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Pruritic dermatosis is a frequent and burdensome disease. The objectives of this study were (1) to assess the willingness to pay (WTP) and the health-related quality of life (HRQoL) in patients with pruritic dermatoses and (2) to compare the results with data on socio-demographic data, and clinical features/symptoms of the patients. One hundred and three patients with pruritic dermatosis had participated in a non-interventional, cross-sectional study. Socio-demographic data, clinical features/symptoms, a health-related quality of life (HRQoL)-based and a dermatology-specific instrument (SF-6D and DLQI, respectively), and two utility indicators such as rating scale (RS) and time-trade-off (TTO) as well as willingness to pay (WTP) were recorded. In our study, there was a significant correlation between DLQI scores and WTP (p < 0.001). Time-trade-off (TTO) was also statistically correlated with SF-6D (p = 0.001). Regression models showed that daily duration and pruritus intensity were associated with lower HRQoL. Furthermore, WTP was the only measure revealing demographic and socio-economic characteristics such as age, education level, family status and income as predicting factors. No significant differences between groups of varying skin diseases were observed. HRQoL and WTP proved to be valid tools to assess the burden of disease in patients with pruritic dermatosis. However, further research with a larger number of patients is needed to validate the present findings.

We describe a patient with painful enlargement and severe nail deformity of both great toes. The patient furthermore presented with some minor diagnostic criteria for psoriasis such as nail pitting and had a positive family history of the disease. In the recent literature, such cases have been recognized as a new entity termed psoriatic onycho-pachydermo-periostitis (POPP). In this case report, POPP is discussed in relationship to other forms of psoriatic arthropathy and with special emphasis regarding its diagnostic criteria and therapeutic implications.

In the present study the action of various cytokines as regulators of human melanocyte growth and differentiation was examined in vitro. Primary melanocyte cultures were obtained in complete medium free of 12-O-tetradecanoylphorbol-13-acetate or serum. First passage melanocytes were treated with various concentrations of recombinant tumour necrosis factor alpha and beta (rTNF-alpha, rTNF-beta), as well as with various recombinant interleukins (rIL-1a, rIL-1b, rIL-2, rIL-3, rIL-4 and rIL-6) for 6 days in complete medium and for 6 and 12 days in a mitogen-reduced medium variant. The 4-methylumbelliferyl heptanoate fluorometric microassay and Ki-67 staining were used for assessing cell proliferation, and the immunophenotype was evaluated using various monoclonal antibodies. Melanocyte proliferation in complete medium was inhibited by rTNF-alpha (-24%), rTNF-beta (-17%), rIL-1a (-21%), rIL-1b (-18%) and rIL-6 (-29%); in contrast, rIL-2, rIL-3 and rIL-4 had no antiproliferative effect. Measurements of Ki-67-positive nuclei confirmed these results. In the reduced medium variant, none of the above cytokines inhibited melanocyte proliferation. Recombinant TNF-alpha and rTNF-beta markedly reduced the expression of the pigment cell-associated antigens HMB-45 and K.1.2, and they enhanced the expression of VLA-2, ICAM-1 and HLA class I antigens and strongly induced HLA-DR. Similar changes were induced by rIL-1a, rIL-b and rIL-6, and rIL-2 decreased the expression of HLA class I antigens and of ICAM-1. In conclusion, several cytokines inhibited the growth and modulated the phenotype of melanocytes in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Aberrant proliferation of tumor cells characterizes cancer growth. Investigations of cellular growth control mechanisms have contributed to our understanding of carcinogenesis and to the identification of compounds with specific antitumor activity. Many cytokines have been found to act on melanoma tumors, either produced by the tumor cells themselves or by infiltrating host cells. Purified cytokines allowed direct comparison of the growth response between normal human melanocytes and malignant melanoma cells. The present paper summarizes results of a series of our own experiments not yet published and data from a review of the recent literature. Proliferation of normal human melanocytes is enhanced by several cytokines, including basic fibroblast growth factor (bFGF), melanoma growth stimulatory activity (MGSA), hepatocyte growth factor (HGF), and mast cell growth factor (MGF). Melanoma cells are additionally stimulated by epidermal growth factor (EGF)/transforming growth factor alpha (TGF-alpha) and nerve growth factor (NGF). Tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta 1 (TGF-beta 1), and interleukin (IL)-6 are all potent inhibitors of melanocyte growth, but they are less effective on melanoma cells or even stimulate their growth. Interferon (IFN)-alpha and IFN-gamma inhibited proliferation of melanoma cells but not of melanocytes, whereas IFN-beta showed antiproliferative effects in both cell types. These findings suggest an alteration in growth control mechanisms during melanocyte transformation and possibly play a role in melanoma pathogenesis.

Experimental animal models have shown that various cytokines, depending of their specific properties, may support growth and metastasis of tumor cells or even lead to tumor rejection. The analysis of expression of cytokine genes by melanoma cell lines indicated that melanoma cells constitutively produce both autostimulatory and inhibitory cytokines. Using reverse transcriptase polymerase chain reaction analysis, simultaneous expression of several cytokines, including interleukin-1 beta (IL-1 beta), IL-6, IL-8, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor, by melanoma cells was found. The same cytokine transcripts were detected in melanocytes, suggesting that cells of the melanocytic lineage express a specific pattern of cytokines in vitro. All these cytokines are known to be able to stimulate effector cells of the host. Additionally, production of mRNA for IL-10, a cytokine with potential immunosuppressive properties, was detected in melanoma cells and melanocytes. These and other cytokines are likely to be involved in the immune response to cancer and at this time it is unknown what the net effects of multiple cytokines are on the outcome of the host response to tumor.