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Paraneoplastic pemphigus (PNP), a clinically and immunopathologically distinct mucocutaneous blistering dermatosis, is a severe form of autoimmune multiorgan syndrome generally associated with poor therapeutic outcome and high mortality. This IgG-mediated disease is initiated by an obvious or occult lymphoproliferative disorder in most cases. Clinically severe mucositis, and polymorphic blistering skin eruptions, and histologically acantholysis, keratinocyte necrosis and interface dermatitis are its hallmark features. A 58-year-old female presented with recurrent, severe, recalcitrant stomatitis and widespread erosions/blistering lesions of one-year duration. Treatment with repeated courses of systemic corticosteroids at a peripheral center would provide temporary relief. She also had fever, productive cough, odynophagia and poor oral intake, herpes zoster ophthalmicus, pain in the abdomen, and watery diarrhea. An array of investigations revealed chronic lymphocytic leukemia (CLL), mediastinal and para-aortic lymphadenopathy, bronchiolitis obliterans, and vertebral osteoporosis/fractures. With the diagnosis of CLL-associated PNP she was managed with dexamethasone-cyclophosphamide pulse (DCP) therapy for 3 cycles initially, followed by COP regimen (cyclophosphamide, vincristine, and prednisolone) for 5 cycles. Remission is being maintained with chlorambucil and prednisolone pulse therapy once in 3 weeks with complete resolution of skin lesions and adequate control of CLL.

Full article can be viewed here: http://www.hindawi.com/crim/dm/2012/207126/

Bullous pemphigoid is an autoimmune blistering skin disease characterized by the presence of circulating autoantibodies which recognize specific proteins of the epidermis and dermoepidermal junction. Diagnosis is based on clinical criteria and laboratory investigations, notably histology, direct and indirect immunofluorescence, and ELISA. This study describes a new immunofluorescence assay for parallel determination of anti-BP180 and anti-BP230 based on recombinant antigenic substrates. The aim of the study was to detect BP180 and BP230 autoantibodies by BIOCHIP technology using both a specially designed recombinant BP180-NC16A protein and cells expressing the BP230-gc antigen fragment. 18 patients with bullous pemphigoid were included in the study. Autoantibodies to BP180 were detected by the BIOCHIP technique in 83.33% of patients with clinical, serological, and immunohistological confirmed bullous pemphigoid while autoantibodies against BP230-gC were detected only in 39% of patients. The detection of anti-BP180-NC16A and anti-BP230-gC by a new biochip-based immunoassay is a suitable alternative to indirect immunofluorescence and ELISA. This method has the advantage of easily discriminating the different autoantibody specificities. The BIOCHIP method is faster, cheaper, and easy to use when compared with the ELISA approach. For this reason, the new method could be used as an initial screening test to identify patients with bullous pemphigoid, and doubtful results could then be confirmed by ELISA.

Full article (free) found here: http://www.hindawi.com/isrn/dermatology/2012/237802/

There are a limited number of reports indicating the role of human leukocyte antigen (HLA) class I alleles in pemphigus vulgaris. This study was designed to highlight the association of HLA class I alleles with pemphigus vulgaris in Iran. Fifty patients with pemphigus vulgaris, diagnosed based on clinical, histological and direct immunofluorescence findings were enrolled into this study. The control group consisted of 50 healthy, age- and sex-matched individuals. HLA typing of class I (A, B and C alleles) was carried out using polymerase chain reaction based on the sequence-specific primer method. This study showed the higher frequency of HLA-B*44:02 (= 0.007), -C*04:01 (< 0.001), -C*15:02 (< 0.001) and -C*16:01 (= 0.027) in the patient group, compared to the controls, while the frequency of HLA-C*06:02 (< 0.001) and -C*18:01 (= 0.008) in the patients with pemphigus vulgaris was significantly lower than the controls. Regarding the linkage disequilibrium between HLA class I alleles, the HLA-A*03:01, -B*51:01, -C*16:02 haplotype (4% vs 0%,= 0.04) is suggested to be a predisposing factor, whereas HLA-A*26:01, -B*38, -C*12:03 haplotype (0% vs 6%, = 0.01) is suggested to be a protective factor. In conclusion, it is suggested that HLA-B*44:02, -C*04:01, -C*15:02 alleles and HLA-A*03:01, -B*51:01, -C*16:02 haplotype are susceptibility factors for development of pemphigus vulgaris in the Iranian population, while HLA-C*06:02, -C*18:01 alleles and HLA-A*26:01, -B*38, -C*12:03 haplotype may be considered as protective alleles.

Full article available here: http://onlinelibrary.wiley.com/doi/10.1111/1346-8138.12071/abstract;jsessionid=B90D811159F2CE1C4C357306A37A9D15.d04t04

american-quarter-horsePemphigus foliaceus (pem-fi-gus foli-a-shus) is an auto immune disease that affects humans and dogs and, to a lesser extent, cats and horses.
In horses, it is characterized by primary lesions that often begin on the head and lower extremities; secondary lesions spread to other areas, with an exudate that dries to a crust. There may be extensive edema (swelling) in the legs and abdomen (called “ventral” edema).
Equine pemphigus foliaceus (EPF) is considered rare and signs and symptoms may resemble those of other conditions such as insect bite allergies (crusty lesions), pigeon fever (ventral edema) or other skin conditions.
The primary way to diagnose EPF is by punch biopsy of the skin which is examined by a veterinary pathologist. The pathologist looks for changes consistent with this diagnosis, while also ruling out other causes.
Horses with EPF may also have systemic signs of illness – fever, depression, loss of appetite, lethargy and weight loss. The skin may be painful to touch and swelling can make it difficult to walk or lie down.
Senear-Usher syndrome or pemphigus erythematosus is a pathology that overlaps clinically and serologically with pemphigus foliaceus and lupus erythematosus. Skin biopsies of patients with pemphigus erythematosus reveal acantholysis and deposits of immunoglobulins in desmosomes, and they are positive in the lupus band test. In the present paper, we determined whether the autoantibodies associated with pemphigus erythematosus targeted a single antigen or multiple antigens as a result of the stimulation of independent B cell clones. Our present paper demonstrates that patients with pemphigus erythematosus produce both antiepithelial antibodies specific for desmoglein 1 and 3 and antinuclear antibodies specific for Ro, La, Sm, and double-stranded DNA antigens. After eluting specific anti-epithelial or anti-nuclear antibodies, which were recovered and tested using double-fluorescence assays, a lack of cross-reactivity was demonstrated between desmosomes and nuclear and cytoplasmic lupus antigens. This result suggests that autoantibodies in pemphigus erythematosus are directed against different antigens and that these autoantibodies are produced by independent clones. Given these clinical and serological data, we suggest that pemphigus erythematosus behaves as a multiple autoimmune disease.

Full article can be viewed on: http://www.hindawi.com/journals/ad/2012/296214/

Screenshot_2Pemphigus foliaceus (PF) is an immune-mediated disease that causes pustules and crusted lesions, most commonly on the pinnae, nasal planum, periocular area, chin, feet of affected cats. Acantholytic cells caused by dehydration of intercellular adhesions are often seen on cytology but are not pathognomic for PF. A definitive diagnosis is made based on histopathology showing subcorneal pustules with nondegenerate neutrophils and acantholytic cells. PF is treated with immunosuppressive doses of corticosteroids alone or in combination with other immunosuppresive medications, such as chlorambucil or cyclosporine. Most patients require lifelong treatment with these medications to keep the disease in remission.

Hershey, a 6-year-old, spayed domestic shorthaired cat weighing 3.4 kg, presented with an acute onset of nonpruritic crusted lesions on the head, ears, nail beds, and nasal

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area. She had a 2-day history of lethargy and anorexia. She had no history of medical disease and was up-to-date on vaccinations.

Full article on: http://mobile.vetlearn.com/Media/images/pdf/2010/PV/PV0510_mckay_Derm.pdf

Puppy-Love-puppies-9460996-1600-1200Pemphigus in Dogs

Pemphigus is the general designation for a group of autoimmune skin diseases involving ulceration and crusting of the skin, as well as the formation of fluid-filled sacs and cysts (vesicles), and pus filled lesions (pustules). Some types of pemphigus can also affect the skin tissue of the gums. An autoimmune disease is characterized by the presence of autoantibodies that are produced by the system, but which act against the body’s healthy cells and tissues — just as white blood cells act against infection. In effect, the body is attacking itself. The severity of the disease depends on how deeply the autoantibody deposits into the skin layers. The hallmark sign of pemphigus is a condition called acantholysis, where the skin cells separate and break down because of tissue-bound antibody deposits in the space between cells.

There are four types of pemphigus that affect dogs: pemphigus foliaceus, pemphigus erythematosus, pemphigus vulgaris, and pemphigus vegetans.

In the disease pemphigus foliaceus, the autoantibodies are deposited in the outermost layers of the epidermis, and blisters form on otherwise healthy skin. Pemphigus erythematosus is fairly common, and is a lot like pemphigus foliaceus, but less afflictive. Pemphigus vulgaris, on the other hand, has deeper, and more severe, ulcers because the autoantibody is deposited deep in the skin. Pemphigus vegetans, which affects only dogs, is the rarest form of pemphigus, and seems to be a gentler version of pemphigus vulgaris, with somewhat milder ulcers.

full article can be found here: http://www.petmd.com/dog/conditions/skin/c_dg_pemphigus?page=show#.UQbd3R3WLXA

Human epidermis shows a non-neuronal cholinergic system including keratinocyte (kc) acetylcholine (Ach) axis which is composed by enzymes and two families of Ach receptors (muscarinic and nicotinic receptors). The activity of these two receptors can regulate the interkeratinocytes and kcs-extracellular matrix adhesion modifying the regulation of intercellular adhesion molecules like cadherins and integrins. Some authors demonstrate that acantholysis in pemphigus depends not only on anti desmogleins antibodies (abs) (mostly IgG) but even on other abs directed against kc membrane antigens (e.g. anti Ach receptors Abs). In the early phase of pemphigus pathogenesis, anti Ach receptors Abs block Ach signaling essential for cell shape and intercellular adhesion and increase the phosphorylation of adhesion molecules. Combined with the action of abs antidesmogleins, anti Ach receptors Abs cause the acantholytic phenomenon. In vitro experiments show that high doses of Ach in acantholytic kcs can rapidly reverse this pathologic event. In vivo experiments using neonatal mice model of Pemphigus have demonstrated that cholinergic agonists reduce these lesions. Therapy with pyridostigmine bromide and Nicotinamide per os or pilocarpine used topically, drugs that present cholinomimetic effects, has

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lead to encouraging results in patients affected by Pemphigus disease. Cholinergic agents could have a strategic role in the therapy of pemphigus since they could be responsible for the early stage of acantholytic diseases.

Full article available at: http://www.ingentaconnect.com/content/ben/aiaamc/2012/00000011/00000003/art00008

Although bacterial pyoderma is among the most commonly encountered dermatologic conditions in dogs, some cases present diagnostic challenges even to experienced clinicians. This article presents several unusual manifestations of pyoderma, including bullous impetigo, superficial spreading pyoderma, mucocutaneous pyoderma, and post-grooming furunculosis. Conditions mimicking pyoderma, including juvenile cellulitis, immunomodulatory-responsive lymphocytic-plasmacytic pododermatitis, and pemphigus foliaceus are also described. Diagnostic techniques used for diagnosing and characterizing pyoderma are also discussed.

Full article available at: http://www.vetsmall.theclinics.com/article/PIIS019556161200143X/abstract?rss=yes

Pemphigus vulgaris (PV) is an autoimmune mucocutaneous disease presenting clinically with blisters or erosions of the skin and mucous membrane. The main histopathologic characteristic of this disease is suprabasal vesicles due to loss of cell–cell adhesion between keratinocytes named acantholysis. Studies have shown that apoptosis is increased in PV. The purpose of this study is to investigate the role of apoptosis in blister formation in PV.

Methods

This cross-sectional study was conducted on 25 specimens of oral PV. The presence of apoptosis was evaluated using the TUNEL technique in the normal perilesional region, vesicle area, and acantholytic cells. Also, the expression of Bax pro-apoptotic marker was assessed by the biotin–streptavidin immunohistochemical method. SPSS software was used for Wilcoxon test analysis. P values <0.05 were considered significant.

Results

The percentage and intensity staining of TUNEL-positive cells were noteworthy. There were statistically significant differences between basal and parabasal) = 0.05 (, tombstone with vesicle roof (= 0.038) and basal with tombstone (= 0.038). However, the expression and staining intensity of pro-apoptotic marker Bax were weak, and no statistically significant differences were observed between the various areas.

Conclusion

The results obtained in the present study suggest that the process of apoptosis occurs early in PV because it was observed in the perilesional normal appearing tissue. Also, the process of apoptosis may cause exacerbation or speeding of the bulla formation. In other words, inhibition of apoptosis in the patients could reduce the severity of the lesions.

Full article available here: http://www.medworm.com/index.php?rid=6781830&cid=c_297_32_f&fid=28436&url=http%3A%2F%2Fonlinelibrary.wiley.com%2Fresolve%2Fdoi%3FDOI%3D10.1111%252Fjop.12022