The 15 references with contexts in paper A. Ershov V., V. Dolgikh T, T. Dolgikh I., S. Morozov V., Yu. Orlov P., A. Reis B., А. Ершов В., В. Долгих Т., Т. Долгих И., С. Морозов В., Ю. Орлов П., А. Рейс Б. (2013) “Мутации Лейдена и течение острого панкреатита тяжелой степени // Leiden Mutation and the Course of Severe Acute Pancreatitis” / spz:neicon:reanimatology:y:2013:i:6:p:36

1
Smelaya T.V., Salnikova L.E., Moroz V.V., Golubev A.M., Zarzhetsky Yu.V., Rubanovich A.V. Genetichesky polimorfizm i chastota razvitiya oslozhnenii pri pnevmonii razlichnogo genezisa. [Genetic polymorphism and the rate of development of complications in pneumonia of varying genesis]. Obshchaya Reanimatologiya. 2011; 7 (2): 10—16. [In Russ.]
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  1. In-text reference with the coordinate start=2107
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    Key words: acute pancreatitis, Leiden mutation. Molecular And Cellular Mechanisms For The Development Of Critical Conditions In recent years the incidence of acute pancreatitis has not undergone any dramatically changes
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    [1]
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    . On one hand this is due to peculiarities of eating habits with increasing consumption of alcohol and its surrogates, cholelithiasis prevalence all resulting in number of patients increased.

2
Moroz V.V., Smelaya T.V., Golubev A.M., Salnikova L.E. Genetika i meditsina kriticheskikh sostoyanii: ot teorii k praktike. [Genetics and medicine of critical conditions: from theory to practice]. Obshchaya Reanimatologiya. 2012; 8 (4): 5—12. [In Russ.]
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  1. In-text reference with the coordinate start=2473
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    On one hand this is due to peculiarities of eating habits with increasing consumption of alcohol and its surrogates, cholelithiasis prevalence all resulting in number of patients increased. On another hand, improvement in clinical, laboratory and instrumental diagnosis of the disease also contributed to constant occurance of the disease
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    [2]
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    . Mortality rate due to destructive forms of acute pancreatitis exceeded 20% both nationally and internationally [3]. Severe disorders of hemostasis in critical illness including acute pancreatitis are caused by many factors where destructive processes in organs and tissues, massive bleeding and transfusions, endotoxemia and hypoxia play a leading role [4, 5].

3
Tarasenko V.S., Kubyshkin V.A., Demin D.B., Volkov D.V., Smolyagin A.I., Chukina O.V. Immunologicheskie narusheniya pri pankreonekroze i ikh korrektsiya. [Immunological disorders in pancreatic necrosis and their correctio]. Khirurgiya. Zhurnal Imeni N.I.Pirogova.2013; 1: 88—95. [In Russ.]
Total in-text references: 2
  1. In-text reference with the coordinate start=2590
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    On another hand, improvement in clinical, laboratory and instrumental diagnosis of the disease also contributed to constant occurance of the disease [2]. Mortality rate due to destructive forms of acute pancreatitis exceeded 20% both nationally and internationally
    Exact
    [3]
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    . Severe disorders of hemostasis in critical illness including acute pancreatitis are caused by many factors where destructive processes in organs and tissues, massive bleeding and transfusions, endotoxemia and hypoxia play a leading role [4, 5].

  2. In-text reference with the coordinate start=3070
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    Increase of blood hemoconcentration and viscosity in pancreatonecrosis cause hypercoagulation and thrombophilia, which significantly contribute to development of disseminated intravascular coagulation
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    [3, 6]
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    . Genetic mutation of genes that control the folate circle and coagulation factors II and V significantly increase the risk of of primary and recurrent venous and arterial thrombosis even in apparently healthy individuals [7, 8].

4
Bianchi M.E.DAMPs, PAMPs and alarmins: all we need to know about danger. J. Leukoc. Biol.2007; 81 (1): 1—5. http://dx.doi.org/10.1189/ jlb.0306164. PMID: 17032697
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  1. In-text reference with the coordinate start=2850
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    Severe disorders of hemostasis in critical illness including acute pancreatitis are caused by many factors where destructive processes in organs and tissues, massive bleeding and transfusions, endotoxemia and hypoxia play a leading role
    Exact
    [4, 5]
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    . Increase of blood hemoconcentration and viscosity in pancreatonecrosis cause hypercoagulation and thrombophilia, which significantly contribute to development of disseminated intravascular coagulation [3, 6].

5
Savelyev V.S., Filimonov M.I., Gelfand B.R. Ostryi pankreatit kak problema urgentnoi khirurgii i intensivnoi terapii. Intensivnaya terapiya v khirurgii. [Acute pancreatitis as a problem of urgent surgery and intensive therapy]. Consilium medicum.2000; 2 (9): 16. [In Russ.]
Total in-text references: 1
  1. In-text reference with the coordinate start=2850
    Prefix
    Severe disorders of hemostasis in critical illness including acute pancreatitis are caused by many factors where destructive processes in organs and tissues, massive bleeding and transfusions, endotoxemia and hypoxia play a leading role
    Exact
    [4, 5]
    Suffix
    . Increase of blood hemoconcentration and viscosity in pancreatonecrosis cause hypercoagulation and thrombophilia, which significantly contribute to development of disseminated intravascular coagulation [3, 6].

6
Vinokurov M.M., Savelyev V.V., Khlebnyi E.S., Kershengolts B.M. Kompleksnaya otsenka urovnya endogennoi intoksikatsii u bolnykh v sterilnoi faze pankreonekroza. [Integrated estimation of the level of endogenous intoxication in patients with sterile-phase pancreatic necrosis]. Khirurgiya. Zhurnal Imeni N.I.Pirogova.2012; 10: 21—26. [In Russ.]
Total in-text references: 1
  1. In-text reference with the coordinate start=3070
    Prefix
    Increase of blood hemoconcentration and viscosity in pancreatonecrosis cause hypercoagulation and thrombophilia, which significantly contribute to development of disseminated intravascular coagulation
    Exact
    [3, 6]
    Suffix
    . Genetic mutation of genes that control the folate circle and coagulation factors II and V significantly increase the risk of of primary and recurrent venous and arterial thrombosis even in apparently healthy individuals [7, 8].

7
Moroz V.V., Golubev A.M., Afanasyev A.V., Kuzovlev A.N., Sergunova V.A., Gudkova O.E., Chernysh A.M. Stroenie i funktsiya eritrotsita v norme i pri kriticheskikh sostoyaniyakh. [The structure and function of a red blood cell in health and critical conditions]. Obshchaya Reanimatologiya. 2012; 8 (1): 52—60. [In Russ.]
Total in-text references: 1
  1. In-text reference with the coordinate start=3309
    Prefix
    Genetic mutation of genes that control the folate circle and coagulation factors II and V significantly increase the risk of of primary and recurrent venous and arterial thrombosis even in apparently healthy individuals
    Exact
    [7, 8]
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    . Only few research studies, however, were devoted to evaluation of pathogenetic significance of the hemostatic system gene alterations in acute pancreatitis. Thereupon, the objective of the present study was to evaluate a pathogenic effect of factor V Leiden mutation in severe acute pancreatitis.

8
Filimonov M.I., Burnevich S.Z.Khirurgiya pankreonekroza: 80 lektsii po khirurgii. [Surgery for pancreatic necrosis: 80 lectures on surgery]. Moscow: Litterra; 2008. [In Russ.]
Total in-text references: 1
  1. In-text reference with the coordinate start=3309
    Prefix
    Genetic mutation of genes that control the folate circle and coagulation factors II and V significantly increase the risk of of primary and recurrent venous and arterial thrombosis even in apparently healthy individuals
    Exact
    [7, 8]
    Suffix
    . Only few research studies, however, were devoted to evaluation of pathogenetic significance of the hemostatic system gene alterations in acute pancreatitis. Thereupon, the objective of the present study was to evaluate a pathogenic effect of factor V Leiden mutation in severe acute pancreatitis.

9
Doix S., Mahrousseh M., Jolak M., Laurent Y., Lorenzini J.L., Binquet C., Zeller M., Cottin Y., Wolf J.E.Factor V Leiden and myocardial infarction: a case, review of the literature with a meta-analysis. Ann. Cardiol. Angeiol. (Paris).2003; 52 (3): 143—149. PMID: 12938565
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  1. In-text reference with the coordinate start=5352
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    The primary disease severity was confirmed by the clinical and laboratory criteria (Table 1) recommended by I. I. Dzhanelidze St. Petersburg Emergency Care Research Institute
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    . The diagnosis of acute destructive pancreatitis in group I (60% cases) and in group II (69% cases) was proved by means of laparoscopy within one day from the time of admission. All patients were treated in the Intensive Care Units of the Surgery and Purulent Surgery Departments at the Municipal Clinical Emergency Hospital No1 and Omsk Clinical Medical and Surgical Center d

10
Folsom A.R., Cushman M., Tsai M.Y., Aleksic N., Heckbert S.R., Boland L.L., Tsai A.W., Yanez N.D., Rosamond W.D.A prospective study of venous thromboembolism in relation to factor V Leiden and related factors. Blood.2002; 99 (8): 2720—2725. http://dx.doi.org/10.1182/ blood.V99.8.2720. PMID: 11929758
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  1. In-text reference with the coordinate start=11073
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    Apparently, this is due to the microvasculature elements dysfunction in destruction of the pancreas caused by a precapillary spasm against catecholamine excess, erythrocytes sludging and deceleration, stasis and local microthrombosis development
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    [10]
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    . It should be emphasized that all factors apart from local microthrombosis in reconstituted conditions must provide the identical effect in both groups. To our opinion, the gene mutation causes more extensive damages to the pancreas facilitating in concert with other factors development of thrombotic complications of the primary disease.

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    Here and in tables 4 and 5: * — P<0,05 while comparison among groups. protein C, as this occurs in the absence of the genetic alteration, but becomes resistant to its effect. Due to resistance to protein C clotting factor V concentration is increased becoming a provocative factor for thrombus formation in organs including the pancreas
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    [10]
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    . Development of microfocal pancreatonecrosis, a mild form of destructive pancreatitis, was detected by 25.6% more often in patients without Leiden mutation than in patients with this mutation.

11
Tolstoi A.D., Goltsov R.V.Vozmozhnosti «obryva» destruktivnogo protsessa na rannikh stadiyakh pankreonekroza. [Possibilities of a «break» in the destructive process in early-stage pancreatic necrosis]. Obshchaya Reanimatologiya. 2005; 1 (3): 58—60. [In Russ.]
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  1. In-text reference with the coordinate start=14609
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    acute pancreatitis is stipulated by late medical care (4—5thday after disease onset), severe violations of water-electrolyte metabolism and acid-base balance, hypovolemia, endotoxicosis, enteric microflora translocation under tissue hypoxia and acidosis against palsy and pancreas microvasculature dysfunction that has been confirmed by pathophysiological and clinical studies
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    . The maximum value of the leukocyte intoxication index was registered in patients of the group II which was higher 15.3-fold and 1.12-fold in control and comparison groups, respectively (Table 6).

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    Bacteriological examination of blood and urine revealed a high growth of both gram-positive (82%) and gram-negative (10%) microflora that included S.aureusincluding MRSA+, S.epidermidis, E.coli, K.pneumoniae. Similar findings have been described earlier
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    [11, 15]
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    . This study revealed significant differences in severe acute pancreatitis course in patients with and without factor V Leiden mutation. Apparently, the changes caused by the mutation lead to alteration within the pancreas in the hemostatic system facilitating the size increasing and appearance of new necrosis foci in the affected organ.

12
Sukach M.S., Dolgikh V.T.Vliyanie geptrala na koagulyatsionnuyu aktivnost krovi pri pankreonekroze. [Effect of heptral on blood coagulation activity in pancreonecrosis]. Obshchaya Reanimatologiya. 2011; 7 (6): 34—39. [In Russ.]
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  1. In-text reference with the coordinate start=7830
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    . (%)25 (50,0)22 (52,4)47 Alcohol abuse, abs. (%)13 (26,0)10 (23,8)23 Diet violation, abs. (%)12 (24,0)10 (23,8)22 Total504292 Table 2 Distribution of patients with acute pancreatitis depending on etiology of the disease indicated time points. Toxicity indicators were determined by standardized methods, such as M. J. Malakhova's method for low and average molecular weight substances
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    and Lowry's method. Genetic mutations were detected by polymerase chain reaction. During the study groups were compared according to final dynamic parameters of disease development, such as the pathology form and its complications, frequency of specific treatment modes application and their efficacy.

  2. In-text reference with the coordinate start=15461
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    The second stage of endotoxemia as determined by accumulation of low and average molecular weight substances both on erythrocytes and in plasma (in accordance to M. J. Malakhova method
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    [12]
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    ) was observed in patients in the group I at the time of admission and during three days of treatment, The third stage of endotoxemia («a complete saturation phase») or reversible compensation of the natural detoxification system clinically manifested by more severe endotoxemia induced apparently by increasing of catabolic processes was observed in patients of the group II at the

13
Savelyev V.S., Filimonov M.I., Gelfand B.R., Burnevich S.Z. Pankreonekroz i pankreatogennyi sepsis. Sostoyanie problemy. [Pancreatic necrosis and pancreatogenetic sepsis: State-of-the-art of the problem]. Annaly Khirurgii.2003; 1: 12—19. [In Russ.]
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  1. In-text reference with the coordinate start=16614
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    Worsening of endotoxemia severity in patients of the group II to 3—6 days was evidently associated with hypercoagulation due to a typical «shock» activation of the blood coagulation system and decrease of anticoagulation system activity as a result of Leiden mutation
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    [13]
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    , as well as developing high intraperitoneal pressure due to enzymatic peritonitis and intestinal paresis resulted from ischemia and hypoxia of the intestinal wall tissues. This created favorable conditions for the intestinal microflora and toxins translocation into the bloodstream during reperfusion and corresponded in terms to purulent infection foci formation in the abdominal cavi

14
Malakhova M.Ya.Endogennaya intoksikatsiya kak otrazhenie kompensatornoi perestroiki obmennykh protsessov v organizme. [Endogenous intoxication as a portrayal of the compensatory rearrangement of metabolic processes in the body]. Efferentnaya Terapiya.2000; 6 (4): 3—14. [In Russ.]
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  1. In-text reference with the coordinate start=17022
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    This created favorable conditions for the intestinal microflora and toxins translocation into the bloodstream during reperfusion and corresponded in terms to purulent infection foci formation in the abdominal cavity
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    [14]
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    . It should be noted there were no any reliable distinctions in respect to the concentration level of the low and average molecular weight substances in the erythrocyte membranes and lymphocytes rate in the group I to the 5—6 days in comparison with the control group.

15
Rantsev M.A., Sarapultsev P.A., Kuznetsov N.N., Chupakhin O.N., Sarapultsev A.P., Khodakov V.V., Sidorova L.P. Korrektsiya gemokoagulyatsionnykh narushenii pri eksperimentalnom pankreonekroze. [Correction of hemocoagulative disorders in experimental pancreatic necrosis]. Uralsky Meditsinsky Zhurnal.2012; 1 (93): 26—29. [In Russ.]
Total in-text references: 1
  1. In-text reference with the coordinate start=19380
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    Bacteriological examination of blood and urine revealed a high growth of both gram-positive (82%) and gram-negative (10%) microflora that included S.aureusincluding MRSA+, S.epidermidis, E.coli, K.pneumoniae. Similar findings have been described earlier
    Exact
    [11, 15]
    Suffix
    . This study revealed significant differences in severe acute pancreatitis course in patients with and without factor V Leiden mutation. Apparently, the changes caused by the mutation lead to alteration within the pancreas in the hemostatic system facilitating the size increasing and appearance of new necrosis foci in the affected organ.