Współistnienie łuszczycy z wypryskiem dłoni i stóp - problem diagnostyczny

Przewlekłe zmiany zapalne zlokalizowane w obrębie dłoni i stóp są poważnym problemem diagnostycznym dla każdego dermatologa. W pierwszej kolejności trzeba brać pod uwagę występowanie zmian wypryskowych, łuszczycy zwykłej oraz łuszczycy krostkowej. Stwierdzenie typowych grudek łuszczycowych w innej lokalizacji bądź dodatnie wyniki testów płatkowych nie wykluczają współistnienia obu procesów chorobowych. Przeanalizowano przypadki 36 chorych hospitalizowanych na Oddziale Dermatologicznym Miejskiego Szpitala Zespolonego w Olsztynie w latach 2005-2008. U połowy chorym (18 osób) wyniki testów płatkowych były dodatnie, najczęściej na nikiel i chrom. U 19 pacjentów wykonano badanie histopatologiczne: u 11 osób stwierdzono wyprysk, u 4 łuszczycę, a u 4 cechy łuszczycy i wyprysku. Dodatnie testy płatkowe występowały u około 50% osób ze stwierdzoną łuszczycą oraz u 75% z nakładaniem się łuszczycy i wyprysku. Powyższe wyniki mogą tłumaczyć, dlaczego chorzy z rozpoznaniem łuszczycy często źle tolerują leczenie miejscowe albo dlaczego działanie alergenu i wywołany tym samym proces zapalny może być objawem Koebnera, który pobudza stale proces łuszczycowy, mimo stosowanego leczenia. Z kolei zmieniony łuszczycowo naskórek staje się bardziej przenikalny dla alergenów, co może skutkować rozwojem alergii kontaktowej

Neutrofilowe zapalenie grzbietów rąk

Neutrofilowe zapalenie grzbietów rąk (NDH) jest rzadką, zlokalizowaną odmianą zespołu Sweeta. W obu jednostkach chorobowych występują: gorączka, neutrofilia, leukocytoza, podwyższenie odczynu Bienackiego i poziomu białka C-reaktywnego oraz zmiany rumieniowo-naciekowe. W NDH dodatkowo mogą występować pęcherze krwotoczne i martwica, podobne jak w piodermii zgorzelinowej. Podobnie jak w zespole Sweeta NDH często wiąże się między innymi z nowotworami złośliwymi, chorobami zapalnymi jelit, nietolerancją leków, chorobami autoimmunologicznymi (reumatycznymi). W artykuleomówiono przypadek pacjenta z neutrofilowym zapaleniem grzbietów rąk związanym z chorobą rozrostową, zlokalizowanąw prawym płucu. Pacjent wykazał dobrą odpowiedź na leczenie ogólne kortykosteroidami i leczenie miejscowe

Stem Cells as Potential Candidates for Psoriasis Cell-Replacement Therapy

Recent years have seen considerable progress in explaining the mechanisms of the pathogenesis of psoriasis, with a significant role played in it by the hyper-reactivity of Th1 and Th17 cells, Treg function disorder, as well as complex relationships between immune cells, keratinocytes, and vascular endothelium. The effect of stem cells in the epidermis and stem cells on T cells has been identified and the dysfunction of various types of stem cells may be a prime cause of dysregulation of the inflammatory response in psoriasis. However, exploring these mechanisms in detail could provide a chance to develop new therapeutic strategies. In this paper, the authors reviewed data on the role played by stem cells in the pathogenesis of psoriasis and initial attempts at using them in treatment

Is the diet important for psoriasis?

Psoriasis is a systemic disease, associated with the occurrence of metabolic disorders (obesity, diabetes, hyperuricemia, lipid disorders) and rapid development of atherosclerosis; therefore diet can be an important adjuvant therapy. A low-calorie diet is an important complement treatment of patients with psoriasis, particularly those with concomitant obesity. There are a lot of studies indicating that obesity is a risk factor for psoriasis and vice versa. Visceral adipose tissue produces numerous proinflammatory cytokines (TNF-α, IL-6, Il-8, Il-17, Il-18), the same ones that participate in development of psoriatic lesions. Important factors in the diet are the essential polyunsaturated omega-3 fatty acids. They have an anti-inflammatory effect because they inhibit the production of proinflammatory cytokines (I-1b, IL-6, IL-8, TNF-α) and adhesion molecules (ICAM-1, VCAM-1). In addition, supplementation of omega-3 and natural antioxidants in the diet may help to reduce "oxidative stress" and systemic inflammation. The use of a gluten-free diet is controversial, but in patients with positive anti gliadin antibodies it seems justified. An essential element of the procedure is to avoid alcohol and all its forms and stimulants that have pro-inflammatory effects. We should advise our patients to avoid grapefruit juice during treatment with cyclosporine and limit the supply of simple sugars, animal fats and alcohol during treatment with retinoids. Dietary recommendations for patients with psoriasis are an important part of a holistic approach to patients who expect comprehensive care, not just the prescription

Skin tags as a symptom of metabolic disorders

Skin tags are classified as benign lesions. They occur mainly on the skin of the neck, eyelids, armpits, and groin as pedicles and soft nodules. Their occurrence is associated with obesity, insulin resistance, atherogenic lipidemia, and metabolic syndrome, as well as increased risk of atherosclerosis. In the pathogenesis factors which are impaired in obesity, such as leptin, insulin resistance associated with obesity (IGF-1), androgens and estrogens believed to stimulate the receptors on keratinocytes and fibroblasts to grow, may play a role. In addition, these receptors are stimulated by tryptase released from the mast cells by mechanical injuries. Probably HPV plays a role as a cofactor. The dermatological literature does not provide much information about this subject, so the authors draw attention to the link between the presence of skin tags and the development of metabolic disorders

Psoriasis as an autoimmune disease

Nowadays it is known that psoriasis belongs to the group of autoimmune diseases and may coexist with other diseases in this group. Most often patients have psoriatic arthritis, rheumatoid arthritis, inflammatory bowel disease, autoimmune thyroid diseases and multiple sclerosis. The coexistence of these disorders can be a diagnostic and therapeutic problem (there is controversy over the use of corticosteroids). The common pathogenesis is still not explained. We know that the loss of immunotolerance leads to formation of autoreactive Th1 and Th17 lymphocytes which recognize self-antigens and lead to their destruction in the target organ. Some features of immune mechanisms, observed in psoriasis, suggest its autoimmune background. In psoriasis the main role is played by the activation of the axis IL-12/Th1/IFN- and Th17/Il-23. Il-12 probably acts on naive T cells and the Th1 response is initiated. Il-23 maintains the Th1-mediated inflammatory reaction, stimulates maturation and effects of Th17, and maintains a certain amount of memory cells. We also observe dysfunction of Treg cells, which are responsible for the destruction of autoreactive lymphocytes. In addition, psoriatic keratinocytes have increased resistance to apoptosis, which eliminate damaged cells so that they cannot be recognized as a foreign antigen. However, researchers have suggested that initially the polyclonal activation of T lymphocytes is induced by superantigens (e.g. streptococcal M protein, peptidoglycan) or skin trauma (Koebner phenomenon), whereas in the later phase self-antigens in the epidermis are recognized by autoreactive T cells (keratin K 17, HPV 5 proteins L1, Pso p27), leading to autoimmunity

The Role of the Neutrophilic Network in the Pathogenesis of Psoriasis

One role of neutrophils, the most abundant innate immune sentinels, is neutrophil extracellular trap (NET) formation, which plays a significant role in immune surveillance. However, NET operation is bidirectional. Recent studies report that NETs may contribute to the development of autoimmune diseases such as psoriasis. The participation of neutrophils in the pathogenesis of that disease is dependent on an autoinflammatory feedback loop between neutrophils, lymphocytes, dendritic cells and keratinocytes. Our aim was to clarify the field of NET research in psoriasis and highlight the main factors required for NET generation, which may be a target of new therapies. This article presents a comphrehensive review concerning studies addressing the participation of neutrophils in the pathogenesis of psoriasis. Based on the available English-language literature, we discuss original papers presenting significant research findings which may help to understand and interpret the NET formation process in psoriasis, as well as the newest systematic reviews on PubMed. Next, the comparison, synthesis and summary of reported results were performed to clearly indicate the specific component of the NET which participates in the development of psoriasis