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Acne vulgaris is a chronic inflammatory disease of multifactorial etiology that affects the pilosebaceal unit. The characteristic period for onset of acne is adolescence with increasing persistence or the appearance of acne in adulthood. The clinical presentation of acne can vary from mild to severe, characterized by a variety of lesions that include comedones, papules, pustules and nodules, scarring and dispigmentation. The etiopathogenesis of acne is complex and involves the interaction of endogenous and exogenous factors. The main pathogenetic mechanisms take place in the pilosebaceal unit and include increased production and altered lipid composition of sebum, hyperkeratinization, reproduction of Cutibacterium acnes bacteria and inflammation. In addition to these factors, today attention is focused on other etiological factors that may contribute to the development of acne, and include diet, stress, the connection of intestinal microflora, brain and skin, sun exposure, premenstrual acne, comedogenic cosmetics and smoking. Given the diversity of etiological factors and the complexity of pathogenesis, finding a single cure with satisfactory effects and good tolerability is not easy. Acne, due to its characteristic clinical features involving the face and causing sometimes permanent scarring, if untreated can lead to negative psychosocial consequences on the individual. Therefore, it is of extreme importance to have a good understanding and knowledge of the etiology and pathogenesis of acne so that these insights can be directed towards the development of effective treatment. [ABSTRACT FROM AUTHOR]

Background: Marjolin’s ulcer is a rare entity related to squamous cell carcinoma of the skin that develops in the area of a chronic wound, and has a more aggressive course, with infiltrative growth, a higher recurrence rate, a higher metastatic potential, and a higher mortality rate. Aim: To raise awareness of the possibility of developing squamous cell carcinoma in the area of chronic wounds, and to discuss therapeutic options, since due to the specifics of Marjolin’s ulcer, there is no unambiguous therapeutic approach. Case Report: A 77-year-old patient was referred to the Dermatovenereology Clinic for an ulcer of her right lower leg. She stated that the ulceration on the lower leg lasted and recurred for many years, and the recent verrucous ulcerated change persisted for more than a year. After two months of unsuccessful conservative therapy, a biopsy of the chronic wound was performed, and the presence of squamous cell carcinoma was found. Due to the large local finding and the absence of metastases, it was decided that the patient receives primary radical radiotherapy. Three months after radiotherapy, a major lower leg defect was described which, compared to the preoperative finding, indicated regression of the tumor process. A week later, a pronounced edge of the change was observed. A biopsy was performed, but no recurrence of the tumor was found. One year after radiotherapy, a chronic wound without recurrence of squamous cell carcinoma but with delayed healing was described. Conclusion: Although Marjolin’s ulcer, an aggressive form of squamous cell carcinoma, is a rare entity, it should be considered when the chronic wound is not healing, in the absence of risk factors for ulceration. Future research is needed to determine a standard therapeutic approach, as well as the optimal follow-up period. [ABSTRACT FROM AUTHOR]

Aim: To analyze the distribution of HLA-DRB1-DQA1-DQB1 haplotypes as well as the extended haplotype Cw*0602-B57-DRB1*07-DQA1*0201-DQB1*0201 in patients with positive and negative family history of psoriasis. Patients and methods: The association of HLA genes classes I and II with psoriasis has been studied in 118 patients with chronic stable psoriasis. The frequency of HLA haplotypes was analyzed by means of serology and hybridization with specific oligonucleotide probes. Results: The group with positive family history showed a significant association with DRB1*07-DQA1*0201-DQB1*0201 and DRB1*07-DQA1*0201-DQB1*0303 as well as with the extended haplotype Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0201 (P = 0,004). The frequency of extended haplotype in the group with negative family history was similar to the control group. Conclusion: Psoriatics with positive family history show stronger association with susceptible HLA haplotypes, thus stressing the role of HLA genes in psoriasis inheritance. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 40-year-old man with foot rash, joint swelling, and low back pain. Topics include yellow pustules with hyperkeratosis consistent with keratoderma blenorrhagicum noted on the plantar surfaces of the feet; and treatment with nonsteroidal antiinflammatory agents, systemic glucocorticoids, and sulfasalazine showing the patient's symptoms abated.

Copyright of Collegium Antropologicum is the property of Croatian Anthropological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Collegium Antropologicum is the property of Croatian Anthropological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lichen planus is recognized as a T-cell-mediated disease. Histologically, it is characterized by the formation of colloid bodies representing apoptotic keratinocytes. The apoptotic process mediated by CD8+ cytotoxic T lymphocytes (CTLs) and NK cells mainly involves two distinct pathways: the perforin/granzyme pathway and the Fas/FasL pathway. So far, little is known regarding the role of perforin-mediated apoptosis in lichen planus. In the present study, the expression and distribution of perforin, T and NK cell subsets in the epidermis and dermis of lesional and nonlesional lichen planus skin were studied. Skin biopsy specimens from lesional and nonlesional skin of ten patients with lichen planus and eight healthy persons were analysed by immunohistochemistry. Significant accumulation of T cells, particularly of CD4+ and CD8+ subsets, was found in both epidermis and dermis of lichen planus lesions compared with nonlesional and healthy skin. There were no significant differences in the incidence of NK cells (CD16+ and CD56+) between lesional, nonlesional and healthy skin. Perforin expression was significantly upregulated in the epidermis of lichen planus lesions. In conclusion, accumulation of perforin+ cells in the epidermis of lichen planus lesions suggest a potential role of perforin in the apoptosis of basal keratinocytes. [ABSTRACT FROM AUTHOR]

Copyright of Collegium Antropologicum is the property of Croatian Anthropological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Collegium Antropologicum is the property of Croatian Anthropological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aim To assess the differences in the way how Slovenian and Croatian health care professionals (HCPs) confront ethical dilemmas and perceive the role of hospital ethics committees (HECs). Methods This cross-sectional, survey-based study involved HCPs from three Slovenian and five Croatian university medical centers (UMC). The final sample sizes were 308 (244 or 79.2% women) for Slovenia and 485 (398 or 82.1% women) for Croatia. Results Compared with Croatian physicians, Slovenian physicians reported a higher share of ethical dilemmas regarding waiting periods for diagnostics or treatment, suboptimal working conditions due to interpersonal relationships in the ward, and end-of-life treatment withdrawal, and a lower share regarding access to palliative care and patient information protection. Compared with Croatian nurses, Slovenian nurses reported a lower share of ethical dilemmas regarding the distribution of limited resources, recognizing the patient's best interests, and access to palliative care. Compared with Croatian other HCPs, Slovenian other HCPs reported a lower burden of ethical dilemmas regarding waiting periods for diagnostics or treatment, distribution of limited resources, and access to palliative care. When encountering an ethical dilemma, all HCPs in both countries would first consult their colleagues. Slovenian and Croatian HCPs recognized the importance of the HECs to a similar extent, but viewed their role differently. Conclusion Croatian and Slovenian HCPs are confronted with different ethical dilemmas and perceive the role of HECs differently. [ABSTRACT FROM AUTHOR]

Alopecia areata (AA) is a frequent disease with nonscarring hair loss on the scalp and/or body. Hair follicle in alopecia areata is not irreversibly destroyed, so potential for hair regrowth remains. Considering unknown etiopathogenesis, treatment of AA is symptomatic and directed toward halting disease activity. Lymphocytic inflammatory infiltrate around hair follicle, increased levels of autoantibodies, cytokine abnormalities and increased prevalence of autoimmune comorbidities, support the hypothesis of AA as an organ-specific autoimmune disorder. Therefore, investigations are directed toward new immunomodulatory or immunosuppressive drugs with induction effect on hair growth. New biologic drugs and their influence on hair growth as well as genetic therapy for alopecia areata are currently under investigation. Contemporary principles in therapy of alopecia areata and treatments available will be discussed in this article.

Psoriasis is a common chronic inflammatory skin disease characterized by hyperproliferation and incomplete differentiation of epidermal keratinocytes as well as by inflammatory infiltrate of T-lymphocytes in dermis and epidermis. Psoriasis is nowadays also recognized as a T cell mediated disease resulting from aberrant activation of both innate and adaptive immunity. The main effector cells in mediating psoriatic phenotype are helper CD4+ T cells and cytotoxic CD8+ T cells. Both, CD4+ and CD8+ T cells, mediate apoptosis via the release of cell granules, perforin and granzymes or by binding of ligands to their death receptors on target cells. The role of cell cytotoxicity mechanisms, particularly those mediated by perforin, in psoriasis is as yet unclear. Perforin is a pore forming molecule, located within the cytoplasm of cytotoxic T cells and natural killer cells, which enables entry of granzymes and other apoptotic molecules into the target cell in order to mediate programmed cell death. The importance of perforin-mediated cytotoxicity has been demonstrated in several autoimmune diseases and in some inflammatory skin diseases. Recent studies claimed its role in the immunopathogenesis of psoriasis as well. Accumulation of perforin-positive cells in psoriatic epidermis close to damaged keratinocytes suggests that T lymphocytes induce damage to keratinocytes by releasing cytolytic molecules. On the other hand, apoptotic keratinocytes might trigger an injury response program causing regenerative hyperplasia of epidermal keratinocytes, a hallmark of psoriasis. Progress in understanding of effector part of cell cytotoxicity in psoriatic plaque might in future enable more specific treatment of psoriatic patients by blocking selectively each of proposed cytolytic mechanisms and molecules as potential new therapeutic targets.

Apoptosis is a physiological process of programmed cell death responsible for homeostasis in the body. In skin, apoptotic process regulates keratinocyte proliferation and differentiation in that way maintaining homeostasis of epidermal compartment. The process of apoptosis is controlled by proteins of the Bcl-2 family, several proapoptotic (Bax, Bak, Bad) and antiapoptotic (Bcl-2, Bcl-x(L)) proteins. Nowadays, it seems that dysfunctional apoptosis has an important role in the pathogenesis of several skin diseases. Psoriasis is a chronic hypeproliferative inflammatory skin disease characterized by abnormal keratinocyte hyperproliferation and differentiation as well as by decreased keratinocyte apoptosis. Based on recent studies, it is likely that apoptosis has an important role in epidermal hyperproliferation of psoriatic lesion. Having in mind the significance of Bcl-2 family proteins in apoptosis, it is important to elucidate their role in psoriasis pathogenesis. Observed upregulation of antiapoptotic and downregulation of proapoptotic Bcl-2 family molecules in psoriatic skin implies their significance in psoriasis development.

Psoriasis is a chronic skin disease characterized by epidermal hyperproliferation that is probably mediated by an immunologic reaction to particular epidermal, dermal or circulating immunogenic peptide. The inheritance of psoriasis within some families suggests the importance of genetic factors in the pathogenesis of the disease. Population based studies revealed that psoriasis is associated with HLA genes class I and II located on the chromosome 6. The highest risk of developing psoriasis carries the HLA-Cw*0602 gene. The analysis of HLA polymorphism in Croatian patients also showed the importance of Cw*0602 allele in psoriasis susceptibility. Until now, eight different gene loci for psoriasis are mentioned in the OMIM (Online Mendelian Inheritance in Men) data base. Even though, the psoriasis association with HLA genes is doubtless, only some carriers of susceptible genes develop the disease. Therefore, some other genes except HLA genes as well as some environmental factors have a role in the pathogenesis of psoriasis.

Psoriasis is a chronic hypeproliferative inflammatory skin disease characterized by abnormal keratinocyte hyperproliferation and differentiation, intra-epidermal accumulation of neutrophil granulocytes, and dermal inflammatory infiltrate that mostly consists of T-cells. Today, psoriasis is definitely recognized as a T-cell-mediated inflammatory disease. Infiltration of T-cells seems to be the primary event that precedes the keratinocyte hyperproliferation. It is suggested that systemic lymphocyte activation is followed by the local accumulation of specific CD4+ T-cells and subsequently by the activation of intradermal CD8+ T-cells. So far, it seems that CD4+ T-cells create an appropriate type-1 cytokine environment for CD8+ T-cells activation that eventually trigger the psoriatic cascade. Thus, T-cells are responsible for initiation and maintenance of psoriasis. The precise mechanism how activated T-cells trigger psoriasis is yet unknown. However, it seems that the specific immune reaction to a putative antigen, mediated by T-cells leads to creation of psoriatic lesions. The immune reaction constantly driven by bacterial superantigens or epidermal self-antigens eventually leads to development of psoriatic lesions. The psoriatic process is a dynamic process that includes interaction between Th1- and Tc1-cells as well as between T-cells and keratinocytes. The better understanding of the immunopathogenesis of psoriasis would allow for development of specific T-cell-targeted and/or cytokine-targeted new therapies.