Role of therapeutic apheresis in infectious and inflammatory diseases: Current knowledge and unanswered questions

Sloan, Steven R.; Andrzejewski, Chester; Aqui, Nicole A.; Kiss, Joseph E.; Krause, Peter J.; Park, Yara A.

doi:10.1002/jca.21370

Cited by 19 publications

(17 citation statements)

References 36 publications

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“…Patients with a profound reduction of ADAMTS13 (defined by an activity < 30%) were compared to patients with less severe suppression of ADAMTS13 activity (≥ 30%) in terms of clinical parameters at the time of inclusion before TPE treatment. Patients with ADAMTS13 activity ≥ 30% showed a trend to less organ dysfunction as indicated by lower SOFA scores (16 (14-19) vs. 19 (17)(18)(19)(20)(21)(22), p = 0.095, Fig. 4a) and comparable severity of hemodynamic shock (NE dose, 0.884 (0.639-1.158) μg/ kg/min vs. 0.667 (0.516-1.273) μg/kg/min, p = 0.529, Fig.…”

Section: Adamts13 and Correlation With Clinical Parameters Of Diseasementioning

confidence: 99%

“…Although uncontrolled, we observed rapid stabilization of hemodynamics, improvement of fluid balances, and reduction of key pro-inflammatory cytokines and permeability factors. We believe that these positive surrogate effects can be attributed to two important aspects: (1) removal of harmful circulating molecules and (2) replacement of protective plasma proteins consumed by the disease process [22].…”

Section: Introductionmentioning

confidence: 99%

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Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock

et al. 2020

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Background: A dysbalanced coagulation system is part of the pathological host response to infection in sepsis. Activation of pro-coagulant pathways and attenuation of anti-coagulant activity ultimately lead to microvascular stasis and consequent organ failure. No treatment approaches specifically targeting this axis are available. We explored the effects of therapeutic plasma exchange (TPE) on microvascular coagulation dysbalance in septic shock. Methods: We conducted a prospective single-center study enrolling 31 patients with early septic shock (onset < 12 h) requiring high doses of norepinephrine (NE > 0.4 μg/kg/min). Clinical and biochemical data, including measurement of protein C; a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13 (ADAMTS13); and von Willebrand factor antigen (vWF:Ag), were obtained before and after TPE against fresh frozen plasma. Results: Antithrombotic acting proteins such as antithrombin-III (ATIII) and protein C were markedly reduced in septic patients, but their activity increased after TPE (ATIII, 51% (41-61) vs. 63% (48-70), p = 0.029; protein C, 47% (38-60) vs. 62% (54-69), p = 0.029). Median ADAMTS13 activity was increased by TPE from 27 (21-42) % before to 47 (38-62) % after TPE (p < 0.001). In contrast, vWF:Ag was elevated and could be reduced by TPE (353 (206-492) IU/dL vs. 170 (117-232) IU/dL, p < 0.001). Regression analysis yielded a correlation between ADAMTS13 activity and platelet count (p = 0.001, R 2 = 0.316). Conclusions: Septic shock was associated with activation of pro-coagulant pathways and simultaneous depletion of anti-coagulant factors. TPE partially attenuated this dysbalance by removing pro-and by replacing anti-coagulant factors. Trial registration: ClinicalTrials.gov, NCT03065751. Retrospectively registered on 28 February 2017.

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Section: Adamts13 and Correlation With Clinical Parameters Of Diseasementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock

et al. 2020

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“…In addition to lysis of red blood cells, Babesia pathogenesis is thought to be caused by host response to infection . After acute infection with babesiosis, there are systemic elevations in cytokines and adhesion molecules including tumor necrosis factor‐alpha (TNF‐α), interferon‐gamma (IFN‐γ), interleukin‐2 (IL‐2), interleukin‐6 (IL‐6), Eselectin, intracellular adhesion molecule 1 (ICAM‐1), and vascular‐cell adhesion molecule 1 (VCAM‐1) . Although moderate production of these pro‐inflammatory cytokines can be protective, excessive production may lead to severe babesiosis .…”

Section: Pathogenesismentioning

confidence: 99%

“…This process of asexual reproduction is asynchronous without the massive hemolysis that results in paroxysmal fevers and rigors in malaria [15]. In addition to lysis of red blood cells, Babesia pathogenesis is thought to be caused by host response to infection [15][16][17]. After acute infection with babesiosis, there are systemic elevations in cytokines and adhesion molecules including tumor necrosis factoralpha (TNF-a), interferon-gamma (IFN-g), interleukin-2 (IL-2), interleukin-6 (IL-6), Eselectin, intracellular adhesion molecule 1 (ICAM-1), and vascular-cell adhesion molecule 1 (VCAM-1) [16,18].…”

Section: Pathogenesismentioning

confidence: 99%

Apheresis for babesiosis: Therapeutic parasite reduction or removal of harmful toxins or both?

Saifee

Krause

2015

J of Clinical Apheresis

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Babesiosis is a potentially life-threatening illness caused by intraerythrocytic protozoan parasites of the genus Babesia that are transmitted most commonly by Ixodes ticks, and rarely from blood transfusion or congenitally. Clinical presentations of babesiosis include asymptomatic infection, mild to moderate disease, or severe disease. Antibiotics such as atovaquone plus azithromycin or clindamycin and quinine can be used effectively to treat this disease in most cases, however in high risk populations, the mortality rate can be as high as 20% despite therapy. Therapeutic exchange transfusion has been used in severe babesiosis and is of apparent therapeutic benefit. It is not entirely clear through what mechanism therapeutic exchange transfusion may help patients. Data suggests that in addition to parasite load reduction, it is possible that therapeutic exchange transfusion removes toxins generated by babesia infection. There are many remaining questions that need to be addressed regarding exchange transfusion for babesiosis. J. Clin. Apheresis 31:454-458, 2016. © 2015 Wiley Periodicals, Inc.

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“…Another literature search using "therapeutic apheresis" only, "donor apheresis" only, and "cellular therapy" only was also performed and the results showed a yearly median of 17 (range: 6-26), 6 (range: [3][4][5][6][7][8][9], and 168 (range: 68-274) articles in each field, respectively during the same time-period. Hence, in 2012, the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the American Society for Apheresis (ASFA) held a sympo-sium to address the need for apheresis research, as well as the barriers to achieving that goal [3][4][5][6]. They concluded that there is a need to establish consortia in apheresis to facilitate research, networking, and collaboration among researchers, especially junior investigators, as well as to promote funding for apheresis research [3].…”

Section: Introductionmentioning

confidence: 99%

Apheresis research–more abstracts should be published as full manuscripts to provide more evidence for clinical practice guidelines

Pham

Jiang

Pan

et al. 2015

J of Clinical Apheresis

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High-quality evidence to support clinical practice is lacking in apheresis medicine compared to other therapeutic modalities. A potential source of evidence comes from the abstracts submitted to the Annual Meetings of the American Society for Apheresis (ASFA). Therefore, the goal of this study is to determine the proportion of abstracts from the 2005 to 2012 ASFA Annual Meetings that subsequently became PubMed-indexed publications. Furthermore, we sought to determine the factor(s) that were associated with the likelihood of abstracts to be published as full manuscripts. During the 8-year study period, 684 abstracts were available for analysis (median: 82/year, range: 64-118). Most abstracts (74%) were from US institutions, and 67% of first authors were affiliated with academic centers. There were more abstracts (64%) on therapeutic versus donor apheresis (20%) and cellular therapy (16%). Overall, 16% of the abstracts have been published in PubMed-indexed journals, with a median time of 17 months from the ASFA Annual Meeting (range: 1-96 months). Abstracts whose first authors were affiliated with academic institutions were 3.14 times more likely to have been published than abstracts with ones affiliated with an apheresis organization and/or a community hospital. However, neither the first author's location nor the type of apheresis procedure significantly affected the publication rate after adjusting for other covariates. In conclusion, the rate of publication is low and authors should be encouraged to follow their presentations at the meeting with peer-reviewed manuscripts. This change is essential to provide more published evidence for future apheresis practice guidelines. J. Clin. Apheresis 31:353-358, 2016. © 2015 Wiley Periodicals, Inc.

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Role of therapeutic apheresis in infectious and inflammatory diseases: Current knowledge and unanswered questions

Cited by 19 publications

References 36 publications

Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock

Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock

Apheresis for babesiosis: Therapeutic parasite reduction or removal of harmful toxins or both?

Apheresis research–more abstracts should be published as full manuscripts to provide more evidence for clinical practice guidelines

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