Activation of the contact system by filtration of platelet concentrates with a negatively charged white cell-removal filter and measurement of venous blood bradykinin level in patients who received filtered platelets

BACKGROUND: Several recent reports have described hypotensive transfusion reactions in patients receiving platelet concentrates (PCs) filtered through white cell-reduction filters. It is well known that a negatively charged surface activates the contact system, consisting of factor XII, prekallikrein, and high-molecular-weight kininogen. STUDY DESIGN AND METHODS: To clarify the mechanisms of these hypotensive reactions, the possibility that white cell-reduction filtration activates the contact system was examined. Venous blood plasma bradykinin levels were also measured in patients receiving PC transfusions through filters. RESULTS: None of the measured values were changed by filtration through a positively charged filter. However, filtration through a negatively charged filter resulted in a decrease in the amounts of prekallikrein and an increase in the amount of bradykinin generated, which indicated the activation of the contact system. The bradykinin level was inversely related to the activity of angiotensin-converting enzyme (ACE) in the PCs and was elevated by addition of an ACE inhibitor. Although the venous blood plasma bradykinin level did not change in two patients with a normal ACE activity during PC transfusion through the negatively charged filter, two patients who had decreased ACE activity, showed a significant increase in bradykinin during the transfusion. CONCLUSION: These results suggest that the generation of a large amount of bradykinin by filtration of PCs through a negatively charged filter might cause hypotensive reactions in patients with decreased ACE activity. The clinical significance of bradykinin generation requires further study.     

White cells in fresh-frozen plasma: evaluation of a new white cell- reduction filter

BACKGROUND: Fresh-frozen plasma (FFP) has generally been regarded as an acellular component. Recently, viable lymphocytes have been detected in this component and the question of irradiation of FFP for certain patients has been raised. Whether the numbers of white cells (WBCs) in FFP are sufficient to require WBC-reduction of acellular components for patients receiving WBC-reduced cellular components has not been determined. WBC numbers in FFP were examined, and the performance of a new commercial WBC-reduction filter for FFP was assessed. STUDY DESIGN AND METHODS: WBC numbers in plasma processed for use as FFP and in thawed FFP were counted before and after WBC-reduction filtration by the use of flow cytometry Fast and slow filtration was used to simulate laboratory and bedside filtration, respectively. Three different methods for plasma harvesting (soft-spin, hard-spin, and second-spin methods) were assessed. The filter capacity was also examined. RESULTS: The numbers of WBCs in plasma covered a three-log10 range (soft-spin method, 0.04-3.6 × 10(6); hard-spin method, 0.47-45.4 × 10(6); second- spin method, 0.4–37.2 × 10(6)). For the hard-spin and second-spin methods which produced the greatest plasma yields, 92 percent and 85.7 percent of bags, respectively, had counts>1 × 10(6) and 43 percent (hard-spin method) and 45.7 percent (second-spin method) had counts>5 × 10(6). There was no significant difference between the counts obtained in plasma and thawed FFP. The filter reduced WBC numbers to <1 × 10(5) in all but 3 of 49 bags. In the remaining three, there were <2 × 10(5) WBCs. Five bags of plasma could be processed effectively through each filter. CONCLUSION: FFP may contain WBC numbers above the threshold at which the use of WBC-reduction filters for cellular components in some patients is necessary. Confirmation of these findings and similar investigations on plasma prepared by other methods may help in defining a role for the use of WBC-reduction filters for FFP     

Intermittent visceral edema induced by long-term enalapril administration

OBJECTIVE: To describe a case of intermittent visceral angioedema associated with long-term enalapril use. CASE SUMMARY: A 72-year-old white woman developed severe abdominal pain as a result of visceral angioedema associated with long-term enalapril therapy. She had been taking enalapril 20 mg/day for 9 years prior to the first reported episodes of abdominal pain. DISCUSSION: Visceral angioedema associated with angiotensin-converting enzyme (ACE) inhibitors is a documented adverse effect. However, onset of symptoms has never been reported after 9 years of use. Not until 2 years after initial presentation were the symptoms correlated to enalapril administration. Since discontinuation of enalapril, the patient has not reported any symptoms for >2 years. An objective causality assessment categorized this adverse drug event as a result of enalapril as possible. CONCLUSIONS: Development of angioedema from ACE inhibitors occurs in <1% of the population. Limited case reports have identified intermittent visceral angioedema from ACE inhibitors. However, it is important to recognize that this adverse effect can also occur in patients who have been treated with ACE inhibitor therapy for several years.     

Cryofiltration apheresis and plasma fractionation causing anaphylactoid reactions in patients receiving angiotensin converting enzyme inhibitors.

Severe anaphylactoid reactions and even death have been reported in hemodialysis patients using certain membrane dialyzers while receiving angiotensin converting enzyme (ACE) inhibitors. We report mild to moderate anaphylactoid reactions in 4 patients receiving plasmapheresis with on-line membrane filters after being placed on ACE inhibitors. Of 21 patients receiving 497 plasma fractionation procedures, only the 2 patients who were receiving ACE inhibitors developed anaphylactoid reactions. Of 28 patients who had 680 cryofiltration procedures, only 2 of 5 patients who were taking ACE inhibitors developed anaphylactoid reactions. All patients developed facial flushing, increased warmth, bradycardia, and hypotension after approximately 1/2 to 1 L of plasma was processed during the procedures. Only a few procedures caused severe hypotension requiring discontinuation of the procedure. We quantified vasodilatory mediators in 1 patient, who developed pronounced symptoms. Results were obtained for 6-keto PGF1alpha, PGD-M, and methyl histamine in plasma. In addition, in the same patient, 2,3 dinor 6-keto PGF1alpha and methyl histamine were quantified in urine samples. Our results showed that plasma and urinary metabolites were not grossly elevated although they did increase slightly. Mild to moderate anaphylactoid reactions were observed in some patients on ACE inhibitors receiving plasma fractionation or cryofiltration apheresis. This was resolved by discontinuing either the ACE inhibitor, plasma fractionation, or cryofiltration apheresis.     

Isolated visceral angioedema: an underdiagnosed complication of ACE inhibitors?

Angiotensin-converting enzyme (ACE) inhibitors are known to cause potentially fatal peripheral angioedema in some patients. ACE inhibitors may also cause isolated visceral angioedema, a rarely reported complication. This article describes 2 patients who experienced this complication. Both patients came to medical attention with episodes of recurrent abdominal symptoms that had occurred while taking ACE inhibitors for hypertension. Each patient had undergone surgical procedures for symptoms that persisted after surgery and were ultimately relieved with cessation of their ACE inhibitors. These cases call attention to what may be an underappreciated cause of abdominal pain in patients presenting to emergency departments.     

Bradykinin-induced cough reflex markedly increases in patients with cough associated with captopril and enalapril.

We studied the effects of angiotensin converting enzyme (ACE) inhibitors on cough responses to bradykinin (BK), substance P (SP) and citric acid in a double blind, random study on 10 hypertensive patients receiving ACE inhibitors. Of these patients, five had reported cough with ACE inhibitors. Cough responses to citric acid were similar between patients with and without cough, and SP up to 10(-5) M did not cause cough in any of the subjects. BK caused cough at 13.4 +/- 1.2 (-log M) in 5 patients with cough associated with ACE inhibitors, but it did not cause cough at concentrations up to 10(-5) M in other 5 patients. One month after the withdrawal of ACE inhibitors, 5 patients were free from cough symptoms, and BK did not cause cough up to 10(-5) M in these patients, except for one who coughed at 10(-9) M, without changes in responses to citric acid. BK caused cough at 14.3 +/- 0.7 (-log M) although BK1-7, a major metabolite of BK by ACE, caused cough at 5.7 +/- 0.7 (-log M) in another 3 patients with cough associated with ACE inhibitor. These results suggest that impaired metabolism of BK induced by ACE inhibitors may relate to the manifestation of cough in hypertensive patients receiving ACE inhibitors.     

Safety of Angiotensin-converting enzyme inhibitors in patients with insect venom allergies

OBJECTIVE: To review the literature with respect to the safety of angiotensin-converting enzyme (ACE) inhibitors in patients allergic to insect venom and those undergoing venom immunotherapy (VIT). DATA SOURCES: A MEDLINE search was conducted (1966-March 2006) using the following search terms: bee sting, venom, insect stings, ACE inhibitors, angiotensin II receptor blockers, immunotherapy, and desensitization. The bibliographies of qualifying articles were also searched for relevant references. DATA SYNTHESIS: Several case reports have described severe allergic reactions, including anaphylaxis, in patients taking ACE inhibitors subsequent to being stung or receiving VIT. Exacerbation of the allergic response by ACE inhibitors is thought to be related to accumulation of bradykinin and inhibition of the formation of angiotensin II. Similar reactions have not been described with angiotensin-receptor blockers, but are theoretically possible. CONCLUSIONS: ACE inhibitors may exacerbate the response to insect venom, resulting in potentially life-threatening allergic reactions to insect stings or VIT. Although this risk is difficult to quantify based only on data from case reports, it seems prudent that patients with documented allergic reactions to insect venom avoid ACE inhibitor therapy, if possible. If, after careful consideration of the risks and benefits, ACE inhibitor therapy is deemed warranted, education regarding measures to minimize exposure to insect stings and training on self-administration of epinephrine should be provided, as with any person with venom allergy. In patients in whom VIT is appropriate, temporary discontinuation of the ACE inhibitor prior to each venom injection may prevent subsequent adverse reactions.     

Donor survey to assess facial flushing during automated red cell collections and medication use

Background: We conducted a donor survey to assess the occurrence of facial flushing and other symptoms during automated 2‐U red cell collections (2RBC) and plateletpheresis (PLT) procedures and evaluated the possible association of the reactions with angiotensin‐converting enzyme (ACE) inhibitors or with the collection technology. Methods: An online survey was developed using Zoomerang to capture details of the donors' experience and medication use after 2RBC or PLT donations in regional blood centers of the American Red Cross. Results: Between 12/16/09 and 4/19/10, 1,299 donors in five American Red Cross blood center regions completed an online survey (739 2RBC, 4.2% total registrations; 560 PLT, 2.3% total registrations). Facial flushing was reported by 29 donors, and was more likely associated with 2RBC than PLT procedures (3.0% vs. 1.3%, P = 0.03). Facial flushing with 2RBC donation was reported by eight of 72 (11%) donors on ACE inhibitors; and 14 of 667 (2%) donors who were not taking ACE inhibitors (P = 0.001). The incidence of facial flushing reactions with PLT donation was less than 2% whether donors reported ACEI inhibitor use or not. More than 95% of the donors reported their intent to donate again, regardless of symptoms. Conclusion: Facial flushing was more often reported by 2RBC donors taking ACE inhibitors than other donors [11% vs. 2%; P = 0.001]; and was uncommon among PLT donors, irrespective of ACE inhibitor use (<2%). All blood donors should be informed of the potential for common, minor side effects of the collection procedure and the possible but rare occurrence of more medically serious complications. J. Clin. Apheresis, 2011. © 2011 Wiley‐Liss, Inc.     

Angiotensin-converting enzyme inhibition and smoking potentiate the kinin response to cardiopulmonary bypass

BACKGROUND: This study tested the hypothesis that angiotensin-converting enzyme (ACE) inhibitors potentiate activation of the kallikrein-kinin system during cardiopulmonary bypass (CPB). METHODS: The effects of CPB on concentrations of bradykinin and its metabolite bradykinin 1-5 (BK1-5) were determined in 31 patients taking an ACE inhibitor who were randomized to continue ACE inhibitors until coronary artery bypass surgery (ACE inhibitor group, N = 19) or to discontinue them 48 hours before surgery (no ACE inhibitor group, N = 12). Arterial and venous blood was sampled before CPB, at 30 minutes of CPB, at 60 minutes of CPB, after separation from CPB, and on postoperative day 1. RESULTS: Arterial bradykinin ( P < .001 [from 22.4 +/- 24.1 fmol/mL to 86.2 +/- 98.7 fmol/mL in the no ACE inhibitor group]) and arterial ( P < .001) and venous ( P = .016) BK1-5 concentrations increased significantly during CPB. Arterial bradykinin concentrations were significantly higher ( P = .017), whereas BK1-5 concentrations ( P = .024) and the molar ratio of BK1-5/bradykinin ( P = .008) were significantly lower in the ACE inhibitor group compared with the no ACE inhibitor group. In addition, arterial bradykinin concentrations were significantly increased in smokers compared with nonsmokers ( P = .015), when we controlled for the ACE inhibitor group. There was no effect of smoking on ACE activity ( P = .597 overall). There was a significant inverse correlation between arterial bradykinin and mean arterial pressure ( r 2 = 0.2137, P = .010) and a significant correlation between arterial bradykinin and tissue-type plasminogen activator antigen concentrations ( r 2 = 0.174, P = .022) during CPB. Tissue-type plasminogen activator antigen was significantly higher in the ACE inhibitor group than in the no ACE inhibitor group (18.0 +/- 7.8 ng/mL versus 12.4 +/- 4.5 ng/mL, P = .016) but not in smokers compared with nonsmokers ( P = .451). CONCLUSION: Preoperative ACE inhibitors and smoking potentiate the kinin response to CPB and may contribute to the hemodynamic and fibrinolytic response observed during CPB.     

Atypical reactions associated with use of angiotensin-converting enzyme inhibitors and apheresis

BACKGROUND: Anaphylactic or atypical reactions, characterized by flushing, hypotension, dyspnea, and bradycardia, have been reported in patients undergoing hemodialysis, low-density lipoprotein apheresis, IgG affinity column apheresis, therapeutic plasma exchange, and desensitization immunotherapy while receiving angiotensin-converting enzyme (ACE) inhibitor therapy. STUDY DESIGN AND METHODS: Records were reviewed of 299 consecutive patients undergoing therapeutic plasma exchange with colloid replacement at the University of North Carolina Hospitals from September 1981 through December 1993. Charts were selected for further analysis if atypical reactions (flushing or hypotension defined as a mean decrease in blood pressure of 20 torr or greater) occurred during apheresis or if there was concurrent administration of an ACE inhibitor. RESULTS: Fourteen (4.7%) of 299 patients were receiving ACE inhibitor therapy at the time of apheresis; all 14 experienced an atypical reaction. In contrast, 20 (7%) of 285 patients not receiving ACE inhibitors developed atypical reactions (p < 0.001). The 14 ACE inhibitor patients accounted for 41 percent (14/34) of all patients having atypical reactions during apheresis. CONCLUSION: Patients receiving ACE inhibitor therapy who are undergoing therapeutic plasma exchange with albumin replacement solutions are at high risk (100%) for atypical reactions. It is recommended that ACE inhibitors be withheld for at least 24 hours before that procedure.     

A case of transfusion-associated graft-versus-host disease not prevented by white cell-reduction filters

A case of transfusion-associated graft-versus-host disease (TA-GVHD) in a patient with non-Hodgkin's lymphoma is reported. The patient, a 67-year-old woman, was diagnosed as having diffuse, mixed type non-Hodgkin's lymphoma, at clinical stage IIIA. She was treated with combination chemotherapy and received multiple blood transfusions for anemia and thrombocytopenia. Although white cells (WBCs) were reduced in the transfused components by WBC-reduction filters, the patient developed TA-GVHD that was confirmed by skin biopsy. It is suggested that the WBC reduction attained with these filters does not prevent TA-GVHD in immunocompromised patients. It is recommended that all blood components should be irradiated before transfusion to such patients.     

Angiotensin II receptor blockers in patients with ACE inhibitor-induced angioedema

OBJECTIVE: To determine the safety of using angiotensin II receptor blockers in patients who have experienced angioedema following treatment with angiotensin-converting enzyme (ACE) inhibitors. DATA SOURCES: Clinical literature identified through MEDLINE (January 1966-August 1999). Key search terms included angioneurotic edema, angiotensin-converting enzyme inhibitors, receptors-angiotensin, and losartan. DATA SYNTHESIS: ACE inhibitor-induced angioedema occurs with an incidence of 0.1-0.5%. Alternative therapy is necessary for patients who experience this potentially life-threatening adverse effect. Since angiotensin II receptor blockers do not increase concentrations of bradykinin, the proposed mechanism of ACE inhibitor-induced angioedema, they were presumed to be safe alternatives. Recent case reports, however, document angioedema following therapy with angiotensin II receptor blockers; 32% of the reported patients experienced a prior episode of angioedema attributed to ACE inhibitor therapy. CONCLUSIONS: Until the exact cause of both ACE inhibitor- and angiotensin II receptor blocker-induced angioedema is determined, angiotensin II receptor blockers should be used with extreme caution in patients with a prior history of angioedema.     

Hypotensive reaction during staphylococcal protein A column therapy in a patient with anomalous degradation of bradykinin and Des-Arg9-bradykinin after contact activation

BACKGROUND: Hypotensive reactions have occurred in patients taking angiotensin converting enzyme (ACE) inhibitors after infusion of blood previously in contact with negatively charged surfaces capable of generating kinins, which accumulate when ACE, a kininase, is inhibited. A patient with anomalous bradykinin (BK) metabolism who experienced hypotension during extracorporeal staphylococcal protein A (SPA) therapy while on an ACE inhibitor was studied. CASE REPORT: A patient with mitomycin-associated hemolytic-uremic syndrome received SPA treatments after her ACE inhibitor, lisinopril, was held. Lisinopril was restarted before her 18th SPA treatment, and immediately after return of treated plasma she developed facial redness and hypotension, which resolved after the return stopped and recurred when restarted. To study formation and degradation of kinins, exposed her plasma to glass beads. We found a normal kinin formation rate but an abnormal degradation and accumulation of Des-Arg9-BK. The kinin degradation enzymes ACE, aminopeptidase P (APP), and carboxypeptidase N (CPN) were measured while on an ACE inhibitor, showing absence of ACE activity, low APP, but normal CPN. CONCLUSION: This patient's vasodilation and hypotension during SPA therapy was associated with a pre- existing anomaly of BK metabolism. Her ACE inhibitor shifted degradation toward Des-Arg9-BK formation, and her low APP was associated with a prolonged t50 and accumulation of the vasoactive Des-Arg9-BK.     

Abdominal pain with rigidity secondary to the anti-emetic drug metoclopramide

We report a case of abdominal pain with rigidity, mimicking an acute abdomen, caused by metoclopramide, a common anti-emetic drug. Extrapyramidal symptoms are commonly reported side-effects of this medication. They generally include involuntary movements of limbs, torticollis, oculogyric crisis, rhythmic protrusion of tongue, trismus, or dystonic reactions resembling tetanus, etc. Abdominal rigidity due to this medication, resembling an acute abdomen, has not been reported previously. This case report illustrates the importance of considering medication side-effects when evaluating a patient with abdominal pain and rigidity.     

Treatment of hypertension in patients with diseases of the aorta and peripheral arteries

Strict antihypertensive therapy for thoracic aortic aneurysm is extremely important. Administration of beta-blocker or angiotensin II receptor blocker (ARB) has been reported to prevent aneurysm enlargement in patients with Marfan's syndrome. While there is no significant association between hypertension and the risk of development of abdominal aortic aneurysm, a large-scale case controlled study showed a lower frequency of ruptured aneurysm in patients treated with ACE inhibitors. The beneficial effects of ACE inhibitor and/or ARB treatment should be confirmed by large-scale randomized controlled-trials. In patients with peripheral arterial disease, administration of beta-blockers has been considered to exacerbate lower limb ischemic symptoms; however they have recently been shown to be used safely in patients exhibiting intermittent claudication.     

A multistate cluster of red blood cell transfusion reactions associated with use of a leucocyte reduction filter

In 2000, the American Red Cross (ARC) received reports of unusual transfusion reactions of unknown aetiology among patients receiving leucocyte-reduced (LR) red blood cell (RBC) units in multiple distribution regions. We evaluated potential risk factors of reactions among patients who received LR-RBC transfusions. A case-patient was defined as any patient with onset of back pain while receiving an LR-RBC transfusion from 1 January to 25 May 2000. Controls were chosen randomly and selected in a 1:3 case : control ratio from healthcare facilities in which case-patients were transfused. Product-specific risk factors of reactions were further determined through nested case-control study, procedural review of blood collection facility and quality-control-testing record review of product processing. Reaction incidence rates were determined through ARC blood product distribution data by region of blood collection and processing. There were 29 reactions detected in patients who received transfusions in 13 healthcare facilities in five states. Eighteen case-patients and 78 controls were included in the case-control study. In univariate analysis, case-patients were more likely than controls to have a haematologic malignancy, to have received the transfusion as an outpatient, to have received an RBC transfusion within the previous 3 months, to have received medication used to prevent reactions or to diminish their intensity upon transfusion (i.e. premedication) or to have received LR-RBC units prepared with the HemaSure r\LS System(HS) rather than two other filters used. In multivariate analysis limited to recipients of HS-filtered RBC units, transfusion premedication [adjusted odds ratio (AOR) = 7; 95% confidence interval (CI) 1.4-37; P = 0.02] and transfusion as an outpatient (AOR = 5; 95% CI 1.1-20; P = 0.03) were independently associated with reactions. The rate of reported transfusion reactions was 2.0 reactions per 10 000 RBC units distributed. A multistate cluster of transfusion reactions was significantly associated with leucocyte filtration of RBC units prepared with a specific product, the HS filter. The reactions also were independently associated with premedication and transfusion as an outpatient; these may be surrogates for an increased risk of reaction or for greater likelihood of detection. The mechanism for these reactions has not been elucidated. This cluster of reactions underscores the importance of surveillance efforts to detect adverse events after transfusion, particularly when new methods to modify blood products are introduced.     

C1 Esterase Inhibitor for Ace-Inhibitor Angioedema: A Case Series and Literature Review

BackgroundAngiotensin-converting enzyme (ACE) inhibitors are a commonly prescribed and effective medication to treat hypertension. Although generally well tolerated, about 1% of patients will experience angioedema, a potentially life-threatening adverse drug reaction. This reaction is thought to be mediated via a buildup of bradykinin and does not typically respond to epinephrine, corticosteroids, or antihistamines. Alternative treatment strategies have been investigated, the bulk of which surround the use of therapies approved for hereditary angioedema.ObjectiveUtilization of C1 esterase inhibitors at our institution was reviewed between 2016 and 2018 for treatment of ACE inhibitor–induced angioedema. We describe the clinical course of case series, along with a review of current literature.DiscussionUtilization of C1 esterase inhibitors for treating ACE inhibitor–induced angioedema is an uncommon therapy and has limited efficacy in our case series. Treatment did not result in rapid improvement of swelling, prevention of intubation, or prevention of intensive care unit admission.ConclusionsBased on our case series, C1 esterase therapy should not be utilized routinely for ACE inhibitor–induced angioedema and is not expected to prevent intubation in severe cases.     

Platelet storage lesion of WBC-reduced, pooled, buffy coat-derived platelet concentrates prepared in three in-process filter/storage bag combinations

BACKGROUND: With the implementation of universal WBC reduction in the United Kingdom, in-process WBC-reduction filters for pooled buffy coat (BC)-derived platelet concentrates (PCs) are used in routine production. The effects of three filter/storage bag combinations on platelet activation and microvesiculation and on the activation of coagulation were investigated. STUDY DESIGN AND METHODS: Using pooled BCs from the same donors, three filter/storage bag combinations (Autostop BC/CLX, Pall Biomedical; Sepacell PLX5/PL2410, Asahi Medical; and Imugard III-PL 4P/Teruflex, Terumo) were compared with unfiltered controls for their effects on microvesiculation and other storage-induced changes in platelets. Process efficiency was measured by platelet yield and residual WBC count. The storage changes were assessed: pH, activation of platelets measured by CD62P on the platelet surface and in supernatant plasma, quantitation of platelet-derived and RBC-derived microvesicles, cellular injury measured by annexin V in the supernatant plasma, and activation of the coagulation system measured by kallikrein-like and thrombin-like activities, prothrombin fragment 1+2, and thrombin-antithrombin complex. RESULTS: All three filters were comparable in terms of platelet recovery and WBC removal, and none induced immediate platelet activation or microvesiculation. With storage, platelet activation or microvesiculation increased in platelets prepared by all three filters and in unfiltered controls, but these effects were significantly less in the Imugard PCs than in controls. These findings were consistent with those for annexin V in the supernatant plasma, which were lower in Imugard PCs than in other products. Sepacell and Imugard filters reduced RBC-derived microvesicles to 50 percent of control levels, but the Autostop filter had no effect. On storage, levels of RBC-derived microvesicles in filtered products remained static, but levels in the unfiltered control doubled. Kallikrein- and thrombin-like activities were generated only by the Autostop filter without any further increment on storage. CONCLUSION: WBC-reduced pooled BC-PCs prepared by various filter/bag combinations were equivalent on Day 1 but differed during storage in terms of platelet activation or microvesiculation.     

Improved removal of white cells with minimal platelet loss by filtration of apheresis platelets during collection

BACKGROUND: Filtration of apheresis platelets to remove white cells (WBCs) requires operator intervention after the collection procedure (postcollection filtration), which may cause variable and unsatisfactory filter performance (WBC removal and platelet loss). The MCS+ LN9000 apheresis system filters platelets through a WBC-reduction filter during each collection cycle (continuous filtration) at a flow rate of 15 to 25 mL per minute. Apheresis platelets obtained by continuous filtration were evaluated in terms of platelet loss, WBC removal, and platelet storage properties and then were compared to unfiltered apheresis platelets and to apheresis platelets that underwent postcollection filtration. Two WBC-reduction filters were tested (LRF6 and LRFXL). STUDY DESIGN AND METHODS: In 70 apheresis platelets, postcollection filtration was performed by using the LRF6 at flow rates of 80 mL per minute (n = 30) and 50 mL per minute (n = 30) and the LRFXL at 50 mL per minute (n = 10). One hundred fifty-eight apheresis platelets underwent continuous filtration through the LRF6 (n = 58) or the LRFXL (n = 100). Unfiltered apheresis platelets (controls) (n = 30) were obtained by the same collection protocol. RESULTS: Estimated platelet loss with continuous filtration was 7 percent for the LRFXL and 3 percent for the LRF6. A reduction in the filtration flow rate from 80 to 50 mL per minute with postcollection filtration through the LRF6 resulted in markedly lower WBC levels, with 10 percent versus 57 percent of the apheresis platelets having WBC counts <1 × 10⁵, respectively. Additional improvements in WBC removal were found with continuous filtration; 85 percent of the apheresis platelets filtered with the LRF6 and 100 percent of the apheresis platelets filtered with the LRFXL had WBC counts <1 × 10⁵. CONCLUSIONS: Continuous or postcollection filtration of freshly collected apheresis platelets resulted in minimal platelet loss. Better WBC removal from apheresis platelets was obtained with continuous filtration than with postcollection filtration, likely because of the slower flow rate. Platelet storage quality was not affected by filtration.