Патоморфогенез сполучнотканинного компоненту шкіри хворих на псоріаз і гіпертонічну хвороб

Abstract

З метою визначення структурних ушкоджень сполучної тканини шкіри хворих на псоріаз в залежності від наявності або відсутності артеріальної гіпертензії у 60 пацієнтів були досліджені біоптати шкіри за допомогою світлооптичної мікроскопії. Встановлено, що морфологічним субстратом ушкодження сполучнотканинного компоненту шкіри у хворих на псоріаз і гіпертонічну хворобу є дифузний фіброз сосочкового шару і фіброеластоз сітчастого шару дерми. Внаслідок коморбідного патоморфогенезу ушкоджень сполучнотканинної основи шкіри у хворих на псоріаз і гіпертонічну хворобу відбуваються значний інтерстиційний набряк сосочкового шару, перифокальна лейкоцитарна інфільтрація, ексудація, транссудація, плазморагії у складі дермальних сосочків, базофільна дегенерація колагенових фібрил, дистрофія еластичного компоненту дерми. Background. Many questions about pathomorphogenesis of damage of the skin connective tissue in patients with psoriasis and hypertension on the background of the skin age changes require clarification and further advance. Objective. The aim of research is to determine the damages of the skin connective tissue in psoriasis patients, depending on the presence or absence of hypertension. Methods. In 60 patients with active psoriasis with and without hypertension skin biopsies were studied using light-optical microscopy. In quantitative morphological study the mitotic index of fibroblasts were calculated. Results. It was found that the morphological basis of damages of the skin connective tissue in patients with psoriasis and hypertension are diffuse fibrosis of the papillary layer and fibroelastosis of reticular layer. It triggers a cascade of typical pathomorphological changes of significantly higher intensity than the skin lesions in psoriasis patients without hypertension. In patients with psoriasis in the active phase with concomitant essential hypertension in areas of damaged skin psoriatic lesions observed distinct fibers papillary and reticular dermis layers. As part of various shapes and sizes buds developed diffuse fibrosis was observed with a sharp predominance of collagen fibers. Single elastic fibers degenerate looked like fragmented structure against the backdrop of significant leukocyte infiltration, exudation, hemorrhage, interstitial edema. Groups of smooth papillae interspersed with high fine papillae, between which most expressive areas were more destructive changes of the epidermis. In the reticular layer of the dermis observed typical signs of advanced fibroelastosis degeneration of collagen fibrils and polymorphic form complexes elastic fibrils on the background of alternating small cells elastosis and elastolysis. On the border between the papillary dermis layers of mesh and observed the formation of connective tissue packs numerous capillary loops around the base, which led to significant narrowing their gaps and deformation capillaries. In contralateral areas of the skin of patients with psoriasis and essential hypertension destructive tissue changes associated with microvascular damage (infiltration, exudation, hemorrhage), were absent, but the diffuse fibrosis of the papillary layer and reticular dermis fibroelastosis manifested as a characteristic feature of systemic damage to the skin. Consisting of two layers of the dermis was observed a statistically significant increase in mitotic activity of fibroblasts (in 34,3-44,9% compared to control) in patients with essential hypertension or psoriasis regardless of the presence or absence of elements of psoriatic damage to the skin surface. When combined with active psoriatic process with hypertension in the skin of patients had a more significant increase in dermal fibroblasts mitotic activity relative to the control level – by 132,8% (p<0,05). Conclusion. Comorbid morphogenesis causes dermal damage in patients with psoriasis and hypertension: significant interstitial edema of papillary layer; perifocal leukocyte infiltration, exudation, extravasations, plasmorrhage consisting of dermal papillae; degeneration of collagen fibrils and dystrophy of elastic components of the dermis.