Role of inflammation and iron exchange disorders in progression of liver cirrosis
| Autor: | S. V. Paducheva, I. A. Bulatova, A. P. Shchekotova |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
chemistry.chemical_classification
medicine.medical_specialty Cirrhosis biology business.industry Inflammation medicine.disease Gastroenterology Pathogenesis Ferritin chemistry Fibrosis Transferrin Internal medicine medicine biology.protein Tumor necrosis factor alpha medicine.symptom Endothelial dysfunction business |
| Zdroj: | Perm Medical Journal. 38:38-45 |
| ISSN: | 2687-1408 0136-1449 |
| Popis: | Objective. To assess the role of the main pathogenetically significant molecules, including tumor necrosis factor alpha (TNF-) and transferrin, as an inflammatory protein, in the progression of chronic diffuse liver diseases (CDLD). Material and methods. The study involved 86 patients with cirrhosis of the liver (LC) of viral, alcoholic and mixed etiology. Inflammatory parameters were studied, including tumor necrosis factor alpha (TNF-), indicators of iron metabolism, -fetoprotein (AFP), vasculoendothelial growth factor (VEGF), and functional liver biochemical tests. The control group consisted of 70 persons. Results. It was revealed that the LC severity class is interrelated with the clinical manifestations of the disease, the severity of biochemical syndromes as well as a significant increase in the concentration of -globulins, CRP, the amount of TNF- up to 3.5 (2.64.7) pg/ ml (p 0.001) and ferritin up to 325.8 (209; 401) ng / ml (p 0.001) compared to the control group. An increase in TNF- and ferritin as inflammatory protein in LC confirms the growth of the activity of inflammation in the liver and correlates with other parameters involved in the pathogenesis of LC: with VEGF, as a marker of endothelial dysfunction, which is involved in the activation of fibrosis and neoangiogenesis, and AFP, reflecting regeneration processes in the liver. Conclusions. The progression of liver damage in cirrhosis is based primarily on the secondary inflammation caused by portal hypertension with the entry of intestinal antigens and toxins into the central bloodstream. At the same time, the perverse circle of the development of the disease is closed. |
| Databáze: | OpenAIRE |
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