본 연구에서 Pemphigus populitransversus 미루나무면충(신칭)을 국내에서 처음으로 보고한다. 이 종의 형태학적 정보, 분포지역, 기주식물, 한국에 분포하는 Pemphigus 속 종들에 대한 분류키를 제공한다.

본 연구에서 Pemphigus bursarius를 국내에서 처음으로 보고한다. 이 종의 분포지역, 기주식물, 형태학적 정보를 제공한다.

A 67 years old female showed diffuse erosive ulceration at left buccal mucosa. She had received tegretol to treat the patient’s pain and anxiety of trigeminal neuralgia for 18 months. Otherwise her medical history was nonspecific. Under the clinical diagnosis of lichen planus she received anti-inflammatory therapies using antibiotics and steroid ointment, which were not effective. Consequently her oral ulceration was gradually expanded and aggravated. In the biopsy examination mucosa epithelium was irregularly keratinized and focally detached from underlying connective tissue by thin cleft spaces, accompanied with inflammatory cell infiltration into the subepithelial area. The epithelium was generally acanthomatous with short rete ridges. Many spots of acantholysis were found in the basal and suprabasal layers of epithelium, into which melanocytes were migrated. Particularly, many keratinocytes not only in the spinous layer but also in the suprabasal layer contained atypical keratohyalin granules in their cytoplasms. In the immunohistochemistry the epithelium was rarely positive for PCNA and IgK, but strongly positive for HSP-70, and many keratinocytes showed strong positive reaction of lysozyme in their cytoplasms. Taken together, with the characteristic cytotoxic changes of keratinocytes, which are usually found in the oral epithelium damaged by certain drug abuse, the present case of pemphigus-like oral lesion was diagnosed as drug-induced pemphigus caused by long time intake of tegretol, carbamazepine derivative. The acute oral drug-induced pemphigus should be differentially diagnosed from oral lichen planus, recurrent aphthous ulceration, oral leukoplakia, candidiasis, autoimmune pemphigus, etc., in order to treat properly in the absence of biohazards of systemic therapeutic drugs

Pemphigus is an autoimmune blistering disease characterized by autoantibodies against epidermal adhesion molecules, desmogleins. Pemphigus vulgaris is most common and shows intraepidermal vesicles caused by the breaking apart of epidermal cells, acantholysis. A 65 years old male patient complained of severe mucosa ulceration on his right mandibular retromolar pad area where traumatic injuries occurred during mastication. He also had multifocal round skin ulcerations, less than 7~8mm in diameter and showed habitual onset and disappeared soon. At this time he was anxious about his oral ulceration with a cancer phobia, thereby a biopsy was made to rule out any malignancy in the ulceration. The histology examination showed multifocal suprabasal splits forming vesicles and erosion. The suprabasal splits were linear and parallel to the basal cell layer. The immunostain of IgK was strongly positive in the vesicular fluid as well as the cell membranes of dissociating keratinocytes, and also positive in many plasma cells infiltrated into the subepithelial zone. TNFα, IL‐1, ‐8, ‐28 for the pro‐inflammatory reaction were weakly expressed, while IL‐6 was strongly positive in the acantholytic keratinocytes of vesicle forming area. β‐defensin‐1, ‐2, ‐3 for the innate immunity were diffusely positive in the involved epithelium. The cell survival proteins, pAKT and HSP‐70 were diffusely positive in the epithelium, while the apoptosis protein, PARP was consistently positive in some acantholytic keratinocytes. These findings indicated that the vesicle formation occurred by autoantibody reaction without the activation of pro‐inflammatory and cell‐mediated immune reactions. The lesion was diagnosed pemphigus vulgaris with abrupt onset of epithelial vesicles at the predisposing areas of traumatic injuries by type II hypersenstitive immune reaction.