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Various infections and autoimmune and reactive skin conditions can present with blisters of varying sizes. Some of these disorders are seen in everyday practice, whereas others are rarely encountered. In many cases, the clinical picture is so typical that the diagnosis is easy and obvious; nevertheless, the significant clinical overlap between many of these diseases can cause frustration in both unexperienced and expert clinicians. We present the most typical clinical clues and offer simplified algorithms to the clinical diagnosis of skin conditions with vesicles and bullae. We focus on several aspects, when assessing a patient with blisters on the skin: age of onset, a history of comorbidities and medications intake, the general condition of the patient, and most importantly, the distribution, number, size, morphology, and evolution of the blisters, the characteristics of the peribullous skin, and the presence of mucosal involvement. Emphasis is put on differentiating between potentially life-threatening blistering eruptions and more benign self-limiting conditions. © 2020 Elsevier Inc. All rights reserved.

Linear IgA bullous dermatosis (LABD) is a subepidermal, vesiculobullous eruption that can be drug induced, often by vancomycin.1 We describe a rare case of an 80-year-old woman with vancomycin-induced LABD whose disease continued to progress despite drug cessation, likely attributable to continued drug elution from vancomycin-loaded bone cement from a recent shoulder arthroplasty revision.

Brunsting-Perry pemphigoid is defined as an autoimmune vesiculobullous eruption typically localized on the head and neck region with minimal or no mucosal involvement. The disease tends to run a chronic and recurrent course with residual scarring. Histological features are characterized by subepidermal bullae and linear IgG deposits at the dermo-epidermal junction. We report a case of a 46-year-old lady who presented with typical features of Brunsting-Perry pemphigoid. Autoantibodies to type VII collagen were identified by using recessive dystrophic epidermolysis bullosa skin which lacks type VII collagen in an indirect immunofluorescence assay. As a result, we diagnosed our patient as having the Brunsting-Perry pemphigoid variant of epidermolysis bullosa acquisita (EBA). This finding led us to review the literature on target antigens in Brunsting-Perry pemphigoid. Only 11 out of the 58 cases reported to date had target antigens identified. Interestingly, type VII collagen was the second most common target antigen/autoantibody (4 cases) detected after BP180 (5 cases). However, 2 further cases of EBA localized to the face with typical features of Brunsting-Perry pemphigoid were found in the literature. Although the target antigens are heterogeneous in Brunsting-Perry pemphigoid, a significant number of cases represent a clinical presentation of localized EBA.

Drug induced linear IgA bullous dermatosis (LABD) is a rare blistering disease that has been shown to be associated with the use of various medications. Although rarely seen together, some of the medications associated with LABD can lead to the syndrome drug reaction with eosinophilia and systemic symptoms (DRESS), which presents with fever, cutaneous eruption, and multi-organ involvement. We present a patient who developed fever and a generalized vesiculobullous eruption after recently starting amlodipine and meloxicam. Initial laboratory tests demonstrated elevated liver function tests, leukocystosis, and eosinophilia. Histopathologic examination of the punch biopsy revealed a bulla with sub-epidermal split and numerous neutrophils. Direct immunofluorescence demonstrated broad deposition of IgA along the dermal-epidermal junction. These findings were consistent with an overlap between LABD and DRESS. Drug induced LABD and DRESS are independently both rare diseases. It is even more uncommon to see the two concurrently in the same patient. In this patient, these two conditions were thought to be triggered by either amlodipine or meloxicam. Given the high mortality rate associated with DRESS, it is important to recognize the presentation and initiate the appropriate treatment plan as soon as possible.

Bullous systemic lupus erythematosus (BSLE) is a rare subepidermal blistering disorder characterized by an acute vesiculobullous eruption in a subset of individuals with systemic lupus erythematosus. BSLE most commonly affects young women and only rarely affects children. Herein we report a rare case of BSLE in a 6-year-old boy.

Linear IgA dermatosis (LAD) is a rare, subepidermal blistering disease with mucocutaneous involvement. It may be idiopathic or drug induced. We describe a 4-year-old girl who presented with a vesiculobullous eruption after she had been treated with cefixime for urinary tract infection. A diagnosis of drug-induced LAD was made based on clinical, histopathological, and immunofluorescence findings. Naranjo adverse drug reaction algorithm was used to assess imputability resulting with a "probable" association. In literature, cephalosporin antibiotics are rarely reported in association with LAD. To our knowledge, this is the first case of a cefixime-induced LAD among adults and children.

Paederus dermatitis is a peculiar irritant dermatitis characterised by appearance of vesicles, bulla and pustules on erythematous base. The disease is provoked by an insect belonging to the genus Paederus. The beetle does not bite or sting, but brushing or crushing the beetle over the skin provokes the release of hemolymph which contains paederin, a potent vesicant agent. We report a case of extensive involvement of the skin by Paederus that mimicked varicella minor.

Mycosis fungoides (MF) represents the most common type of cutaneous T-cell lymphoma (CTCL). CTCL often progresses through patch, plaque and tumor stages but can also manifest with varied clinical presentations. MF rarely presents in vesiculobullous fashion, in which vesicles or bullae develop in pre-existing plaques or on the trunk or proximal extremities. We report a patient who presented with a vesiculobullous eruption on the palms and soles, resembling dyshidrotic dermatitis, which we believe represents dyshidrotic MF. Diehl J, Sarantopoulos GP, Chiu MW. Dyshidrotic mycosis fungoides.

A previously healthy 20-year-old man presents with a mildly pruritic, progressive rash. The eruption began in his scalp and subsequently spread over 9 days’ time to his neck, back, and chest. He had been seen in the emergency department andprescribedoral cephalexin for theeruption, with no improvement. He denies any other use of medication (including prescription or over-the-counter medications, herbal supplements, andvitamins) in thedays,weeks, or months prior to onset. He denies any travel or illicit drug use. The patient otherwise feels well, without fever, chills, or systemic symptoms.Hehas receivedappropriate immunizations,hasnorelevant family history, and has never experienced similar episodes. The physical examination is notable for numerous grouped vesicles and relatively monomorphic tensebullae, coalescing intomarkedly annular plaques, superimposedon erythematous baseswith central clearing and scale. Theeruption isgeneralizedandsymmetricbutpredominatesonhisposterior neck, back, chest andupper arms (Figure 1), and inner thighs.He is otherwise afebrile and appears well. Quiz at jama.com A B

Senel, Engin/0000-0001-8098-1686; WOS: 000286472500021 PubMed: 21455431 Clarithromycin is a macrolide antibiotic. In clinical trials, adverse drug reactions of clarithromycin are usually mild and transient. Only 1 of the adverse reactions are severe. Herein, we present a case with vesiculobullous skin reaction and vein thrombosis caused by administration of intravenous clarithromycin.

Linear IgA Bullous Dermatosis (LABD) is an immune-mediated subepidermal vesiculobullous eruption characterized by linear deposits of IgA at the basement membrane zone. Most cases are idiopathic but medications, infections, and malignancies have also been reported to induce LABD. We report the case of a 54-year-old woman who developed LABD shortly after receiving an influenza vaccination.

A 37-year-old woman presented with a pruritic, vesiculobullous eruption on her neck in the region of an ebony pendant. Acute allergic contact dermatitis was suspected and treated with oral prednisone and hydroxyzine ([Figure 1][1]A and Figure 1B). Two months later, we performed a patch test on her

Exaggerated reactions to insect bites are characteristic of patients with haemoproliferative disorders, particularly chronic lymphocytic leukaemia (CLL). Skin lesions usually appear after the diagnosis of leukaemia and seem unrelated to laboratory findings, disease course or therapy. Rarely, the eruption may precede the diagnosis of the haematologic malignancy. The patients usually do not recall of insect bites, and the diagnosis may require histological and laboratory investigations to exclude specific lesions or autoimmune bullous diseases. Lesions may run a chronic course and represent a therapeutic challenge. Here, we report an adult patient with CLL who developed itchy recurrent papulovesicular and bullous lesions. Differential diagnosis was made with cutaneous specific lesions of CLL, bullous pemphigoid and pemphigus vulgaris, but laboratory and histological investigations confirmed the diagnosis of an insect bite reaction. The patient was treated with oral H1 anti-histamines and topical corticosteroids under occlusion, with marked improvement after 10 days.

Herpes zoster is an acute vesiculobullous eruption estimated to affect 10% to 20% of the population. The diagnosis usually can be based on clinical features alone, but laboratory studies may be needed for definitive diagnosis, particularly in atypical presentations.

Auteur(s) : Giacomo CALDAROLA1 giacomocaldarola@libero.it, Luca FANIA1, Emanuele COZZANI2, Claudio FELICIANI1, Clara DE SIMONE1 1 Department of Dermatology, Catholic University of Sacred Heart, Largo Francesco Vito, 8 – 00168 Rome, Italy 2 Section of Dermatology, Di.S.E.M., University of Genoa, Genoa, Italy A 31-year-old Caucasian man was referred with a one-week-old extensive vesiculobullous eruption. Physical examination showed multiple tense blisters on the trunk and extremities, [...]

Blister beetle dermatosis is a distinctive vesiculobullous eruption that occurs after contact with three major groups of beetles (Order: Coleoptera). It is caused by a vesicant chemical contained in the body fluids of the beetles. The smallest and least known family is the Oedemer-idae. Although there are few references in the medical literature, blister beede dermatosis caused by oedemerids may be more common and widespread than currently recognized. The best known family is the Meloidae with numerous species worldwide causing blistering. The vesicant chemical in both Oedemeridae and Meloidae is cantharidin. The third group of blister beetles includes species of the genus Paederus (Family: Staphylinidae). The clinicopatho-logic picture differs because this genus contains a different vesicant agent, pederin. The clini-copathologic features of oedemerid blister beetle dermatosis are described. The world medical and relevant entomologie literature is reviewed.

Herpes gestationis (HG) is an uncommon autoimmune bullous disease that appears during pregnancy or in association with trophoblastic tumors. It is characterized by an intensely pruritic vesiculobullous eruption that develops during the later part of pregnancy or during the immediate postpartum period. Direct immunofluorescence reveals linear deposits of C3 along the basement membrane zone in all patients with active disease.1Although it is generally accepted that HG in the mother is not associated with an increased fetal risk, there is a tendency for premature and small-for-gestationalage babies to occur. Only a few studies have specifically addressed this issue. We have studied all patients diagnosed with HG at our Department of Dermatology since direct immunofluorescence became available; the issue of fetal complications was examined. Patients and Methods. All patients with HG seen at the Hospital Clinic, Barcelona, Spain, between February 1972 and November 1994 were included and retrospectively studied. The

Occurrence of bullous disease in patients with chronic lymphocytic leukemia (CLL) leads to a high suspicion of an autoimmune blistering disorder, especially bullous pemphigoid or paraneoplastic pemphigus. However, the possibility of a characteristic vesiculobullous eruption associated with CLL must be kept in mind. 1,2 We report two cases of this rare entity extensively studied by immunohistology. Report of Cases Case 1 . In 1978, a 70-year-old man was diagnosed with CLL and IgM monoclonal gammopathy. In 1982, he had a pruritic blistering eruption consisting of a few infiltrated erythematous plaques, with some of them covered with vesiculae. The coalescence of vesiculae resulted in large tense bullae, several centimeters in diameter ( Figure 1 ). Each plaque was fixed and healed in 3 to 5 days, sometimes leaving hyperpigmentation but no scar or milia. No bullae occurred on normal skin or on the mucosa. The course of the cutaneous disease was characterized by spontaneous

• Reports of pemphigus following ionizing radiation exposure are rare. We report two cases and review the literature regarding this association. Characteristics common to these cases include a prodromal persistent non-specific dermatitic eruption that is often interpreted as radiation dermatitis, and latency of variable duration before the onset of a vesiculobullous eruption that begins at the portal of irradiation. Direct immunofluorescence is positive for intercellular IgG, while indirect immunofluorescence is commonly positive only at low titers; HLA correlations have not been studied. Documentation of clinical course and laboratory confirmation of the diagnosis, including hematoxylin-eosin, direct and indirect immunofluorescence, and HLA determinations (if available), should be recorded to enable further clarification of this entity. ( Arch Dermatol . 1990;126:1319-1323)

Brunsting-Perry cicatricial pemphigoid is a chronic recurrent vesiculobullous eruption that occurs predominantly on the head and neck. Because of the clinical, histologic, and immunologic similarity to cicatricial pemphigoid, it has been suggested that Brunsting-Perry cicatricial pemphigoid represents the cutaneous counterpart of cicatricial pemphigoid and should be included as a member of the pemphigoid spectrum of diseases. The concurrence of Brunsting-Perry cicatricial pemphigoid and bullous pemphigoid, as seen in the patient in this report, supports this viewpoint.

We describe a new case of lipoid proteinosis (LP) in a child and discuss its different clinical presentations, especially in its early erosive stage, as well as its prognosis and therapy. A 3.5-year-old healthy girl presented with a chronic and recurrent vesiculobullous skin eruption since early childhood. She had developed hoarseness of the voice during the first few months of life. Cutaneous examination revealed the presence of multiple non-pruritic tense vesicles and erosions on a non-erythematous base on her face, hands and elbows with a waxy thickening of the skin on her face. Histologic examination confirmed the diagnosis of LP. The patient was then regularly followed in our department for therapy for her disease.

Cicatricial pemphigoid is a chronic, scarring, vesiculobullous eruption, with a theoretical autoimmune cause. It is closely related to bullous pemphigoid, yet unlike bullous pemphigoid, no circulating antibodies have been found. We present here a patient with cicatricial pemphigoid with circulating antibodies to the basement membrane zone of the skin, thus giving more evidence for it being an immunologic disease and for rationale for treatment.

• A unilateral vesiculobullous eruption associated with fever was seen on the neck, shoulder, and upper part of the chest of a 7-year-old boy. Although three dermatomes in all were involved, the lesions resembled herpes zoster. The patient had had varicella in infancy. Culture of fluid from several bullae yielded echovirus 6; however, and serum neutralizing antibody to this virus rose in titer from 1:32 to 1:640. It is suggested that echovirus 6 and other enteroviruses may cause a number of vesicular eruptions that resemble herpes zoster and similar infections. Viral culture, while often difficult to obtain, is the only way to identify the cause of eruptions like this one. ( Am J Dis Child 133:283-284, 1979)

SUMMARY A vesiculobullous eruption with clinical and histological features of bullous pemphigoid developed in a 38-year-old woman with proved systemic lupus erythematosus. The patient had a sulphone responsive blistering disease that was characterized by pruritic subepidermal bullae and linear, predominantly IgA basement membrane zone deposition and IgA pemphigoid antibodies in her sera. Because both diseases are associated with immune complexes of special immunoglobulin classes, this association may not be entirely fortuitous.

Four patients with systemic lupus erythematosus developed a nonpruritic vesiculobullous eruption that was unresponsive to high-dose systemic corticosteroid therapy. In three patients the eruption was not associated with a flare of systemic disease. Biopsy results showed neutrophilic microabscesses at the dermal papillary tips and perivascular lymphohistiocytic infiltrates. Direct immunofluorescence of normal appearing skin not exposed to the sun was positive in all four patients. Due to the unresponsiveness to corticosteroid therapy and the striking histologic resemblance to dermatitis herpetiformis, each of the patients was treated with dapsone. Within 24 hours each patient had prompt cessation of the appearance of new lesions. Improvement of the eruption did not correlate with improvement of the systemic manifestations of their lupus erythematosus. The rapid response to dapsone therapy suggests that dapsone is useful in treating bullous lesions of systemic lupus erythematosus.

REPORT OF A CASE A 60-year-old woman with a three-month history of a mildly pruritic vesiculobullous eruption involving the extensor surfaces of the extremities, abdomen, and sacral region was referred to the Department of Dermatology at University Hospitals, University of Iowa, Iowa City. A diagnosis of bullous pemphigoid had been made by the referring physician on the basis of the initial clinical presentation and histologic findings of a subepidermal split in a lesional skin biopsy specimen. Direct immunofluorescence of perilesional skin had been performed and showed weak, focal C3 and strong continuous fibrinogen at the basement membrane. Initially, the patient showed a good response to 50 mg of prednisone orally once daily. Azathioprine (Imuran) therapy in a dosage of 50 mg twice daily orally was started four weeks before we saw her; after azathioprine therapy was started, the dosage of prednisone was gradually decreased. She did well until the daily

• Six patients with a vesiculobullous eruption of the type described by Brunsting and Perry as benign pemphigoid were studied by direct and indirect immunofluorescence. All six showed linear deposits of IgG but not IgM or IgA at the epidermal-dermal junction. One case also showed C3 deposition and one patient had circulating antibasement membrane zone antibodies in a titer of 1280. These data provide strong evidence that this condition belongs to the cicatricial pemphigoid-bullous pemphigoid spectrum of disease. ( Arch Dermatol 113:1403-1405, 1977)

• A vesiculobullous eruption with clinical and histological features of bullous pemphigoid developed in a 28-year-old woman with proven systemic lupus erythematosus (SLE). Serum of this patient contained elevated titers of antinuclear antibodies but basement membrane antibodies could not be detected at first, though they did appear in blister fluid. Normal monkey skin explants cultured on this patient's sera gave positive direct immunofluorescence (IF) at the basement membrane zone (BMZ) for IgG deposits. The use of tissue culture methods may be helpful because of the capability of this test system to reveal the presence of the antibodies to the BMZ despite the presence of the antinuclear antibodies that appear to interfere with their demonstration in standard indirect IF tests. (Arch Dermatol114:1187-1190, 1978)