No abstract available.
Funnel Chest*

No abstract available.
Adult* ; Female* ; Humans

We report a case of MALT lymphoma in a 49-year-old woman. Her disease occurred simultaneously in the mucosa of her right upper eyelid conjunctiva and in her left nostril as ulcerating tumors associated with itchy ichthyosiform skin lesions on the trunk, hyperkeratotic palms and soles, and dystrophic nails. Histopathological examinations revealed consistent findings of MALT lymphoma with dissemination; i.e., diffuse infiltrates of lymphoplasmacytoid cells with a few Russel body-like structures, eosinophils, some shoddy granulomas under the irregularly hyperplastic epidermis, and diffuse infiltrates of CCL ( centrocyte-like ) cells and small lymphocytes inside and outside many lymphoid follicle-like structures in the subcutaneous tissue forming florid lymphoepithelial lesions. She died after 27 months duration of her disease with worsening of ichthyosiform skin lesions and dystrophic nails in spite of total excision of the tumors. We discuss the clinical and histopathologic features of MALT lymphoma with dissemination and the various similar diseases to differentiate.
Conjunctiva ; Eosinophils ; Epidermis ; Eyelids* ; Female ; Glycogen Storage Disease Type VI ; Granuloma ; Humans ; Lymphocytes ; Lymphoma, B-Cell, Marginal Zone* ; Middle Aged ; Mucous Membrane ; Skin ; Subcutaneous Tissue ; Ulcer

No abstract available.
Encephalitis, Herpes Simplex* ; Herpes Simplex*

No abstract available.
Encephalitis, Herpes Simplex* ; Herpes Simplex*

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.
Actins ; Bowen's Disease ; Carcinogenesis ; Carcinoma in Situ ; Carcinoma, Squamous Cell ; Epidermis ; Keratoacanthoma ; Keratosis, Actinic ; Prognosis ; Proliferating Cell Nuclear Antigen*

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.
Actins ; Bowen's Disease ; Carcinogenesis ; Carcinoma in Situ ; Carcinoma, Squamous Cell ; Epidermis ; Keratoacanthoma ; Keratosis, Actinic ; Prognosis ; Proliferating Cell Nuclear Antigen*

PURPOSE:This study was performed to investigate the status of cardiac structure and function and to assess their alterations after growth hormone(GH) treatment in children with growth hormone deficiency(GHD). METHODS:Interventricular septal thickness and left ventriclular posterior wall thickness, ejection fraction(EF), fractional shortening(FS), systolic time interval(STI) of left ventricle were measured by two-dimensional and M-mode echocardiography in sixteen children with GHD and age, sex matched sixteen children with GH normal short stature as control. The measure were done before GH treatment and at 6 and 12 months of GH treatment, respectively. RESULTS: 1)Left ventricular posterior wall thickness in GHD group was significantly thinner than that of control group(P<0.05). 2)Interventricular septal thickness and left ventricular posterior wall thickness were increased with GH treatment from 10.4+/-1.7mm, 8.1+/-1.8mm before GH treatment to 11.0+/-0.9mm, 8.7+/-0.7mm and 11.2+/-1.7mm, 9.7+/-1.8mm at 6 and 12 months of GH treatment, respectively. The increment of left ventricular posterior wall thickness after 12 months GH treatment revealed statistic significance(P<0.05). 3)There was no significant alterations of EF, FS, STI of left ventricle after GH treatment at 6 months and 12 months, respectively. CONCLUSION: Left ventricular posterior wall thickness in GHD group was significantly thin compared to that of control group(P<0.05). GH treatment in GHD children for 12 months, resulted statistically significant increase(P<0.05) in posterior wall thickness. There is no evidence of hypertrophic cardiomyopathy after GH treatment. But we could not exclude the possibility of these alterations were induced by an increased overall body size and body surface area after GH treatment. To clarify the exact alterations of cardiac structures and function in children with GHD after GH treatment, long term follow-up studies should be necessary.
Body Size ; Body Surface Area ; Cardiomyopathy, Hypertrophic ; Child* ; Echocardiography ; Follow-Up Studies ; Growth Hormone* ; Heart ; Heart Ventricles ; Humans

PURPOSE:There were many controversies whether constitutional delay of growth and puberty(CDGP) is simple varient of normal growth pattern, or one of the cause of growth disturbance induced by the disturbance of growth hormone secrtion or its function. So we studied about the difference in serum peak growth hormone level after insulin, L-dopa provocation test, and serum IGF-I leve between constitutional delay of growth and puberty(CDGP) and familial short stature(FSS). METHODS:Measurement of serum peak growth hormone and insulin like growth factor-I(IGF-I) level after insulin, L-dopa provocation test were performed in 33 children with costitutional delay of growth and puberty (CDGP). Two groups of children with familial short stature (FSS) whose height were below 10 percentile for chronologic age of Korean national height standards were included as control groups. RESULTS: 1)There were no significant difference of serum peak growth hormone level between children with CDGP and children with FSS and these results were similar in both sex. 2)The mean serum IGF-I level of children with CDGP were 125.69+/-4.06 ng/ml(71.53-189.34ng/ml) in male, 157.7+/-3.17ng/ml(81.9-279.2ng/ml) in female. Both results were significantly lower to those of FSS children by chronologic age group because the mean serum IGF-I level of FSS children were 190.19+/-7.97ng/ml (87.64-297.6ng/ml) in male, 205.47+/-15.87ng/ml(61.7-433.1ng/ml) in female. But compared to FSS children by bone age of 72-96 months, there were no significant difference noted because the mean serum IGF-I level of children with FSSwere130.47+/-0.27ng/ml(63.24-198.2ng/ml)inmale,162.35+/-9.43ng/ml(54.9-217.53 ng/ml) in female. CONCLUSIONS:The results of this study showed that the serum peak growth hormone level after insulin, L-dopa provocation test with children of CDGP revealed no significant difference with those of FSS children in both sex. Serum IGF-I level of CDGP children was lower significantly to those of FSS children by chronologic age group, but no much difference with FSS children of bone age group.
Adolescent ; Child* ; Female ; Growth Hormone* ; Humans ; Insulin* ; Insulin-Like Growth Factor I ; Levodopa* ; Male ; Puberty*

No abstract available.
Embryonic Structures* ; Humans*