Full article can be viewed here: http://www.hindawi.com/crim/dm/2012/207126/
Full article (free) found here: http://www.hindawi.com/isrn/dermatology/2012/237802/
Full article can be viewed on: http://www.hindawi.com/journals/ad/2012/296214/
Pemphigus 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
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.
Pemphigus 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
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
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.
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.
The percentage and intensity staining of TUNEL-positive cells were noteworthy. There were statistically significant differences between basal and parabasal) P = 0.05 (, tombstone with vesicle roof (P = 0.038) and basal with tombstone (P = 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.
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.