C

C. Chapman

Pennine Acute Hospitals NHS Trust

Publishes on Blood transfusion and management, Blood groups and transfusion, Blood donation and transfusion practices. 96 papers and 3.3k citations.

96Publications
3.3kTotal Citations

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Top publicationsby citations

Ten years of hemovigilance reports of transfusion‐related acute lung injury in the United Kingdom and the impact of preferential use of male donor plasma
C. Chapman, D. Stainsby, Hilary Jones et al.|Transfusion|2009
Cited by 350

BACKGROUND AND METHODS: From 1996 through 2006, 195 cases were reported as transfusion-related acute lung injury (TRALI) to the Serious Hazards of Transfusion scheme and from 1999 onward classified by probability, using clinical features and HLA and/or HNA typing. From late 2003, the National Blood Service provided 80 to 90 percent of fresh-frozen plasma (FFP) and plasma for platelet (PLT) pools from male donors. RESULTS: Forty-nine percent of reports were highly likely/probable TRALI, and 51 percent possible/unlikely. Of 96 investigations, donor antibodies recognizing recipient antigens were found in 73 cases (65%), with HLA Class I in 25 of those (40%), HLA Class II antibodies in 38 (62%), and granulocyte antibodies in 12 (17%). A review in 2003 revealed that the TRALI risk/component was 6.9 times higher for FFP and 8.2 times higher for PLTs than for red blood cells, and that in donors of implicated FFP/PLTs, white blood cell antibodies were found 3.6 times more often than by chance (p <or= 0.0001), with all implicated donors being female. Provision of male plasma was associated with a reduction in TRALI reports from 36 in 2003 to 23 in each of 2004 and 2005 and 10 in 2006. Highly likely/probable cases reduced from 22 in 2003 to 13, 6, and 3 [corrected] in the 3 subsequent years, with cases implicating FFP or PLTs with positive donor serology [corrected] falling from 16 to 9, 3, and 1 respectively. CONCLUSIONS: The risk of highly likely/probable TRALI due to FFP has fallen from 15.5 per million units issued during 1999 through 2004 to 3.2 per million during 2005 through 2006 (p = 0.0079) and from 14.0 per million to 5.8 per million for PLTs.

Single hospital experience of TRALI
Jonathan P. Wallis, A. Lubenko, A. W. Wells et al.|Transfusion|2003
Cited by 158

BACKGROUND: TRALI is a serious adverse effect of blood transfusion. There is evidence that the condition is underrecognized and underreported. STUDY DESIGN AND METHODS: This study was an observational study carried out in a single hospital. RESULTS: Eleven cases of TRALI were recognized over 12 years. In 10 cases the implicated donor unit was FFP and in 1 case uncertain. All implicated donors were parous women. In 4 cases the presumed causative antibodies were to an HLA class II antigen only. Specific anti-neutrophil antibodies, possibly causative, were detected in 1 case only. Ten of the 11 cases required mechanical ventilatory support. Five persons died as a result of the TRALI. The observed incidence of TRALI caused by FFP is 1 in 7900 units transfused. CONCLUSION: TRALI is the most common serious adverse effect of blood transfusion in our hospital. Antibodies to HLA class II antigens should be looked for routinely when investigating a possible case of TRALI.

The impact of universal leukodepletion of the blood supply on hemovigilance reports of posttransfusion purpura and transfusion‐associated graft‐versus‐host disease
Lorna M. Williamson, D. Stainsby, Hilary Jones et al.|Transfusion|2007
Cited by 131Open Access

BACKGROUND: The pathogenesis of posttransfusion purpura (PTP) and transfusion-associated graft-versus-host disease (TA-GVHD) involves patient exposure to donor platelets (PLTs) and T lymphocytes, respectively, which are removed during blood component leukodepletion (LD). STUDY DESIGN AND METHODS: Reports of PTP and TA-GVHD to the UK hemovigilance scheme Serious Hazards of Transfusion (SHOT) from 1996 to 2005 were compared before and after implementation of universal LD during 1999. RESULTS: There were 45 reports of PTP, with a mean of 10.3 per year before universal LD and 2.3 per year afterward (p < 0.001). All patients had received red cells, but before universal LD, only 1 of 31 (3%) cases had also received PLTs, compared to 8 of 14 (57%) afterward (p < 0.001). Thirty-four cases (76%) had human platelet antigen (HPA)-1a antibodies, whereas 11 had antibodies to other HPA specificities, only 1 of which occurred after LD. Two cases reported before LD also had heparin-dependent PLT antibodies. There were 13 reports of TA-GVHD, all fatal, of which only 2 cases of undiagnosed immunodeficiency met current UK criteria for irradiated components. Eight others had one or more risk factors: B-cell malignancy (6), steroids (1), fresh blood (1), and donor-recipient HLA haplotype share (4). Eleven cases were due to non-LD and 2 to LD components (p < 0.001). No cases have been reported since 2001. In an additional 405 cases, nonirradiated components were transfused in error to high-risk recipients, mainly on fludarabine, but none developed TA-GVHD. CONCLUSIONS: These findings suggest that universal LD has further reduced the already low risk of TA-GVHD in immunocompetent recipients and has altered the profile of PTP cases.