Tinea Incognito Due to Trichophyton Rubrum – A Case Report

Tinea incognito is a dermatophyte infection modified by inappropriate and often prolonged use of topical steroids. We present a case of tinea incognito in a 72-year-old woman, referred by her family physician who had unsuccessfully treated the lesions for 3 weeks with topical steroid cream. Physical examination revealed multiple nummular scaly papules and plaques which spread over her arms and trunk. The lesions were circular, erythematous, sharply demarcated with raised scaly edge some coalescing to form moderately infiltrated areas. Direct microscopy was positive for fungal hyphae. Fungal culture on Sabouraud’s agar grew Trichophyton rubrum. The patient was successfully treated with oral terbinafine 250mg daily and 1% clotrimazole cream twice daily. The present case highlights the importance of considering a dermatophytosis when clinical presentation of dermatosis is atypical. Disseminated scaly infiltrate lesions should be investigated for fungal infection in patients previously treated with steroids, as to avoid misdiagnosis and spread of infection

Epidermal Malignant Tumors: Pathogenesis, Influence of UV Light and Apoptosis

Basal cell carcinoma and squamous cell carcinoma, collectively termed non-melanoma skin cancers are the most commonmalignant tumors in humans. Basal cell carcinoma grows slowly and metastatic spread is very rare. Squamous cell carcinoma is characterized by infiltrative, destructive growth and metastasis. Long-term exposure of skin to UV light has a great impact on development of these epidermal malignancies. UV light induces cascade of events like well known DNA damage of keratinocytes as well as still completely undetermined influence on apoptotic process through expression of proapoptotic and antiapoptotic molecules. The major role in development of skin cancer is given to proapoptotic p53 molecule or tumor suppressor gene which mutation due to UV exposure leads to resistance of DNA-damaged cell to apoptosis. Other proapoptotic molecules such as Fas ligand (FasL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are strongly expressed in basal cell carcinoma and squamous cell carcinoma that could be explained by the ability of tumor to escape the attack of immune system

Dermatophyte infections in Primorsko-goranska County, Croatia: a 21-year survey

This study examined the frequency of dermatophytoses in the Primorsko-Goranska County, a north-western part of Croatia, over a period of 21 years (1988-2008). All fungal samples were microscopically examined with 20% potassium hydroxide (KOH) solution. Fungal infections were confirmed in 26.9% cases. Out of these, dermatophytes were isolated in 38.3%, Candida spp. infection in 55.1% cases, while non-dermatophyte molds were identified in 6.6% isolates. The most frequently isolated dermatophyte was Trichophyton (T.) mentagrophytes var. interdigitalis (55.4%), followed by Mycrosporum (M.) canis (36.9%), T. violaceum (3.2%), M. gypseum (2.2%), and T. verrucosum (1.3%). Epidermophyton (E.) floccosum (0.9%) and T. rubrum (0.1%) were identified only sporadically. The most common dermatophytosis diagnosed in the 21-year period was tinea pedis (26.2%) followed by tinea capitis (21.8%) and tinea corporis (20.1%). Toenail onychomycosis (14.5%) was more common than fingernail onychomycosis (2.0%). T. mentagrophytes var. interdigitalis was the major pathogen causing tinea pedis (86.6%) as well as toenail onychomycosis (93.9%), while M. canis was most frequently isolated in tinea capitis (98.6%), tinea corporis (62.1%), and tinea faciei (40.2%). With regard to age and sex, T. mentagrophytes var. interdigitalis infections were predominant in middle-aged men. M. canis affected mostly children up to 9 years with a slight predominance in girls. Data from epidemiological trend analysis such as presented in our study are important for evidence-based public health measures for the prevention and control of dermatophytoses.</p

THE ROLE OF PERFORIN MEDIATED CELL CYTOTOXICITY IN PSORIASIS

Psorijaza je kronično-recidivirajuća upalna bolest kože obilježena poremećajem diferencijacije i proliferacije keratinocita te upalnim infiltratom, mahom T-limfocita u dermisu i epidermisu. Dosadašnje spoznaje upućuju da je psorijaza genski poremećaj proliferacije keratinocita posredovan T-limfocitima koji nastaje zbog poreme}ene aktivacije čimbenika stečene, ali i prirođene imunosti. Glavne populacije izvršnih stanica u psorijatičnom imunosnom odgovoru su pomagački CD4+ i citotoksični CD8+ T-limfociti. Obje vrste izvršnih T-limfocita djeluju na ciljne stanice, bilo putem lučenja citotoksinâ (perforina i granzima) ili pak putem molekula vezanih na membranu citotoksičnih stanica poput liganda za molekulu Fas (FasL). Za sada, uloga mehanizama stanične citotoksičnosti u patogenezi psorijaze, napose onih posredovanih perforinom, još nije dovoljno istražena. Perforin je citolitički protein pohranjen u citoplazmatskim granulama citotoksičnih T-limfocita i priro|eno ubilačkih stanica s osnovnom ulogom stvaranja perforinskih pora čime se otvara prolaz za ulaz granzima i drugih proapoptotskih molekula u ciljnu stanicu i izaziva njezina smrt apoptozom. Povečana ekspresija molekula perforina utvrđena je u oboljelih od nekih autoimunosnih bolesti kao što su multipla skleroza, autoimunosni tireoiditis te reumatoidni artritis. Novija istraživanja govore u prilog uključenosti ovih mehanizama i u imunopatogenezu psorijaze. Nakupljanje perforin-pozitivnih (P+) stanica u psorijatičnom epidermisu tik do apoptotski promijenjenih keratinocita upučuje da upravo T-limfociti oslobađanjem citolitičkih molekula uništavaju psorijatične keratinocite. S druge strane, apoptotski keratinociti mogli bi aktivirati regenerativni program cijeljenja uzrokujuči hiperplaziju keratinocita, što je ujedno i glavno obilježje psorijaze. Napredak u poznavanju izvršnog dijela stanične citotoksičnosti u psorijatičnom plaku možda će u budućnosti omogućiti da se odabirno zaustave određeni citolitički mehanizmi i molekule čime se uspostavlja potpuno nov i specifičniji pristup u liječenju psorijaze.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

THE ROLE OF BCL-2 FAMILY PROTEINS IN PSORIASIS

Apoptoza je fiziološki proces programirane smrti stanica odgovoran za održavanje homeostaze u organizmu. U koži se procesom apoptoze nadzire proliferacija i diferencijacija keratinocita te tako održava homeostaza unutar epidermisa. Proces programirane stanične smrti nadziru proteini porodice Bcl-2 uključujući više proapoptotskih (Bax, Bak, Bad) i protuapoptotskih molekula (Bcl-2, Bcl-xl). Danas se smatra da poremećaj procesa apoptoze ima važnu ulogu u razvoju mnogih kožnih bolesti. Psorijaza je kroničnorecidivirajuća upalna bolest kože obilježena poremećajem diferencijacije i proliferacije keratinocita te sniženom apoptozom keratinocita unutar epidermisa. Na temelju dosadašnjih spoznaja o ulozi programirane stanične smrti u nastanku psorijaze, čini se da apoptoza ima važnu ulogu u razvoju epidermalne hiperproliferacije psorijatične lezije. Budući da proteini porodice Bcl-2 nadziru proces apoptoze, važno je razjasniti njihovu ulogu u patogenezi psorijaze. Naime, uočena povećana ekspresija protuapoptotskih, a sniženo izražavanje proapoptotskih molekula porodice Bcl-2 u psorijatičnoj koži upućuju na njihovu važnost u razvoju bolesti.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-xL) 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

THE ROLE OF PERFORIN MEDIATED CELL CYTOTOXICITY IN PSORIASIS

Psorijaza je kronično-recidivirajuća upalna bolest kože obilježena poremećajem diferencijacije i proliferacije keratinocita te upalnim infiltratom, mahom T-limfocita u dermisu i epidermisu. Dosadašnje spoznaje upućuju da je psorijaza genski poremećaj proliferacije keratinocita posredovan T-limfocitima koji nastaje zbog poreme}ene aktivacije čimbenika stečene, ali i prirođene imunosti. Glavne populacije izvršnih stanica u psorijatičnom imunosnom odgovoru su pomagački CD4+ i citotoksični CD8+ T-limfociti. Obje vrste izvršnih T-limfocita djeluju na ciljne stanice, bilo putem lučenja citotoksinâ (perforina i granzima) ili pak putem molekula vezanih na membranu citotoksičnih stanica poput liganda za molekulu Fas (FasL). Za sada, uloga mehanizama stanične citotoksičnosti u patogenezi psorijaze, napose onih posredovanih perforinom, još nije dovoljno istražena. Perforin je citolitički protein pohranjen u citoplazmatskim granulama citotoksičnih T-limfocita i priro|eno ubilačkih stanica s osnovnom ulogom stvaranja perforinskih pora čime se otvara prolaz za ulaz granzima i drugih proapoptotskih molekula u ciljnu stanicu i izaziva njezina smrt apoptozom. Povečana ekspresija molekula perforina utvrđena je u oboljelih od nekih autoimunosnih bolesti kao što su multipla skleroza, autoimunosni tireoiditis te reumatoidni artritis. Novija istraživanja govore u prilog uključenosti ovih mehanizama i u imunopatogenezu psorijaze. Nakupljanje perforin-pozitivnih (P+) stanica u psorijatičnom epidermisu tik do apoptotski promijenjenih keratinocita upučuje da upravo T-limfociti oslobađanjem citolitičkih molekula uništavaju psorijatične keratinocite. S druge strane, apoptotski keratinociti mogli bi aktivirati regenerativni program cijeljenja uzrokujuči hiperplaziju keratinocita, što je ujedno i glavno obilježje psorijaze. Napredak u poznavanju izvršnog dijela stanične citotoksičnosti u psorijatičnom plaku možda će u budućnosti omogućiti da se odabirno zaustave određeni citolitički mehanizmi i molekule čime se uspostavlja potpuno nov i specifičniji pristup u liječenju psorijaze.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