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High CSF transforming growth factor β levels after subarachnoid haemorrhage: association with chronic communicating hydrocephalus
  1. M R Douglas1,2,
  2. M Daniel1,
  3. C Lagord1,
  4. J Akinwunmi3,
  5. A Jackowski4,
  6. C Cooper1,
  7. M Berry1,
  8. A Logan1
  1. 1
    Molecular Neuroscience Group, University of Birmingham, Edgbaston, Birmingham, UK
  2. 2
    Department of Clinical Neuroscience, University of Birmingham, Edgbaston, Birmingham, UK
  3. 3
    Department of Neurosurgery, Brighton and Sussex Medical School, University of Sussex, Brighton, UK
  4. 4
    Department of Spinal Surgery, Royal Orthopaedic Hospital, Birmingham, UK
  1. Professor A Logan, Molecular Neuroscience Group, School of Clinical and Experimental Medicine, Institute of Biomedical Research (West), University of Birmingham, Edgbaston, Birmingham B15 2TT, UK; a.logan{at}


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

Methods: Temporal changes in total (latent plus active) TGFβ1/β2 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 with those that did not.

Results: Mean (SD) CSF levels of total TGFβ1 were 97 (42) pg/ml and total TGFβ2 were 395 (39) pg/ml in control patients with (non-haemorrhagic) hydrocephalus. For days 1–5 post-subarachnoid haemorrhage (dph), levels of 1427 (242) pg/ml and 976 (191) pg/ml were seen for total TGFβ1 and TGFβ2, respectively. Beyond 5 dph, total TGFβ1/β2 levels declined but remained significantly elevated (p<0.01) above control patient values for at least 19 dph. Haemorrhagic patients that went on to develop chronic communicating hydrocephalus had significantly higher levels of total TGFβ1 (p<0.01) and TGFβ2 (p<0.05) between 1 and 9 dph, compared with those of haemorrhagic patients that did not.

Conclusions: Acutely measured levels of TGFβ1/β2 in the CSF of patients with subarachnoid haemorrhage are thus potential prognostic biomarkers for the subsequent development of chronic communicating hydrocephalus, indicating likely dependency on CSF shunting.

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  • M R Douglas and M Daniel contributed equally.

  • Competing interests: None.

  • Ethics approval: Ethics approval was obtained from the South Birmingham Health Authority Ethics Committee.