Background: Psoriasis can be described as a T-cell-mediated disease, with a complex role for variety of cytokines and other factors. Among the inflammatory molecules influencing the keratinocites, TNF-α appears critical in sustaining most of the clinical manifestations of psoriasis. It is postulated that changes in cytokine production both locally and systemically could be useful in monitoring disease activity. Objective: The aim of the study was to evaluate serum levels of tumor necrosis factor alpha (TNF-α) in patients with psoriasis and the healthy subjects, and also to assess a possible association between TNF-α, clinical type and severity of disease. Methods: We studied the levels of serum TNF-α in 60 patients with psoriasis and in the serum of helthy 20 controls. According to the clinical type of disease, patients with psoriasis were divided into four groups: chronic plaque psoriasis (CPP), erythrodermic psoriasis (EP), pustular psoriasis (PP) and psoriatic arthritis (PA). Blood samples were collected from all psoriasis patients and from healthy control subjects. Serum level of TNF-α were measured by an enzyme-linked immunosorbent assay (ELISA) technique. The severity of CPP was assessed by Psoriasis Area and Severity Index (PASI). Results: Serum levels of TNF-α in patients with psoriasis were significialy higher than in the control group (3.25+1.74 pg/mL vs 0.20+0.01pg/mL, respectively). Significantly elevated serum TNF-α was in patients with PP type (7.39+6.92 pg/mL). There was statistically significant difference between the mean level of TNF-ɑ compared to the clinical type of psoriasis (p<0.05). The mean PASI score in patients with CPP was 0.56±12.45. It was not found statistically significant correlation between serum level of TNF-ɑ and PASI score in patients with CPP (p>0,05). Conclusion: Our results have demonstrated the imortance of determining serum levels of TNF-ɑ in patients with psoriasis. Further investigations are required to clarify the pathogenic role and clinical significance of TNF-ɑ, and these findings may provide important clues to assist in the development of new therapeutic strategies for patients with psoriasis.

Background: Androgenetic alopecia (AGA) is an androgen-related condition that develops in genetically predisposed individuals. The condition is characterized by the progressive loss of terminal hairs on the scalp in a characteristic distribution. Trichoscopy represents the dermoscopy imaging of the scalp and hair. Structures which may be visualized by trichoscopy include hair shafts, hair follicle openings, perifollicular epidermis and cutaneous microvessels. Objective: The aim of this prospective study was to identify the trichoscopic features of androgenetic alopecia. Methods: Hundred-four patients with AGA and 80 healthy subjects were enrolled in this study. Data on age, gender, personal and family history, clinical type and duration of disease were collected and analyzed. Control group consisted of 80 generally healthy subjects. Trichoscopic examination was performed using either videodermatoscope or handheld dermatoskope. Trichoscopy results were obtained in frontal, occipital and both temporal areas of the scalp, including number of yellow dots and vellus hairs, number of hairs in one pilosebaceous unit and percentage of follicular ostia with perifollicular hyperpigmentation. The data were statistically evaluated. Results: The number of yellow dots, pilosebaceous units with only one hair and with perifollicular hyperpigmentation was significantly increased in androgenetic alopecia (p<0.05). The percentage of thin hairs (<0.03 mm) in AGA was significantly higher than in healthy controls (p<0.05). Conclusion: Our study has shown the significances of trichoscopy of patients with AGA. Regular clinical and trichoscopical follow-ups are very important to monitor disease activity and treatment tolerance.

Introduction: Psoriasis is a common chronic skin disorder characterized by inflammation and abnormal epidermal proliferation. Its severity ranges from a chronic plaque psoriasis (CPP) to generalized psoriatic erythroderma (PE). The cause of psoriasis is unknown although most evidence supports the hypothesis that psoriasis is an immunologically mediated disease. The T-helper (Th) 1 and Th17 cells are responsible for the inflammation of psoriasis. Immunoglobulin E (IgE) is a class of immunoglobulin essential for the allergic response. There is some evidence that IgE may take a part in the pathogenesis of psoriasis. Aim: The aim of the study was to compare serum levels of total IgE between patients with psoriasis and healthy subjects, and to assess the difference between localized form (CPP) and extensive form of disease (PE). Methods: Seventy-five patients with psoriasis and 30 healthy subjects were enrolled in this study. Data on age, gender, personal and family history, clinical type and duration of disease were collected and analyzed. Serum levels of IgE were measured using nephelometric method. Results: Serum levels of total IgE were significantly higher in patients than in controls (46.7% vs.. 10%; p<0.05). Statistical difference of IgE concentration was also observed between CPP and PE. Comparison between patients and controls with regard to the median of the serum level of total IgE levels showed a statistically highly significant elevation in patients (425 IU/ml) compared with controls (54.5 IU/ml) (p<0,05). A higher total IgE concentration was observed in the group of patients with a longer period of skin changes. No relation was found between the serum level of IgE and family history of psoriasis, age or sex (p>0.05). Conclusions: This study supports the evidence that elevation of total serum IgE is associated with psoriasis. The exact role of serum IgE in psoriasis should be additionally investigated in future studies.

A noninvasive diagnostic procedure that allows for in vivo microscopic examination of the epidermis, the dermoepidermal junction, and the papillary dermis. This aids in the identification of specific diagnostic patterns related to color and cell structure to aid in differentiating malignant and benign lesions.

Introduction: Basal cell carcinoma (BCC) is a non-melanocytic skin malignancy arising from basal cells of epidermis or follicular structures. Etiology of BCC is a multifactorial combination of genotype, phenotype, and environmental factors. There are several clinical variants of BCC including nodular, cystic, superficial, morphoeic, keratotic, pigmented and micronodular. Aim: The aim of our study was to analyze the recent clinical trends of basal cell carcinoma by reviewing a single institution’s experience. Methods: Total number of 422 patients clinically diagnosed with basal cell carcinoma were included in the study. Data on age, gender, skin type, personal and family history, duration of disease, localization of lesions, clinical type of lesions, and recurrence rate were collected and analyzed. The data were statistically evaluated. Results: More than 80% of all BCC’s were located on sun-exposed skin areas (p<0.05).The male /female ratio was 1:0.92. The nodular BCC was the most frequent type (59.2%), followed by the superficial (16.1%), pigmented (15.2%) and morphoeic (9.5%) types. The nodular and pigmented types were predominant located on the head and neck, whereas the trunk was the most common location for the superficial type (p<0.05). The tumor is commonly found in concomitance with skin lesion related to chronic sun exposure, such as actinic keratoses, solar lentigines and facial telangiectasia. During this study period, 41 cases showed recurrence of the cancer as the overall recurrence rate was 9.7%. There were no cases with metastasis or fatal outcome. Conclusions: The factors related to the development of BCC were older age and exposure to ultraviolet rays both in recreational and in occupational form. The prevention of BCC is based on the knowledge of risk factors, early diagnosis and treatment, particularly in susceptible populations.

Background: Allergic contact dermatitis (ACD) is a delayed type of hypersensitivity from contact with a specific allergen to which the patients has developed a specific sensitivity. The aim of the study was to evaluate the results of epicutaneous patch testing with standard series of contact allergen in patients suspected to have ACD. Methods: 355 cases of ACD were included in the study. Test substances were applied on the upper part of the patient’s back, on clinically uninvolved and untreated skin. All patients were free from therapy with oral antihistamines, steroids and immunosuppressants. The patch test was removed and reaction were evaluated after 48 h and 72 h. Grading of negative (-) to positive (+ to ++++) patch test was done according to the International Contact Dermatitis Research Group. Statistical data analysis was performed by using χ2–test. Results: Of the 355 cases, 146 patients were male (41.1%) and 209 were female (58.9%). The youngest patients in the study was 16 years of age and the oldest was 67 years of age. The commonest age group affected was 41-50 years. Hands were the most common site of involvement. The occupational character of skin lesions was find in 75 (21.1%). The most common positive reactions were recorded to nickel sulphate 99 (27.8%), cobalt chloride 46 (12.9%), thimerosal 31 (8.7%), colophony 23 (6.5%), carba mix 21 (5.9%), potassium dichromate 20 (5.6%), acid chromici 19 (5.3%), fragrance mix 18 (5%), balsam of Peru 13 (3.7%), formaldehyde 9 (2.5%), and other allergens 26 (7.3%). Females were significantly more likely to show a positive response to two or more allergens (p<0.05). There was no statistically significant impact of age, occupation and duration of disease on results of patch testing (p>0.05). Conclusions: Our results indicate that nickel sulphate, cobalt chloride and thimerosal are the most common allergens responsible for induction of ACD. These findings are crucial in the treatment, long term management, an education of patients with ACD.

Alopecia areata (AA) is a non-scarring inflammatory disease of the hair follicle. Although it usually presents as asymptomatic localized hair loss, it is a disese of very broad spectrum. Alopecia universalis (AU) is an uncommon form of AA that involves the loss of all haed and body hair and is estimated to account approximately 5% of all alopecia cases [1]. The cause of disease is unknown, although there is evidence to suggest that the link between lymphocytic infiltration of the follicle and the disruption of the hair follicle cycle in AA may be provided by a combination of factors, including cytokine release, cytotoxic T-cell activity, and apoptosis [2,3]. It is also considered that a disequilibrium in the production of cytokines, with a relative excess of proinflammatory and Th1 types, vs. anti-inflammatory cytokines may be involved in the persistence of AA lesions, as shown in human scalp biopsies [4]. The immune response presented in AU is associated with aberrant lesional expression of interferon-gamma (IFN-γ), interleukin-2 (IL-2) and IL-1β, and overexpression of ICAM-1 and MHC molecules on hair follicle keratinocytes and dermal papilla cells [5].