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Lichen planus is a chronic inflammatory mucocutaneous disorder commonly affecting the skin, nails, hair, and mucous membranes (1). Although its main cause is still unclear, lichen planus is defined as a T cell- mediated inflammatory disease (2). CD8+ T lymphocytes activate their cytotoxic armamentarium and induce basal keratinocyte apoptosis (2). The susceptibility of basal keratinocytes to CD8+ T lymphocytes is enhanced through MHC class I expression on keratinocytes triggered by interferon (IFN)- gamma (3). The cytotoxic process is mainly mediated by the release of lytic molecules, such as perforin, granzyme B, and granulysin (GNLY) (4–8). The upregulation of perforin and granzyme B has been previously demonstrated in the peripheral blood and lesional skin of patients with lichen planus (4–8). GNLY is a member of the saposin-like lipid-binding protein (SAPLIP) family and has a cytotoxic effect on tumour cells and a variety of microorganisms (9, 10). It is located in the cytotoxic granules of T cells, which are released upon antigen stimulation, and in the cytotoxic granules of natural killer (NK) cells. GNLY presence has only recently been observed in lichen planus lesions, but the expression level of this molecule in peripheral blood and subsequent determination of cells that express this molecule in blood and lesions remains unknown (8). In this study we examined the dynamics of GNLY expression in different cytotoxic subtypes of peripheral blood lymphocytes and in the skin lesions of patients with lichen planus.

Case report of a patient developing severe bullous hemorrhagic Sweet syndrome following application of the first dose of the SARS- CoV-2 Oxford AstraZeneca vaccine.

Targeted biologics have been successfully used for the treatment of moderate to severe psoriasis1 . However, in parallel to the increasing use of biological agents, the number of paradoxical adverse events (PAEs) is increasing as well2 . Herein, we report a case of a palmoplantar pustular reaction in a patient with severe psoriasis treated with ixekizumab. A 50-year-old-woman with a 30-years-history of psoriasis was referred to our Department due to progressive exacerbation of severe chronic plaque psoriasis (PASI 16.8) in spite of methotrexate therapy. Thus, ixekizumab at scheduled dosage was started. Initially, a rapid improvement of psoriatic lesions was observed.

Psoriasis is a recurrent, chronic, immune-mediated, systemic inflammatory disease of the skin, joints, and other organic systems. After atopic dermatitis, chronic stationary psoriasis is the most common inflammatory skin disease, affecting an average of 2–4% of the world’s population. The disease carries a significant burden due to its numerous comorbidities and the major impact on patients’ social and emotional aspects of life. According to current knowledge, psoriasis is a multifactorial disease that occurs in genetically predisposed individuals under various environmental factors, which trigger an immune response disorder with a series of complex inflammatory cascades. The disease is initiated and maintained by mutual interaction of the innate and adaptive immune cells, primarily dendritic cells, T lymphocytes, and keratinocytes, whose leading role alternates at different stages of the disease, consisting mainly in the IL-23/Th17 pathway. Inflammatory events result in consequent epidermal and dermal changes and evolution of the characteristic psoriatic phenotype, respectively. This paper aims to present a comprehensive overview of current knowledge on psoriasis genetic and environmental etiological factors, immunopathogenesis, and the leading cellular and cytokine participants in the inflammatory pathways of this disease.

Pojavnost atopijskog dermatitisa (AD) tijekom posljednjih desetljeća u porastu je, što je osobito izraženo u zemljama zapada. Smatra se da je uzrok smanjena izloženost mikroorganizmima tijekom najranijeg djetinjstva i posljedično smanjena stimulacija imunološkog sustava. Budući da crijevna mikroflora predstavlja prvi i najveći izvor mikrobnog opterećenja, promjene u njezinu sastavu i raznovrsnosti smatraju se čimbenikom nastanka AD-a. To je razlog zašto se probiotici, zahvaljujući svojoj sposobnosti manipulacije sastavom mikroflore i imunomodulatornim učincima, smatraju mjerom prevencije i liječenja atopijskog dermatitisa. Dosadašnje studije ukazuju na njihov preventivni potencijal, no kao terapijska intervencija nisu pokazali pozitivne učinke. Ipak, primjena probiotika u AD-a za sada je ostala predmetom istraživanja, a buduće studije trebale bi razjasniti zaslužuju li oni mjesto među ostalim preventivnim i terapijskim mjerama te razriješiti nedoumice glede njihove primjene., The prevalence of atopic dermatitis (AD) has risen over the past decades, and this is especially expressed in western countries. Reduced microbial exposure during infancy and therefore reduced stimulation of immune system is considered to be the cause for this rising prevalence. Intestinal microbiota represents the first and major source of microbial exposure and therefore the changes in its composition and diversity are considered to be responsible for development of AD. That is why probiotics are, owing to their ability to manipulate the composition of microbiota and their immunomodulatory effects, considered to be a promising prevention and therapeutic intervention of atopic dermatitis. Former studies indicate that they have a preventing potential, but their therapeutic effects have not been proven. However, probiotic use in AD is a subject of reasearches at the moment, and future studies should clearify if they deserve a place among the other preventive and therapeutical measures and resolve uncertanities regarding their administration.

TNF-related apoptosis-inducing ligand (TRAIL) is recognized as an important regulator of immune responses during infections and various autoimmune-mediated pathologies. Its role in inflammatory dermatoses is largely unknown. We aimed to investigate the expression of TRAIL and its receptors DR4 and DR5 in psoriasis vulgaris. Immunohistochemistry for TRAIL, DR4 and DR5 was performed on samples of lesional (n = 10) and non-lesional (n = 10) skin of patients with plaque psoriasis and skin of healthy volunteers (n = 10). Expression of TRAIL and its receptors was further examined by means of double immunofluorescence staining and co-localization with CD4, CD8, CD11c, CD68, CD16 and CD56 markers. Immunohistochemical staining for TRAIL was significantly enhanced in psoriatic lesional as well as non-lesional epidermis compared to the epidermis of healthy skin. Lesional epidermis also showed increased immunoreactivity for DR5. In addition, expression of TRAIL and both of its receptors was significantly increased in the dermis of lesional skin. As evidenced by double immunofluorescence, TRAIL was readily expressed by most of the examined cells of the inflammatory infiltrate in psoriatic lesions. In contrast, the expression of DR4 was found mostly among CD4+ and CD8+ cells but was only nuclear, while DR5 showed cytoplasmic staining in rare CD16+, CD56+ and CD68+ cells. According to abundant in situ presence of TRAIL and its receptors in lesional psoriatic skin, it seems that this cytokine participates in the complex interplay between keratinocytes and cells of the dermal infiltrate and thus contributes to the inflammatory cycle in psoriasis vulgaris.

It is well known that several psychiatric disorders may be related to childhood psychological trauma. Recent studies have associated childhood exposure to trauma to some skin diseases. Our study aimed at exploring whether psoriasis is related to the reported positive and negative traumatic life events in different age intervals beginning from early childhood to adulthood. Furthermore, we investigated differences between psoriatics with early and late onset according to traumatic experiences in different age intervals. Also, we investigated the possible correlation of traumatic experiences with the disease severity. One hundred patients with psoriasis and 101 controls (patients with skin conditions considered to be "non-psychosomatic") were enrolled in the study. All participants completed a specific questionnaire measuring traumatic life experiences (Traumatic Antecedents Questionnaire, TAQ). The TAQ assesses positive personal experiences (competence and safety) and negative personal experiences (neglect, separation, secrets, emotional, physical and sexual abuse, trauma witnessing, other traumas and exposure to alcohol/drugs) from early childhood to adulthood. The severity of psoriasis was estimated according to the Psoriasis Area and Severity Index (PASI), a standardized measuring instrument. The amount of positive experiences did not differ significantly among groups, except for safety scores that were higher in controls compared with both psoriatic groups (early and late onset). On the other side, negative traumatic experiences appeared more frequently in patients with psoriasis during all developmental periods. We found no correlation between severity of psoriasis and traumatic experiences. The present study demonstrates an increased history of childhood and adulthood negative traumatic experiences in patients with psoriasis compared to the control group. Our findings suggest a relationship between retrospectively reported negative traumatic experiences and psoriasis.

Psoriasis is a chronic papulosquamous skin disease, histologically characterized by epidermal hyperproliferation and dermal infiltration of inflammatory cells. The majority of T lymphocytes infiltrating dermis are CD4+ T lymphocytes secreting type 1 and type 17 cytokines. These cytokines are responsible for triggering keratinocyte proliferation as well as chemokine secretion and subsequent migration of other inflammatory cells in the skin. Contrarily, lymphocytes that accumulate in epidermis are mainly CD8+ T lymphocytes. According to the recent findings, these cells can also secrete type 1 and type 17 cytokines. However, it is demonstrated so far that epidermal CD8+ T lymphocytes contain higher amounts of cytolytic molecules, such as perforin, granzyme B and granulysin whose role in psoriasis pathogenesis is still unknown. Therefore, in this article we hypothesize the active involvement of cell mediated cytotoxicity in killing the proliferating keratinocytes as a mechanism of potential self-defense and possible brake in psoriatic plaque formation, maintaining skin homeostasis.

The aim of the study was to analyze the Microsporum canis infections in the Rijeka area, Croatia, observed between 1990 and 2001. A total of 724 cases of dermatophytosis caused by M. canis were diagnosed in 320 individuals with the tinea capitis and 404 with tinea corporis. The M. canis infections constituted 32.8% of all dermatophytes isolated during the study period.

Zusammenfassung Die Haufigkeit von Dermatomykosen und ihr Erregerspektrum im Raum Rijeka, Nordwestkroatien, wurde im Zeitraum vor und wahrend des Krieges 1990– 1994 sowie in der Nachkriegszeit 1995– 1999 analysiert. Insgesamt 20463 Patienten mit klinisch manifesten Dermatomykosen wurden an der Klinik fur Dermatovenerologie in Rijeka untersucht. Im Zeitraum 1990-1994, waren 2462 Proben positiv, im Zeitraum 1995– 1999. waren 2250 Proben positiv. Die am haufigsten isolierten Dermatophyten waren Trichophyton mentagrophytes und Microsporum canis, gefolgt von Microsporum gypseum, Epidermophyton floccosum, Trichophyton verrucosum und Trichophyton rubrum. Die grossere Anderung im Dermatophytenspektrum wurde in der Nachkriegszeit beobachtet, verursacht durch die Bevolkerungswanderung aus den anderen Regionen nach Rijeka. Dies zeigte sich mit dem Verschwinden von T. verrucosum und T. rubrum und dem Auftauchen von Trichophyton violaceum. Diese antropophile Art wurde die dritthaufigste. Unsere Befunde wurden mit denen aus fruheren Studien in der selben Region und mit den aus anderen Landern verglichen.

The Hair Follicle (HF) is a vital component of mammalian skin and represents a unique, highly regenerative system that undergoes phases of rapid growth, regression, and resting periods. The hair cycling is of profound clinical relevance since majority of the hair growth disorders occur as a result of cycle changes. The influence of many molecules governing the formation of HF has been investigated and many of important cycle mediators have been identified. Cellular and molecular events during cycling are controlled by a network of sequential activation of autocrine, paracrine and endocrine signaling pathways. This implies variations in the expression or activity of the Wnt family molecules, Fibroblast Growth Factor (FGF), Transforming Growth Factor β (TGF-β), Hedgehog pathway, β-Catenin pathway, noggin, transcription factor Stat3, Epidermal Growth Factor (EGF), Insulin Growth Factor-1 (IGF- 1), Vascular Endothelial Growth Factor (VEGF), Thyrotropin Releasing Hormone (TRH), Polyamine, Spermidine, Neurotrophins (NT3, NT4), prolactin, retinoids, Bone Morphogenetic Protein 4 (BMP4), cathepsin L, 17-β estradiol, dihydrotestosterone and many others. Despite considerable progress in this area, the key elements of cycle control have not been identified. Therefore, for the most common hair disorders several agents are available, even none of these is curative or preventive. The one of the prime challenges of hair research is a better understanding of the molecular controls of hair cycling and developing drug which would effectively manipulate the cycle. Future therapy strategies will be based on new and better knowledge about the HF biology. Until than, alopecia areata, telogen effluvium and androgenetic alopecia, will remain unsolved medical problems.

This open study was conducted in 72 outpatients with acne vulgaris, to compare the clinical efficacy and tolerability of azithromycin and minocycline. Azithromycin was administered as a single oral dose (500 mg/day) for 4 days in four cycles every 10 days and minocycline was administered 100 mg daily for 6 weeks. Improvement was assessed 6 weeks after initiation of treatment with a four-graded scale. A satisfactory clinical response was observed in 75.8% of the patients treated with azithromycin and in 70.5% of those treated with minocycline. There were no significant differences between these two acne treatments in terms of reduction of the number of lesions (p> 0.05). Both agents were well tolerated and mild side effects were reported in 10.3% of azithromycin and 11.7% of minocycline treated patients. We conclude that azithromycin is at least as clinically effective and well tolerated as minocycline as treatment of facial comedonic and papulopustular acne.

The aim of this study was to determine the prevalence of true local anesthetic (LA) allergy among patients referred for suspected hypersensitivity and to describe the main characteristics of adverse drug reactions (ADR) induced by LA in our population. We retrospectively analyzed the medical files of patients referred to the Department of Dermatovenereology, University Hospital Center Rijeka, Rijeka, Croatia, for the investigation of LA hypersensitivity in the period between January 2000 and December 2012. A total of 331 patients underwent skin testing and, in cases of negative results, subcutaneous exposition to LA. In patients with suspected delayed reaction, patch test was performed. Altogether, 331 patients reported 419 independent ADR occurring during 346 procedures. Most commonly, patients reported having only one ADR, but 41 (12.4%) of them had two reactions, 14 (4.2%) had three, five (1.5%) had four and in one patient (0.3%) five ADR to LA were observed. The majority of reactions occurred during dental procedures when most commonly lidocaine and articaine were used. Local reactions were reported in 44 patients, whereas 490 general symptoms occurred during 375 independent ADR in 287 patients. The most common symptoms were cardiovascular system reactions in 89 patients (18.2%). Allergic reaction was detected in three patients (0.91%). One patient showed immediate-type reaction to bupivacaine and two patients had a delayed-type reaction to lidocaine. Adverse reactions to LA are common and are mostly due to their pharmacological properties and drug combinations or psychogenic origin. Allergic accidents to LA are rare.

Psoriasis is probably as old as mankind. Today, it is a well defined skin disease, in which genetic, environmental and immunologic factors participate in etiopathogenesis. However, despite its frequency, chronicity and visibility, it is quite hard to find a description of psoriasis in the works of the ancient physicians. Dermatology developed slowly, first with appearance of the protodermatologists at the end of the 18th century, and continued with the arrival of the first dermatologists. From those times psoriasis became a distinct entity. However, until the last century, the descriptions of disease considered «morbi in pulchredine», were rather vague, the denomination not standardized and the translation from one language to others discrepant. Different authors called the disease with various names, while diverse diseases had the same names. The confusion in terminology and description of psoriasis lasted for centuries.

Background: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) has been implicated in the pathogenesis of various inflammatory pathologies and cancer. We aimed to investigate its expression in normal human skin, inflammatory skin diseases and epidermal neoplasms. Methods: Immunohistochemistry for TWEAK was performed in samples of healthy skin, plaque psoriasis, lichen planus, prurigo nodularis, discoid lupus erythematosus, lichen sclerosus, seborrheic keratosis, common warts, actinic keratosis, Bowen’s disease, keratoacanthoma and basal and squamous cell carcinoma. Double immunofluorescence was used to investigate co-localization of TWEAK with cytokeratin-10 and proliferating cell nuclear antigen (PCNA). Results: TWEAK was robustly expressed in the epidermis of healthy skin and decreased in inflammatory conditions, both in the context of epidermal hyperplasia and atrophy. Decreased TWEAK immunoreactivity was regularly observed in common warts, actinic keratosis and Bowen’s disease, particularly in areas of marked proliferation as evidenced by PCNA-positive nuclei. In squamous cell carcinoma, expression of TWEAK ranged from strong to completely absent, and it mostly corresponded with the expression of cytokeratin-10. TWEAK was absent in keratoacanthoma and basal cell carcinoma. Conclusions: TWEAK is a constitutively expressed epidermal protein whose downregulation might be an early indicator of disturbed differentiation or pathologic proliferation of keratinocytes that accompany inflammatory and neoplastic skin diseases.

Current research in pathogenesis of psoriasis vulgaris suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained by T cells. However, the question of lymphocyte being an initiator of psoriatic events remains open so far. Clinical observations such as plaque symmetry, stress-induced onset or exacerbations, pruritus, and possibility of generalization, suggest a role of the nervous system and neurogenic inflammation in pathogenesis. A key to understanding the role of melanocyte in psoriasis is their ability to act as regulatory cell in maintaining epidermal homeostasis. In suggested hypothetic event, melanocyte, acting as a local "stress sensor", provide communicatory link between CNS and skin. The disease probably begins with so far unknown signal directed through neuronal network to the melanocyte, placed in the center of epidermal unit. That signal governs keratinocyte cellular activities and lead to reactive abnormal epidermal differentiation and hyperproliferation. Increased proliferation of basal keratinocytes and high metabolic demands creates angiogenesis in papillary dermis and elongation of dermal papillae. Stimulated melanocytes and basal keratinocytes become an important source of proinflammatory cytokines that attract lymphocytes in dermis. In conclusion, according to our hypothesis, lymphocyte infiltrate in psoriasis is secondary event rather than vice versa as presented in the literature.

Generally, the cumulative UV exposure correlates with the site-specific incidence of skin cancer but more detailed analysis showed that the frequency of BCC of some facial regions cannot be explained with site-specific UV exposure. Apoptosis plays a central role in cancer development due to suppressed process of programmed cell death. Anatomic localization, UV and senescence can influence expression of apoptosis related molecules resulting in advantage of cancer cells development and tumor progression. Anti-tumor immune response, as an important factor in elimination of cancer cells, is also modified by UV radiation and aging, further contributing to cancer progression and its development. Hypothesis: UV radiation, senescence and proliferation intensity influence the expression of apoptosis related molecules in normal keratinocytes. Mutated cells express altered molecules with different degree of antigenicity. We propose that small differences in the expression of pro- and anti-apoptotic molecules in the keratinocytes in association with the local immune reaction (modulated also by UV radiation) determine the type of the non-melanoma skin cancer as well as their frequency (site-specific incidence). In vitro and in vivo models could explain how the modulation of UV can influence the apoptotic system and local immune reaction, while animal experiments could explain different site-specific incidence (frequency) of the same tumor. Better understanding of these mechanisms could lead to development of different therapeutic approaches for early elimination of cancer prone cells or cells in early stages of cancer development. The same model could be used to explain the site-specific localization of other types of cancer (i.e. melanoma) or benign tumors.

Granuloma annulare (GA) is a common dermatosis characterized by an annular arrangement of erythematous papules, plaques, rarely nodules or patches. It is a type of non-infectious granuloma with unknown etiology. Hypothesis. The immune reaction always begins with the foreign-body granuloma formation. However, if during the process the antigen is recognized as too small the immune reaction stops the granuloma development. In the case of GA the dysfunctional control mechanism continues to sustain the granulomatous formation. Because the target does not exist anymore, the initiated process starts the "search" for a new target (circular spreading). Different histological and clinical presentations depends on which gene of the control mechanism is dysfunctional, while the distribution depends on the type of antigen and its distribution at the start of the immune reaction. The disappearance of GA after biopsy, that occurs in some cases, could be attributable to the specific defective gene involved (the biopsy can disrupt only some type of GA). So, new therapies for solitary GA formations could be directed to the disruption and creation of a new and healthy immune response from the point of disruption. A comparative analysis of the gene expression of GA and the foreign-body granuloma in the same patient, and GA among different patients could clarify which genes are involved in granulomatous formations. The cells affected by those genetic defects are probably histiocytes and lymphocytes (both always present in GA). Because of some similarity, necrobiosis lipoidica could also be a specific type of GA.

Keloids are a hyperproliferative response of connective tissue in response to trauma. The mechanism by which this occurs is poorly understood and currently no successful treatment exists. Hypothesis: Senescent fibroblasts form during wound repair, as the result of oxidative stress. They have a major role in the control of fibroblast proliferation and extracellular matrix synthesis, acting as inhibitors. The defective induction of stress-induced senescent phenotype (SIPS) creates an insufficient number of senescent cells, diminishing the inhibitor effect, causing the uncontrolled hyperproliferation and keloid formation. In the proposed mechanism of keloid formation, fibroblasts have a major role, but it is also possible that other cells are involved, like keratinocytes and melanocytes. Accepting the hypothesis to be correct, a therapy that induces senescence can be used to prevent the keloid formation. Current therapies are only partially effective because they either induce senescence in too few cells or in enough number of cells, but at the same time inducing death (apoptosis and necrosis) of other cells. Dead cells are probably the source of a new repair cycle (proliferation), therefore the process of keloid formation is only postponed but not blocked. A more efficient prevention of keloid formation could be achieved using specific drugs or physical methods that induce senescence and not cell death. Therapies based on photodynamic and PUVA therapy, capable to induce predominantly cell senescence, can be possibly effective. The magnitude of oxidative stress, created during photodynamic therapy, can be reduced and used to produce sublethal doses, to cause senescence instead of cell death. Except standard photosensitizers, other drugs could be used, that are not so powerful in inducing oxidative stress, i.e. amphotericin B in combination with UV light.

Multiple warts in a 32-year-old-man are reported that developed after tattooing and remaining exclusively confined to that area. The tattooing was done 2.5 years earlier by a professional tattoo artist. It was previously a lesion-free tattoo, but when damaged by sunburn developed multiple skin warts. The ability of a latent virus to induce warts after cutaneous ultraviolet exposure was discussed.

There is not even a single report in the literature of a case that can connect retinal detachment and childbirth in myopic women. However, myopia is considered as an indication for cesarean section in some European countries. Our retrospective study comprised all women diagnosed with myopia during or before pregnancy, who delivered during period 1993– 2002 in the Department of Obstetrics and Gynecology, University Clinical Hospital Rijeka. Our study confirms the practice of myopia as indication for cesarean section in Croatia, although strong recommendations to allow high myopic patients deliver spontaneously arose as far back as 1985. It is essential to recognize scientific or non-scientific criteria for operative delivery in order to avoid the surgical overtreatment.

Clinical observations suggest that the nervous system, including psychological factors, can influence the onset and course of alopecia areata (AA). The aim of this study was to determine whether stressful life events, stress perception, and trait-anxiety are risk factors in the onset and course of AA. A group of 45 patients diagnosed with AA and a group of 45 healthy controls were participants in the study. The patients with AA were divided into two subgroups: patients with a first episode of AA and patients with recidivism of the disease. All participants completed questionnaires addressing sociodemographic, clinical and psychological aspects of their disorder. The frequency and types of stressful life events experienced over the previous six months were recorded. Lemyre and Tessier's Mesure de Stress Psychologique was used to measure emotional, cognitive, behavioral, and physiological aspects of distress. Anxiety was evaluated by the Spielberg's Trait Anxiety Inventory. The subgroups of AA and the control group, using the same numbers of subjects matched for age and sex, education level, marital and employment status, were statistically compared. The number of patients with four stressful life events over the previous 6 months was significantly higher in the group of AA patients with recidivism of disease compared to the control group (P=0.004). There were no differences among the other groups with respect to the frequency of life events. Examination of the relationships between the two groups regarding anxiety, as well as perceived distress, revealed that the groups differed significantly with respect to psychosocial variables studied. A significantly higher degree of trait-anxiety and perceived distress were observed among patients in both AA subgroups (first onset and recidivism of AA) than in the healthy control group. The highest scores for anxiety and stress perception among examined groups were obtained in the group with recidivism of AA (33.42 +/- 12.71 and 90.32 +/- 50.74, respectively). Trait-anxiety and stress perception constitutes risk factors that may influence the onset and exacerbation of AA. The present study does not provide evidence of a significant role of stress in the onset of AA. Life events may play an important role in triggering of some episodes.

The objective of the study was to evaluate the health beliefs and knowledge about acne among acne patients and family physicians. A total of 100 patients referred to a dermatologist for management of acne vulgaris and 120 family physicians completed questionnaires. The questionnaires consisted of questions about health beliefs, the natural course of the disease, the causes of acne, and a set of questions about the knowledge of acne therapy. Acne was considered as a trivial and transitory condition by 52% of the acne patients and 44% of the family physicians. The overall score of correct answers pertaining to the causes of acne among the acne patients and family physicians was 11 and 15%, respectively. The percentage of correct answers regarding the natural course of the disease was 6% for both subsets of subjects. Acne was believed to be curable by 96% of acne patients. Most patients (66%) believed that acne would improve immediately after the first treatment. The knowledge of isotretinoin teratogenecity was reasonable among family physicians (55% correct answers), but it was much lower for other side effects (9%). The overall score of correct answers regarding antibiotic therapy among family physicians was only 21%. Impact of the disease was underestimated by family physicians and also by acne patients. Overall knowledge pertaining to the causes, natural course and therapy was very low. Myths and misconceptions still exist among patients but also among family physicians.

An open, noncomparative study was performed to establish the efficacy of azithromycin in the treatment of early syphilis. Sixteen patients were treated with oral azithromycin: 1g the first day and then 500 mg for the following 8 days. Two patients were excluded from the study, leaving 14 patients for the evaluation of the efficacy. Venereal Disease Research Laboratory (VDRL) negativity was observed in 3 out of 6 patients treated for primary syphilis after 3 months and in all patients after 6 months. Two of 8 patients treated for manifest or early latent secondary syphilis had VDRL negativity after 3 months and 4 patients after 6 months. This study demonstrates that azithromycin is effective in the treatment of early syphilis. Two patients experienced gastrointestinal side effects which did not require treatment interruption.

Psoriasis is a chronic hyperproliferative skin disease characterized by keratinocyte hyperproliferation and inflammation. It is generally considered as an autoimmune disease mediated by T cells. The precise mechanism of triggering keratinocyte hyperproliferation is as yet unknown. Apoptosis seems to be important in the maintenance of skin cell homeostasis as well as in the pathogenesis of some skin diseases. We hypothesize how apoptosis mediated by cytolytic mechanisms could be involved in initiating and maintenance of psoriatic plaque. Increased keratinocyte hyperproliferation might develop as a consequence of failure to remove self-reactive T cells by apoptosis that in other way cause significant keratinocyte damage. Apoptotic keratinocytes might trigger an injury response program causing regenerative hyperplasia of epidermal keratinocytes. Another possibility is that the failure to eliminate these abnormal keratinocytes could result in the persistence of chronic inflammatory conditions constantly recruiting specific T cells. Increased epidermal thickness in psoriasis could be also explained by imbalance between the expression of pro- and anti-apoptotic proteins. Epidermal keratinocytes have the ability to produce cytolytic molecules, thus they might also have the potential to protect the epidermis from T cell-mediated damage. In conclusion, hyperproliferation of psoriatic keratinocytes might be partly due to changes in the keratinocyte expression of pro- and anti-apoptotic genes, partly to the damaged keratinocytes triggering an inappropriate wound repair response and partly by the failure to eliminate these abnormal keratinocytes resulting in the persistence of chronic inflammation. Each of the proposed mechanisms might be a possible therapeutic target mainly by new immunomodulatory agents.

This single-blind (investigator) comparative study was designed to determine the efficacy and tolerability of 1 g of azithromycin vs 500 mg of ciprofloxacin both given as a single oral dose in patients with gonorrhea, who were constantly on the move. One hundred eight patients (59 men and 49 women) with clinically suspected gonococcal infection, confirmed by Gram-stain and culture, were enrolled. Data of 50 patients treated with azithromycin and 51 with ciprofloxacin were evaluable for efficacy and tolerability at the end of the study. After 2 weeks clinical and microbiological cure rates were 96.0% (48 out of 50) for the patients treated with azithromycin and 92.15% (47 out of 51) for the patients treated with ciprofloxacin (p > 0.05). Adverse reactions were reported in 5 patients treated with azithromycin and 6 with ciprofloxacin. In conclusion, 1 g azithromycin is at least as clinically and microbiologically effective and well tolerated as 500 mg of ciprofloxacin in the treatment of gonococcal infections. The drug is particularly useful for sailors and people constantly on the move.