Sensitivity to estrogen has been described previously. The clinical picture is varied with pruritus, either generalized or localued or as urticaria. The hallmark of estrogen dermatitis is the cyclic premenstrual flare. The patient reported here had cyclic erythema multiforme-like lesions and showed a positive intradermal skin test to estrogen. A 20-year-old female patient presented with a periodic 5 year duration of skin lesions on both hands. The eruption commenced in the second half of the menstrual cycle, worsened through the luteal phase but the lesion almost disappeared during menstruation. An intradermal skin test to estrone showed positive results. However, a skin test with medroxyprogesterone acetate was negative. After systemic steroid and antihistamine therapy, the lesions were found to be significantly improved.
Dermatitis* ; Erythema ; Erythema Multiforme ; Estrogens* ; Estrone ; Female ; Hand ; Humans ; Luteal Phase ; Medroxyprogesterone Acetate ; Menstrual Cycle ; Menstruation ; Pruritus ; Skin ; Skin Tests ; Urticaria ; Young Adult

BACKGROUND: A presumptive diagnosis of cutaneous tuberculosis can be made on the basis of patients' history, clinical and histologic findings. However, isolation of Mycobacerum tuberculosis is required for a definitive diagnosis and confirmation can be difficult with traditional techniques, including the direct visualization in tissue and growth in culture. OBJECTIVE: We used polymerase chain reaction(PCR) for the detection of mycobacterial DNA from routinely prepared formalin-fixed, paraffin-embedded skin specimens to evaluate its usefulness as a diagnostic tool. METHOD: We studied typical cases of localized cutaneous tuberculosis. Ten paraffin-embedded biopsy samples obtained from 2 patients with scrofuloderma, lupus vulgaris and tuberculosis verrucosa cutis were analyzed by PCR, respectively. RESULTS: M. tuerculosis DNA was demonstrated in all 10 specimens. CONCLUSION: This study shows that the PCR will be a useful method for the confirmation of the diagnosis in localized cutaneous tuberculosis and many skin lesions thought to be related to M. tuberculosis infection.
Biopsy* ; Diagnosis ; DNA* ; Humans ; Lupus Vulgaris ; Mycobacterium tuberculosis* ; Mycobacterium* ; Paraffin* ; Polymerase Chain Reaction* ; Skin* ; Tuberculosis ; Tuberculosis, Cutaneous*

An IgM anti-phenolic glycolipid-I(PGL-I) antibodies in leprosy was measured using specimens of dried capillary blood collected on filter paper from the skin smear site instead of sera from venous blood. We also measured IgM antibodies from venous blood collected on filter paper. The correlation among the three samples was good. So I concluded the collection of capillary blood on filter paper is a convenient method for handling, mailing and storage of samples.
Antibodies* ; Capillaries* ; Immunoglobulin M* ; Leprosy ; Postal Service ; Skin

BACKGROUND: Chronic actinic dermatitis comprises a spectrum of chronic photosensitivity disorders. Treatment includes avoidance of UV light, application of broad-spectrum topical sunscreens, PUVA therapy, corticosteroid, azathioprine and cyclosporine. OBJECTIVE: Our purpose was to determine the efficacy of cyclosporine in the treatment of chronic actinic dermatitis. METHODS: Six patients with chronic actinic dermatitis refractory to conventional treatment were treated with cyclosporine 100-200mg a day for four to eighteen weeks. RESULTS: In all six patients improvement of the skin lesions and itching were dramatic, but in three of them hyperterision developed during the cyclosporine treatment. After stopping the cyclosporine therapy, their blood pressures normalized within two to five weeks. Other side effects of cyclosporine were not found. Although the skin lesions of all of the six patients were aggravated more or less after stopping the cyclosporine therapy, we could maintain their improved states with topical corticosteroids and oral antihistamines. CONCLUSION: 1. Cyclosporine is a good alternative in treating chronic actinic dermatitis patients who are suffering from severe symptoms refractory to conventional therapy. 2. Hypertension is the frequent side effect of cyclosporine.
Adrenal Cortex Hormones ; Azathioprine ; Cyclosporine* ; Histamine Antagonists ; Humans ; Hypertension ; Photosensitivity Disorders* ; Pruritus ; PUVA Therapy ; Skin ; Sunscreening Agents ; Ultraviolet Rays

A 51-year-old female developed a distinctive perioral rash, conisting of discrete or confluent erythematous papules for one and a half years. Histopathologic examiriation revealed upper dermal granulomas admixed with lymphoytes. Pieces of hair shaft were staincd peri-dish by AFB in the center of granuloma, which might play a role in the formation of the granuloma She also had used corticosteroid ointment intermittently duririg this time. There were no associated systemic abnormalities. The lesions resolved after two month treatment with oral corticosteroid and tetrac cline.
Dermatitis, Perioral* ; Exanthema ; Female ; Granuloma ; Hair ; Humans ; Middle Aged

Dyschromatosis universalis hereditaria is a rare pigmentary disorder characterized by widespread mothed hyperpigmentation and hypopigmentation. We report a 40-year-old male patient with numerous hyperpigmenter, and hypopigmented macules all over the body except on the palms and soles. The family history revealed similar pigmentary changes in 5 other members through 4 generations, and we could guess the hereditary pattern of the disease of this family to be autosomal dominant inheritance.
Adult ; Family Characteristics ; Humans ; Hyperpigmentation ; Hypopigmentation ; Male ; Moths ; Wills

Cerebriform intradermal melanocytic nevus is a cause of cutis veticis gyrata, a morphologic term which describes the hypertrophy and folding of the skin, typically occurring on the scslp, to present a gyrate or cerebriform appearance. We report a 37-year-old woman with a 17 x 22cm soft, convoluted mass over most of the occipital, parietal, and temporal scalp. At birth, she had a small brownish macide on the occipital scalp that enlarged to form this extensive lesion. Histologically, nests of nevus cells were shown in the upper and the mid dermis.
Adult ; Dermis ; Female ; Fibroadenoma ; Humans ; Hypertrophy ; Nevus ; Nevus, Pigmented* ; Parturition ; Rabeprazole ; Scalp ; Skin

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: At the present time, more than 100 cases of squamous cell carcinoma (SCC) developing in neurotrophic ulcers of leprosy have been reported. But the histopathologic features and the differences between SCC in leprosy and de novo SCC was not described. OBJECTIVE: The purpose of this study was to evaluate the characteristics of SCC in leprosy and to investigate growth dynamics of SCC in ulcers in leprosy. METHODS: We reviewed the clinical features and the degree of histopathologic differentiation of 13 cases of SCC in ulcers of leprosy patients presenting at the KLCA from 1986 to 1998. And immunohistochemical staining with PCNA(proliferating cell nuclear antigen) and TUNEL staining were done in paraffin-embedded tissue sections from 18 sites of 13 cases of SCC in ulcers of leprosy. RESULTS: 1. The average duration of leprosy and of an ulcer prior to diagnosis of SCC was 43 years and 19 years, respectively. 2. Histopathologic grading of 13 cases was performed as follows:10 cases were well-differentiated and 3 cases were moderately-differentiated. 3. The PCNA LI(labelling index) was 47.26+/-7.38% in well-differentiated group and 48.86+/-9.39% in moderately -differentiated group. 4. The apoptotic index(AI) was 45.57+/-8.68% in well- differentiated group and 29.38+/-1.06% in moderately differentiated group. The AI in de novo SCC was 45.09+/-6.18%. CONCLUSION: (1) Malignant change in chronic ulcer in leprosy may be found more often if patients are examined with care. (2) Our leprosy case with SCC is a 63-year-old male with past history of lepromatous leprosy of 43 year duration having ulcer problems for 19 years before presenting with SCC on an average. (3) High-degrees of malignancy in SCC of leprosy patients might be caused by extended cell survival due to decreased apoptosis rather than increased cell proliferation.
Apoptosis ; Carcinoma, Squamous Cell* ; Cell Proliferation ; Cell Survival ; Diagnosis ; Humans ; In Situ Nick-End Labeling ; Leprosy* ; Leprosy, Lepromatous ; Male ; Middle Aged ; Proliferating Cell Nuclear Antigen ; Ulcer*