14 research outputs found
ΠΠ°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π° β ΡΠ½ΠΈΠ²Π΅ΡΡΠ°Π»ΡΠ½ΡΠΉ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠ°ΠΊΡΠΎΡ Π² ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠΈ ΠΎΡΠ³Π°Π½ΠΎΠ² ΠΈ ΡΠΈΡΡΠ΅ΠΌ ΠΏΡΠΈ COVID-19
Relevance. The pathogenesis of COVID-19 remains one of the most pressing. The literature discusses the role of iron as a factor supporting inflammatory processes, hypercoagulability and microcirculation crisis in severe COVID-19.The aim of study. was to identify changes in iron metabolism in patients with severe COVID-19 and hyperferritinemia.Material and methods. In this study, we used a content analysis of available scientific publications and our own observations of the peculiarities of the clinical picture and laboratory parameters in patients with a severe course of COVID-19 who had hyperferretinemia at the height of the disease. The main group consisted of 30 patients hospitalized in the Department of Anesthesiology, Resuscitation and Intensive Care of N.A. Semashko City clinical Hospital No. 38 with the diagnosis COVID-19, bilateral polysegmental pneumonia, severe course and hyperferritinemia. The diagnosis of a new coronavirus infection was confirmed by visualization of bilateral viral lung lesions with chest CT-scan, positive PCR test for SARS-CoV-2 and the presence of immunoglobulins to SARS-CoV-2. The control group consisted of 20 healthy volunteers. The study evaluated the biochemical parameters of iron metabolism, fibrinolysis and markers of inflammation. Changes associated with impaired iron metabolism were assessed by the level of serum iron, transferrin, daily and induced iron excretion in the urine. Statistical processing was carried out using nonparametric methods.Results. All patients with severe COVID-19 and hyperferritinemia showed signs of impaired iron metabolism, inflammation and fibrinolysis β a decrease in the level of transferrin (p<0.001), serum iron (p><0.005), albumin (p><0.001), lymphocytes (p><0.001) and an increase in leukocytes (p><0.001), neutrophils (p><0.001), CRP (p><0.005), IL-6 (p><0.001), D-dimer (p><0.005), daily urinary iron excretion (p><0.005) and induced urinary iron excretion (p><0.001). Conclusions The study showed that in the pathogenesis of the severe course of COVID-19, there is a violation of iron metabolism and the presence of a free iron fraction. The appearance of free iron can be caused by damage to cells with the βreleaseβ of iron from cytochromes, myoglobin, hemoglobin, or violation of the binding of iron to transferrin, which may be the result of a change in the protein structure or violation of the oxidation of iron to the trivalent state. When assessing the degree of viral effect on the body, one should take into account the effect of various regulators of iron metabolism, as well as an assessment of the level of free iron not associated with transferrin. Keywords: new coronavirus infection, COVID-19, SARS-CoV-2, iron metabolism, free iron, ferritin, transferrin, NTBI, nontransferrin bound iron>Λ0.001), serum iron (pΛ0.005), albumin (pΛ0.001), lymphocytes (pΛ0.001) and an increase in leukocytes (pΛ0.001), neutrophils (pΛ0.001), CRP (pΛ0.005), IL-6 (pΛ0.001), D-dimer (pΛ0.005), daily urinary iron excretion (pΛ0.005) and induced urinary iron excretion (pΛ0.001).Conclusions. The study showed that in the pathogenesis of the severe course of COVID-19, there is a violation of iron metabolism and the presence of a free iron fraction. The appearance of free iron can be caused by damage to cells with the βreleaseβ of iron from cytochromes, myoglobin, hemoglobin, or violation of the binding of iron to transferrin, which may be the result of a change in the protein structure or violation of the oxidation of iron to the trivalent state. When assessing the degree of viral effect on the body, one should take into account the effect of various regulators of iron metabolism, as well as an assessment of the level of free iron not associated with transferrin.Β ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. ΠΠΎΠΏΡΠΎΡ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π° COVID-19 ΠΎΡΡΠ°Π΅ΡΡΡ ΠΎΠ΄Π½ΠΈΠΌ ΠΈΠ· ΡΠ°ΠΌΡΡ
Π°ΠΊΡΡΠ°Π»ΡΠ½ΡΡ
. Π Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΠ΅ ΠΎΠ±ΡΡΠΆΠ΄Π°Π΅ΡΡΡ ΡΠΎΠ»Ρ ΠΆΠ΅Π»Π΅Π·Π° Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΡΠ°ΠΊΡΠΎΡΠ°, ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠΈΠ²Π°ΡΡΠ΅Π³ΠΎ Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΏΡΠΎΡΠ΅ΡΡΡ, Π³ΠΈΠΏΠ΅ΡΠΊΠΎΠ°Π³ΡΠ»ΡΡΠΈΡ ΠΈ ΠΊΡΠΈΠ·ΠΈΡ ΠΌΠΈΠΊΡΠΎΡΠΈΡΠΊΡΠ»ΡΡΠΈΠΈ ΠΏΡΠΈ ΡΡΠΆΠ΅Π»ΠΎΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠΈ COVID-19.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ. ΠΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π° Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19 ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π Π½Π°ΡΡΠΎΡΡΠ΅ΠΌ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Ρ ΠΊΠΎΠ½ΡΠ΅Π½Ρ-Π°Π½Π°Π»ΠΈΠ· ΠΈΠΌΠ΅ΡΡΠΈΡ
ΡΡ Π½Π°ΡΡΠ½ΡΡ
ΠΏΡΠ±Π»ΠΈΠΊΠ°ΡΠΈΠΉ ΠΈ ΡΠΎΠ±ΡΡΠ²Π΅Π½Π½ΡΠ΅ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ Π·Π° ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡΠΌΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½Ρ ΠΈ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΡΡ
ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΎΠ² Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19, ΠΈΠΌΠ΅Π²ΡΠΈΡ
Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΡ Π² ΠΏΠ΅ΡΠΈΠΎΠ΄ Π½Π°ΠΈΠ±ΠΎΠ»ΡΡΠΈΡ
ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΡΠ½ΠΎΠ²Π½Π°Ρ Π³ΡΡΠΏΠΏΠ° ΡΠΎΡΡΠΎΡΠ»Π° ΠΈΠ· 30 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ², Π³ΠΎΡΠΏΠΈΡΠ°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
Π² ΠΎΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ Π°Π½Π΅ΡΡΠ΅Π·ΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ, ΡΠ΅Π°Π½ΠΈΠΌΠ°ΡΠΈΠΈ ΠΈ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π‘ΠΠ± ΠΠΠ£Π Β«ΠΠΎΡΠΎΠ΄ΡΠΊΠ°Ρ Π±ΠΎΠ»ΡΠ½ΠΈΡΠ° β 38 ΠΈΠΌ. Π.Π. Π‘Π΅ΠΌΠ°ΡΠΊΠΎΒ» Ρ Π΄ΠΈΠ°Π³Π½ΠΎΠ·ΠΎΠΌ Β«COVID-19, Π΄Π²ΡΡΡΠΎΡΠΎΠ½Π½ΡΡ ΠΏΠΎΠ»ΠΈΡΠ΅Π³ΠΌΠ΅Π½ΡΠ°ΡΠ½Π°Ρ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ, ΡΡΠΆΠ΅Π»ΠΎΠ΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅Β» ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ. ΠΠΈΠ°Π³Π½ΠΎΠ· Π½ΠΎΠ²ΠΎΠΉ ΠΊΠΎΡΠΎΠ½Π°Π²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΏΠΎΠ΄ΡΠ²Π΅ΡΠΆΠ΄Π°Π»ΡΡ Π²ΠΈΠ·ΡΠ°Π»ΠΈΠ·Π°ΡΠΈΠ΅ΠΉ Π΄Π²ΡΡΡΠΎΡΠΎΠ½Π½Π΅Π³ΠΎ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ Π»Π΅Π³ΠΊΠΈΡ
ΠΏΡΠΈ ΠΊΠΎΠΌΠΏΡΡΡΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ Π³ΡΡΠ΄Π½ΠΎΠΉ ΠΊΠ»Π΅ΡΠΊΠΈ, ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠΌ ΠΠ¦Π -ΡΠ΅ΡΡΠΎΠΌ Π½Π° SARS-CoV-2 ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΠ³Π»ΠΎΠ±ΡΠ»ΠΈΠ½ΠΎΠ² ΠΊ SARS-CoV-2. ΠΡΡΠΏΠΏΡ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΈ 20 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ±ΡΠΎΠ²ΠΎΠ»ΡΡΠ΅Π². Π ΡΠ°Π±ΠΎΡΠ΅ Π΄Π°Π½Π° ΠΎΡΠ΅Π½ΠΊΠ° Π±ΠΈΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π°, ΡΠΈΠ±ΡΠΈΠ½ΠΎΠ»ΠΈΠ·Π° ΠΈ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ. ΠΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ, ΡΠ²ΡΠ·Π°Π½Π½ΡΠ΅ Ρ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π°, ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ ΠΏΠΎ ΡΡΠΎΠ²Π½Ρ ΡΡΠ²ΠΎΡΠΎΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π°, ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½Π°, ΡΡΡΠΎΡΠ½ΠΎΠΉ ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ. Π‘ΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΡΡ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΡ ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΠ»ΠΈ Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π½Π΅ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ².Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π£ Π²ΡΠ΅Ρ
ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19 ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ ΠΎΡΠΌΠ΅ΡΠ°Π»ΠΈΡΡ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΠ΅ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ ΠΈ ΡΠΈΠ±ΡΠΈΠ½ΠΎΠ»ΠΈΠ·Π° β ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½Ρ ΡΡΠ²ΠΎΡΠΎΡΠΎΡΠ½ΠΎΠ³ΠΎ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½Π° (p<0,001), ΠΆΠ΅Π»Π΅Π·Π° (p><0,005) ΠΈ Π°Π»ΡΠ±ΡΠΌΠΈΠ½Π° (p><0,001), Π»ΠΈΠΌΡΠΎΡΠΈΡΠΎΠ² (p><0,001) Π² ΠΊΡΠΎΠ²ΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ Π² Π½Π΅ΠΉ Π»Π΅ΠΉΠΊΠΎΡΠΈΡΠΎΠ² (p><0,001), Π½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΠΎΠ² (p><0,001), Π‘Π Π (p><0,005), ΠΠ-6 (p><0,001), D-Π΄ΠΈΠΌΠ΅ΡΠ° (p><0,005), Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΡΡΠΎΡΠ½ΠΎΠΉ (p><0,005) ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ (p><0,001). Π·Π°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ ΠΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ, ΡΡΠΎ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ ΡΡΠΆΠ΅Π»ΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ COVID-19 ΠΈΠΌΠ΅Π΅Ρ ΠΌΠ΅ΡΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π° ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠ°ΠΊΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π° ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π²ΡΠ·Π²Π°Π½ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ Ρ Π²ΡΡΠ²ΠΎΠ±ΠΎΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΆΠ΅Π»Π΅Π·Π° ΠΈΠ· ΡΠΈΡΠΎΡ
ΡΠΎΠΌΠΎΠ², ΠΌΠΈΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π°, Π³Π΅ΠΌΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π° Π»ΠΈΠ±ΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² ΡΠ²ΡΠ·ΡΠ²Π°Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ, ΡΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠΌ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΡΡΡΠΊΡΡΡΡ Π±Π΅Π»ΠΊΠ° ΠΈΠ»ΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Π² ΡΡΠ΅Ρ
Π²Π°Π»Π΅Π½ΡΠ½ΠΎΠ΅ ΡΠΎΡΡΠΎΡΠ½ΠΈΠ΅. ΠΡΠΈ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π½Π° ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌ ΡΠ»Π΅Π΄ΡΠ΅Ρ ΡΡΠΈΡΡΠ²Π°ΡΡ ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠΎΠ² ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡΠ΅Π½ΠΊΡ ΡΡΠΎΠ²Π½Ρ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ, Π½Π΅ ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠ³ΠΎ Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠ»ΡΡΠ΅Π²ΡΠ΅ ΡΠ»ΠΎΠ²Π°: Π½ΠΎΠ²Π°Ρ ΠΊΠΎΡΠΎΠ½Π°Π²ΠΈΡΡΡΠ½Π°Ρ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡ, COVID-19, SARS-CoV-2, ΠΎΠ±ΠΌΠ΅Π½ ΠΆΠ΅Π»Π΅Π·Π°, ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ΅ ΠΆΠ΅Π»Π΅Π·ΠΎ, ΡΠ΅ΡΡΠΈΡΠΈΠ½, ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½, NTBI, nontransferrin bound iron>Λ0,001), ΠΆΠ΅Π»Π΅Π·Π° (pΛ0,005) ΠΈ Π°Π»ΡΠ±ΡΠΌΠΈΠ½Π° (pΛ0,001), Π»ΠΈΠΌΡΠΎΡΠΈΡΠΎΠ² (pΛ0,001) Π² ΠΊΡΠΎΠ²ΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ Π² Π½Π΅ΠΉ Π»Π΅ΠΉΠΊΠΎΡΠΈΡΠΎΠ² (pΛ0,001), Π½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΠΎΠ² (pΛ0,001), Π‘Π Π (pΛ0,005), ΠΠ-6 (pΛ0,001), D-Π΄ΠΈΠΌΠ΅ΡΠ° (pΛ0,005), Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΡΡΠΎΡΠ½ΠΎΠΉ (p0,005) ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ (pΛ0,001).ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ, ΡΡΠΎ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ ΡΡΠΆΠ΅Π»ΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ COVID-19 ΠΈΠΌΠ΅Π΅Ρ ΠΌΠ΅ΡΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π° ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠ°ΠΊΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π° ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π²ΡΠ·Π²Π°Π½ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ Ρ Π²ΡΡΠ²ΠΎΠ±ΠΎΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΆΠ΅Π»Π΅Π·Π° ΠΈΠ· ΡΠΈΡΠΎΡ
ΡΠΎΠΌΠΎΠ², ΠΌΠΈΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π°, Π³Π΅ΠΌΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π° Π»ΠΈΠ±ΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² ΡΠ²ΡΠ·ΡΠ²Π°Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ, ΡΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠΌ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΡΡΡΠΊΡΡΡΡ Π±Π΅Π»ΠΊΠ° ΠΈΠ»ΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Π² ΡΡΠ΅Ρ
Π²Π°Π»Π΅Π½ΡΠ½ΠΎΠ΅ ΡΠΎΡΡΠΎΡΠ½ΠΈΠ΅. ΠΡΠΈ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π½Π° ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌ ΡΠ»Π΅Π΄ΡΠ΅Ρ ΡΡΠΈΡΡΠ²Π°ΡΡ ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠΎΠ² ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡΠ΅Π½ΠΊΡ ΡΡΠΎΠ²Π½Ρ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ, Π½Π΅ ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠ³ΠΎ Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ ΠΆΠ΅Π»Π΅Π·Π°.
Secondary hemophagocytic syndrome in adult patients. Study of 91 patients
Background. Secondary hemophagocytic lymphohystiocytosis (sHLH) is a hyperinflammatory reaction provoked by some trigger (cancer, autoimmune or infection). The majority of affected patients are at high risk of fatal multiple organ failure without getting immunsupressive treatment.Objective. Clinical and laboratory profile of sHLH patients.Materials and methods. Retrospective study included clinical, instrumental and lab data from the 91 patients followed between June 2009 and June 2019. Diagnosis sHLH had been based on HLH-2004 and H-Score criteria. The analyzed parameters had been fever chart, liver and spleen enlargement, changes in the bone marrow; values levels of glutamic pyruvic transaminase, serum glutamic oxaloacetic transaminase, alkaline phosphatase, bilirubin, triglycerides, total ferritin with percentage of glycosylation. All patients with rheumatic disorders or malignancies had received either immunosuppressive or cytotoxic therapy. Febrile patients received anti-infective treatment according to the local routine protocols.Results. The data from 91 patients (41 male and 50 female) had been analyzed. Median age was 58 (2β90) years. The sHLH trigger-diseases spectrum included leukemia/lymphoma (n = 52), infection diseases (n = 11), autoimmune disorders (n = 5), allogenic bone marrow transplantation (n = 13), unidentified (n = 10). A fever with an unknown origin and refractory to antibacterial treatment had been observed in 87 (96 %) patients. Morphological hemophagocytic evidences in the bone marrow had been found in 83 %. Breath shortening, liver failure, neurologic disturbances, systemic effusions, rash, heart failure had been registered in 83 % patients. Detected splenomegaly presented in 56 %. Laboratory changes, median were as following: serum glutamic-pyruvic transaminase (alanine aminotransferase, SGPT) β 92 (39.2β1060.8) IU/L; serum glutamic oxaloacetic transaminase (aspartate aminotransferase, SGOT) β 105 (40β4177) IU/L; alkaline phosphatase β 225 (120.9β989) IU/L; bilirubin β 50.5 (22β559) Β΅mol/L; triglycerides β 3.2 (1.95β8.6) mmol/L; total ferritin β 10000 (597β255000) ng/mL with glycosylation percentage β 20.45 (0β37.8) %. 71 patients received various of HLH-directed therapy courses. The overall survival rate was 27 %, median follow-up β 540 days.Conclusion. The main clinical and instrumental findings in sHLH are fever, refractory to anti-infective treatment, elevation of transaminases, serum alkaline phosphatase, triglycerides, total ferritine with low glycosylated fraction. Early diagnosing and immunesupression are the main factors of survival
Discrimination between Complete versus Non-Complete Pathologic Response to Neoadjuvant Therapy Using Ultrasensitive Mutation Analysis: A Proof-of-Concept Study in <i>BRCA1</i>-Driven Breast Cancer Patients
Neoadjuvant chemotherapy (NACT) for breast cancer (BC) often results in pathologic complete response (pCR), i.e., the complete elimination of visible cancer cells. It is unclear whether the use of ultrasensitive genetic methods may still detect residual BC cells in complete responders. Breast carcinomas arising in BRCA1 mutation carriers almost always carry alterations of the TP53 gene thus providing an opportunity to address this question. The analysis of consecutive BC patients treated by NACT revealed a higher pCR rate in BRCA1-driven vs. BRCA1-wildtype BCs (13/24 (54%) vs. 29/192 (15%), p BRCA1 mutation carriers were available for the study. While TP53 mutation was identified in all chemonaive tumors, droplet digital PCR (ddPCR) analysis of the post-NACT tumor bed revealed the persistence of this alteration in all seven pCR-non-responders but in none of five pCR responders. Eleven patients provided to the study post-NACT tissue samples only; next-generation sequencing (NGS) analysis revealed mutated TP53 copies in all six cases without pCR but in none of five instances of pCR. In total, TP53 mutation was present in post-NACT tissues in all 13 cases without pCR, but in none of 10 patients with pCR (p < 0.000001). Therefore, the lack of visible tumor cells in the post-NACT tumor bed is indeed a reliable indicator of the complete elimination of transformed clones. Failure of ultrasensitive methods to identify patients with minimal residual disease among pCR responders suggests that the result of NACT is a categorical rather than continuous variable, where some patients are destined to be cured while others ultimately fail to experience tumor eradication