Bullous Pemphigoid-like Eruption Research Articles

Autoimmune bullous dermatoses in cancer patients treated by immunotherapy: a literature review and Italian multicentric experience.

Cutaneous immune-related adverse events are frequently associated with immune checkpoint inhibitors (ICIs) administration in cancer patients. In fact, these monoclonal antibodies bind the cytotoxic T-lymphocyte antigen-4 and programmed cell death-1/ligand 1 leading to a non-specific activation of the immune system against both tumoral cells and self-antigens. The skin is the most frequently affected organ system appearing involved especially by inflammatory manifestations such as maculopapular, lichenoid, psoriatic, and eczematous eruptions. Although less common, ICI-induced autoimmune blistering diseases have also been reported, with an estimated overall incidence of less than 5%. Bullous pemphigoid-like eruption is the predominant phenotype, while lichen planus pemphigoides, pemphigus vulgaris, and mucous membrane pemphigoid have been described anecdotally. Overall, they have a wide range of clinical presentations and often overlap with each other leading to a delayed diagnosis. Achieving adequate control of skin toxicity in these cases often requires immunosuppressive systemic therapies and/or interruption of ICI treatment, presenting a therapeutic challenge in the context of cancer management. In this study, we present a case series from Italy based on a multicenter, retrospective, observational study, which included 45 patients treated with ICIs who developed ICI-induced bullous pemphigoid. In addition, we performed a comprehensive review to identify the cases reported in the literature on ICI-induced autoimmune bullous diseases. Several theories seeking their underlying pathogenesis have been reported and this work aims to better understand what is known so far on this issue.

Systemic Treatment of Cutaneous Adverse Events After Immune Checkpoint Inhibitor Therapy: A Review.

As treatment with immune checkpoint inhibitors (CPIs) for cancer increases, so has the incidence of immune-related cutaneous adverse events (irCAEs). These toxicities can significantly impact quality of life and may be dose-limiting. Current guidelines for irCAEs offer only corticosteroids or CPI discontinuation. Evidence supports biologic immunomodulatory therapies when corticosteroids fail or need avoidance. A review of literature from 2010 to 2020 yielded 45 articles, resulting in 185 irCAEs, including bullous pemphigoid-like eruption (n = 55), psoriasis/psoriasiform dermatitis (n = 41), and maculopapular rash (n = 31). Treatments included immunomodulators, intravenous immunoglobulin, aprepitant, acitretin, tetracyclines, and biologic agents. Overall, 92.3% of patients saw improvement or resolution of their rash. Bullous pemphigoid-like eruptions were treated with a tetracycline +/- niacinamide (94.7% success [18/19]), omalizumab (100% success [7/7]), and rituximab (100% success [10/10]). Although prospective research is required, this review provides a comprehensive list of successful, non-corticosteroid treatment options for irCAEs to improve compliance with lifesaving cancer therapy.

Bullous Pemphigoid-like Eruption Triggered by Targeted Therapy for Metastatic Melanoma.

Bullous Pemphigoid-like Eruption Triggered by Targeted Therapy for Metastatic Melanoma.

Bullous Pemphigoid-like Skin Eruption during Treatment with Rivaroxaban: A Clinical Case Study.

Little has been documented about hypersensitivity reactions caused by treatment with rivaroxaban. This paper reports a bullous pemphigoid-like skin eruption that occurred in a 76-year-old female patient during rivaroxaban treatment. This case highlights the vigilance required by healthcare workers in recognising potential adverse effects of newly marketed drugs and in making medication changes when necessary. A bullous pemphigoid-like eruption due to treatment with rivaroxaban has not, to the best of the Authors’ knowledge, been reported previously in the literature.LEARNING POINTSRivaroxaban can cause a bullous eruption apparently similar to epithelial toxic necrolysis (or to Stevens-Johnson syndrome).There is an apparent similarity between skin adverse events caused by the different anticoagulants.The anticoagulant responsible for the skin side-effects can be identified on clinical grounds by the correct differential diagnosis.

Bullous Scabies Simulating Pemphigoid

Scabies is a contagious infestation affecting subjects of all ages, races, and social conditions. We report a case of a 79-year-old man who developed a bullous pemphigoid-like eruption. He presented to our unit 4 months after the onset of symptoms. An autoimmune bullous disease was suspected. Direct immunofluorescence on a skin specimen and anti-desmoglein 1, anti-desmoglein 3, and anti-bullous pemphigoid antigen 180 were negative. Surprisingly, the histology of a skin lesion demonstrated the presence of scabies, which was successfully treated with benzyl benzoate 20%. The diagnosis of bullous scabies should be considered for any bullous eruptions accompanied by papules and itching resistant to steroid treatment and with negative immunopathologic findings.

Orf-induced immunobullous disease: A distinct autoimmune blistering disorder

Many complications have been reported after orf infection, including lymphadenopathy, secondary bacterial infection, and erythema multiforme. Rare associations with papulovesicular eruptions, including a bullous pemphigoid-like eruption, have also been described. Our purpose was to clinically, histologically, and immunologically characterize two cases of orf-induced blistering disease, and to determine whether this condition represented a novel disease entity distinct from known immunobullous diseases. Two patients were clinically described and skin biopsy specimens were collected for routine histology, direct immunofluorescence studies, and polymerase chain reaction analysis to detect orf viral DNA. Patients' sera were assessed for autoantibodies by indirect immunofluorescence studies using normal-appearing human salt-split skin, by Western blot analysis using keratinocyte extracts, dermal extracts, and recombinant type VII collagen, and immunoprecipitation studies of extracts from biosynthetically radiolabeled human keratinocytes. Two distinctive cases of severe, diffuse blistering eruptions after orf infection are described. In one patient, orf virus DNA was detected in the inciting orf lesion, but not in blistered skin, ruling out disseminated orf infection as a cause of the blisters. In both cases, histology revealed subepidermal blisters with mixed inflammatory cell infiltrates containing neutrophils and eosinophils, direct immunofluorescence microscopy studies demonstrated IgG and C3 deposited at the dermoepidermal junctions of perilesional skin, and indirect immunofluorescence studies demonstrated circulating antibasement membrane IgG that bound the dermal side of salt-split skin. Extensive immunoblot and immunoprecipitation studies failed to reveal a consistent, identifiable autoantigen. We describe only two cases. The autoantigen recognized by circulating autoantibodies was not identified. Orf-induced immunobullous disease is a unique disease entity that is clinically and immunologically distinct from bullous pemphigoid, epidermolysis bullosa acquisita, and other known immunobullous conditions.

A case of crusted scabies with a bullous pemphigoid‐like eruption and nail involvement

We report a case of a 71-year-old man infected at a nursing home who developed a bullous pemphigoid-like eruption with nail involvement. He was diagnosed by his family doctor as suffering from eczema and was treated with topical corticosteroids, then blisters started appearing. He was next diagnosed as suffering from bullous pemphigoid and treated with oral prednisolone, which worsened his condition. He was finally diagnosed as having crusted scabies with bullous pemphigoid-like eruptions and nail involvement at our clinic. He was then prescribed oral ivermectin (two doses of 12 mg ivermectin with a 1-week interval) and topical lindane (1%gamma-BHC in petrolatum) for scabies with 5% salicylic acid in plastibase as an additional treatment for the crusted lesions on his soles. He showed remarkable improvement in 2 weeks, and his nails showed complete recovery after 7 weeks of occlusive dressing treatment with 1%gamma-BHC. One and a half years later, the patient showed no sign of a recurrence of scabies. The histology of a blister taken from this patient was similar to that of bullous pemphigoid. Direct immunofluorescence showed immunoglobulin (Ig)G and C3 deposition at the dermoepidermal junction similar to that of bullous pemphigoid, but indirect immunofluorescence was negative. The bullous symptoms of this patient were considered to be due to the scabies, because the patient recovered completely after receiving treatment for scabies. Indirect immunofluorescent study is important to distinguish between scabies with blister formation and true bullous pemphigoid.

A bullous pemphigoid-like skin eruption after a chemical burn

Bullous pemphigoid is a blistering disorder characterized by antibody deposition in the lamina lucida of the basement membrane zone. In addition to the idiopathic form, there are many agents that have been implicated in inducing bullous pemphigoid or bullous pemphigoid-like lesions. We describe a patient who developed a bullous pemphigoid-like eruption after a chemical burn. (J Am Acad Dermatol 1998;38:337-40.)

Association of scabies with a bullous pemphigoid-like eruption

We describe a patient with scabies who had an associated bullous pemphigoid-like eruption. Previous reports of this association have appeared in the literature. However, most case reports have described negative or nonspecific findings with direct immunofluorescence in contrast to the intense linear homogenous band of IgG and C3 found in our patient.

Paraneoplastic pemphigus appearing as bullous pemphigoid-like eruption after palliative radiation therapy

Paraneoplastic pemphigus is a recently described disease in which patients have polymorphous skin lesions suggestive of both erythema multiforme major and pemphigus vulgaris in association with internal neoplasms, especially non-Hodgkin's lymphoma. These patients have characteristic autoantibodies that bind specific epidermal proteins. A Nikolsky-negative bullous pemphigoid-like eruption developed within the radiation therapy field in a 72-year-old man receiving palliative treatment for recurrent large cell lymphoma. The eruption rapidly progressed to a Nikolsky-positive bullous process more typical of pemphigus vulgaris with extensive involvement of respiratory epithelia. Despite aggressive treatment with high-dose corticosteroids and antibiotics, the patient rapidly succumbed. Results of immunofluorescence studies and autopsy findings confirmed the diagnosis of paraneoplastic pemphigus.

Angiotensin-converting enzyme inhibitors as possible exacerbating drugs in psoriasis

Angiotensin-converting enzyme (ACE) inhibitors are approved for the treatment of hypertension. ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasopressor, by competing with kininase II, the converting enzyme, for binding sites in the lung. As a result of this competitive inhibition, increased levels of biologically active kininase II are present. This is significant because kininase II prevents the catabolism of bradykinin, an enzyme that promotes vasodilatation. Bradykinin is part of the complex kinin system responsible for the delayed phase of acute inflammatory responses. [-4 Thus ACE inhibitors may have an indirect proinflammatory effect that may flare preexisting psoriasis. Several cutaneous adverse effects have been reported with the use ofACE inhibitors. These include a maculopapular eruption with eosinophilia, which is usually mild, transient, and responds to a reduction in dose or treatment with antihistamines, a bullous pemphigoid-like eruption, and rosacea. Angioedema of the extremities, face, lips, tongue, and larynx has also been described.i There are several isolated reports of a pityriasis rosea-like eruption.' and exfoliative dermatitis. ACE inhibitors have not been reported to exacerbate psoriasis. The following case reports suggest that psoriatic flares may be induced by ACE inhibitor use.

Scabies presenting as bullous pemphigoid-like eruption

Several diseases, at times, may be confused with scabies. We report the diagnosis and treatment of scabies in two patients. Their eruptions recurred and persisted and eventually developed blisters. The skin biopsy specimens submitted for light microscopy and immunofluorescence were considered to be consistent with bullous pemphigoid. Both patients were treated successfully with lindane and remained disease free for up to 6 months of follow-up.

Bullous pemphigoid-like eruption induced by amoxycillin

Bullous pemphigoid-like eruption induced by amoxycillin

Penicillamine-induced bullous pemphigoid-like eruption

Penicillamine-induced bullous pemphigoid-like eruption