Plasmapheresis in the treatment of antiphospholipid syndrome

1. Antiphospholipid syndromein general somaticpractice
 
Recently, there is growing interestin thisautoimmunevascular diseasethat manifests itselfinthe developmentof recurrentthrombosisof the venousand arterialsystemsof various organs[1]. The frequency ofpulmonary embolismas a resultof deep vein thrombosisreaches500,000cases per year, most of which are fatal. Insidiousnessof these complicationsisalmost completelyasymptomaticduringtheirup to the timeof thromboembolism in50% of patients[2]. Deep vein thrombosisis often(up to 29%) develop also after surgery, and after surgery for malignanttumorsthe frequencyreaches66%[3].

Most oftenit is a questionofantiphospholipid syndrome, first describedin 1983G.R.Hughes [4]. Antiphospholipid (aPL) antibodies areheterogenous groupof autoantibodies withdifferent properties, including differentspecificphospholipid-associated proteins, as well as reactivephospholipidmolecules. There are basic proteins, which are considered as antigensb2-glycoprotein I,prothrombin,protein C, proteinS,kininogen, annexinV.The various mechanismsinvolvedin the pathogenesisof aPL syndrome, including the effect ofaPLautoantibodiestoproteinCsystemandantithrombinIII, as wellasplatelets, endothelialcells andmonocytes[5, 6].

In particular, these antibodies disruptthe interaction of plateletswiththe endothelium ofblood vessels[7].It was experimentallydemonstrated thatisolated fr om patientswith aPLsyndromeantibodies bindphospholipids andb2-glycoprotein 1 membrane of vascular endothelial cellsand platelets, leading to their activationandthe subsequentpredisposes tothrombosisinsuch exposure[8]. Elevated levels ofantibodies tothe antigenANCA – componentof the cytoplasmof neutrophils andendothelial cellspromotes the development ofvasculopathiesof different typeswithan increased tendency tothrombosis[9].

Endothelialcells play a centralrole in preventingunwanted activationof the coagulation cascadeinintactvessels.Antiphospholipid antibodies of sera fr om patientswith systemic lupus erythematosusin the presence oflow doses ofTNF-astimulateprocoagulantactivity of the cultureof endothelial cells[10].Endothelial damagecontributes tothe release oflarge amountsof von Willebrand factorand fibronectin, thatdue to lowernaturalanticoagulantactivityof antithrombin IIIalso contributes toa hypercoagulable[11]. The sharp increase infactor VIII and vWFwithcommonvenousthrombosisalsonotedS.A.Vasilevet al.(12).  

That's whya lot of connectionsbetween theseautoantibodiesandcoagulationdisorders, including the impact onco-factors, b2-glycoprotein I,whichregulate the processes ofblood clotting. The nature of suchrelationsis unclear,but apparentlytheir influence onimmunodependentmechanismsof coagulation.These patientshave a higher riskof thrombosisand theirrecurrence.

There is the mostdangerousthrombosisof cerebral vesselswith the appearance ofstrokes[13]. In 25% of young patients with stroke it can be foundanticardiolipin antibodies[14, 15]. It is also conceivablethatsome of the manifestationsof migrainecouldbe explained byvascular disordersfor the same reasons. In particular, there may be repeated episodes oftransientischemicbrain disorders, accompanied by headaches[16]. There can communicateaPL syndromewithamyloid depositsin the walls ofcerebral vesselswith a localweakening ofthe mechanicalproperties oftheirwaytotears,is the cause ofhemorrhagic stroke in 10-15% of cases [17].

It is believed thatthe age of onsetof cerebral ischemiaassociatedwith aPL antibodies, a few tens ofyears younger than in the population ofa typicalcerebral ischemia. Perhaps there are developmentthe venoussinusthrombosis also. It can not be excludeddueto vasculardementiadisorders caused byaPL antibodies.The same appliesto cases oflate-onsetepilepsy, which once again highlights the need foran immunological studyofpatients withneurological symptoms, especially young women[18]. Neurological disordersare describedin thebackground of an increasedlevelof anticardiolipin antibodies without causingvisiblevascular lesions[19]. There relations is possiblealso ofsome mental disorderswithaPLsyndrome[20].

Antiphospholipidantibodies maybe the cause ofcoronary heart disease andmyocardial infarction,hepatic lesions[21, 22, 23].In this case,myocardial infarctiondue tocoronary arterydamageaswell ason the backgroundof coagulationdisorders of lipid metabolismandhypercholesterolemia,can occur evenin young adults[24. It describes the development ofmyocardial infarction andduring pregnancyin women withaPLsyndrome causedmiscarriagealso, although not excludedfetalantigenimmunization[25]. Anticardiolipin antibodiesare detected inmore than 70% of patients with coronary arterydiseaseat a young age.

Impactof aPL antibodiesonb2-glycoprotein I, whichisanti-atherogenicfactormayplay a complementaryrole in promotingatherosclerosis in patients withaPL syndrome[26].Patientswith antiphospholipidsyndrome have agreatertendency toatherogenesis[27, 28]. Oxidationof plasma proteinsandendothelial damageoxidant-dependentreducephysiologicalanticoagulantendothelial function[29].Antiprothrombin antibodiesincrease the riskof myocardial infarction, and antibodies againstb2-glycoprotein Icontribute toincreasingplatelet aggregation. It is possible thataPLantibodiesoccur as a resultof systemic arterialinflammatory processand are the part ofan autoimmune responseto the appearance ofdifferent antigens, modifiedatheroscleroticvascularwall[6].

Thrombosisin patients with systemiclupus erythematosusare also associatedwith aPLantibodies, with antibodies tob2-glycoprotein I is muchmore commonly associatedwith suchclinical manifestationsof aPL syndromethananticardiolipin antibodies[30]. Antiprothrombin autoantibodies, even withoutotherantiphospholipid antibodies, may beto blame for thedevelopment ofportal veinthrombosis[31].

Thrombosisoccurin the kidneys also -thrombotic microangiopathy[32]. Glomerularcapillarythrombosispasses intoglomerulosclerosiswith chronic renal failure. It perhaps the developmentthenephrotic syndrome also.

Similar processesin the livercontribute tothe development ofBudd-Chiari syndrome–thrombosisof the hepaticveinswith hepatomegaly, ascites, hepaticcongestioninthe sinuses, hepatocellularnecrosisandsubsequent fibrosis. No lessdangerous arealso themesenteric arterial thrombosis, botharteriesandveins, accompanied by catastrophiccomplications.Ischemicneuropathyof the optic nerveandretinal vascularocclusionmay also beconsequences ofantiphospholipid syndrome[33, 34].

Level riseantiphospholipidantibodiescan also be observedin patients with cancer, up to the development ofsymptomsof multiple organ failurewith highhospitalmortality rateof up to 72% [35].

In some cases, it may developcatastrophic antiphospholipidsyndrome, first described R.A.Ashersonin 1992 (36),when there are arise vascularocclusionof many organsin a short periodof time– fr om a few hoursto several days,leading to acuterespiratory distress syndrome, CNS lesions, myocardial andintestineinfarctionwith the development ofsevereorgan failureand death[11,37, 38, 39]. With the help ofplasmapheresison the backgroundof glucocorticoids andlow molecular weight heparin it is possible toreliefalsosuch a seriouscomplications.

Separately there is differentiatedSneddon syndrome, which is alsocharacteristic ofischemic strokes, peripheral thrombosiswith specificmanifestations-skinlivedo–thrombosisof smalldermalvesselstraveling inthe form ofspider veinson the surface ofthe skin, usually of the lower limbs. Histologicalstudy identifiesnoninflammatorythrombosisof small arteriesand veins of theskin and subcutaneous tissue. Cerebralmanifestationsare characterized byheadaches,focalneurologic symptoms, progressive dementia[41]. Cutaneous manifestationsmay be the firstsymptomsof aPL syndrome. In 37% of these patients subsequentlydevelop systemicthrombosis. At the same time, along with the lupus anticoagulantand anticardiolipin antibodiesare detected tothe vascular endothelium  also [42].

Antiphospholipid syndromecan beprimary or secondary, combined with systemic lupus erythematosus, Raynaud's phenomenon, Sjogren'ssyndrome, Behcet's uveitisandiridocyclitis, as well as malignant neoplasms. Since one of theaPL antibodiesislupus anticoagulant, it is not surprisingthat patientswith systemic lupus erythematosusare prone tothromboticcomplicationsoccurringin children, even in 17% of cases [43]. The main manifestationsarethromboticvascular lesionsof glomeruli ("non-inflammatory renalmicroangiopathy", lupusvasculitisorangiitis)withvascular intimal hyperplasia, which leads to hypertensionin antiphospholipid syndrome. There are frequentconcomitantvalvularlesionsandperipheral vascular diseaseby type ofRaynaud's phenomenon[44].

Antiphospholipid antibodiesaffectplateletmembrane phospholipidswith the excitation ofaggregation, leading tothrombocytopenia andtriggermechanisms for the developmentof DIC. On the otherhand,these antibodiesact onphospholipidmembranesof vascular endothelial cells, promoting their degradation andthrombosis.Furthermore, it is inhibitedplasminogenactivators[45].The first signof antiphospholipid syndromeoccursunexplainedtime of activatedpartial thromboplastin time, which requires a morein-depthresearch, which can help youidentify alsoincreasethe content ofanticardiolipin antibodies, which, of course, is more sensitive andspecific testof this pathology[46] .

Therefore, among thetherapeutic measures it predominatemethodsimpacton the mechanisms ofcoagulation. There are usedanticoagulantssuchas heparin, acetylsalicylic acid (reducing agent of platelet aggregation), ticlopidine, dipyridamole. However,casesare describedalsothe progression ofthrombosiswithgangreneof limbsduring treatment withheparin orwarfarin, which is associatedwith the development ofheparin-induced thrombocytopenia(in 1-3% of cases) aboutthe 5th dayof heparin therapy.

Platelet activationunder the influenceof heparinleads to the formationheparin-dependentIgG-antibodies to damagethe vascular wallof arteriesaswell asveins,andsmall vesselthrombosisdevelopedwith the adventof surfaceskinnecrosis[47].In thepast 50 years,heparinis widely usedin thetreatment of pulmonary embolismand coronarythrombosisin coronary heart diseaseandother indications, but these factsrequirecautionin theuse of heparin, especially in cases of aPL syndrome.

Recently, more andmoreare used such drugs as low molecular weight heparin(dalteparin sodium, enoxaparin sodium),administeredby the patients themselvessubcutaneouslytwice a daywith little or nolaboratory monitoring[48].These drugsdo not causeseriousthrombocytopenia, andthereforesafer, includingforself-administrationat home[2].

Thrombotic complicationsin aPL syndromestimulatedactivation of lipid peroxidation, as seen by the increase inthe level ofisoprostanes(markers of oxidative stress). Sois justified also the takeof antioxidants[49].


Nevertheless, given the autoimmune nature of the disease, most pathogenetically justified is plasmapheresis with removal of the course up to 3.8 liters of plasma, which reduces the frequency of recurrent thrombosis [50]. A.P. Elchaninov et al. (51) in 41 patients with acute central neuroischemic processes on the background of identified features of aPL syndrome was able to make more rapid regression of brain disorders using plasmapheresis, compared with the control group of patients treated only with the help of instenon. Plasmapheresis with the success has been used for the relief of cerebellar ataxia on the background of aPL syndrome [19]. Plasmapheresis has proved effective in the treatment of widespread thrombosis in the background of an increased level of lupus anticoagulant and also factor VIII and von Willebrand factor [12 Vasiliev S.A. et al. 2001]. Plasmapheresis is especially shown during a catastrophic antiphospholipid syndrome with multiple organ failure [11, 37, 38, 39 ].

We must assume that in cases of pulmonary embolism, especially in the chronic course of recurrent episodes, what matters is not so much true thromboembolism, as pulmonary vascular thrombosis in situ with the progression of pulmonary hypertension. There is the primary factor in vascular endothelial injury, which can further lead to thrombosis also in such places. And plasmapheresis pathogenetically is more justified than only anticoagulant therapy, because it can prevent such primary vascular damage. And this tactic has its confirmation.

Thus E.B.Orel et al. (40) report on the use of plasma exchange in patients with acute pulmonary embolism with subtotal (90%) thrombosis of the inferior vena cava, which was held on 29 (!!!) plasmapheresis procedures (10 inpatient, 19 outpatient). After the treatment there were normalized levels of factors VIII and W, fibrinogen content. Recurrent thrombotic events were observed for 13 months. A similar positive result of plasmapheresis in a patient with pulmonary embolism on a background of widespread thrombosis of the jugular, subclavian vein and the other described V.Ya.Rudakova et al. (52). The use of plasmapheresis led to recanalization of previously thrombosed veins of the lower extremities with the restoration of the microcirculation in the lungs after pulmonary thromboembolism.

S. Otsudo et al. (53) cited a case wh ere the use of warfarin and prednisone was not able to arrest the thrombotic symptoms and only after cascade plasmapheresis decreased titers of antibodies to beta2-glycoprotein 1 and anticardiolipin IgG-antibodies.

2. Antiphospholipid syndrome in obstetrics.  
In addition to deep-vein thrombosis there are observed and spontaneous abortions ("habitual miscarriage"). This problem is one of the most pressing problems in obstetrics. Their frequency is 15-20% of all pregnancies, and the incidence of infertility – in 5-11% of marriages [54]. In 30-40% of these abortions are "unexplained» [55].

And among the causes of miscarriage play an important role antiphospholipid autoantibodies (aPL). Known for their association with habitual spontaneous abortion, intrauterine growth retardation, "missed abortion", preeclampsia, thrombocytopenia [56]. Antiphospholipid most often include two types of autoantibodies –  anticardiolipin and lupus anticoagulant.Their detected at about 2% of women with normal pregnancy. At the same time, in pregnant women with preeclampsia incidence of antiphospholipid antibodies reaches 63.5% [57], and the combination of intrauterine growth retardation with hypertensive disorders in pregnancy, this rate reaches 90% [58].

Non-organ specific autoantibodies and, especially, aPL, are one of the causes of recurrent miscarriage. Immunopathogenetic mechanism which leads to early miscarriage in patients with APA may be determined utero-placental thrombosis and vasoconstriction due to the coupling of antibodies to the phospholipid membrane, as well as endothelial cells and platelets. This reduces the production of prostacyclin by endothelial cells, increased platelet thromboxane production, reduced the activity of S-protein, which is a physiological anticoagulant, inactivating procoagulants – factor Va and VIIIa [55]. This leads to instability of the membrane, increased platelet aggregation and inhibition of endothelial prostacyclin synthesis. In addition, the process can cause inhibition of prekallikrein and release endothelial plasminogen. It may also affect the process of embryo implantation in the endometrium.

N. Gleicher et al. (59) also examined the relationship between unexplained infertility and miscarriages with autoimmune disorders. Autoantibodies were detected such as lupus anticoagulant, anti-cardiolipin, anti-phosphatidylserine, anti-phosphatidylethanolamine, histones, against DNA, and poly-dioksitimidil acid – 88% of infertile patients and 70.8% with miscarriages. They reported also about the unusual frequency gammopathy (type IgM) in 38.5% and 45.8% of these patients, respectively. They concluded that some patients with unexplained infertility and miscarriages suffer polyclonal activation of B-lymphocytes and thus confirmed the causal relationship of autoimmune disorders with this obstetric pathology. Even in cases wh ere the autoantibodies for whatever reason can not be determined, increased by 1.5-2 times the level of the CIC indirectly, may also indicate an autoimmune nature of the "unexplained" infertility [60].

Many researchers believe the leading anti-β2-glycoprotein I in the genesis of thrombophilia [61]. There is the most frequent and more severe in also preeclampsia [62]. R.Roubey (63) considered the detection of antibodies to β2-glycoprotein I the most reliable and early sign of the presence of antiphospholipid syndrome.

It is usually assumed that the spontaneous abortions in the first trimester of pregnancy are the result of a chromosomal abnormality. However, damage to the aPL antibody phospholipids of cell membranes villous trophoblast "discovers" them for the impact of cytotoxic immune cells mother in the first trimester, to the 8th week of pregnancy [64]. Circulation of aPL antibodies is often detected in the group of early miscarriage in 43.1% of patients, and even in the group of early pre-embryo losses (35.7%) than in the group of late miscarriages (22.4%). Characteristically, the majority of these women initially treated for infertility, while 15% of them have been repeated attempts to in vitro fertilization [65].

Clinical studies have shown that in the early miscarriages reasons were not anticardiolipin or anti-phosphatidil serine, and anti-phosphatidilethanolamine antibody. Phosphatidylethanolamine is one of the major components for both peripheral and inner layers of the cell membranes. However, these specific antibodies contribute not so much direct damage phosphatidylethanolamine as much damage high molecular weight kininogen, factor XI or prekallikrein. Thus kininogen-dependent antibodies stimulate anti-phosphatidylethanolamine thrombin induced platelet aggregation [66].

Histologically identified salient features peri-villous thrombosis, vascular desolation of terminal villi, their chronic inflammation. In addition to thrombosis and hemorrhage there are detected in the intervillous spaces, retroplacental hematoma, extensive infarction and necrosis of the placenta [48]. This leads to early thrombosis of uteroplacental vessels with fetal malnutrition and death of the embryo.

Besides influence violations receptors of endothelial cells and trophoblast function, as well as the impact of intrauterine autoantibodies that affect embryonic development of the fetus that are the cause of repeated implantation failures, which are not rightly interpreted as infertility [67]. In addition to blood supply and nutrition disorders of the fetus, it can occur also direct effects of antiphospholipid autoantibodies. So, L.F.Akanli et al. (68) described 5 cases of cerebral infarcts in neonates whose mothers showed increased concentrations of anticardiolipin antibodies.

Antiphospholipid antibodies can bind to the trophoblast cells and damage them in violation of the placental barrier, which becomes passable for CIC, viruses, bacteria, and iso-immune auto-antibodies. Antiphospholipid antibodies are a class of IgG-globulin and cross the placenta, giving the fetus the same effect as in the mother's body [61].

Transplacental transfer of maternal antibodies to the fetus can cause vascular thrombosis of any location, including the aorta, renal arteries, cerebral arteries, the superior sagittal sinus and into the portal system. In this case, aPL antibodies in the blood of the newborn may be delayed for a period of 3-6 months. On the other hand, in the "reverse" direction through impaired placental barrier can penetrate fetal antigens of the fetus, the mother contribute to sensitization with the development of fetal antibodies, which further exacerbates the development of the fetus. [48].

The surface of the apical membrane of placental villi, converted to the uterine intervillous circulation, normally covered with a special anticoagulant protein –  Annexin-V. In studying these villi in the placenta, a checked for caesarean section, J.H.Rand et al. (69) found that in patients with aPL syndrome content Annexin-V is much less than in healthy women. Upon incubation of tissue culture placental villi of normal placentas with aPL IgG for 24 hours showed a significant reduction of apical annexin-V. Furthermore, inhibition of cell proliferation observed human umbilical vein endothelial cell in culture, containing anticardiolipin antibodies [70].

Available block Annexin V specific anti-annexin-V antibodies are described in connection with recurrent miscarriage and systemic lupus erythematosus. These antibodies can facilitate the transition of anionic phospholipids on the inner and outer shell membranes promote apoptosis umbilical vein endothelial cells. When this occurs and the yield on the membrane surface of procoagulant phospholipid –  phosphatidylserine [71]. Such "externalizing" phosphatidylserine upon activation of platelets and macrophages leads to activation of their surface coagulation factors X and V, and also  prothrombin [72].
Removing annexin V under the influence of aPL antibodies on the surface of trophoblast makes it procoagulant. In addition, they inhibit the formation of syncytia, hormone production and invasion of the decidua. This results in a placental insufficiency, leading to stop development of the fetus, preeclampsia and abortion [73, 74]. In aPL syndrome prematurity observed in 2.5 times more often, in 3 times more common the malnutrition in newborns and wasting all cases of malnutrition III level [57].
Antiphospholipid syndrome predisposes to severe preeclampsia also [75]. In addition, there is possible development also the so-called catastrophic aPL syndrome with severe progressive multiple organ failure [76]. In preeclampsia on the background of aPL syndrome in 71.5% of cases there were signs of placental insufficiency with intrauterine growth retardation [77].

Failure of implantation of fertilized embryos extracorporeal B.Fisch et al. (78) explained the possible effect of ovarian hyperstimulation – stimulating effect of high doses of estrogen on the development of autoantibodies. They determined the level of AFA during the early follicular phase, during the expected peak level of E2 and 14 days after the egg retrieval. But these findings show also high initial level and AFA before treatment.

As in the pathogenesis of complications of pregnancy in aPL syndrome plays a certain role hypercoagulation, there are widely used anticoagulant and disaggregants on the background of corticosteroids [79]. Nevertheless, the conventional therapy with corticosteroids suppress immunological reactivity and correction of hemostatic disorders of anticoagulants and antiplatelet agents are not always effective and fraught with acute exacerbation of chronic endometritis with the risk of intrauterine infection of the fetus. Moreover, there is evidence that glucocorticoids administered to a pregnant woman can cause a delay of growth and development of the fetus, which was confirmed in special experiments on animals [80].

Antiphospholipid syndrome, in addition to the danger of recurrent miscarriage, may be accompanied also by pulmonary vessels thromboembolism in the development of deep vein thrombophlebitis of the lower limbs and pelvis, the frequency of which varies from 1.5 to 2.7 per 1,000 pregnant women and from 2.8 to 18.3% in of maternal mortality [81].

C.A. Laskin et al. (82) attempted to use prednisone and acetylsalicylic acid in pregnant women with APA and do not succeed, because the frequency of live births did not increase significantly, but the premature in the study group was 62% compared with 17% in the control. In addition, there is information on the effects of aspirin on the fetus, causing hemorrhagic condition in newborns. Furthermore, more likely there are developed hypertension (13% vs. 5%) and diabetes (15% versus 5% in control group).

S. Cowchock (83), leaving the possibility of the use of heparin in the presence of signs of thrombosis, urged caution with the appointment of prednisone and immunosuppressive therapy (including immunoglobulins) in pregnancy.

It should be emphasized the dangers of hormone therapy during pregnancy yet. Thus, G. Celsi et al. (84) have shown that the penetration of glucocorticoids across the placenta contributes to slowing the growth of the fetus and the appearance of hypertension in them as adults. There is described dysfunction of the hypothalamic-pituitary-adrenal system in children whose mothers received during pregnancy hormone therapy.

This was confirmed in the experiments wh ere the use of dexamethasone in pregnant animals led to a decrease in body weight infants, malnutrition and reducing renal glomeruli compared to the control. It is believed that the reduction in the number of nephrons decrease in glomerular filtration area, which contributes to the development of essential hypertension. Obviously this explains the higher levels of blood pressure (130 ± 4 vs. 107 ± 1 mmHg in the control) in the experimental animals were born.

G. Framton et al in 1987 (85) described a case of when, after 10 unsuccessful attempts to continue the pregnancy only after the introduction of plasmapheresis in the complex of therapeutic measures it was managed to prolong pregnancy up to 34 weeks with the healthy delivery. Later D. Fulcher et al (86), also after repeated unsuccessful attempts to save the pregnancy and fetal life with the help of prednisone and aspirin, have been successful only with the help of six sessions plasma exchange, which led to a significant reduction of anticardiolipin antibodies and stabilized the level of placental blood flow, followed by the birth of a living child.

Experience of the Scientific Center for Obstetrics, Gynecology and Perinatology of Russian Academy of Sciences [74, 87] in the treatment of 147 patients using plasmapheresis sessions showed the possibility to obtain a reduction of activity of the autoimmune process with a significant reduction, up to complete disappearance of lupus anticoagulant, CIC levels (26%), and immunoglobulin E, M, G (for 16-21%), normalization hemostasiogram, the disappearance of DIC markers. There are normalized indicators of oxygen transport, PaO2 and hemoglobin oxygen saturation. In 76% of these patients took timely delivery, and 6% at term 32-34 weeks – weighing 2.6-3.9 kg newborn, and all the children were alive [88].

Moreover, it was useful to introduce a course of plasmapheresis (three-fold in a day) also in the scheme of preparation for in vitro fertilization (IVF) and embryo transfer in 62 women with tubal-peritoneal infertility. Percentage of pregnancy is based on one embryo transfer at the same time was 51.6%, while in the comparison group (50 women who have had a drug therapy only) – 42% (p <0.05). Of the pregnancies there was resulted in births of 84.4% (with 71.4% in the control group, p <0.05), with the birth of viable children in 100% of patients. After the preparation for IVF using plasmapheresis incidence of ovarian hyperstimulation syndrome was 8%, while in the comparison group, it developed three times more likely (28%) [89, 90].

In Ukraine, the Donetsk regional center of maternity and childhood courses of plasmapheresis were performed in 80 pregnant women with aPL syndrome who have managed to get the 78 (97.5%) of viable children, while in the comparison group (60) had been 14 pregnancies (23, 3%) in the I trimester, 10 (16.67%) – in the II trimester, 5 neonates died from respiratory distress syndrome and cerebral blood flow disorders [91].

Moreover, courses of plasmapheresis in 33 women with preeclampsia on the background of aPL syndrome contributed to relief of hypercoagulable syndrome with decreased fibrinogen levels by 17%, the normalization of prothrombin ratio, activated thrombin time, a decrease in the degree of platelet aggregation by 18%, a decrease in levels of markers of DIC – D dimers and fibrin monomer complexes in the 2.5-3 times, while in the comparison group (30 women with traditional drug therapy) was observed in only a trend towards normalization of these parameters [48]

K. Abou-Nassar (92) in a patient with systemic lupus erythematosus plasmapheresis used prophylactically during pregnancy every month with the birth of a healthy baby. In such patients found the use of immunosorption also [93] Positives results plasmapheresis noted by other authors [77, 94, 95], as well as on our experience of own [96, 97].

CONCLUSION

All these facts show that the antiphospholipid syndrome occurs much more frequently than it is usually fixed, and this leads to the use of the most belated pathogenetically justified plasmapheresis, or even ignored. This problem is still waiting for its decision and further research.
In our opinion, if you suspect the possibility of such autoimmune disorders there is requires its timely verification and confirmation when it is advisable to perform plasmapheresis without waiting for its manifesting symptoms.

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