Diagnosis
Pemphigus defines a group of autoimmune intraepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug-induced pemphigus, Senear Usher syndrome, and endemic pemphigus foliaceus exist, and are recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons, and eye doctors, as lesions can affect the eyes and mucous membranes of the oral cavity. Intraorally, it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone" appearance. Definitive diagnosis also requires the demonstration of antidesmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire.
There can be vestibular dysfunction, such as some minor hearing loss after using the medication for 2 to 4 months. A certain block effect of neuromuscular. Can cause allergic reactions: rash, drug fever, facial flushing or pale, asthma, palpitations, sense of suppression in the chest, abdominal pain, anaphylactic shock. Interactions
Combined with an aminoglycoside, it can increase the possibility of ototoxicity, nephrotoxicity and neuromuscular blockage, result in some hearing loss or can continue to deafness. It could be a temporary symptom, but often be permanent. Neuromuscular blockade can lead to skeletal muscle weakness and respiratory depression or paralysis (apnea). Using anti-cholinesterase or calcium salts may release this block. Combined with amphotericin B, vancomycin, bacitracin, paromomycin, cyclosporine, kanamycin, cisplatin, bumetanide, etoric acid, furosemide: Would Increase the possibility of ototoxicity and nephrotoxicity. Combined with antihistamines, buclizine, cyclizine, meclizine, phenothiazines, thioketones, trimethamine, and capreomycin: can ameliorate the symptoms of tinnitus, dizziness or vertigo and other ototoxic symptoms. Combined with anti-neuromuscular block drugs: can antagonize the effect of the anti-neuromuscular block drugs on the skeletal muscle (so need to adjust the dose of the drugs for anti-muscle weakness. Combined with ethyl sulfide isoniazid: may increase the side effects. Combined with methoxyflurane or polymyxin injection: may increase renal toxicity or neuromuscular blockade effect. Combined with opioid: The effect of central respiratory inhibition may increase, lead to prolonged respiratory inhibition or respiratory paralysis (apnea). History
Capreomycin, an antiphlogistic antibiotic which was produced in the United States in 1960, and be applied in clinic in 1968.