| Abstract [eng] |
Dissertation topic: the damage to dermal blood vessels and connective tissue during systemic sclerosis. The aim of this dissertation was to determine the sequence in the development of vascular damage and fibrosis by studying vascular changes in the skin and connective tissue of systemic sclerosis patients with vascular atresia characteristic of this pathology and by comparing it with other conditions, where there is no vascular atresia (systemic lupus erythematosus), and with conditions, which are characterised by vascular function instability (Raynaud’s phenomenon). This was a retrospective study, which analysed 60 patients with the aforementioned diseases, 20 with each disease, and a control group of 20 skin biopsies. In addition to routine histochemical stains, a series of immunohistochemical signs and electron microscopic examination were used. It was determined that damage to the vascular endothelium and increased permeability of the vascular walls appear earlier than expressed fibrosis in the skin of systemic sclerosis patients and that the abundant expression of vascular endothelial growth factor (VEGF)-A and its receptor FLT-1 and especially HSP-47 (heat shock protein, a collagen-specific chaperone that induces fibrosis) and eNOS endothelial nitric oxide synthase are immunohistochemical signs of endothelial injury in the early stage of systemic sclerosis. It was determined that in the pathogenesis of the early stage of systemic sclerosis, damage to the small blood vessels predominates in the skin and that it is expedient to consider this when prescribing treatment for systemic sclerosis based on pathogenesis. The use of a skin biopsy is recommended as an auxiliary diagnostic method when differentiating between the early stages of systemic sclerosis, systemic lupus erythematosus, and Raynaud’s phenomenon. |
