78 Correspondence

samples which were supposed to have normal levels. This is probably due to the fact that some of these ‘normal’ NEQAS samples have C6PD assay values at the lower end of the normal range; as the colorimetric kit is sensitive to slightly reduced enzyme levels these samples will thus be rcad as deficient or intermediate. Differences in sensitivity between the colorimetric and visual fluorescence kits d o not account for the occasional reporting of a normal result on a grossly deficient sample, and such cases are probably due to errors on the part of the participant, in either perform- ing the test or in recording the result.

Our study demonstrated that the incubation step in the fluorescent screen should be carried out at 37°C as this appears to maximize the difference in intensity of reaction between low and normal samples, thus reducing the risk of an incorrect interpretation.

In a further study on normal bloods no significant differences were seen in quantitative assay values between samples collected into EDTA, heparin or ACD, and both the screening kits gave the correct responses with these bloods irrespective of which anti- coagulant was used. There were no differences in reaction when the samples were freshly drawn and after overnight Storage at 4°C.

As a result of these findings, Sigma have undertaken to make appropriate changes in the instruction inserts which accompany the kits.

Acknowledgements

This work was supported by the DHSS. A full report of the study is available on request to NHS Procurement Directorate, DHSS, 14 Russell Square, London WCl .

References

BEUTLER E.. BLUMF K.G., KAPLAN J.C., LOHK G.W., R A M ~ T B. & VALENTINE W.N. (1977) International Committee for Standardization in Haematology: Recommended methods for red-cell en7yme analysis. Br. J . Huemot. 35,

GALEN R.S. & GAMBINO S.R. (1975) Beyond Normalily: [hi, Predictive Value and Efjicienq of’ M e d i d Dirrjinosis, pp 10-14, Wiley, New York

33 1-340

S.M. Lewis K.J. Sanders

National External Quulity Assessment Schurnu Royal Posrgraduute Medical School Du Cane Road London W12 ONN

Progressive multifocal leucoencephalopathy in patients with chronic lymphocytic leukaemia

Sir: We read with interest the case report of McNally, Taylor & Wood [Clin. lab. Huemut. (1988) 10, 229-2331, We have also seen a case of progressive multifocal leucoencephalopathy (PML) in a patient with chronic lymphocytic leukaemia (CLL). A 64-year-old woman was noted to have early CLL on a routine blood count following a traumatic fracture in 1981. The disease was initially stable, but 2 years later showed evidence of progression requiring treatment. The disease was only partially responsive and over the next 3 years she received a variety of cytotoxic therapy, including chlorambucil, prednisolone, high- dose pulsed methylprednisolone and splenic irradiation. In June 1986, whilst taking oral prednisolone, she was reported by her son to have become vague and withdrawn over the preceding 2 weeks. She was disorientated in time with a mild mixed dysphasia. A clinical diagnosis of PML was confirmed by CAT scan and brain biopsy. Her mental state slowly deteriorated and there was evidence of progression of her CLL with a rising WBC and increasingly severe thrombocytopenia. She died of a chest infection 6 months after the diagnosis of PML. It is interesting that in common with the reported case (McNally el al. 1988), PML occurred in a patient with advanced CLL requiring further cytotoxic therapy. Although it is important to investi- gate such patients, to exclude potentially remedial disorders (such as subdural haematomas), we suspect that in advanced CLL the combined immunological defect associated with the disease, in conjunction with the need for on-going cytotoxic therapy, would render such patients refractory to treatment with antiviral therapy.

Reference MCNALLY P.G., TAYLOR J.M. & WOOD J.K. (1988)

Case report. Progressive multifocal leuco- encephalopathy associated with chronic

Correspondence 79

lymphocytic leukaemia. Clin. lab. Haemaf. 10, 229-233

Peter Flanagan, MRCP, MRCPath Christine Costello, MRCP, MRCPath

Department of Haemutology Sr Stephen’s Hospilal London S WlO

Guidelines for autologous transfusion

Sir: Having read ‘Guidelines for autologous transfusion’ [Clin. lab. Haemat. (1988) 10, 193 2011 I am filled with admiration at the ingcnuity with which the distinguished working party has obfuscated a simple exercise.

What is the donor/patient to think when told that the advantages of autologous blood are that it is incapable of stimulating antibodies and carries no risk of transmitting infections such as hepatitis o r AIDS yet he is asked to consent to his blood being tested for HBsAg, anti-HIV and syphilis and he may learn that his blood will be crossmatched with his own blood to determine compatibility? He may be astonished to learn that should his blood be positive for HBsAg or anti-HIV the donation will be wasted and not transfused to him: he may well ask what possible harm would the blood do to him. He will certainly be astounded if he learns that his donation has to be treated as a pariah and kept in a refrigerator separate from the normal blood bank.

I should think that most of the testing recommended in the Guidelines is unneces- sary and can only lead to false-positive results and that the working party has missed the boat in not recommending the use of a unique numbering system, used for years by several hospitals for heterologous blood transfusion; this uses sets of replicate numbers unique to each transfusion which link the donor, the donation and the documents unambiguously. It obviates the possibility of transfusing the patient with the wrong donation.

Reference

BRITISH COMMITTEE FOR STANDARDIZATION IN HAEMATOLOGY BLOOV TRANSFUSION TASK

FORCE (1988) Guidelines for autologous trans- fusion. Clin. lab. Haemat. 10, 193-201

F.G. Bolton 47 Mill Street Kidlington Oxfiwd OX5 2EE

Response to Dr Bolton’s letter

Sir: Dr Bolton is not alone in questioning the need to ABO and Rh(D) type predeposited autologous blood and to undertake tests for anti-HIV and for HBsAg. However, the issues are not as simple as he suggests and experience has shown that neither unique numbering systems nor any other check in which human error can play a part are foolproof.

The primary concern which prompted the inclusion of these recommendations in the Guidelines was the recognition that clerical mistakes can and do occur and that patients do occasionally get blood intended for someone else. The inclusion of the ABO and Rh(D) types in the documentation and labelling provides an important additional safety check, particularly if patients with similar names and illegible signatures are dealt with at the same time.

One obvious possible hazard of receiving the wrong blood is viral transmission. HBsAg and anti-HIV testing of every autologous donor can eliminate this. In addition, it is important to bear in mind the safety of those handling blood in the laboratory, in theatre and on the ward, who should be able to have the same confidence in the microbiological status of autologous blood as they have with blood supplied by the Transfusion Service. To seek consent for such tests is no more than current practice.

The task of the multidisciplinary Working Party was to prepare guidance for those wishing to carry out autologous blood transfusion against the background of claims that the procedure is, if not completely safe, at least considerably safer than transfusion with homologous blood. The safety record of blood transfusion in the UK is a notable one, and in seeking to provide guidelines for an alterna- tive, no detail which might contribute to safety can be overlooked. If the opportunity for an error exists, however remote the possibility, then sooner or later that error will occur. We recognize this in the way we manage