Leucocyte-depleted Blood Research Articles

Randomised comparison of leucocyte-depleted versus buffy-coat poor blood transfusion and complications after colorectal surgery

Randomised comparison of leucocyte-depleted versus buffy-coat poor blood transfusion and complications after colorectal surgery

The effects of cardioplegic arrest and reperfusion on the microvasculature of the heart.

Despite laboratory evidence of leucocyte involvement in reperfusion injury, cardiac surgical clinical trials do not support the therapeutic effectiveness of leucocyte filtration. Furthermore, the direct effects of crystalloid cardioplegia and reperfusion on the capillaries of the heart have yet to be elucidated. We tested the effects of cardioplegic arrest and reperfusion both with and without leucocyte depletion, in a model of cardiopulmonary bypass that mimics clinical cardiac surgical conditions. Four groups of Landrace pigs were studied. Group A (n = 6) underwent 30 min of hypothermic (28 degrees C) cardiopulmonary bypass. Groups B (n = 6), C (n = 6) and D (n = 6) also had 90 min of cardioplegic arrest. Group C was then reperfused with whole blood, while Group D was reperfused with leucocyte-depleted blood. Microvascular methylmethacrylate corrosion casts were made at the end of the experimental period. Myocardial vascular anatomy was defined by electron microscopy and capillary abundance derived from this and from the weight of casts from representative areas. Leucocyte deposition was assessed using radioisotope-labelled leucocytes. Ischaemic damage to tissues was graded according to light and electron microscopic findings. In Group A the mean (+/- S.D.) vascular cast weight/volume of myocardium (density) was 125 +/- 9 mg/mm3. After cardioplegic arrest (Group B), it fell to 74 +/- 7 mg/mm3 (P < 0.0001) due to absence of capillaries, although arterioles, venules and non-nutritive bypass vessels remained patent. Following reperfusion with whole blood (Group C), capillary numbers partially recovered but luminal diameters were reduced with a cast density of 94 +/- 5 mg/mm3 (P < 0.0001 versus Group A and B). Leucocyte-depleted (87-92%) reperfusion in Group D did not affect cast density (90 +/- 3 mg/mm3; P = 0.17). Coronary vascular resistances in Groups C and D rose slightly, but not significantly, during reperfusion. Following cardioplegic arrest, microvascular changes are marked. These changes are partially reversed by 30 min reperfusion. Leucocyte depletion does not ameliorate these effects in this model.

Specificities of anti-platelet antibodies in multitransfused patients with haemato-oncological disorders.

The clinical condition and the formation of platelet-reactive antibodies influence the post-transfusion platelet increment. We analysed the specificities of platelet-reactive antibodies in 81 multitransfused patients with haemato-oncological diseases refractory to platelet transfusions, or prior to a scheduled stem cell transplantation. In 17 additional patients we prospectively determined the development of platelet-reactive antibodies at the time of chemotherapy in weekly intervals. Sera were tested by the monoclonal antibody-specific immobilization of platelet antigens (MAIPA)-technique for antiplatelet antibodies against HLA class I antigens, the human platelet-specific alloantigens (HPA)-1, -2, -3, -5, and the platelet membrane glycoproteins (GP) Ia/IIa, Ib/IX, IIb/IIIa (panreactive). Platelet reactive antibodies were found in 54% of blood samples. They were frequent in patients with a history of possible previous immunization, particularly if patients were refractory to platelet transfusions. Platelet-reactive HLA antibodies were the most common antibodies. Even patients without a known risk of primary immunization who received exclusively leucocyte-depleted blood products formed antibodies. By the MAIPA technique, even LCT-negative sera were found to contain platelet-reactive antibodies.

Randomised comparison of leucocyte-depleted versus buffy-coat-poor blood transfusion and complications after colorectal surgery

Allogeneic blood transfusion is associated with an increased frequency of postoperative infection. We studied whether such events can be avoided by the intraoperative and postoperative use of leucocyte-depleted blood. 589 consecutive patients scheduled for elective colorectal surgery were randomised to receive buffy-coat poor (n = 299) or filtered leucocyte-depleted red-cells (n = 290) when transfusion was indicated. 260 patients actually received blood transfusion. Three patients were excluded from analysis. The 142 patients randomised to and transfused with buffy-coat-poor blood had a significantly higher frequency of wound infections and intra-abdominal abscesses than the 155 patients who were allocated to this group but who were not transfused. (12 vs 1%, p < 0.0001) and (5 vs 0%, p = 0.005), respectively. Those receiving buffy-coat-poor blood also had a significantly higher frequency of wound infections and intra-abdominal abscesses than the 118 randomised to and receiving leucocyte-depleted blood (12 vs 0%, p < 0.0001) and (5 vs 0%, p = 0.017), respectively. Postoperative pneumonia occurred at a significantly higher rate in patients receiving buffy-coat-poor blood: 23 versus 3% in non-transfused patients (p < 0.0001), and 23 versus 3% in patients transfused with leucocyte-depleted blood (p < 0.001). The mortality rate between the groups was not statistically different. Our data suggests that the association between allogeneic blood transfusion and postoperative infection is limited to allogeneic blood products that are not adequately depleted of immunosuppressive leucocytes. This undesirable effect can be reduced by leucocyte depletion with high-efficiency filters.

An overview of laboratory and clinical aspects of leucocyte-depleted blood components

Blood component therapy has enabled us to successfully support the increasing demands for treatment of haematological abnormalities. Continuous efforts are made to minimize or prevent immediate side effects of transfusion but the long-term effects of component therapy will remain unknown for some time. There is always a need for products with special qualities (i.e. no CMV, no HLA immunization etc.) however when considering adverse effects it is important to look for alternative strategies which produce minimal alteration in the cellular and fluid components of blood while maintaining optimal clinical efficacy. Continuous education of clinicians and laboratory scientists is needed so that the best possible products are provided reliably and with consistency. This review focused on some of the important debatable issues on the laboratory/microbiology aspects and clinical practice. It is clear that the presence of leucocytes is associated not only with reduced quality, based on the morphological and functional integrity of blood components but also reduced post-transfusion response in some specified cases. A stringent regular QA program is required for the assessment of the trend as both differences between filter batches and slight changes in laboratory operations contribute to the lack of reliability of the system in use. While until recently the main goal of leucocyte depletion for red cells was to prevent NHFTR in specified patients it appears that currently a more ambitious goal of avoiding other important leucocyte-induced transfusion complications are considered with some success, without leaving aside alternative strategies and their practical benefits. In respect to cost-effective transfusion strategies, in multiply-transfused patients, both induction of antibodies against HLA class I antigens and the development of leucocyte-associated virus infections could be prevented by using modern filters which lead to effective components with leucocytes below the threshold reported in the Edinburgh consensus meeting 3 whereas gamma-irradiation of blood components before transfusion, that decreases the mitogen induced stimulation of the lymphocytes is the best strategy for the prevention of post-transfusion GVHD. Many advances have been made in methods of detection of a low level of leucocytes, (Nageotte chamber, flow cytometry, PCR) and the storage lesion induced by the residual leucocytes, 7 helping to better define product quality. A considerable degree of cooperation is also seen between clinicians, scientists and other disciplines and manufacturers of the diverse technologies.

Clinical aspects of platelet transfusion therapy.

Platelet transfusions are established as effective treatment for thrombocytopenic bleeding. However, the indications for prophylactic platelet transfusions are being reconsidered because of the greatly increased demand for platelet concentrates. Platelet refractoriness is the main clinical problem associated with repeated platelet transfusions. This is most frequently due to HLA alloimmunisation or non-immune platelet consumption associated with clinical factors such as septicaemia. The initial management of refractory alloimmunised patients is to use HLA-matched platelet transfusions. If there is no improvement with HLA-matched platelet transfusions, platelet crossmatching may identify the cause of the problem and help with the selection of compatible donors. Other measures used to improve responses to platelet transfusions are usually ineffective. There has been considerable interest in methods to prevent HLA alloimmunisation and platelet refractoriness and particularly in leucocyte depletion of blood components. The use of leucocyte-depleted blood components has other benefits for multitransfused patients, but further studies are needed before the routine use of leucocyte-depleted blood components can be recommended for patients likely to receive repeated platelet transfusions.

Impact of leucocyte‐depleted blood components on the haematological recovery and prognosis of patients with acute myeloid leukaemia

Use of leucocyte-depleted blood components reduces refractoriness to platelet transfusions, but the cost-effectiveness of this policy has been in doubt. We retrospectively analysed data of 115 patients with acute myeloid leukaemia (AML), treated according to a standardized cytostatic protocol. Fifty patients had received standard (STD) platelet concentrates (PCs) and red blood cell concentrates (RBCs). Sixty-five patients had received leucocyte-depleted (L-D) components, with fewer than one million leucocytes per unit. Refractory patients (22% of the STD group and 3% of the L-D group) were excluded from further observations. There were no differences between the groups during the first cytostatic treatment period. Thereafter, significantly fewer PCs and RBCs were transfused to the L-D group. In the L-D group, granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 50 x 10(9)/l) were shorter, the lowest leucocyte counts were higher, serious infections were less common (44% v 59%), and the patients spent fewer days in hospital. The median relapse-free survival (RFS) was longer in the L-D group than in the STD group. We conclude that leucocyte depletion of blood components has favourable effects on the recovery of haematopoiesis, consumption of blood components, occurrence of serious infections, and relapse-free survival in AML.

Clinical aspects of platelet transfusions

Refractoriness is the most important complication of platelet transfusion therapy, occurring in about 50% of patients receiving repeated transfusions. The major causes are HLA alloimmunization and non-immune platelet consumption associated with clinical factors such as septicaemia. DIC and splenomegaly. Initial management of alloimmunized patients who are refractory to platelet transfusions from random donors is the use of HLA-matched platelet transfusions, which improve responses to transfusions in about 65% of patients. It may be difficult to provide effective platelet transfusion support for alloimmunized patients not responding to HLA-matched transfusions. There has been much interest in methods for the prevention of HLA alloimmunization. Primary HLA alloimmunization is dependent on the presence of HLA class II antigen-bearing cells in transfusions; pure platelet transfusions are non-immunogenic as platelets only express HLA class I antigens. The use of leucocyte-depleted blood components in multitransfused patients has resulted in a reduction in HLA alloimmunization and platelet refractioness. Improvements in the techniques for leucocyte-depletion of red cell and platelet concentrates and the possibility of inactivation of HLA class II antigen-bearing cells by UV irradiation makes prevention of alloimmunization an attainable goal.

Leucocyte-Depleted Blood: A Comparison of Cell-Washing Techniques

Leucocyte-Depleted Blood: A Comparison of Cell-Washing Techniques

Recovery of blood neutrophils after acute peripheral depletion.

Blood neutrophil recovery in the dog appears to be qualitatively similar whether leucopenia is achieved by injection of leucocyte antiserum to remove the cells in vivo or by exchange transfusion with leucocyte-depleted blood. Return to the control level after antiserum injection occurs within 3–5 hours with neutropenias in excess of about 50% and is followed by neutrophilia of variable degree with restoration of the normal count usually by 24 hours. There is reason to think that recovery is accomplished in large part by an accelerated release of cells from marrow. This conclusion, which is based mainly upon the appearance of numerous band cells in the periphery, is supported by the results obtained in x-irradiated animals and is consistent with related observations by others and with theoretical considerations of neutrophil balance. The extent of release of nonsegmented cells is related more to the relative (percentage) change than to the absolute decrease in neutrophils. These observations can be interpreted to mean that the number of mature cells available for release from the marrow reservoir is a function of the normal steady state level in blood. Possible mechanisms of compensation for the decline in cells in the periphery are discussed and exploratory studies are reported. It is suggested that the control system may include a suppressor feedback between mature neutrophils and blood-forming sites.