A pemphigus foliaceus-like eruption associated with the use of ampicillin in a cat.
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Ampicillin↗
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Acantholysis and spongiosis are associated with loss of syndecan-1 expression.
BACKGROUND: Syndecan-1, a heparan sulfate proteoglycan present on the membrane of keratinocytes, functions in intercellular adhesion. Acantholysis and spongiosis are both characterized by diminished intercellular adhesion that may lead to blister formation. In spongiotic conditions, desmosomal stretching occurs prior to cell separation while in acantholytic conditions, cell separation occurs without stretching. While many of the structural relationships have been described, the molecular interactions regulating keratinocyte to keratinocyte adhesion are not yet fully understood. METHODS: Sections from ten cases of Grover's disease, two pemphigus vulgaris, one pemphigus foliaceus, one bullous pemphigoid, two herpes simplex, and ten spongiotic dermatitis were stained with BB-4, a monoclonal anti-syndecan-1 antibody. RESULTS: Nine of ten Grover's, all three pemphigus, and both herpes cases showed absent or markedly decreased syndecan-1 expression by acantholytic keratinocytes, with a sharp delineation from adjacent unaffected skin. The remaining Grover's case showed moderate loss of syndecan-1 expression. The pemphigus foliaceus case showed retention of staining along the basal cell layer, but expression was lost in the mid stratum spinosum. All ten spongiotic cases showed a diffuse mild decrease in staining, with loss of syndecan-1 expression surrounding microvesicles. Bullous pemphigoid, as expected, did not show loss of syndecan expression. CONCLUSIONS: The loss of syndecan-1 expression evident in acantholytic conditions and, to a lesser extent in spongiotic conditions, may contribute to the decreased intercellular adhesion characteristic of these lesions.
Acantholysis↗
Ultraviolet-induced acantholysis in pemphigus.
Ultraviolet irradiation produced an acantholytic phenomenon in normal skin of seven patients with pemphigus foliaceus. In six of the seven patients, this reaction was manifested by a positive Nikolsky sign and was confirmed by biopsy in four. Friction alone, infrared irradiation, occlusive dressing, and a rubefacient failed to produce a similar reaction. The thermal burn in the skin of patients having pemphigus was of subepidermal type. Ultraviolet-induced acantholysis was inhibited by chloroquine phosphate, taken orally, in the two patients tested. Prednisone had no such effect. It is concluded that ultraviolet light is a major aggravating stimulus for pemphigus foliaceus.
Acantholysis↗
[Analysis of HLA-DR in Mexican patients with pemphigus].
UNLABELLED: Pemphigus are a group of bullous skin disorders histologically characterized by intraepidermal acantholytic and circulating antibodies blisters due to directed against the cellular surface of keratinocytes. In Mexican patients with pemphigus, HLA antigens have not been studied as they have been for other populations; for this reason, a comparative, prospective, transversal and observational study has been done with 25 patients, 18 with pemphigus vulgaris and the other seven with pemphigus foliaceus. DNA was extracted by the salting-out method and HLA-DR was determined by amplification with PCR and allele-specific oligonucleotides (ASO). RESULTS: HLA-DR14 (DR6) is more common in patients with pemphigus vulgaris than in the healthy population, which corroborates with previous reports. On the other hand, as reported we also found that HLA-DR1 in Mexican population represents a higher risk for pemphigus foliaceus.
Adult↗
Studies on etiologic factors in pemphigus.
A survey of 234 cases of pemphigus yielded three observations which suggest that different forms of pemphigus may have different etiologies. 1. While the incidence of pemphigus in the age group of 21 and over was essentially the same in males and females (108 and 113) the incidence was significantly higher in females in the age group under 20. Only two of 13 patients in this group were males. Also pemphigus foliaceus and erythematosus was reported in a significantly higher proportion of the cases in the age group of 2 1/2 to 20 thus suggesting that the juvenile form of the disease differs from the adult form. 2. In four of a group of 15 cases identified as pemphigus foliaceus the disease appeared to be provoked by minor physical insults, a frequency which is significantly higher than the five cases with similar histories in the group of 198 cases identified as pemphigus vulgaris. 3. In the entire group of 234 cases two patients with pemphigus both proven by immunofluorescence had relatives with pemphigus. Also a third patient had a blood relative with bullous pemphigoid. This frequency of three per 234 is higher than would be expected by chance. Studies of one family (not included in this survey) with multiple skin antibodies suggest that such familial predispositions may be due to abnormal immune responses.
Adolescent↗
Pemphigus as a paradigm of autoimmunity and cell adhesion.
Pemphigus is a group of autoimmune blistering diseases of the skin and mucous membranes that are characterized histologically by intraepidermal blisters due to the loss of cell-cell adhesion of keratinocytes and immunopathologically by the finding of pathogenic IgG autoantibodies directed against the cell surface of keratinocytes. Identification of the target antigens has redefined pemphigus as an autoimmune disease against desmosomal cadherin or desmoglein. The IgG autoantibody-mediated functional inhibition of desmoglein which plays an important role in the cell-cell adhesion of keratinocytes results in blister formation. Patients with pemphigus vulgaris and pemphigus foliaceus have IgG autoantibodies against desmoglein3 and desmoglein1, respectively. Even complex clinical variations of pemphigus vulgaris and foliaceus are now logically explained by the desmoglein compensation theory. As an extension of this theory, the exfoliative toxin produced by Staphylococcus aureus, which causes staphylococcal scalded skin syndrome and bullous impetigo, was found to specifically cleave desmoglein1 and induce the identical histology to pemphigus foliaceus. Another recent innovation has been the development of an active disease mouse-model for pemphigus using autoantigen knockout mice, in which self-tolerance of the defective gene product is not acquired. When splenocytes from desmoglein3 knockout mice are adoptively transferred into mice expressing desmoglein3, anti-desmoglein3 IgG is stably produced in the recipient mice that develop the phenotype of pemphigus vulgaris. This model will be valuable not only for dissecting the cellular and molecular mechanisms in pathogenic antibody production but also for developing novel therapeutic strategies.
Animals↗
Diabetes mellitus induced in a dog after administration of corticosteroids and methylprednisolone pulse therapy.
An 8-year-old ovariohysterectomized Chow Chow was referred because of dermatologic lesions diagnosed as pemphigus foliaceus. Intolerance to orally administered corticosteroids necessitated the use of methylprednisolone pulse therapy. One week after treatment, diabetes mellitus was diagnosed on the basis of blood and urine test results. For 3 years after treatment, the dog has remained a well-regulated diabetic. Complete remission of pemphigus foliaceus is maintained by alternate-day, orally administered prednisone (0.5 mg/kg of body weight).
Administration, Oral↗
Bullous lesions in scleroderma.
BACKGROUND: The occurrence of bullous lesions in localized or systemic scleroderma is rare. Three histologic patterns have been reported: lichen sclerosus et atrophicus-like, lymphangiectatic blisters and autoimmune blistering diseases. OBJECTIVE: To investigate the frequency, clinical, and immunopathologic features of patients with scleroderma and bullous eruptions and to review the literature regarding this rare condition. METHODS: A retrospective study of 53 cases of scleroderma (localized, generalized, and systemic) in the dermatology and rheumatology clinics at one institution over an 8-year span. Clinical, serologic, and immunopathologic findings were analyzed in four cases. RESULTS: Four of 53 patients exhibited bullous lesions in association with scleroderma. The first case illustrates lymphangioma-like clinical and pathologic presentation. The second case demonstrates bullous lichen sclerosus et atrophicus-like pattern. The other two cases exemplify a superimposed autoimmune skin disease, epidermolysis bullosa acquisita and penicillamine induced pemphigus foliaceus after treatment for systemic scleroderma. CONCLUSIONS: Of the 53 original patients, we have described four cases of bullous scleroderma (7.5%) Illustrating several pathogenetic mechanisms of bulla formation. inflammatory (lichen sclerosus et atrophicus), fibrotic/obstructive (lymphangiomatous), autoimmune (epidermolysis bullosa acquisita), and pemphigus foliaceus. The final case illustrates bullae as a complication of therapy for the underlying scleroderma.
Adult↗
Pemphigus IgG, but not bullous pemphigoid IgG, causes a transient increase in intracellular calcium and inositol 1,4,5-triphosphate in DJM-1 cells, a squamous cell carcinoma line.
It is still unclear what kinds of mechanisms are involved in blister formation after antibodies bind to the antigens in pemphigus and bullous pemphigoid. The effects of IgGs from pemphigus vulgaris, pemphigus foliaceus, and bullous pemphigoid sera on intracellular calcium concentration ([Ca++]i) and inositol 1,4,5-trisphosphate were examined in a human squamous cell carcinoma cell line (DJM-1 cells) and in cultured human keratinocytes to clarify whether signal transduction via calcium is involved. IgGs were purified with protein A affinity column from the sera of five pemphigus vulgaris patients, three pemphigus foliaceus patients, eight bullous pemphigoid patients, and 14 normal volunteers. Keratinocytes were cultured in Eagle's minimum essential medium containing 1.8 mM Ca++ and loaded with fura-2/AM, followed by addition of the IgGs. Subsequently, [Ca++]i was determined by measuring the fluorescence ratio (F340/F360) with videomicroscopy. Pemphigus IgGs (seven of eight cases) induced a rapid and transient increase in [Ca++]i in both the cells, whereas a [Ca++]i increase was caused by very few IgGs from bullous pemphigoid (one of eight cases) and normal sera (two of 14 cases). The pemphigus IgG-induced transient [Ca++]i increase was not affected by chelating extracellular Ca++ with ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetracetic acid. In addition, monoclonal antibodies acid. In addition, monoclonal antibodies against 180-kD and 230-kD antigens did not exert this change. Pemphigus IgGs that caused a [Ca++]i increase induced rapid and transient production of inositol 1,4,5-trisphosphate, peaking at 20 seconds. These findings suggest that IgG from pemphigus induces Ca++ mobilization by inositol 1,4,5-trisphosphate from internal stores, and that mechanisms of antibody-transmitted signaling in pemphigus may differ from those in bullous pemphigoid.
Adult↗
Antibody deposits in Tzanck smears in pemphigus vulgaris.
Forty-three patients, including 24 males and 19 females between 5 and 62 years of age, having pemphigus vulgaris (27), pemphigus foliaceus (1), bullous pemphigoid (3), chronic benign bullous dermatosis of childhood (2) and herpes zoster (10) were included in this study. Tzanck smears were prepared from the floor of the blisters in these patients by deroofing the bullae, and the slides were stored without fixation at room temperature for 1 to 10 days. Immunofluorescence staining was done with FITC-conjugated anti-human IgG. Twenty-one cases having pemphigus vulgaris and 1 case having pemphigus foliaceus showed bright green fluorescence on the membrane of acantholytic cells. No epithelial cells were seen in smears from bullous pemphigoid and chronic benign bullous dermatosis of childhood, whereas epithelial cells were seen in 10 cases of herpes zoster. These stained negative with anti-IgG. Storage of the prepared smears for 1-10 days did not seem to affect the results of immunofluorescence. Tzanck smears can be used as an easy substitute for skin/mucosal biopsy for the direct immunofluorescence test.
Adolescent↗
Tissue immunoglobulin G subclasses observed in immune-mediated dermatopathy, deep pyoderma and hypersensitivity dermatitis in dogs.
A panel of monoclonal antibodies has been used to define three of the four subclasses of canine immunoglobulin G (IgG2, IgG3 and IgG4) in formalin-fixed tissues. These reagents, together with a polyclonal antiserum specific for the Fc region of canine IgG, were used in an immunohistochemical study of biopsies of skin from five normal dogs and from the lesions of canine pemphigus foliaceus in seven dogs, discoid lupus erythematosus in eight dogs, bullous pemphigoid in one dog, cutaneous drug eruption in two dogs, deep pyoderma in 13 dogs and hypersensitivity dermatitis in eight dogs. IgG autoantibody was identified in the skin of all the dogs with immune-mediated dermatoses by using the polyclonal reagent, and antibody of the IgG2 and/or IgG4 subclass was identified in the epidermis of three of the dogs with pemphigus foliaceus, two of those with discoid lupus erythematosus and in the dog with bullous pemphigoid. In all the lesions, the infiltrate of dermal plasma cells consisted of similar numbers of IgG2 and IgG4 bearing cells, with relatively few IgG3 positive cells. The total number of these cells was generally approximately the same as or greater than the number of cells labelled with the polyclonal reagent. There was no significant difference between the IgG-bearing plasma cell infiltrate in German shepherd dogs with deep pyoderma and that in dogs of other breeds. The infiltration of IgG2 and IgG4 bearing plasma cells into the skin of dogs with a range of cutaneous disorders was related to the selectively enhanced serum levels of these subclasses in the diseased dogs.
Animals↗
Immunohistochemical analysis of the distribution of desmoglein 1 and 2 in the skin of dogs and cats.
OBJECTIVE: To compare the distribution of desmoglein (Dsg) 1 and 2 in skin specimens obtained from dogs and cats to provide information about the possible role of the density of Dsg 1 and 2 in the localization of lesions attributable to pemphigus foliaceus in these 2 species. SAMPLE POPULATION: Skin biopsy specimens obtained from 4 dogs and 4 cats. PROCEDURE: Biopsy specimens were collected from the muzzle, bridge of the nose, ear, dorsum, abdomen, area adjacent to the teats, and footpads of each animal. Immunohistochemical analysis was performed on formalin-fixed, paraffin-embedded skin samples by use of a biotinylated mouse monoclonal anti-Dsg 1 and 2 antibody raised against bovine muzzle. Color development was performed by use of the streptavidin-biotin-peroxidase method with a chromogenic substrate. RESULTS: Immunohistochemical staining yielded a positive reaction in skin samples obtained from all anatomic sites. The intensity and distribution of staining were related to the number of layers of the stratum spinosum. No differences were detected between samples obtained from dogs and cats. CONCLUSIONS AND CLINICAL RELEVANCE: No differences in intensity of Dsg 1 and 2 antigen were observed in the stratum spinosum between skin samples obtained from dogs and cats. Analysis of this result suggests that factors other than the distribution of Dsg may be responsible for the differences in localization of primary clinical lesions in dogs and cats with pemphigus foliaceus.
Amino Acid Sequence↗
Immunoglobulin E-bearing cells and mast cells in skin biopsies of horses with urticaria.
The pathogenesis of equine urticaria is not well understood. In man, urticaria has been associated with immunological and nonimmunological mechanisms leading to the release of various mediators by mast cells. Skin biopsies of 32 horses with a history of urticaria were stained with toluidine blue, a double-labelling method for chymase and tryptase, and immunohistochemistry for immunoglobulin (Ig)E. These horses were compared with horses with pemphigus foliaceus, insect bite hypersensitivity and control horses with healthy skin. Neither formalin fixation time nor biopsy site influenced the staining methods. No chymase-positive cells were found. In all groups of horses, cells staining with toluidine blue and for tryptase and IgE were found in the epidermis and hair follicle papilla and significantly more positively staining cells were observed in the subepidermal dermis compared with the deep dermis. Horses with urticaria had significantly more IgE-bearing cells in the subepidermal dermis than control horses. However, horses with urticaria had significantly fewer toluidine-blue-stained mast cells in both subepidermal and deep dermis compared with the insect bite hypersensitivity and pemphigus foliaceus groups. This study suggests that IgE-mediated reactions play a role in the pathogenesis of urticaria.
Animals↗
[Pemphigus].
Pemphigus is an infrequent, organ-specific, autoimmune bullous disease, which affects the skin, mucous membranes and appendages. Histopathologically, it is characterized by acantholysis. Pemphigus has classically been divided into two major groups, pemphigus vulgaris and pemphigus foliaceus, with their respective clinical variants pemphigus vegetans and pemphigus erythematosus. In recent years, new variants of pemphigus have been described: paraneoplastic pemphigus, IgA pemphigus and pemphigus herpetiformis. This article reviews the epidemiology, etiopathogenesis, clinical symptoms, diagnosis, treatment and prognosis of pemphigus. Advances in molecular biology techniques have made it possible to more precisely identify the different antigens against which antibodies are directed, and to fine-tune ELISA diagnostic techniques. Treating pemphigus vulgaris and foliaceus with general steroids has modified their prognosis; it is estimated that mortality in recent decades is less than 10 %. Managing the clinical complications that appear during the evolution of the pemphigus has contributed to reducing morbidity and mortality.
Humans↗
Usefulness of enzyme-linked immunosorbent assay using recombinant desmogleins 1 and 3 for serodiagnosis of pemphigus.
Pemphigus is an autoimmune blistering disease with two major subtypes, pemphigus vulgaris (PV) and pemphigus foliaceus (PF). Patients with pemphigus have circulating antidesmoglein (Dsg)1 and/or anti-Dsg3 IgG autoantibodies. We have previously developed enzyme-linked immunosorbent assays (ELISAs) using recombinant Dsg1 and Dsg3 expressed by baculovirus as a diagnostic tool for pemphigus. The purpose of this study was to evaluate the practical application of these ELISAs for clinical use with a large number of serum samples. We used 81 PV sera, 48 PF sera, 114 bullous pemphigoid (BP) sera, 124 collagen disease sera, nine sera of other non-pemphigus bullous diseases and 179 normal control sera. A cut-off value was determined by receiver-operating-characteristic plots. Forty-seven of 48 PF sera (97.9%) were positive in the Dsg1 ELISA and 79 of 81 PV sera (97.5%) were positive in the Dsg3 ELISA, while only two (1. 1%) and four (2.2%) of 179 normal sera were positive in Dsg1 and Dsg3 ELISAs, respectively. However, some disease control sera of BP and collagen diseases exceeded the cut-off value. Introduction of a grey zone helped to decrease the number of these false-positive sera. Furthermore, in three patients studied, the respective Dsg1 and Dsg3 ELISA scores showed parallel fluctuation with the disease activity along the time course. We conclude that Dsg1 and Dsg3 ELISAs provide a simple, sensitive and highly specific assay for the diagnosis of patients with PV and PF and that these ELISAs may be a valuable tool to monitor the disease activity. We also propose diagnostic criteria for pemphigus based on ELISA reactivity: if a serum is positive against Dsg3 it indicates a diagnosis of PV, regardless of reactivity against Dsg1; if a serum is negative for Dsg3 and positive for Dsg1, it indicates a diagnosis of PF.
Aged↗
Pemphigus vulgaris exacerbated by exposure to sunlight.
We report two cases of pemphigus vulgaris who showed exacerbation of their bullous skin lesions after exposure to sunlight. These cases indicate that ultraviolet light is an aggravating factor, not only for pemphigus foliaceus, but also for pemphigus vulgaris.
Adult↗
Further experience with pemphigus in children.
Seven children had pemphigus: six had pemphigus vulgaris and one pemphigus foliaceus. Four who had pemphigus vulgaris were administered dexamethasone pulses. Follow-up from six months to one year was uneventful; the disease was under control and there were no complications due to therapy. Our observations suggest that the clinical features, course, and principles of therapy for pemphigus in children are essentially the same as those in adults.
Adolescent↗
Fixation of pemphigus vulgaris and foliaceus antibodies in shedding snake epidermis.
The fixation of pemphigus antibodies was revealed by indirect immunofluorescence in shedding grass snake epidermis. The antibodies of patients with pemphigus vulgaris (PV) were specifically binding to the antigenic substance which appears in the snake epidermis at the initial stage of integument change. At the peak of shedding, the fixation of PV antibodies was observed only in the upper layers of the 'old' epidermis, although the intensity of fluorescent staining was considerably reduced. At the same stage of shedding, there was marked fixation of antibodies of patients suffering from pemphigus foliaceus (PF). The specific binding of PF antibodies was noted predominantly on the cell membranes of the 'old' keratinocytes, localized in the upper layers of the epidermis. In contrast to bullous pemphigoid antibodies, PV and PF antibodies failed to fix in the skin of the snake prior to or after physiologic shedding. The data obtained suggest that pemphigus may have an atavistic origin.
Adult↗