25 research outputs found
ΠΠ°Π»Π΅ΠΊΡΠΈΠ½Ρ 1 ΠΈ 3 Π² ΠΌΠ΅Ρ Π°Π½ΠΈΠ·ΠΌΠ°Ρ ΡΠ΅ΠΊΡΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΡ Π³ΡΠ°Π½ΡΠ»ΠΎΡΠΈΡΠΎΠ² Π² ΠΎΠΏΡΡ ΠΎΠ»Π΅Π²ΡΡ ΡΠΊΠ°Π½Ρ ΠΏΡΠΈ ΡΠ°ΠΊΠ΅ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ°
Background: Gastric and colon tumors are often associated with eosinophilic infiltration of tumor tissue, the significance of which is still not entirely clear. The recruitment of eosinophils into the tissues can be in part regulated by galectins β galactose-binding proteins which are expressed by a variety of tissues and are capable of exerting a broad range of effects.
Aims: To evaluate the expression of galectin-1 and galectin-3 in tumor tissue, and gal-3 gene mRNA expression in blood eosinophils in patients with gastric and colon cancer with or without tissue eosinophilia.
Materials and methods: The study included a total of 107 patients (84 males and 23 females, average age 60,9 6,8) with verified gastric cancer (52 persons) and colon cancer (55 persons), who underwent treatment or were registered at the dispensary at the regional medical institution Tomsk Regional Oncology Center (Tomsk, Russia). The control group consisted of 15 men and 11 women of comparable age. The materials of the research included samples of gastric and colon tumors obtained during surgery, and eosinophilic granulocytes isolated from whole blood by immunomagnetic separation. Galectin-1 and galectin-3 expression in tumor tissue was evaluated by immunohistochemistry. The expression of gal-3 gene mRNA in eosinophils was determined by real-time reverse transcription polymerase chain reaction. Statistical analysis of the results was carried out using the non-parametric Mann-Whitney U test for independent samples with Benjamini-Hochberg procedure for multiple comparisons, and the Chi-square Pearson criterion with Yates correction.
Results: In patients with gastric cancer and colon cancer, regardless of the presence of tissue eosinophilia, low expression of galectin-3 in the tumor tissue and high expression of gal-3 gene mRNA in peripheral blood eosinophils were found. Gastric and colon cancer patients with eosinophilic infiltration of tumor tissue were characterized by low expression of galectin-1 within tumor cells (in 64.0% cases, 2 = 4.890, Ρ = 0.029; and in 73.9% cases, 2 = 5.981, p = 0.031 respectively). There was a statistically significant connection between the level of galectin-1 expression by tumor cells and the presence of tissue eosinophilia both in gastric ( = 0.307) and colon cancer ( = 0.330).
Conclusion: Low expression of galectin 1 and 3 by tumor cells in gastric and colon cancer with tissue eosinophilia indicates the lack of a significant effect of these proteins on the process of recruiting eosinophilic granulocytes into tumor tissue. Increased expression of galectin-3 in blood eosinophils in gastric and colon cancer is not associated with the presence of eosinophilic infiltration of tumor tissue.ΠΠ±ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠ΅. ΠΡΠΈ ΡΠ°ΠΊΠ΅ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° Π²Π΅ΡΡΠΌΠ° ΡΠ°ΡΡΠΎ ΠΎΠ±Π½Π°ΡΡΠΆΠΈΠ²Π°Π΅ΡΡΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½Π°Ρ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ, Π·Π½Π°ΡΠ΅Π½ΠΈΠ΅ ΠΊΠΎΡΠΎΡΠΎΠΉ Π΄ΠΎ ΡΠΈΡ
ΠΏΠΎΡ Π½Π΅ΡΡΠ½ΠΎ. Π ΡΠ΅Π³ΡΠ»ΡΡΠΈΠΈ ΡΠ΅ΠΊΡΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΎΠ² Π² ΡΠΊΠ°Π½Ρ Π½ΠΎΠ²ΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΈΠ½ΠΈΠΌΠ°ΡΡ ΡΡΠ°ΡΡΠΈΠ΅ Π³Π°Π»Π΅ΠΊΡΠΈΠ½Ρ β Π±Π΅Π»ΠΊΠΈ, ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΠ΅ΠΌΡΠ΅ ΠΌΠ½ΠΎΠ³ΠΈΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ ΠΈ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΠΈΠ΅ΡΡ ΡΠΈΡΠΎΠΊΠΈΠΌ ΡΠΏΠ΅ΠΊΡΡΠΎΠΌ ΡΠ²ΠΎΠΉΡΡΠ².
Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ β ΠΎΡΠ΅Π½ΠΈΡΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ Π³Π°Π»Π΅ΠΊΡΠΈΠ½ΠΎΠ² 1 ΠΈ 3 Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΈ ΠΌ-Π ΠΠ Π³Π΅Π½Π° Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-3 Π² ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»Π°Ρ
ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΈ ΡΠ°ΠΊΠ΅ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° Ρ ΡΠΊΠ°Π½Π΅Π²ΠΎΠΉ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠ΅ΠΉ ΠΈ Π±Π΅Π· Π½Π΅Π΅.
ΠΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 107 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² (84 ΠΌΡΠΆΡΠΈΠ½Ρ ΠΈ 23 ΠΆΠ΅Π½ΡΠΈΠ½Ρ, ΡΡΠ΅Π΄Π½ΠΈΠΉ Π²ΠΎΠ·ΡΠ°ΡΡ 60,9 6,8 Π»Π΅Ρ) Ρ Π²Π΅ΡΠΈΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ Π΄ΠΈΠ°Π³Π½ΠΎΠ·ΠΎΠΌ ΡΠ°ΠΊΠ° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° (52 Π±ΠΎΠ»ΡΠ½ΡΡ
) ΠΈ ΡΠ°ΠΊΠ° ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° (55 Π±ΠΎΠ»ΡΠ½ΡΡ
), ΠΊΠΎΡΠΎΡΡΠ΅ ΠΏΡΠΎΡ
ΠΎΠ΄ΠΈΠ»ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π² ΠΠΠΠ£Π Π’ΠΎΠΌΡΠΊΠΈΠΉ ΠΎΠ±Π»Π°ΡΡΠ½ΠΎΠΉ ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄ΠΈΡΠΏΠ°Π½ΡΠ΅Ρ (Π’ΠΎΠΌΡΠΊ). Π Π³ΡΡΠΏΠΏΡ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ Π²ΠΎΡΠ»ΠΈ 15 ΠΌΡΠΆΡΠΈΠ½ ΠΈ 11 ΠΆΠ΅Π½ΡΠΈΠ½ ΡΠΎΠΏΠΎΡΡΠ°Π²ΠΈΠΌΠΎΠ³ΠΎ Π²ΠΎΠ·ΡΠ°ΡΡΠ°.
ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ: ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΠ΅ Π³ΡΠ°Π½ΡΠ»ΠΎΡΠΈΡΡ, Π²ΡΠ΄Π΅Π»Π΅Π½Π½ΡΠ΅ ΠΈΠ· ΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΠΌΠ°Π³Π½ΠΈΡΠ½ΠΎΠΉ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠΈ, ΠΈ ΠΎΠ±ΡΠ°Π·ΡΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ°, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ Π² Ρ
ΠΎΠ΄Π΅ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π²ΠΌΠ΅ΡΠ°ΡΠ΅Π»ΡΡΡΠ²Π°. ΠΠΊΡΠΏΡΠ΅ΡΡΠΈΡ Π³Π°Π»Π΅ΠΊΡΠΈΠ½ΠΎΠ² 1 ΠΈ 3 Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΠΈ. ΠΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌ-Π ΠΠ Π³Π΅Π½Π° Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-3 Π² ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΡ
Π³ΡΠ°Π½ΡΠ»ΠΎΡΠΈΡΠ°Ρ
ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ°Π·Π½ΠΎΠΉ ΡΠ΅ΠΏΠ½ΠΎΠΉ ΡΠ΅Π°ΠΊΡΠΈΠΈ Π² ΡΠ΅ΠΆΠΈΠΌΠ΅ ΡΠ΅Π°Π»ΡΠ½ΠΎΠ³ΠΎ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΎΠ±ΡΠ°ΡΠ½ΠΎΠΉ ΡΡΠ°Π½ΡΠΊΡΠΈΠΏΡΠΈΠΈ. ΠΠ»Ρ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² ΠΏΡΠΈΠΌΠ΅Π½ΡΠ»ΠΈ Π½Π΅ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΠΉ U-ΠΊΡΠΈΡΠ΅ΡΠΈΠΉ ΠΠ°Π½Π½Π°Π£ΠΈΡΠ½ΠΈ Π΄Π»Ρ Π½Π΅Π·Π°Π²ΠΈΡΠΈΠΌΡΡ
Π²ΡΠ±ΠΎΡΠΎΠΊ Ρ ΠΏΠΎΠΏΡΠ°Π²ΠΊΠΎΠΉ ΠΠ΅Π½Π΄ΠΆΠ°ΠΌΠΈΠ½ΠΈΠ₯ΠΎΡ
Π±Π΅ΡΠ³Π° Π΄Π»Ρ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ ΠΈ ΠΊΡΠΈΡΠ΅ΡΠΈΠΉ Ρ
ΠΈ-ΠΊΠ²Π°Π΄ΡΠ°Ρ ΠΠΈΡΡΠΎΠ½Π° Ρ ΠΏΠΎΠΏΡΠ°Π²ΠΊΠΎΠΉ ΠΠ΅ΠΉΡΡΠ°.
Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π£ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠ°ΠΊΠΎΠΌ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠ°ΠΊΠΎΠΌ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° Π²Π½Π΅ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π½Π°Π»ΠΈΡΠΈΡ ΡΠΊΠ°Π½Π΅Π²ΠΎΠΉ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠΈ ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° Π½ΠΈΠ·ΠΊΠ°Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-3 Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΈ, Π½Π°ΠΏΡΠΎΡΠΈΠ², Π²ΡΡΠΎΠΊΠΈΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌ-Π ΠΠ Π³Π΅Π½Π° Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-3 Π² ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΡ
Π³ΡΠ°Π½ΡΠ»ΠΎΡΠΈΡΠ°Ρ
ΠΏΠ΅ΡΠΈΡΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ. Π£ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠ°ΠΊΠΎΠΌ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° Ρ ΡΠΊΠ°Π½Π΅Π²ΠΎΠΉ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠ΅ΠΉ Π·Π°ΡΠ΅Π³ΠΈΡΡΡΠΈΡΠΎΠ²Π°Π½Π° Π½ΠΈΠ·ΠΊΠ°Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-1 (Π² 64,0% ΡΠ»ΡΡΠ°Π΅Π², 2 = 4,890, Ρ = 0,029, ΠΈ Π² 73,9% ΡΠ»ΡΡΠ°Π΅Π², 2 = 5,981, p = 0,031 ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ). ΠΠΎΠΊΠ°Π·Π°Π½Π° Π°ΡΡΠΎΡΠΈΠ°ΡΠΈΡ Π³ΠΈΠΏΠΎΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-1 Ρ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠ΅ΠΉ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ( = 0,307) ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° ( = 0,330).
ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠ΅ΡΠΈΡΠΈΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ Π³Π°Π»Π΅ΠΊΡΠΈΠ½ΠΎΠ² 1 ΠΈ 3 Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΏΡΠΈ ΡΠ°ΠΊΠ΅ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ°, ΡΠΎΠΏΡΠΎΠ²ΠΎΠΆΠ΄Π°ΡΡΠΈΠΉΡΡ ΡΠΊΠ°Π½Π΅Π²ΠΎΠΉ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΠΈΠ΅ΠΉ, ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΠ΅Ρ ΠΎΠ± ΠΎΡΡΡΡΡΡΠ²ΠΈΠΈ Π·Π½Π°ΡΠΈΠΌΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π΄Π°Π½Π½ΡΡ
Π±Π΅Π»ΠΊΠΎΠ² Π½Π° ΠΏΡΠΎΡΠ΅ΡΡ ΡΠ΅ΠΊΡΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΡΡ
Π³ΡΠ°Π½ΡΠ»ΠΎΡΠΈΡΠΎΠ² Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ ΡΠΊΠ°Π½Ρ. ΠΠΎΠ²ΡΡΠ΅Π½Π½ΡΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ Π³Π°Π»Π΅ΠΊΡΠΈΠ½Π°-3 ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»Π°ΠΌΠΈ ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ
ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΈ ΡΠΎΠ»ΡΡΠΎΠ³ΠΎ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ° Π½Π΅ Π·Π°Π²ΠΈΡΠΈΡ ΠΎΡ Π½Π°Π»ΠΈΡΠΈΡ ΡΠΎΠ·ΠΈΠ½ΠΎΡΠΈΠ»ΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ
Cardiac damage in liver cirrhosis in alcohol abusers
Aim: To estimate the contribution of liver cirrhosis (LC) to the development of heart diseases in alcohol abusers. Subjects and methods: The investigation included 80 patients with alcoholic LC without a history of cardiovascular and respiratory diseases and, as a control group, 32 alcohol abusers without a history of chronic diseases of the liver and cardiovascular and respiratory systems; 45 patients with alcoholic cardiomyopathy (ACM) and congestive heart failure without a history of coronary heart disease and valvular diseases, among whom 11 patients were found to have LC. In addition to standard clinical examination, all the patients underwent electrocardiography, by estimating the corrected QT interval (QTc), standard echocardiography; and those without ACM underwent estimation of left ventricular (LV) kinetics using speckle-tracking echocardiography. Results: The patients with alcoholic LC were found to have a higher LV ejection fraction and a more obvious impairment of LV global longitudinal deformity, and more commonly LV diastolic dysfunction. 16 of the 80 patients with LC were observed to have moderate pulmonary hypertension while the mean pulmonary artery pressure (MPAP) was within the normal range in all the patients without LC. A prolonged QTc interval was revealed in the patients with LC. The duration of QTc was directly correlated with the MELD severity of LC. The patients with chronic heart failure in the presence of ACM and CL showed a more obvious LV diastolic dysfunction, as estimated by E/E', a greater LV mass index, and a higher MPAP than those with ACM without LC. Conclusion: The LC patients both with ACM and without a history of diseases of the heart were noted to have its more evident disorders as diastolic dysfunction and elevated MPAP. Those without ACM were observed to have impaired LV global deformity and a prolonged QTc interval
Cardiac damage in liver cirrhosis in alcohol abusers
Aim: To estimate the contribution of liver cirrhosis (LC) to the development of heart diseases in alcohol abusers. Subjects and methods: The investigation included 80 patients with alcoholic LC without a history of cardiovascular and respiratory diseases and, as a control group, 32 alcohol abusers without a history of chronic diseases of the liver and cardiovascular and respiratory systems; 45 patients with alcoholic cardiomyopathy (ACM) and congestive heart failure without a history of coronary heart disease and valvular diseases, among whom 11 patients were found to have LC. In addition to standard clinical examination, all the patients underwent electrocardiography, by estimating the corrected QT interval (QTc), standard echocardiography; and those without ACM underwent estimation of left ventricular (LV) kinetics using speckle-tracking echocardiography. Results: The patients with alcoholic LC were found to have a higher LV ejection fraction and a more obvious impairment of LV global longitudinal deformity, and more commonly LV diastolic dysfunction. 16 of the 80 patients with LC were observed to have moderate pulmonary hypertension while the mean pulmonary artery pressure (MPAP) was within the normal range in all the patients without LC. A prolonged QTc interval was revealed in the patients with LC. The duration of QTc was directly correlated with the MELD severity of LC. The patients with chronic heart failure in the presence of ACM and CL showed a more obvious LV diastolic dysfunction, as estimated by E/E', a greater LV mass index, and a higher MPAP than those with ACM without LC. Conclusion: The LC patients both with ACM and without a history of diseases of the heart were noted to have its more evident disorders as diastolic dysfunction and elevated MPAP. Those without ACM were observed to have impaired LV global deformity and a prolonged QTc interval
Analysis of the localization and timing of the hernias formation in anterior abdominal wall after colostomy
Background. Despite the many studies conducted, the problem of choosing the
prevention of parastomal hernias remains relevant. Nowadays, no studies have been presented
in the available literature on the timing of the parastomal hernias formation after removal
of the colostomy and localization of the hernia in the projection of the intestinal stoma.
The purpose of this study is to evaluate the results of stoma treatment to establish the
average time of formation of parastomal hernia and its localization in the projection of the
intestinal stoma. Materials and methods. The analysis of 22 patients with various abdominal
surgical pathology requiring removal of a colostomy in 2017β2022, who subsequently
developed a parastomal hernia, was carried out. Results. The study did not establish
a statistically significant difference in the timing of the formation of parastomal hernia. A
statistically significant difference was obtained among patients with different localization
(lateral-caudal and circular location) (p < 0.05) of parastomal hernia. Conclusions. The revealed
fact of the formation of parastomal hernias in the absolute majority of cases, lateralcaudal
localization, directs the surgeon to perform preventive measures to further strengthen
this zone in order to prevent hernias during the formation of a colostomy