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High CSF TGFß levels after subarachnoid haemorrhage: association with chronic communicating hydrocephalus
  1. Michael R Douglas (m.r.douglas{at}blueyonder.co.uk)
  1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom
    1. Matija Daniel (m-daniel{at}runbox.com)
    1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom
      1. Catherine Lagord (catherinelagord{at}yahoo.co.uk)
      1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom
        1. James Akinwunmi (neuro.akin{at}googlemail.com)
        1. Department of Neurosurgery, University of Sussex Medical School, United Kingdom
          1. Andre Jackowski (debbie.bagnall{at}roh.nhs.uk)
          1. Department of Spinal Surgery, Royal Orthopaedic Hospital, Birmingham, United Kingdom
            1. Caroline Cooper (csflood{at}yahoo.com)
            1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom
              1. Martin Berry (m.berry{at}bham.ac.uk)
              1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom
                1. Ann Logan (a.logan{at}bham.ac.uk)
                1. Molecular Neurosciences Group, University of Birmingham Medical School, United Kingdom

                  Abstract

                  Background: Chronic communicating hydrocephalus is a common sequela of subarachnoid haemorrhage and develops when the flow and drainage of cerebrospinal fluid (CSF) are impaired after fibrosis in the subarachnoid space. Transforming growth factor (TGF)β1/β2 are potent fibrogenic agents released by platelets into the CSF after subarachnoid haemorrhage, which may promote post-haemorrhagic fibrosis after chronic communicating hydrocephalus.

                  Methods: Temporal changes in total (latent plus active) TGFß1/ß2 CSF levels of post-haemorrhage patients developing acute hydrocephalus were measured using ELISA to discover if titres were higher in patients that subsequently developed chronic communicating hydrocephalus, compared to those that did not.

                  Results: Mean ±SD CSF levels of total TGFβ1 were 97±42pg/ml and total TGFβ2 were 395±39pg/ml in control patients with non-haemorrhagic hydrocephalus at 1-5 days post-haemorrhage (dph). Levels rose to a peak of 1427±242pg/ml and 976±191pg/ml for total TGFß1 and TGFß2, respectively. Beyond 5dph, total TGFß1/ß2 levels declined, but remained significantly elevated (p<0.01) above control patient values for at least 19dph. Subarachnoid haemorrhage patients that went on to develop chronic communicating hydrocephalus had significantly higher levels of total TGFß1 (p<0.01) and TGFß2 (p<0.05) between 1-9dph, compared to those of haemorrhagic patients that did not.

                  Conclusions: Acutely measured levels of TGFß1/ß2 in the CSF of subarachnoid haemorrhage patients are thus potential prognostic biomarkers for the subsequent development of chronic communicating hydrocephalus, indicating likely dependency on CSF shunting. Furthermore, both cytokines are potential targets for acute anti-fibrotic therapies aimed at ameliorating post-haemorrhagic chronic communicating hydrocephalus.

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