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The Role of Focal Infections in the Pathogenesis of Psoriasis and Chronic Urticaria

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The Role of Focal Infections in the Pathogenesis of Psoriasis and Chronic Urticaria Original paper The role of focal infections in the pathogenesis of psoriasis and chronic urticaria Paweł Łukasz Brzewski 1, Magdalena Spałkowska 2, Magdalena Podbielska 2, Joanna Chmielewska 2, Marta Wołek 1, Katarzyna Malec 3, Anna Wojas-Pelc 1 1Department of Dermatology, Jagiellonian University Medical College, Krakow, Poland Head: Prof. Anna Wojas-Pelc MD, PhD 2Students’ Scientific Society, Jagiellonian University Medical College, Krakow, Poland Head: Prof. Anna Wojas-Pelc MD, PhD 3Department of Otolaryngology, Head and Neck Surgery, 5 th Military Hospital with Polyclinic, Krakow, Poland Head: Andrzej Kozak MD, PhD Postep Derm Alergol 2013; XXX, 2: 77 –84 DOI: 10.5114/pdia.2013.34155 Abstract Introduction: The Focal Infection Theory, originally presented at the beginning of the 20 th century, postulates that systemic diseases can be caused by microorganisms that arise from the focus of infection. Foci of infections have been described as sinuses, adenoids, tonsils, teeth, genitourinary tract, gall bladder and kidneys. A focus of infec - tion is defined as the area that can occur in any part of the body, contains a pathogen (microorganism) and is usu - ally asymptomatic. There are discordant opinions about the role of focal infections in the pathogenesis of psoria - sis and urticaria. Aim: To establish whether there is a higher incidence of focal infections in patients with chronic urticaria and pso - riasis. Material and methods: We retrospectively reviewed 129 patients with a history of psoriasis and chronic urticaria: 58 women and 71 men treated in the Department of Dermatology of the Jagiellonian University Medical College in Krakow. Results: In the analyzed group, 11 patients had a dental consultation, 58 – laryngological consultation and 29 women had a gynecological consultation. The most common examples of focal infection were tonsillitis, upper respiratory tract infections, sinusitis, dental caries and genitourinary tract infections. Aggravating factors were similar to pre - viously described. Conclusions: A high incidence of focal infections in patients with psoriasis and urticaria suggests that infections may play a significant role in the pathogenesis of these skin disorders. Treatment of infection foci may play the key role in the remission of skin changes. Key words: focal infection, urticaria, psoriasis. Introduction Chronic urticaria The Focal Infection Theory, originally presented at the Chronic urticaria is defined by the presence of urticaria, beginning of the 20 th century, postulates that systemic dis - on most days of the week, for at least 6 weeks. The diag - eases can be caused by microorganisms that arise from the nosis is made by description of its clinical features (typi - focus of infection. Foci of infections have been described as cal urticarial lesions ± angioedema) with the criteria of time. sinuses, adenoids, tonsils, teeth, genitourinary tract, gall blad - Approximately 40% of the patients with chronic urticaria der and kidneys. A focus of infection is defined as the area have episodes of angioedema [1]. Urticaria is classified into that can occur in any part of the body, contains a pathogen immunological mediated (IgE-dependent and non-IgE (microorganism) and is usually asymptomatic. dependent) and non-immunological mediated ones. Phys - Address for correspondence: Paweł Łukasz Brzewski MD, PhD, Department of Dermatology, Jagiellonian University Medical College, 8 Skawińska St, 31-066 Krakow, Poland, phone: +48 12 424 79 99, ext. 7400, e-mail: [email protected] Received: 16.11.2012, accepted: 19.02.2013. Postępy Dermatologii i Alergologii XXX; 2013/2 77 P. Ł. Brzewski, M. Spałkowska, M. Podbielska, J. Chmielewska, M. Wołek, K. Malec, A. Wojas-Pel c ical urticaria is caused by physical exertion, mechanical, t oimmune response, histamine releasing factors theory and electromagnetic or thermal stimuli (such as water, UV light, cellular defects theory. Autoimmune theory claims that cold, heat, pressure) with nonspecific activation of mast autoantibodies and serum factor present in blood cause cells [2-4]. The most common form of chronic urticaria is release of histamine from skin mast cells and basophiles. the idiopathic form (80-90%), where the external allergic The main argument against this theory is that antibodies cause or disease cannot be found [5-7]. There are sever - found in chronic urticaria (autoantibodies to IgE, Fc εRI) are al theories trying to explain the pathogenesis of urticaria. not specific to the disease. The other theory is supported Chronic urticaria is usually self-limited with a duration of by the fact that some patients with chronic idiopathic 2-5 years. Approximately 30-50% of patients with chron - urticaria demonstrate excessive production of platelet- ic idiopathic urticaria have circulating auto antibodies to derived clotting factors. This could support the theory that the high-affinity IgE receptor, Fc εRI, on the mast cells and there are histamine releasing factors in the plasma. The basophils releasing histamine or antibodies to IgE [8]. This cellular defects theory claims that patients with urticaria subgroup of chronic urticaria is called autoimmune have mast cell defects (in signaling, trafficking, function) urticaria. The best in vivo clinical test for detection of in [19-23]. vitro basophil histamine releasing activity with 65-71% sen - sitivity and 78-81% specificity is the autologous serum skin Psoriasis test (ASST) [9]. Skin lesions in urticaria are well-circum - Psoriasis is a common and chronic inflammatory skin scribed, raised above the surface of the skin, pale in the disease with an incidence of 2.5% in Caucasians and 1.3% middle, with a smooth surface and extreme purities. in African-Americans [24, 25]. Psoriasis has high potential The shape of the skin changes (plaques, wheals) varies: to reduce the quality of life of the patient. Patients with they can appear as round, polycyclic, annular, geographic psoriasis reported reduction in physical functioning and lesions [10]. Angioedema in chronic urticaria is an episod - mental functioning comparable to patients with cancer, ic swelling of the mucosa or subcutaneous tissue, asym - arthritis, heart disease, hypertension, diabetes and depres - metric, developing in a few minutes to a few hours, com - sion [26]. Psoriasis is characterized by the presence of thick, mon in the area of the face [11]. Aggravating factors include red skin with flaky, silver-white patches (scales) derived from physical factors (hot, cold, humidity, etc.), NSAIDS, stress, excessive growth of skin epithelial cells. In psoriasis we dis - diet (e.g. spicy meals) [12, 13]. Many autoimmune disorders tinguish the following types: plaque (psoriasis vulgaris), are associated with chronic urticaria. Patients with chron - guttate, pustular, inverse (flexural psoriasis, intertriginous ic urticaria have an increased odds ratio for hypothyroidism, psoriasis) and erythrodermic (exfoliative psoriasis) [27]. Pso - hyperthyroidism, antithyroid antibodies. There is a sig - riasis is characterized by flare-ups and remissions. Main nificantly higher incidence of rheumatoid arthritis, Sjögren factors triggering psoriasis are: skin injuries (e.g. scratch - syndrome, celiac disease, type I diabetes mellitus, and sys - ing), medications, stress, smoking, alcohol, streptococcal temic lupus erythematosus among female patients with infections, HIV and hormonal changes [28-31]. High pre - chronic urticaria. All examined patients had a high mean valence of obesity has been reported in patients with pso - platelet volume, positive rheumatoid factor, and antinu - riasis [32]. In differential diagnosis of psoriasis, the following clear antibodies. The common mechanism in previously diseases should be considered: atopic keratoconjunctivi - mentioned diseases is a high prevalence of autoantibod - tis, atopic dermatitis, adult blepharitis, dry eye syndrome, ies and the presence of a chronic inflammatory process contact dermatitis, seborrheic dermatitis, diaper der - (high mean platelet volume). 9.8% of examined patients matitis, onychomycosis, squamous cell carcinoma, num - had hypothyroidism, 2.6% – hyperthyroidism (0.6% and mular eczema, lichen planus, lichen simplex chronicus, 0.5%, respectively, in controls) [14]. Thyroid autoantibod - mycosis fungoides, subcorneal pustulosis, pustular erup - ies (esp. anti-TPO antibodies, antimicrosomal antibodies) tions pityriasis alba, pityriasis rosea, sicca keratocon - are found 2-3 times more often among patients with chron - junctivitis, syphilis, reactive arthritis, gout and pseudogout ic urticaria than in controls [15, 16]. The exact role of autoan - and tinea [33]. Psoriasis is an autoimmune disease with tibodies remains unknown. It is suggested that patients a great role of genetic and environmental factors in its with chronic urticaria have a higher tendency to develop pathogenesis [34]. Factors playing a key role in the patho - autoantibodies [17]. Focal bacterial, viral, parasite infections genesis of psoriasis are: T cells, antigen presenting cells may play the key role in autoimmunity. In the differential (APCs), keratinocytes, Langerhans’ cells, macrophages, nat - diagnosis of the chronic urticaria, disorders that should be ural killer cells (NKs), an array of Th1 type cytokines, growth taken into consideration are complement-mediated dis - factors (VEGF, KGF) and others. The main hypothesis orders, malignancies, cutaneous or systemic mastocyto - assumes that the disease starts with the activation of
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