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Öğe Androgen receptor status in lesional and normal skin of patients with rosacea(Blackwell Publishing Ltd, 2004) Erkek, E.; Bozdogan, O.; Kocak, M.; Birol, A.; Atasoy, P.…Öğe Bcl-2-related proteins, (alpha)-smooth muscle actin and amyloid deposits in aggressive and non-aggressive basal cell carcinomas(Taylor & Francis As, 2002) Bozdoğan, Ö.; Erkek, E.; Atasoy, P.; Koçak, M.; Birol, A.; Caydere, M.Aberrant expression of bcl-gene products has been implicated in the development of non-melanoma skin cancers. Recently, altered expression of alpha-smooth muscle actin has been proposed as predictive of tumour behaviour in basal cell carcinomas. The purpose of this study was to compare the aggressive and non-aggressive basal cell carcinomas in terms of bcl-gene products and alpha-smooth muscle actin expression. Fifty excisional biopsy samples were studied by immunohistochemical technique for the differential expressions of bcl-2, bax, bcl-x and alpha-smooth muscle actin. Bcl-2, bcl-x and bax were expressed in 34 (68%), 38 (76%) and 41 (82%) specimens, respectively. Immunoreactivity for alpha-smooth muscle actin was noted both in tumour nests (64%) and within the stroma (54%). There was a significant difference between aggressive and non-aggressive basal cell carcinomas in terms of bcl-2 and stromal alpha-smooth muscle actin immunoreactivity. Non-aggressive basal cell carcinomas display a concordant expression of bcl-family proteins, whereas aggressive tumours reveal a discordant pattern. An increased expression of stromal alpha-smooth muscle actin with a concomitant decrease or loss of bcl-2 expression may be highly suggestive of aggressiveness in basal cell carcinoma.Öğe A case of pemphigus vulgaris possibly triggered by quinolones(European Acad Dermatology & Venereology, 2002) Anadolu, R.Y.; Birol, A.; Bostanci, S.; Boyvatt, A.Pemphigus vulgaris is an autoimmune blistering disorder in which both genetic and environmental factors, mainly drugs, are thought to play a part in its aetiopathogenesis. Although some drugs that contain thiol groups, such as D-penicillamine and captopril, and non-thiol drugs, such as cephalosporin, have been reported to trigger or induce pemphigus, there are no previous reports regarding the influence of quinolones in triggering this disease. Here we present a case of pemphigus possibly triggered by quinolones.Öğe Dermatomal lichenoid graft-versus-host disease within herpes zoster scars(Blackwell Publishing Ltd, 2003) Sanli, H.; Anadolu, R.; Arat, M.; Ekmekci, P.; Birol, A.; Erdem, C.; Koc, H.Case 1 A 23-year-old woman was diagnosed with chronic myelogenous leukemia in 1997. In 1999, she underwent allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor after induction chemotherapy with cyclophosphamide and busulfan. At day 46 after BMT, she was discharged with a medication regimen which included cyclosporine, fluconazole, acyclovir, and trimethoprim/sulfamethoxazole. Five months later she developed clusters of vesicles and pain over the right inframammary and right infrascapular areas corresponding to the T5 - T6 dermatomes. Herpes zoster infection was diagnosed clinically and acyclovir therapy ( 3 x 10 mg/kg/day) was started. All lesions healed within 2 weeks leaving atrophic cicatrices and postinflammatory hyperpigmentation. Eight months after BMT, she presented with erythematous and hyperpigmented macules on the malar areas. Follicular hyperkeratosis on the chest and interscapular area, reticulated white plaques on the buccal mucosa, and significant xerosis were also observed on dermatologic examination. Dermatopathologic examination of a biopsy specimen obtained from the lesions on the face was evaluated to be consistent with "atrophic folliculocentric lichen planus." Two weeks later she was admitted again for new lesions on the trunk. Flat, violaceous, slightly scaly papules were located exactly on the dermatomes of the previous herpes zoster infection ( Fig. 1). A biopsy specimen of these lesions showed a dense, subepidermal, band-like, lymphocytic inflammatory infiltrate, vacuolar degeneration of the basal cell layer, and scattered dyskeratotic cells in the epidermis, confirming the diagnosis of lichenoid graft-versus-host disease (GVHD) (Fig. 2a and 2b). Case 2 A 47-year-old woman was diagnosed with chronic myelogenous leukemia in 1998. She underwent allogeneic BMT from an HLA-matched sibling donor after a preoperative chemotherapy regimen with cyclophosphamide and busulfan in 1999. At day 20, she developed erythema and a burning sensation on her palms and soles and erythema, hyperpigmentation, and desquamation on her face and neck. The lesions increased gradually within 3 weeks. Dermatologic examination on day 40 revealed widespread violaceous, lichenoid papules and plaques on the face, neck, trunk, upper extremities, and genital region. There were also reticulated, white plaques on the buccal mucosa. A biopsy obtained from the lesions on the neck showed findings consistent with both acute and lichenoid GVHD. The skin lesions resolved within 1 month after prednisolone therapy leaving postinflammatory hyperpigmentation. Seven months later, she developed herpes zoster infection involving the right neck, shoulder, chest, and scapular area corresponding to the C3 - C4 dermatomes. She was treated with famcyclovir for 10 days and the lesions healed completely. Three months after this infection, new, violaceous, lichenoid papular lesions were noted which remained confined to the dermatomes affected by the herpes zoster infection ( Fig. 3). Dermatopathologic examination revealed dyskeratotic cells, focal vacuolization in the basal cell layer, and a superficial band-like lymphocytic infiltrate in the papillary dermis, consistent with lichenoid chronic GVHD.Öğe Examination of Bcl-2, Bcl-X and bax protein expression in psoriasis(Blackwell Publishing Ltd, 2003) Koçak, M.; Bozdogan, O.; Erkek, E.; Atasoy, P.; Birol, A.Background Psoriasis is an inflammatory skin disease characterized by epidermal hyperplasia and greatly accelerated epidermal turnover. The blockage of normal apoptotic process in the epidermis is one of the factors implicated in the pathogenesis of psoriasis. Objective The purpose of the present study was to elucidate whether bcl-family proteins are significantly involved in the hypothetical antiapoptotic cascade in lesional psoriatic epidermis. Methods Twenty-six lesional biopsy samples of 26 patients with psoriasis and five control specimens from normal skin were studied by immunohistochemical method for the differential expression of pro-apoptotic bax and antiapoptotic bcl-2 and bcl-x proteins. Results Compared with the normal epidermis, bcl-2 expression was significantly reduced, whereas bax and bcl-x were significantly overexpressed in the psoriatic epidermis. The localization of bcl-2/bax/bcl-x proteins in the psoriatic epidermis did not show a significant deviation from that in the normal epidermis. Conclusion These findings indicate a discordant expression of bcl-2 and bax/bcl-x in psoriatic epidermis. Increased bcl-x expression might contribute to the antiapoptotic response in psoriatic keratinocytes. The presence of strong bax expression with a concomitant decrease in bcl-2 expression suggests either a functional defect in bax protein or an inherent/acquired resistance to bax-mediated apoptosis in psoriatic keratinocytes.Öğe Focal acral hyperkeratosis: A rare cutaneous disorder within the spectrum of costa acrokeratoelastoidosis(Wiley, 2004) Erkek, E.; Kocak, M.; Bozdogan, Ö.; Atasoy, P.; Birol, A.Acrokeratoelastoidosis and focal acral hyperkeratosis share similar clinical features and identical histologic epidermal alterations. These disorders are distinguished solely on the basis of the absence of elastorrhexis in the latter. We present a case of focal acral hyperkeratosis in a 9-year-old girl. The lesions consisted of translucent polygonal papules clustered on the thenar regions of the palms and over the metacarpophalangeal and interphalangeal joints. Histopathologic examination revealed orthohyperkeratosis within focal clavus-like depressions of the epidermis and prominent hypergranulosis. There was no evidence of alterations in elastic tissue. The clinicopathologic distinction between focal acral hyperkeratosis and acrokeratoelastoidosis is blurred. There is enough evidence to consider the former as a histologic variant of Costa acrokeratoelastoidosis syndrome, and a better nomenclature for this disorder would be "acrokeratoelastoidosis without elastorrhexis."Öğe Keloid secondary to therapeutic cupping: an unusual complication(Wiley, 2005) Birol, A.; Erkek, E.; Kurtipek, G. S.; Koçak, M.…Öğe A simple clinical scoring system to improve the sensitivity and standardization of the diagnosis of mycosis fungoides type cutaneous T-cell lymphoma: logistic regression of clinical and laboratory data(Blackwell Publishing Ltd, 2003) Stevens, S.R.; Ke, M.S.; Birol, A.; Terhune, M.H.; Parry, E.J.; Ross, C.; Cooper, KD..Background The diagnosis of mycosis fungoides (MF) is notoriously difficult to establish because in the early stages, histological features may be nonspecific or merely suggestive. Objectives To standardize the diagnosis of MF. Methods We studied 138 patients with suspected MF referred over a 7-year period to a university department of a dermatology-based cutaneous lymphoma clinic. Six diagnostic criteria were evaluated: clinical morphology, clinical distribution, skin biopsy T-cell receptor gene rearrangement (TCR-GR), skin biopsy pan T-cell marker loss greater than or equal to 2, skin biopsy CD4/CD8 ratio greater than or equal to 6, and skin biopsy diffuse epidermal HLA-DR expression. These six clinical and laboratory criteria were compared by logistic regression analysis in patients with histologically diagnosed MF and those with benign disease. Results Of the 138 patients, 74 had histology of MF, 47 of benign dermatoses and 17 were indeterminate. Close associations were found between a histological diagnosis of MF and TCR-GR (odds ratio 14.4), classical morphology (7.5), classical distribution (2.5) and diffuse epidermal HLA-DR expression (2.8). Logistic regression models were developed depending on the availability of data (either TCR-GR or HLA-DR). Probabilities for correctly diagnosing MF compared with histology as the 'gold standard' were derived from these logistic regression models. A scoring system assigning point values based on these probabilities was then created in order to assist the clinician in making the diagnosis. If using TCR-GR data, a positive TCR-GR = 2.5 points, the presence of classical morphology = 2.0 points, and the presence of classical distribution = 1.5 points. A total score of greater than or equal to 3.5 points assigns a high probability (> 85%) of having MF. If using HLA-DR expression, then the presence of classical morphology = 2.5 points, a positive diffuse epidermal HLA-DR expression = 2.0 points, and the presence of classical distribution = 1.5 points. In this case, a total score of greater than or equal to 4.0 points assigns a high probability (> 85%) of MF. Conclusions The logistic regression models and scoring systems integrate clinical and laboratory assessments, allow rapid probability estimation, and provide a threshold for the diagnosis of MF in an objective, standardized manner.
