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Articles by M. J Griffiths
Total Records ( 2 ) for M. J Griffiths
  M. J Griffiths , E Chow , M. D Panting , C Ford and R. Gama
  Background

National guidelines for cerebrospinal fluid (CSF) analysis and its reporting in suspected subarachnoid haemorrhage (SAH) were published in 2003, but revised in 2008 to give greater clarity in interpretation. It is not known whether the less ambiguous reporting of 2008 guidelines may lead to a false assurance and adversely affect patient outcome. We, therefore, re-interpreted scans reported under the 2003 guidelines, using the 2008 guidelines and compared these reports against final diagnosis and patient outcome obtained from a retrospective case-note review audit.

Methods

We identified requests for CSF xanthochromia studies from the laboratory system between September 2006 and August 2007. Spectroscopy scans were then retrieved and re-interpreted using the 2008 guidelines. The original reports and re-interpreted scans were compared against diagnosis and patient outcome using case-note review.

Results

We received 93 requests for CSF spectroscopy on 90 patients. Fourteen requests were not processed due to insufficient sample, but of these three patients had a repeat lumbar puncture (LP). Two further requests were not processed at the request of the clinician as they were no longer clinically indicated. Therefore, 77 spectroscopic scans were re-interpreted. The revised guidelines re-classified 11 previously equivocal scans into the not supportive of SAH category. On case-note review, one patient had a subsequent fatal SAH. The remaining 10 were given non-SAH final diagnoses and none had similar further inpatient episodes for at least 12 months and up to 18 months following LP.

Conclusions

The revised (2008) national guidelines for the analysis of CSF in suspected SAH offer greater clarity in reporting without adversely affecting patient outcome.

  A. E Fry , A Ghansa , K. S Small , A Palma , S Auburn , M Diakite , A Green , S Campino , Y. Y Teo , T. G Clark , A. E Jeffreys , J Wilson , M Jallow , F Sisay Joof , M Pinder , M. J Griffiths , N Peshu , T. N Williams , C. R Newton , K Marsh , M. E Molyneux , T. E Taylor , K. A Koram , A. R Oduro , W. O Rogers , K. A Rockett , P. C Sabeti and D. P. Kwiatkowski
 

The prevalence of CD36 deficiency in East Asian and African populations suggests that the causal variants are under selection by severe malaria. Previous analysis of data from the International HapMap Project indicated that a CD36 haplotype bearing a nonsense mutation (T1264G; rs3211938) had undergone recent positive selection in the Yoruba of Nigeria. To investigate the global distribution of this putative selection event, we genotyped T1264G in 3420 individuals from 66 populations. We confirmed the high frequency of 1264G in the Yoruba (26%). However, the 1264G allele is less common in other African populations and absent from all non-African populations without recent African admixture. Using long-range linkage disequilibrium, we studied two West African groups in depth. Evidence for recent positive selection at the locus was demonstrable in the Yoruba, although not in Gambians. We screened 70 variants from across CD36 for an association with severe malaria phenotypes, employing a case–control study of 1350 subjects and a family study of 1288 parent–offspring trios. No marker was significantly associated with severe malaria. We focused on T1264G, genotyping 10 922 samples from four African populations. The nonsense allele was not associated with severe malaria (pooled allelic odds ratio 1.0; 95% confidence interval 0.89–1.12; P = 0.98). These results suggest a range of possible explanations including the existence of alternative selection pressures on CD36, co-evolution between host and parasite or confounding caused by allelic heterogeneity of CD36 deficiency.

 
 
 
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