The objective of the present work was to study the pathogenetic mechanisms underlying nasal bleeding (NB) in the patients presenting with arterial hypertension (AH). A total of 47 patients with AH suffering from NB were available for the examination of whom 28 experienced a single bleeding episode and 19 had recurrent bleeding. 11 of them were treated by endonasal surgical intervention for the achievement of hemostasis. Simultaneously, mucoperichondreal biopsies were taken from the anterior septal portions and used for histological and ultrastructural investigations. The laboratory examination of all the patients has demonstrated hyperfibrinogenemia and the enhanced level of soluble monomeric fibrin complexes in the blood (especially in the patients with recurrent nasal bleeding) despite the normal platelet levels, prothrombin and thrombin times. These findings gave reason to characterize the hemostasiological status of the patients as chronic compensated disseminated intravascular coagulation (DIC) syndrome. The histological study revealed hyaline, erythrocyte-rich and fibrin thrombi in the vessels of the microcirculatory system whereas ultrastructural studies showed desquamation of endothelial cells, massive desendothelization, and disintegration of the basal membrane with the exposure of subendothelium. It is supposed that these changes provoked the development of thrombosis and focal necrosis in nasal mucosa. The authors conclude that the cause of nasal bleeding associated with arterial hypertension is directly related to the lesions of vascular endothelial, microcirculatory disorders, and modification of the blood coagulation processes rather than to the mechanical rupture of blood vessels. These changes are believed to be responsible for the development of local intravascular coagulation.
Myelodysplastic syndrome is a group of myeloid neoplasms that arise from the action of damaging factors on hematopoietic stem cells, which are based on somatic mutations, which leads to the formation of clonal hematopoiesis. we know from epidemiological data that old age, male gender, and smoking are in themselves independent risk factors for myelodysplastic syndrome. These factors can potentiate the occurrence of mutations in the genome. In young people and children, myelodysplastic syndrome is a direct consequence of genetic abnormalities. There is an assumption that epigenetic regulatory genes are subject to frequent mutations. The chromatin of malignant cells acquires epigenetic abnormalities affecting tumor resistance, which explains their response to treatment with epigenetic drugs in combination with other therapies The appearance of new mutations potentiates hematopoiesis, which is accompanied by the shutdown of apoptosis and the transformation of myelodysplastic syndrome into acute myeloid leukemia. It is suggested that mutations in the genes of epigenetic regulators have functional effects on pluripotent hemopoietic stem cells. Epigenetic profiling of patients had a significant impact on understanding the molecular basis of etiology, pathogenesis, and patterns of transformation of myelodysplastic syndrome into acute myeloid leukemia, but it is not known which genes are the most clinically significant for their final use in laboratory diagnostics and targeted hypomethylating therapy. Despite the multitude of mutations in epigenetic regulators in myelodysplastic syndrome, the creation of prognostic models based on them requires a detailed study that includes not only analysis of the frequency of such mutations, but also the establishment of a relationship with clinically significant outcomes. The aim of this review is to study the prevalence of the mutational status of epigenetic regulation in patients with myelodysplastic syndrome.
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