Funda Tamer
Turgut Özal University
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Featured researches published by Funda Tamer.
Our Dermatology Online | 2018
Funda Tamer
Seborrheic dermatitis is a chronic inflammatory skin disease which is characterised by erythematous scaly plaques on the sebaceous areas like forehead, eyebrows, glabella, nasolabial folds, scalp, chest, and back. The prevalence of seborrheic dermatitis among adults in the general population is 1-10%. It is more common in men than in women. The disease usually presents between the ages of 30 and 40 years [1]. The incidence of seborrheic dermatitis is similar between ethnic groups [2]. The exact cause of this condition remains unknown. However, numerous factros including Malassezia yeasts, sex hormones like androgens, sebum levels, immune response, neurogenic factors and stress have been implicated in the etiopathogenesis of seborrheic dermatitis [3].
Dermatology practical & conceptual | 2018
Funda Tamer; Mehmet Eren Yuksel; Evren Sarifakioglu; Yavuz Karabag
Background Seborrheic dermatitis is an inflammatory skin disease that affects 1–3% of the general population. The Malassezia species has been implicated as the main causative agent; however, the bacterial flora of the skin may also play role in the etiopathogenesis. Therefore, we investigated the most common bacterial agent of the skin flora of patients with seborrheic dermatitis. Materials and Methods Fifty-one patients with seborrheic dermatitis and 50 healthy individuals are included in this study. Sterile cotton swabs were rubbed on the scalp of the participants for bacterial culture. Colonial morphology was identified with gram stain and catalase test. Results Staphylococcus aureus was isolated from 25 (49%) patients with seborrheic dermatitis and 10 (20%) healthy individuals within the control group. Coagulase-negative staphylococci were isolated from 24 (47.1%) patients with seborrheic dermatitis and 17 (34%) healthy individuals within the control group. Diphtheroids were present in 2 (3.9%) patients and 1 (2%) subject within the control group. Gram-negative bacilli were present only in 1 (2%) patient. Hemolytic streptococci and bacilli were identified in 1 (2%) subject from each group. Colonization of coagulase-negative staphylococci, diphtheroids, gram-negative bacilli, hemolytic streptococci, and bacillus did not differ between patients and healthy controls. However, S. aureus colonization was significantly more common in patients with seborrheic dermatitis than in healthy controls. Conclusion Within this study we revealed that S. aureus colonization was significantly higher among the patients. Therefore, we propose that, in addition to the Malassezia species, S. aureus may play a role in the etiopathogenesis of seborrheic dermatitis.
Indian Dermatology Online Journal | 2017
Funda Tamer; Evren Sarifakioglu; Ozge Mine Orenay; Umran Yildirim
© 2017 Indian Dermatology Online Journal | Published by Wolters Kluwer Medknow Sir, Pityriasis rosea is an acute inflammatory skin disease characterized by erythematous scaling macules, papules, and plaques predominantly on the trunk and proximal extremities. It has been suggested that viral infections, including human herpes virus 6 (HHV6) and HHV7, upper respiratory tract infections, and drugs such as isotretinoin, D‐penicillamine and terbinafine may be associated with pityriasis rosea. In addition to its characteristic clinical features, the disease may rarely present with atypical lesions.[1]
Our Dermatology Online | 2016
Mehmet Eren Yuksel; Funda Tamer
A 61-year-old Caucasian male presented with a breast lump for futher clinical evaluation. The patient admitted that the slowly growing mass had been present for a year. The lesion was asymptomatic, however the patient was concerned about the risk of malignancy. The past medical history and family history were both unremarkable. The physical examination of the patient revealed a skin coloured, well-defined, firm, subcutaneous nodule with a punctum and telangiectasias on the surface (Fig. 1). The lesion was located on the trunk, laterally to the right areola measuring 3x2.5 cm. There was no axillary lymphadenopathy. The lesion was surgically removed without any complications (Fig. 2). The histopathological examination of the specimen revealed an epidermal cyst.
Indian Journal of Dermatology, Venereology and Leprology | 2016
Funda Tamer; Mehmet Eren Yuksel
1. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res 1988;16:1215. 2. Lamartine J, Munhoz Essenfelder G, Kibar Z, Lanneluc I, Callouet E, Laoudj D, et al. Mutations in GJB6 cause hidrotic ectodermal dysplasia. Nat Genet 2000;26:142‐4. 3. Smith FJ, Morley SM, McLean WH. A novel connexin 30 mutation in Clouston syndrome. J Invest Dermatol 2002;118:530‐2. 4. Baris HN, Zlotogorski A, Peretz‐Amit G, Doviner V, Shohat M, Reznik‐Wolf H, et al. A novel GJB6 missense mutation in hidrotic ectodermal dysplasia 2 (Clouston syndrome) broadens its genotypic basis. Br J Dermatol 2008;159:1373‐6. 5. Liu YT, Guo K, Li J, Liu Y, Zeng WH, Geng SM. Novel mutations in GJB6 and GJB2 in Clouston syndrome. Clin Exp Dermatol 2015;40:770‐3. 6. Kellermayer R, Keller M, Ratajczak P, Richardson E, Harangi F, Mérei E, et al. Bigenic connexin mutations in a patient with hidrotic ectodermal dysplasia. Eur J Dermatol 2005;15:75‐9. 7. Radhakrishna U, Blouin JL, Mehenni H, Mehta TY, Sheth FJ, Sheth JJ, et al. The gene for autosomal dominant hidrotic ectodermal dysplasia (Clouston syndrome) in a large Indian family maps to the 13q11‐q12.1 pericentromeric region. Am J Med Genet 1997;71:80‐6.
Acta dermatovenerologica Alpina, Pannonica, et Adriatica | 2016
Ozge Mine Orenay; Funda Tamer; Evren Sarifakioglu; Umran Yildirim
Our Dermatology Online | 2017
Funda Tamer; Mehmet Eren Yuksel
European Medical, Health and Pharmaceutical Journal | 2015
Mehmet Eren Yuksel; Funda Tamer
Our Dermatology Online | 2018
Funda Tamer; Mehmet Eren Yuksel
Our Dermatology Online | 2018
Funda Tamer; Mehmet Eren Yuksel