41-1.59]; pFDR = 0.0039). CD8+ T cells showed no change after correction. CXCL9 showed a non-significant decreasing trend (pFDR = 0.249); no ELISA marker remained significant after FDR correction. NB-UVB exerts a pronounced effect on cellular immunity (reductions in TRM and memory T cells) with limited cytokine suppression, with site-divergent Treg pattern.

Pemphigus foliaceus is a rare autoimmune blistering disease characterized by superficial intraepidermal blister formation and chronic relapsing disease activity. Although systemic immunosuppressive therapy remains the cornerstone of treatment, adherence to both systemic and topical therapies may influence disease control, skin barrier integrity, and susceptibility to secondary infections. We present the case of a 73-year-old man with a history of hypertension, type 2 diabetes mellitus, and chronic ischemic heart disease who developed pemphigus foliaceus confirmed by clinical and histopathological findings. The disease initially manifested with vesicles and flaccid bullae involving the face and chest that progressed to erosions with serohematic crusts. The patient initially received systemic corticosteroids, antihistamines, and topical therapy without adequate response, requiring hospitalization and treatment with intravenous immunoglobulin. Therapy was later adjusted to include mycophenolic acid and corticosteroid tapering, achieving partial clinical improvement. During follow-up, the patient experienced multiple relapses associated with inconsistent adherence to topical therapy and unsupervised discontinuation of systemic corticosteroids. Despite reintroduction of immunosuppressive therapy, intermittent cutaneous activity persisted. On his final hospital admission, he developed secondary cutaneous and urinary infections caused by Klebsiella pneumoniae and Enterococcus faecalis, progressing to septic shock despite advanced medical management. This case highlights the challenges of treatment adherence in pemphigus foliaceus and emphasizes the multifactorial nature of severe disease progression in elderly patients with multiple comorbidities. Inadequate adherence, persistent disease activity, chronic immunosuppression, skin barrier dysfunction, and secondary infections may collectively contribute to unfavorable clinical outcomes. Reinforcement of patient education, close follow-up, and careful monitoring remain essential components in the management of autoimmune blistering diseases.

White pine blister rust disease (WPBR), caused by Cronartium ribicola, ranks among the most destructive pathogens of five-needle pines. We developed a hydroxynaphthol blue (HNB)-based Loop-mediated isothermal amplification (LAMP) assay enabling rapid, visual detection of C. ribicola directly following DNA extraction. LAMP primers targeting the internal transcribed spacer (ITS) region were designed and validated through in silico comparison with related Cronartium species and in vitro testing against sympatric forest fungi. The optimized 25 μL reaction contained 8.0 mM Mg2+, 1.0 mM dNTPs, and an inner-to-outer primer ratio of 8:1, with amplification conducted at 62 °C for 40 min. Positive amplification produced a distinctive color transition from purple to sky blue, enabling visual interpretation without instrumentation. Under the tested conditions, the assay achieved a detection limit of 460 ± 3.2 fg/μL genomic DNA-a 10-fold improvement over conventional PCR in concentration-based sensitivity. Assay applicability was evaluated using 211 field-collected Pinus armandii samples sourced from China. Detection efficiency varied significantly across tissue types. Symptomatic bark exhibited a substantially higher positive detection rate (68.97%, 95% CI: 49.2-84.7%) compared to needles from symptomatic trees (18.75%, 95% CI: 4.1-45.7%). Among asymptomatic samples, 3.75% of bark samples tested positive for C. ribicola DNA, whereas all needle samples were negative. Geographically, positive detections clustered at several discrete sampling sites in southwestern China, predominantly at elevated elevations. The established LAMP-HNB assay provides a rapid, visually interpretable diagnostic tool for early detection and quarantine monitoring of WPBR following DNA extraction. Beyond its practical utility, this assay establishes valuable baseline data for targeted disease surveillance in the context of evolving climate conditions.

Bullous systemic lupus erythematosus (BSLE) is a rare autoimmune blistering manifestation of systemic lupus erythematosus (SLE), typically regarded as a cutaneous variant with limited prognostic significance. However, its relationship to systemic disease activity and therapeutic response remains incompletely defined. We present a 42-year-old male patient with known SLE and recently diagnosed BSLE, who developed progressive, widespread blistering lesions with mucosal involvement, dyspnea, and constitutional symptoms despite ongoing therapy. Physical examination revealed extensive tense bullae, erosions, and ulcerative plaques involving the extremities, face, and oral mucosa. Laboratory evaluation demonstrated positive autoimmune serologies consistent with SLE, while infectious and thromboembolic etiologies were excluded. Histopathology and direct immunofluorescence confirmed the diagnosis of BSLE. Despite treatment with systemic corticosteroids, hydroxychloroquine, dapsone, and rituximab, the patient experienced continued clinical deterioration requiring hospitalization and escalation of care. This case underscores BSLE as more than a cutaneous manifestation, instead suggesting its role as a marker of aggressive, treatment refractory systemic disease. The persistence and progression of skin lesions despite appropriate immunosuppression paralleled ongoing systemic activity, indicating that refractory cutaneous findings should prompt reassessment of overall disease control rather than be dismissed as isolated dermatologic involvement. Early recognition of this pattern may support timely therapeutic escalation and closer multidisciplinary management, with potential to improve clinical outcomes.

A 52-year-old woman presented with a three-month history of pruritic scaly palmoplantar eruptions that progressed to tense bullae over trunk and extremities along with genital mucosal involvement. Serology confirmed syphilis (VDRL reactive at 1:16 and TPHA positive), and biopsy with direct immunofluorescence (DIF) established bullous pemphigoid (BP). Treatment with benzathine penicillin led to resolution of palmoplantar and genital lesions, but there was no improvement of bullous lesions. Treatment with oral doxycycline and prednisolone significantly resolved the bullous eruptions. In adults, secondary syphilis can rarely be present as bullous eruptions, which may mimic autoimmune blistering disorders like BP, thereby posing a diagnostic dilemma. This case uniquely demonstrates BP persisting despite successful syphilis treatment (8-fold VDRL decrease), requiring ongoing immunosuppression. Unlike previously reported cases where bullous lesions resolved with antibiotics alone, this differential response confirms that syphilis can trigger independent, self-sustaining autoimmune bullous disease.