scholarly journals A Case of Bullous Rash Apparently Triggered by Meningococcal and Rotavirus Vaccines in an Infant: Focus on Infantile Bullous Pemphigoid

2021 ◽  
Vol 8 (1) ◽  
pp. 33-36
Author(s):  
Iria Neri ◽  
Valeria Evangelista ◽  
Alba Guglielmo ◽  
Andrea Sechi ◽  
Annalucia Virdi

Bullous pemphigoid (BP) is an autoimmune bullous disease and is a rare condition in childhood. Acquired tense acral bullae and fixed urticarial annular lesions on the trunk are diagnostic clues of infantile BP. Diagnosis is supported by immunosorbent assay (IgG anti-BP180 and BP230) and direct immunofluorescence (linear deposition of IgG at the dermo-epidermal junction). Topical and/or systemic corticosteroids are the first-line treatment. The prognosis is good with a self-limited clinical course. Differential diagnoses include impetigo and other bullous diseases in children, such as dermatitis herpetiformis, linear IgA bullous dermatosis and erythema multiforme. The etiopathogenesis is still unknown, and the role of antigen stimuli such as infections, drugs and vaccination is still debated.

2020 ◽  
Author(s):  
Aakaash Varma ◽  
Annette Czernik ◽  
Jacob Levitt

Less common immunobullous diseases include cicatricial pemphigoid, epidermolysis bullosa acquisita, and linear IgA bullous dermatosis. Diagnosis of these entities are made through direct immunofluorescence, sometimes requires salt-split skin, as well as, in the case of cicatricial pemphigoid, mucosal scarring. As in pemphigus vulgaris and bullous pemphigoid, common therapies include rituximab, prednisone, and IVIg. Dapsone can be particularly effective in linear IgA bullous dermatosis and bullous lupus. Dermatitis herpetiformis is a rare cutaneous manifestation of gluten sensitivity, characterized by pruritic vesicles on extensor surfaces, that responds to dapsone and gluten avoidance. This diagnosis is confirmed with biopsy and positive serology for anti-tissue transglutaminase IgA. Blistering hypersensitivity reactions include TEN, SJS, erythema multiforme, and fixed drug eruption. All are characterized by varying degrees of keratinocyte necrosis. Common to the management of all include cessation of the offending agent. TEN can be managed by cyclosporine, TNF-inhibition, or—more controversially—IVIg. SJS can be effectively managed with systemic steroids. EM responds variably to a number of agents, including antiviral nucleoside analogues, prednisone, thalidomide, apremilast, and tofacitinib. Infectious causes of blisters include Staphylococcus aureus, HSV, and varicella zoster virus. Epidermolysis bullosa comprises a variety of genetically defective structural proteins of the skin. Recessive variants and those affecting deeper proteins carry more severe phenotypes. Management is best achieved at specialty centers and involves careful wound care as well as prevention of friction. Gene therapy is on the horizon for these disorders. Other blistering entities, mechanical or inflammatory in nature, are also discussed at the end of this chapter. This review contains 13 figures, 1 table, and 86 references. Keywords: Blisters, bullae, bullous, pemphigoid, necrolysis


2010 ◽  
Vol 2 (4) ◽  
pp. 137-142
Author(s):  
Đorđi Gocev ◽  
Katerina Damevska ◽  
Suzana Nikolovska ◽  
Ljubica Pavlova ◽  
Nada Petrova

Abstract Linear IgA bullous dermatosis is a chronic, acquired, autoimmune subepidermal vesiculobullous disease. Both children and adults are affected. It is characterized by direct immunofluorescence findings of linear immunoglobulins class A (IgA) deposits along the dermal-epidermal junction (basement membrane zone). In children, the disease is commonly referred to as chronic bullous disease of childhood and it mostly affects children between 2 and 5 years. The onset of the disease is acute; the first episode is the most severe, while recurrences tend to wax and wane in severity and last till puberty or even longer. Diaminodiphenylsulfone is the treatment of choice, although systemic corticosteroids are reported to be very effective as well. We report a 3-year-old boy with a vesiculobullous eruption which developed one week following administration of cephalexin for upper respiratory infection. He was referred to our Clinic from other health institutions as treatment failure for suspected strophulus or impetigo bullosus. On admission, the patient had fever and numerous vesiculobullous and erosive lesions distributed on the face and trunk. After immunohistological verification, the treatment with prednisone 25 mg/d was introduced, due to rapid progression of the disease and the fact that diaminodiphenylsulfone was not available. Improvement occurred after 2 weeks, so the dose was carefully tapered, taking into account the possibility of adrenal suppression. The medication was completely excluded within the next three months. No serious side effects were observed, except transitory hirsutism. The patient has had no relapses over the last 20 months of clinical follow-up.


2020 ◽  
Author(s):  
Annette Czernik ◽  
Aakaash Varma ◽  
Jacob Levitt

Less common immunobullous diseases include cicatricial pemphigoid, epidermolysis bullosa acquisita, and linear IgA bullous dermatosis. Diagnosis of these entities are made through direct immunofluorescence, sometimes requires salt-split skin, as well as, in the case of cicatricial pemphigoid, mucosal scarring. As in pemphigus vulgaris and bullous pemphigoid, common therapies include rituximab, prednisone, and IVIg. Dapsone can be particularly effective in linear IgA bullous dermatosis and bullous lupus. Dermatitis herpetiformis is a rare cutaneous manifestation of gluten sensitivity, characterized by pruritic vesicles on extensor surfaces, that responds to dapsone and gluten avoidance. This diagnosis is confirmed with biopsy and positive serology for anti-tissue transglutaminase IgA. Blistering hypersensitivity reactions include TEN, SJS, erythema multiforme, and fixed drug eruption. All are characterized by varying degrees of keratinocyte necrosis. Common to the management of all include cessation of the offending agent. TEN can be managed by cyclosporine, TNF-inhibition, or—more controversially—IVIg. SJS can be effectively managed with systemic steroids. EM responds variably to a number of agents, including antiviral nucleoside analogues, prednisone, thalidomide, apremilast, and tofacitinib. Infectious causes of blisters include Staphylococcus aureus, HSV, and varicella zoster virus. Epidermolysis bullosa comprises a variety of genetically defective structural proteins of the skin. Recessive variants and those affecting deeper proteins carry more severe phenotypes. Management is best achieved at specialty centers and involves careful wound care as well as prevention of friction. Gene therapy is on the horizon for these disorders. Other blistering entities, mechanical or inflammatory in nature, are also discussed at the end of this chapter. This review contains 13 figures, 1 table, and 86 references. Keywords: Blisters, bullae, bullous, pemphigoid, necrolysis


2019 ◽  
Vol 12 (7) ◽  
pp. e230037 ◽  
Author(s):  
Giulia Tadiotto Cicogna ◽  
Martina Ferranti ◽  
Daniele Vaccari ◽  
Mauro Alaibac

A 68-year-old woman was referred to the unit of dermatology for a large basal cell carcinoma on the chin. She was treated with imiquimod cream 5%, and 4 weeks after she developed isolated and grouped tense serum-filled vesicles and bullae on lips, nose, scalp, ankles and lumbar area, and then expanded to the whole body. Histological examination was consistent with a subepidermal bullous dermatosis. Moreover, direct immunofluorescence showed linear deposition of IgA at the basement membrane zone supporting the diagnosis of linear IgA bullous dermatosis (LABD). Dapsone 50 mg/day was administered, and the lesions gradually improved within some weeks, and no new lesions appeared. The temporal relationship between the application of the drug and the development of the disease indicates a role of this topical agent in triggering LABD.


2022 ◽  
Vol 36 ◽  
pp. 205873842110212
Author(s):  
Alberto Corrà ◽  
Veronica Bonciolini ◽  
Lavinia Quintarelli ◽  
Alice Verdelli ◽  
Marzia Caproni

Linear IgA bullous dermatosis (LABD) is a mucocutaneous autoimmune blistering disease affecting both adults and children. It is caused by IgA antibodies targeting multiple antigens along the basement membrane zone, leading to disruption of dermoepidermal junction and development of bullous lesions which often presents in characteristic arrangement. Although most LABD cases have been reported to be idiopathic, different triggers have been described, including several drugs and infection. However, the occurrence of vaccine-induced cases of LABD is not widely known and accepted due to the few reports available. We present two cases of LABD occurred following different triggers, rising the suspicion for a possible pathogenetic role of vaccines.


2013 ◽  
Vol 5 (1) ◽  
pp. 31-36
Author(s):  
Kristina Kostić ◽  
Lidija Kandolf Sekulović ◽  
Radoš D. Zečević

Abstract Bullous pemphigoid is an autoimmune blistering disease that predominantly affects elderly persons and rarely children. We present a 12-year-old girl with sudden appearance of tense blisters on an erythematous base on the trunk, neck, hands and legs with intense pruritus. Standard laboratory test results were within the normal range except for blood eosinophilia of 12% of the total white cell count. Skin biopsy specimens showed evolving subepidermal blisters with perivascular lymphohistiocytic, eosinophil and neutrophil infiltrations in the papillary dermis. Direct immunofluorescence of perilesional skin showed linear, continuous deposits of IgG and C3 along the dermoepidermal junction. Indirect immunofluorescence showed circulating anti-basement membrane zone IgG autoantibodies at a titer of 1:80. We started treatment with systemic corticosteroids, methylprednisolone 0,5 mg/kg per day and 500 mg erythromycin 4 times a day during 10 days. After 3 days 50 mg dapsone (DDS, 4,4-diaminodiphenylsulphone) per day was added. After a few days, there were no new changes on the skin and pruritus disappeared completely.


2019 ◽  
Vol 2 (2) ◽  
Author(s):  
Florica Sandru ◽  
Mihai Dumitrascu ◽  
Daniel-Vasile Balaban ◽  
Razvan-Cosmin Petca ◽  
Adelina Popa ◽  
...  

Linear IgA bullous dermatosis (LABD) is a rare, immune-mediated cutaneous pathology, characterized by IgA deposits along the basal membrane. Clinically, it manifests as an eruption, consisting of vesicles and bullae, with herpetiform distribution, on erythematous and/or normal skin. The lesions are located symmetrically, at the level of the trunk and extremities. Clinically, diagnosis can be difficult because it can be easily mistaken with dermatitis herpetiformis or bullous pemphigoid.     We present the case of a 79-years-old woman, without significant comorbidities, who developed a vasculo-bullous eruption, intensely itchy, located symmetrically on trunk and extremities, evolving for 4 years. We performed a skin biopsy, with histopathological examination and direct immunofluorescence, which revealed: sub epidermal vesicular-bullous lesion and dermal infiltrate with numerous neutrophils and eosinophils; IgA - continuous linear positivity at the dermal-epidermal junction. Thus, the diagnosis of LABD was established. The treatment consisted of systemic corticosteroids, colchicine, and antihistamines, with favorable evolution.    The management of these patients can be challenging, as LABD can be induced by certain drugs, and may also be associated with lymphoid malignancies.


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