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Sampogna F.,Istituto Dermopatico dellImmacolata
Current Problems in Dermatology (Switzerland) | Year: 2013

In order to give a practical meaning to a concept, it is necessary to measure it. In this chapter, some guidelines for the creation of a life course questionnaire are given, starting from the concept of measurement and all the properties (validity, reliability, responsiveness and interpretability) that an instrument must have, to be defined as a measurement tool. The first step is to define the construct to be measured. Cumulative life course impairment (CLCI) assumes impairment over time of the life course of individuals; key concepts of CLCI are accumulation of risk as well as timing of risk exposure. CLCI is a longitudinal construct, and in order to measure it, it is imperative to take the role of time into account. Questionnaires administered at a certain moment during the patient's life will investigate the impact the disease had on his/her life from the beginning until that moment. Items to be assessed in patients suffering from chronic condition will be, among others, physical and psychological comorbidities, feelings of stigmatization and coping style. Together with the given personality, and other personal and clinical characteristics, they may contribute to changes in the life trajectory compared to a hypothetical 'unaffected average life course'. At the end of the chapter, an example of life course questionnaire is proposed. Copyright © 2013 S. Karger AG, Base. Source


Sampogna F.,Istituto Dermopatico dellImmacolata
Current Problems in Dermatology (Switzerland) | Year: 2013

The concepts of cumulative life course impairment (CLCI) and health-related quality of life (QoL) are analyzed, in order to find shared and divergent aspects. The concept of QoL includes the patients' perception of their health and their personal experiences concerning the psychosocial impact of the disease on their life. CLCI aims to investigate the impact of a chronic disease on the milestones of life, such as education, work, relationships, children, social life, (briefly - on the whole trajectory of life) and on how the disease influenced the possibility of patients of living their life up to its full potential. QoL is a cross-sectional measure, while CLCI takes into account the lifetime. However, it is clear that the possibility of reaching one's full life potential and QoL at a certain time are correlated. There are few studies in dermatology in this field; however, both in the case of atopic dermatitis and of vitiligo it has been shown that patients with a severe condition in childhood endured severe psychosocial and physical consequences in adulthood and experienced a profound negative impact of the disease on their current quality of life. It is thus important to take into account both CLCI and QoL when evaluating the impact of a chronic condition on a patient's life. Copyright © 2013 S. Karger AG, Base. Source


Guerra L.,Tissue Engineering and Cutaneous Pathophysiology Laboratory | Dellambra E.,Tissue Engineering and Cutaneous Pathophysiology Laboratory | Brescia S.,Tissue Engineering and Cutaneous Pathophysiology Laboratory | Raskovic D.,Istituto Dermopatico dellImmacolata
Current Drug Metabolism | Year: 2010

Vitiligo is a multifactorial disorder characterized by the appearance of white maculae that may spread over the entire body skin. Depigmentation arises from the loss of functioning melanocytes. Non segmental vitiligo (NSV) is the most common form of the disease: it is usually progressive and may be associated with familiarity and autoimmunity. Segmental vitiligo (SV) frequently stabilizes few years after its onset. Vitiligo etiology involves multiple pathogenetic factors, most of them working in concert. Impaired antioxidative defences lead to accumulation of reactive oxygen species (ROS), which affect melanocytes. Mitochondrial membrane lipid peroxidation may participate to ROS overproduction. A temporal sequence may connect oxidative stress and autoimmunity. Overall, a genetic predisposition renders vitiligo melanocytes more susceptible to precipitating factors than normal healthy melanocytes. The definition of isolated or superimposed manifestations of polygenic skin disorders has been proposed for SV and SV-NSV association. Keratinocytes and melanocytes are both affected and apoptosis, ageing or melanocythorragy are the ultimate effects of the complex deregulation in vitiligo skin. Pathogenetic therapies mainly act by inducing immunosuppression and stimulation of melanocyte proliferation and migration. Here the most popular hypotheses for the pathogenesis of vitiligo are summarized. Fundamental cellular, biochemical and molecular alterations accounting for melanocyte destruction in vitiligo are also described. Last, pathogenetic approaches in the treatment of such a complex disease are discussed, with particular consideration on the cellular and molecular targets of the current therapies. © 2010 Bentham Science Publishers Ltd. Source


Madonna S.,Laboratory of Experimental Immunology | Scarponi C.,Laboratory of Experimental Immunology | Pallotta S.,Istituto Dermopatico dellImmacolata | Cavani A.,Laboratory of Experimental Immunology | Albanesi C.,Laboratory of Experimental Immunology
Cell Death and Disease | Year: 2012

Because of their genetically determined capacity to respond to pro-inflammatory stimuli, keratinocytes have a crucial role in the pathogenesis of psoriasis. Upon IFN-γ and TNF-α exposure, psoriatic keratinocytes express exaggerated levels of inflammatory mediators, and show aberrant hyperproliferation and terminal differentiation. The thickening of psoriasic skin also results from a peculiar resistance of keratinocytes to cytokine-induced apoptosis. In this study, we investigated on the molecular mechanisms concurring to the resistance of psoriatic keratinocytes to cell death, focusing on the role having suppressor of cytokine signaling (SOCS)1 and SOCS3, two molecules abundantly expressed in IFN-γ/TNF-α-activated psoriatic keratinocytes, in sustaining antiapoptotic pathways. We found that SOCS1 and SOCS3 suppress cytokine-induced apoptosis by sustaining the activation of the PI3K/AKT pathway in keratinocytes. The latter determines the activation of the anti-apoptotic NF-κB cascade and, in parallel, the inhibition of the pro-apoptotic BAD function in keratinocytes. For the first time, we report that phosphorylated AKT and phosphorylated BAD are strongly expressed in lesional psoriatic skin, compared with healthy or not lesional skin, and they strictly correlate to the high expression of SOCS1 and SOCS3 molecules in the psoriatic epidermis. Finally, the depletion of SOCS1 and SOCS3, as well as the chemical inactivation of PI3K activity in psoriatic keratinocytes, definitively unveils the role of PI3K/AKT cascade on the resistance of diseased keratinocytes to apoptosis. © 2012 Macmillan Publishers Limited All rights reserved. Source


Kimball A.B.,Harvard University | Gieler U.,Justus Liebig University | Linder D.,University of Padua | Sampogna F.,Istituto Dermopatico dellImmacolata | And 2 more authors.
Journal of the European Academy of Dermatology and Venereology | Year: 2010

Psoriasis is associated with significant physical and psychological burden affecting all facets of a patient's life - relationships, social activities, work and emotional wellbeing. The cumulative effect of this disability may be self-perpetuating social disconnection and failure to achieve a 'full life potential' in some patients. Health-related quality of life studies have quantified the burden of psoriasis providing predominantly cross-sectional data and point-in-time images of patients' lives rather than assessing the possible cumulative disability over a patient's lifetime. However, social and economic outcomes indicate there are likely negative impacts that accumulate over time. To capture the cumulative effect of psoriasis and its associated co-morbidities and stigma over a patient's life course, we propose the concept of 'Cumulative Life Course Impairment' (CLCI). CLCI results from an interaction between (A) the burden of stigmatization, and physical and psychological co-morbidities and (B) coping strategies and external factors. Several key aspects of the CLCI concept are supported by data similar to that used in health-related quality of life assessments. Future research should focus on (i) establishing key components of CLCI and determining the mechanisms of impairment through longitudinal or retrospective case-control studies, and (ii) assessing factors that put patients at increased risk of developing CLCI. In the future, this concept may lead to a better understanding of the overall impact of psoriasis, help identify more vulnerable patients, and facilitate more appropriate treatment decisions or earlier referrals. To our knowledge, this is a first attempt to apply and develop concepts from 'Life Course Epidemiology' to psoriasis research. © 2010 The Authors. Source

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