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#46
05.12.2009, 00:01
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почему берём капиллярную кровь, честно сказать, не знаю, детского отделения в больнице нет, к педиатрии отношения не имеем. безусловно с венозной кровью попроще.
у меня вопрос: а что такое 3diff? 
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#47
05.12.2009, 00:03
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Ну раз уж начал говорить, то мысль закончу. Аппаратуры сейчас выпускается много. И она становится все более специализированной и создается под конкретные задачи. И использовать ее не под те задачи, под которые она производителем заточена - это наживать себе проблемы на пустом месте.
Вот и для вашего анализатора есть своя определенная ниша. Ему место в экспресс лаборатории, например в приемном отделении. Привезли пациента с острым животом, и помимо всего прочего, сразу ему кровушку взяли, в соседнюю комнату отнесли и анализ сделали - сразу можно прикинуть что и как. У хирурга есть нужная ему информация. А если это лаборатория и рутинные клинические анализы крови, так там другой совсем анализатор-то нужен.
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#48
05.12.2009, 00:09
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3 diff - это значит, что анализатор может делить лейкоциты на 3 популяции: гранулоциты, лимфоциты, моноциты (ну или в случае вашего, то нейтрофилы, лимфоциты и все прочее). Полноценной формулы (нейтрофилы, базо, эоз, лимф, моно - 5 diff) он по определению не считает.
И еще насчет венозной крови. Дело тут вовсе не в том, что проще. Для рутинных анализов нужно использовать только венозную кровь. Это должно быть правилом. Капиллярная кровь (при рутинном тестировании), только для спец задач, когда венозную взять затруднительно.
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#49
05.12.2009, 01:02
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Цитата:
Prior studies of pseudothrombocytopenia (PTCP) Previous reports have documented the occurrence of PTCP in up to 0.2% of the healthy population and in 1.9% of hospitalized patients [12, 13 and 14]. Although PTCP is an infrequent condition, it accounts for a sizable fraction (7.5 to 15.3%) of all cases of “thrombocytopenia” that are referred to hematologists for further evaluation [15]. The phenomenon of PTCP that occurs in the absence of abciximab therapy is due to platelet autoantibodies that recognize usually cryptic platelet antigens that are exposed in vitro. The presence of certain anticoagulants (especially EDTA), low temperatures and prolonged time intervals between blood draws and assays are factors that enhance the occurrence of PTCP [16, 17, 18 and 19]. The autoantibodies are usually IgG or IgM with the most commonly reported antigenic target being platelet glycoprotein IIb [16] although other antigens including phospholipids have been described [18]. Ethylene diamine tetra acetic acid is the most commonly reported anticoagulant to induce PTCP. The calcium chelating activity of EDTA is thought to remove calcium from binding sites within Gp IIb or Gp IIIa, resulting in exposure or conformational alteration of the molecule(s), thereby allowing the previously cryptic antigen to interact with the autoantibody [17]. As a result of the frequent association with EDTA anticoagulant a commonly recommended method to screen for this phenomenon and the method most commonly used in the studies in this report is to obtain simultaneous platelet counts in EDTA and sodium citrate anticoagulants. However, the term “EDTA-dependent PTCP” has been rejected by some investigators, since PTCP has been observed in citrate anticoagulants and even in nonchelating anticoagulants such as hirudin and D-phenylalanine-proline-arginine-chloromethyl ketone [19]. Bizzaro et al. [17] noted that in 15 of their 93 cases (10.8%) with PTCP and antiplatelet antibodies, agglutination occurred in citrate at room temperature [17]. In this study, 14 of the 117 cases of PTCP that occurred during abciximab therapy were documented to occur in the presence of citrate anticoagulant. Since the autoantibodies that induce PTCP often are most active in a time-dependent fashion at 4 to 20° C, it has been suggested that the most reliable way to obtain accurate platelet counts is to perform platelet counts on blood at 37° C [17]. However, even this method will cause a few cases to be mislabeled since approximately 17% of autoantibodies are reactive at 37°C in the presence of anticoagulants [17]. The autoantibodies that are reactive at 37°C and in citrate are more likely to be of the IgM class [17]. The gold standard for differentiating PTCP from thrombocytopenia may, therefore, be to perform a platelet count on nonanticoagulated blood obtained by finger stick, in which case a normal platelet count should be obtained. In contrast, a blood smear prepared from EDTA-anticoagulated blood typically reveals platelet clumping. The source of the autoantibodies that are thought to cause PTCP is unknown. Sakurai et al. [20] reported that a group of patients who developed PTCP during hospitalization had been treated with antibiotics 4 to 10 days before the onset of this condition. They hypothesized that the autoantibodies first arose to antibiotics then cross-reacted to platelet membranes. They demonstrated that presupplementation of EDTA tubes with aminoglycosides prevented PTCP and that aminoglycosides added after the onset of platelet clumping could dissociate the aggregates [20]. However, there was no apparent correlation between the antibiotic that the patient had taken therapeutically and the antibiotic that was most effective in inhibiting platelet clumping, casting doubt on the theory that antiplatelet antibodies arise from cross-reacting antibodies to these drugs. Another theory for the origin of the autoantibodies directed to platelets is that they are involved in removing senescent circulating platelets [17]. Potential mechanisms for abciximab-induced PTCP The etiology of the increased prevalence of PTCP in abciximab-treated patients is also obscure. Christopoulos and Machin [10] performed flow cytometric analysis of platelet surface IgG in platelets from two patients with abciximab-induced PTCP and demonstrated a time- and room temperature-dependent increase in surface IgG, which was not present on EDTA samples taken before the infusion of c7E3 or in citrate anticoagulated samples taken during the infusion [10]. Among 19 patients receiving c7E3-Fab, the one with the most severe PTCP also had the most surface IgG [10]. This finding led Christopoulos and Machin to propose that there might be naturally occurring anti-Fab antibodies and that these might bridge platelets to form agglutination. Another possibility is that the binding of the Fab fragment to the beta3 component of the fibrinogen receptor could alter the conformation of the molecule and, in concert with the anticoagulant-induced changes, enhance access of autoantibodies to Gp IIb or other platelet antigens. Abciximab is known to induce the expression of conformational changes in the fibrinogen receptor, as detected by the expression of novel antigens (ligand induced binding sites [LIBS]) [21 and 22]. The potential for abciximab-induced conformational changes in the fibrinogen receptor and the ability of some platelet autoantibodies to react at 37° C also raises the possibility that the mechanisms for PTCP and thrombocytopenia during abciximab therapy could be related. Thus, it is possible that abciximab alone, in the absence of anticoagulants, is adequate to expose the cryptic epitope for warm-reacting platelet autoantibodies, leading to the immune-mediated clearance of platelets and thrombocytopenia. This hypothesis is consistent with the observation that the induction of LIBS epitopes on platelets after abciximab therapy is inversely correlated with the platelet count [21]. This possibility is also attractive because of the relative high frequency of PTCP as a cause of low platelet counts with abciximab therapy and by the fact that the mechanism for abciximab-induced thrombocytopenia remains unknown. Am Coll Cardiol. 2000 Jul;36(1):75-83. Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy.
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#50
05.12.2009, 12:40
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denson
благодарю за подробнейший ответ. кстати, недавно заведующая говорила, что собираются для лаборатории приобретать ещё один анализатор, правда ещё не знаю какая марка, когда приобретут, обязательно отпишусь
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#51
05.12.2009, 15:11
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на счёт анализатора понятно, остаётся только ждать изменения ситуации в лучшую сторону, а пока, к сожалению, что имеем-так и работаем
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#52
05.12.2009, 17:19
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Цитата:
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#53
05.12.2009, 18:18
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Вот и итальянцы говорят, что ложнозаниженное определение числа тромбоцитов из капиллярной крови во многом зависит от техники взятия крови лаборантом:
Mean Plt counts differed of 37 x 10(9)/l less for capillary approach in the first series of comparisons, but decreased to 10 x 10(9)/l less in the second series due to a greater expertise of operators in capillary sampling. --- Vox Sang. 2009 Sep 17. Evaluation of the analytical performances of a portable, 18-parameter hemometric system using capillary blood samples for blood donor enrollment. Pierelli L et al.
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#54
10.12.2009, 20:46
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Цитата:
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#55
10.12.2009, 20:56
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Все зависит от того, ручной анализ крови забирается с цитратом или др. антикоагулянтом: цитрат добавляется к крови в соотношении 1:9 и поэтому гемоглобин в цитратной крови на 10% ниже, чем с ЭДТА. Также еще, если прокол скарификатором недостаточно хорош и кровь течет медленно, то ретивые лаборанты надавливают из пальца кровь вместе с тканевой жидкостью, что тоже способствует ложнозаниженному гемоглобину...
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#56
12.12.2009, 16:47
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Цитата:
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#57
12.12.2009, 16:53
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Цитата:
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#58
15.12.2009, 22:21
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denson
помоги пожалуйста с таким вопросом, сегодня брал у пациента кровь и анализатор выдал следующее: Hb-175 Эр-5,75 Лц-6,4 по лейкоцитарной формуле сказать ничего не могу, т.к. не видел по ней результатов. у меня такой вопрос возле Hb и Эр появился знак"+", что он означает на анализаторе Sysmex-kx-21? заранее благодарю за ответ
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#59
15.12.2009, 22:49
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Цитата:
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#60
20.12.2009, 10:46
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Цитата:
благодарю за ответ
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Линейный вид
