Alan D. Kitchen
NHS Blood and Transplant
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Featured researches published by Alan D. Kitchen.
Vox Sanguinis | 2012
Samreen Ijaz; Renata Szypulska; K. I. Tettmar; Alan D. Kitchen; Richard S. Tedder
Dear Editor, We read with interest the letter from Baylis et al., [1] reporting on the detection of hepatitis E virus (HEV) RNA and antibody in plasma fractionation pools, which originated from several regions across the globe. The authors report that 10% of the pools were HEV RNA positive and discuss the transmission risk through the use of plasmaderived medicinal products. We recently reported evidence of current HEV infection in English and Welsh blood donors indicating a turnover of the virus in the donor panel and the potential for transfusion-associated transmission [2]. To ascertain further the risk of HEV to the English blood supply, serological and molecular investigations were undertaken in plasma minipools collected in 2007. Each mini-pool was made up of 48 individual donors and had originally been prepared for hepatitis C RNA screening. Extraction and detection of HEV RNA was carried out on 880 mini-pools (equivalent to approximately 42 000 individual donors) as previously described [2]. Six of the 880 pools (0Æ7%) had detectable HEV RNA. As expected, viral loads in the HEV RNApositive pools were low (£ 2000 GEq ⁄ ml). Additional HEV antibody (anti-HEV) testing found all 6 (100%) and 1 ⁄ 6 (17%) of the HEV RNA-positive pools to be anti-HEV IgG and IgM reactive respectively. Of the 100 HEV RNA-negative pools tested, 73% and 0% were HEV IgG and IgM reactive respectively. The high incidence of asymptomatic infection with HEV gives ample opportunity for blood donors to infect recipients. Studies undertaken in the general English population indicate an anti-HEV seroprevalence of 13% and estimate that 60 000 cases occur per year [3]. It is therefore perhaps unsurprising that our study demonstrates a high antiHEV IgG prevalence in the mini-pools tested. The detection of HEV RNA and anti-HEV IgM demonstrates current HEV infections. In contrast, Baylis et al. [1] found HEV IgG only in the pools from Asia, which is very surprising given the UK seroprevalence. They also report eightfold higher rates of HEV RNA in tested pools from Europe but do not disclose the pool size. Some of these differences may be explained by variations in the make up of the pools and in the detection assays used. Collectively, these reports provide evidence of the potential to transmit HEV from blood ⁄ blood components and products. However, the extent of HEV transmission posttransfusion and the outcome of receiving HEV-containing transfusion products remain poorly explored. The risks of transfusion-associated HEV deserves due consideration in light of emerging data on the significant harm of persistent HEV in the immunosuppressed [4, 5]. It is estimated that 75% of UK blood ⁄ blood components are given as haematological support to this population. The issue of HEV and blood safety therefore warrants further studies and debate.
Transfusion | 2008
Philip W. Tuke; Paul Grant; James Waite; Alan D. Kitchen; Roger P. Eglin; Richard S. Tedder
BACKGROUND: The detection of hepatitis C virus (HCV) infection is of major importance for the prevention of transfusion‐transmitted hepatitis. The testing of donations by nucleic acid testing (NAT) techniques may not be feasible or economic. Combined antigen and antibody assays are now available, and the performance of two combined assays on window‐phase donations is evaluated.
Transfusion | 2017
Richard S. Tedder; Samreen Ijaz; Alan D. Kitchen; Ines Ushiro‐Lumb; Kate I. Tettmar; Patricia Hewitt; Nick Andrews
Infection with hepatitis E virus (HEV) Genotype 3 is recognized as a food‐borne zoonosis in developed countries where it usually causes a mild self‐limited acute hepatitis. It may cause a persistent infection in the immunosuppressed human that can progress to cirrhosis. To protect the patient from transfusion‐acquired HEV infection, steps have been taken in the United Kingdom to provide for at‐risk patients only components from donors screened for HEV viremia. This strategy does not protect from dietary exposure and calls into question estimation of relative risk between blood transfusion and diet.
Vox Sanguinis | 2014
Alan D. Kitchen; P. L. Chiodini; J. Tossell
The English transfusion service has screened donations from malaria‐risk donors for malarial antibodies for over 10 years. The donor population includes migrants from many malaria‐endemic countries and, from our experiences with post‐transfusion malaria, some of these may remain parasitaemic and need clinical review.
Transfusion | 2012
Alan D. Kitchen; Patricia Hewitt; Peter L. Chiodini
BACKGROUND: Trypanosoma cruzi is a parasitic infection endemic in Central and Southern America, but is spreading into nonendemic countries with migration of infected individuals from endemic countries. The parasite is transmitted by transfusion or transplantation and donation screening is performed routinely in endemic countries to prevent transmission. In situations where migrants from endemic countries have settled in nonendemic countries and present as donors (blood or other cellular products), intervention is required to prevent transfusion or transplantation transmission.
Transfusion | 2014
Gillian K. Rosenberg; Sam Lattimore; S. R. Brailsford; Patricia Hewitt; Kate I. Tettmar; Alan D. Kitchen; Samreen Ijaz; Richard S. Tedder
Hepatitis B virus (HBV) remains the infection most frequently recognized by donation testing in blood donors. It is usually a persistent infection and mostly reflects the country of origin of the donor or the donors family. There are, however, a minority of acute infections and this study undertook their phylogenetic analysis to determine the likely source of infection.
Vox Sanguinis | 2018
C. A. Reynolds; K. L. Davison; N. Andrews; P. Patel; Alan D. Kitchen; S. R. Brailsford
The rate of confirmed hepatitis C virus (HCV) cases, in first‐time donors, is much lower in 2015 than 20 years ago. We investigate reasons for the decline.
Transplantation | 2018
Ines Ushiro-Lumb; Mhairi Webster; Alan D. Kitchen
Background In the UK, the Advisory Committee on Microbiological Safety of Blood, Tissues, Organs and Cells (SaBTO) recommends discretionary T. cruzi antibody screening of donors with identified risk factors for American trypanosomiasis. Centralised T. cruzi antibody screening of deceased organ donors was introduced by the single organ procurement organisation, NHS Blood and Transplant (NHSBT), in 2014. In England, blood donors have been tested on a discretionary basis since 2009, with a current incidence of 0%. Aims To describe the strategy for assessment of donor risks for Chagas disease in a non-endemic country and report results of donor screening implementation. Methods Indication for testing is identified through interview with next of kin (NoK) and medical history obtained from the donor’s general practitioner. T. cruzi antibody screening should be undertaken in donors that meet any of the criteria shown in box 1. Requests submitted for T. cruzi Ab from deceased organ donors in England, N Ireland and Wales between July 2014 - July 2017 were reviewed for data collection. Bio kit Chagas Antibody® initially and then Abbott Architect Chagas ® assays were used as per manufacturer’s instructions. Results Risk of exposure to T. cruzi was identified in approximately 94/5100 consented deceased organ donors (1.84%), a higher proportion than that identified amongst blood donors in England (0.07%). Indications for testing are summarized in table 1. The commonest indication was travel to potentially endemic areas (72.3%), whilst residency in endemic areas accounts for 35.5% of requests. There were no seropositive results. Discussion Identification of risk is based largely on demographic and travel information obtained from the NoK at the time of donation, which is less precise when compared to live donor history, resulting in a lower specificity of selection. True risk of infection is associated with distinctive factors and prolonged exposure in rural, endemic or hyper endemic areas; donor or family history of conditions compatible with Chagas disease may also be present and must be noted. The risk of T. cruzi in our donor population remains very low, reflecting the composition of migrant populations in the UK. The commonest indication for testing is travel to endemic areas, whereas the higher risk indicators are seen in 36% of those tested. In the setting of a non-endemic area, emphasis has been on detailed donor history, with immediate post-donation screening as prompt identification of infected donors in the immediate post-transplant period will still inform modified recipient management and allow mitigation of morbidity through appropriate monitoring and pre-emptive treatment, as required. Table. No title available.
Transfusion Medicine | 2017
Alan D. Kitchen; Patricia Hewitt; P. L. Chiodini
Dear Sir, A male repeat blood donor, born in 1985 and UK resident from birth, contacted NHS Blood and Transplant (NHSBT) on 14 September 2011 to notify them that he had donated blood on 5 July 2011, had subsequently become ill and on 24 August 2011 had been diagnosed with Plasmodium vivax malaria. The door had returned from a visit to India on 17 August 2010 and had not travelled to a malarious area since then. Following UK blood donor deferral guidelines (http://www .transfusionguidelines.org.uk/dsg), the donor was deferred for 6 months, returning to donate on 8 March 2011. The donor declared himself well and, following the pre-donation interview was deemed eligible to donate, with the requirement for malarial antibody testing (MAT) of the donation. The UK Guidelines allow donation 6 months after last return from a malarious area if MAT is performed. The donation was screen negative and released to inventory, and the donor returned to normal donation status. He donated again on 5 July 2011 in good health, and with no further relevant travel, no additional testing was required, and the donation was released to inventory. Following the July 2011 donation, the donor remained well until 10 August 2011 when he developed fever and vomiting. Symptoms persisted for nearly 2 weeks, and investigations identified malaria parasites, confirmed as P. vivax, in a routine blood film. Treatment was given, and symptoms resolved. The donor was deferred for the minimum 3 years required by UK Guidelines, with consideration for reinstatement after that period dependent on negative MAT results. The donor’s notification of his malaria diagnosis triggered a case review that identified the need, although unlikely, to consider possible malaria transmission from the donations prior to diagnosis. The components prepared from both donations were traced. The red cells from the March donation were transfused into a female surgical patient, discharged mid-April 2011, who was alive in September 2011 with no indication of having acquired malaria. The red cells from the June donation were transfused to a female cardiology patient who died from her underlying condition soon after the transfusion started. The FFP from both donations were unused and recalled. As part of NHSBT’s investigations, the available plasma archives of the donor’s previous donations, back to March 2009, were retrieved and tested retrospectively for malarial antibody. In addition, follow-up (f/u) samples were obtained from the donor in November 2011, February 2012, October 2014 and
Isbt Science Series | 2016
K. I. Tettmar; P. W. Tuke; M. Webster; Sam Lattimore; Alan D. Kitchen; T. F. Schulz; Richard S. Tedder
Human herpesvirus 8 (HHV‐8) is the causative agent of Kaposis sarcoma which is of concern in organ transplantation due to transmission through either the donor organ or any associated blood components to immunologically susceptible patients. The prevalence of HHV‐8 in the UK has not been widely investigated. In this study, the seroprevalence of HHV‐8 in English blood donors was measured and the performance of confirmatory assays evaluated.