Acute generalized exanthematous pustulosis (AGEP): A review and update.

Acute generalized exanthematous pustulosis is a severe cutaneous adverse reaction characterized by the rapid development of nonfollicular, sterile pustules on an erythematous base. It is attributed to drugs in the majority of cases. Antibiotics are the most common cause of acute generalized exanthematous pustulosis; however, a wide variety of drugs has been associated with this condition. Typically, within 48 hours of ingesting the causative medication, there is acute onset of fever and pustulosis with leukocytosis. In severe cases there can be mucous membrane and systemic organ involvement. Histologic findings include intracorneal, subcorneal, and/or intraepidermal pustules with papillary dermal edema containing neutrophils and eosinophils. Treatment focuses on removal of the causative drug, supportive care, infection prevention, and the often beneficial use of a potent topical steroid.

Pustular eruption induced by etanercept in a patient with ankylosing spondylitis: a rare side effect.

Etanercept is a tumor necrosis factor alpha (TNF-a) antagonist with anti-inflammatory effects. It is used in the treatment of dermatologic and rheumatologic diseases such as rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. However, etanercept has various cutaneous and systemic side effects. Herein, we report a case of generalized pustular eruption due to etanercept therapy in an ankylosing spondylitis patient and review pustular diseases.

p53 Protein and Proliferating Cell Nuclear Antigen Expression in Epidermal Keratinocytic Neoplasms / 대한피부과학회지

BACKGROUND: Although actinic keratosis and Bowens disease ar considered as carcinoma in situ, most of them are biologically benign and dont progress to invasive squamous cell carcinoma. It is little known why they take the benign courses and which factors are involved in the tumorigenesis. Keratoacanthoma, self-regresi;ing benign tumor, may be sometimes or fused morphologically with well-differentiated squamous cell carcinoma. So it is necessary to find a useful marker to help us distinguish them. OBJECTIVES: We performed this study to gain a better understani ling of biologic behaviour and tumerigenesis of epidermal keiatinocytic neoplasms. METHODS: We investigated the expression of p53 protein and priliferating cell nuclear antigen (PCNA) by an immunohistochemical method on the formalin-fixed, araffinembedded tissue specimens of epidermal keratinocytic neoplasms. RESULTS: Fourteen out of 20 cases of squamous cell carcinoma(70.0%), 14 out of 22 cases of actinic keratosis(63.6%), and 13 out of 20 cases of Bowens disease(65.0%) showed p53 protein expression, but keratoacanthoma was negative. All the tumors studied sho ved significantly increased numbers of PCNA-positive eells when compared with normal epidermis and characteristic distribution pattern. of PCNA-positive cells. Most cases of actinic keratosis exhibited the basal dysplastic pattern, but Bo wenoid variants showed diffuse dysplastic pattern. Karatoacanthoma revealed the marginal pattern and Bowens disease showed the diffuse dysplastic pattern. Well-differentiated squamous cell carcinoria showed the basal dysplastic pattern, while poorly differentiated squamous cell carcinoma revealed d ffuse dysplastic pattern. CONCLUSION: Our results suggest that p53 mutation is a common and early genetic change in the epidermal tumorigenesis and may be used as a good marker for malignan transformation, but it does not seem to correlate with the biollagic behavior or prognosis of epidermal neoplasms. PCNA, which is considered as a proliferation-relaited marker, was expressed with chavaceristic distribution patterns according to the type of tumors, but the frequency of PCNA expression is unlikely to reflct the malignant potential of epidermal neoplasms.

p53 Protein and Proliferating Cell Nuclear Antigen Expression in Epidermal Keratinocytic Neoplasms / 대한피부과학회지

BACKGROUND: Although actinic keratosis and Bowens disease ar considered as carcinoma in situ, most of them are biologically benign and dont progress to invasive squamous cell carcinoma. It is little known why they take the benign courses and which factors are involved in the tumorigenesis. Keratoacanthoma, self-regresi;ing benign tumor, may be sometimes or fused morphologically with well-differentiated squamous cell carcinoma. So it is necessary to find a useful marker to help us distinguish them. OBJECTIVES: We performed this study to gain a better understani ling of biologic behaviour and tumerigenesis of epidermal keiatinocytic neoplasms. METHODS: We investigated the expression of p53 protein and priliferating cell nuclear antigen (PCNA) by an immunohistochemical method on the formalin-fixed, araffinembedded tissue specimens of epidermal keratinocytic neoplasms. RESULTS: Fourteen out of 20 cases of squamous cell carcinoma(70.0%), 14 out of 22 cases of actinic keratosis(63.6%), and 13 out of 20 cases of Bowens disease(65.0%) showed p53 protein expression, but keratoacanthoma was negative. All the tumors studied sho ved significantly increased numbers of PCNA-positive eells when compared with normal epidermis and characteristic distribution pattern. of PCNA-positive cells. Most cases of actinic keratosis exhibited the basal dysplastic pattern, but Bo wenoid variants showed diffuse dysplastic pattern. Karatoacanthoma revealed the marginal pattern and Bowens disease showed the diffuse dysplastic pattern. Well-differentiated squamous cell carcinoria showed the basal dysplastic pattern, while poorly differentiated squamous cell carcinoma revealed d ffuse dysplastic pattern. CONCLUSION: Our results suggest that p53 mutation is a common and early genetic change in the epidermal tumorigenesis and may be used as a good marker for malignan transformation, but it does not seem to correlate with the biollagic behavior or prognosis of epidermal neoplasms. PCNA, which is considered as a proliferation-relaited marker, was expressed with chavaceristic distribution patterns according to the type of tumors, but the frequency of PCNA expression is unlikely to reflct the malignant potential of epidermal neoplasms.