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PWE-107 Bone disease in primary biliary cirrhosis – is the risk higher than previously thought?
  1. L Corless,
  2. F Majeed,
  3. G Abouda
  1. Gastroenterology, Hull and East Yorkshire Hospitals NHS Trust, Hull, UK


Introduction Primary biliary cirrhosis (PBC) is common in gastroenterology practice. Bone disease is more common and fracture risk higher than the general population, although overall prevalence is unknown and risk generally assumed to be considerably lower in those without cirrhosis/severe cholestasis.1,2Since poor bone health can impact both quality of life and mortality, guidelines recommend assessment by bone densitometry (DEXA) for all with PBC, and consideration of calcium and vitamin D (Ca/vitD) supplementation.2We measured bone health in our patients and reviewed performance against guidelines.

Method We performed a retrospective review of all patients (n = 121) with confirmed PBC in our centre. Both prevalence and development of bone disease were measured by including only those with at least 5 years follow up (n = 67).

Results Our cohort was representative of the PBC population; the majority (92.4%) were female and older, and progression to cirrhosis uncommon (7.5%). 26.8% had evidence of chronic liver disease (CLD), and 2/3 had evidence of disease progression during follow up. 61% were on appropriate weight based dose of ursodeoxycholic acid; 10.4% were on no therapy.

DEXA was performed in 66.7% at some time during follow up. Of those, 65.9% had bone disease (17 osteopenia, 12 osteoporosis). Fracture prevalence was 10.4%; most were not on prior bone protection (data not available n = 2). 53% of the cohort were on no bone protection, including 5 with osteopenia.

The cohort was divided into those with/without CLD. Of those with CLD, (n = 18), 13 had DEXA of whom 69.2% were osteopenic/osteoporotic; most were on bone protection. Of those with no DEXA, only one was receiving Ca/vitD. Even in those with no evidence of CLD (n = 36), 44.4% were osteopenic/osteoporotic. Again, a notable proportion (33.3%) had no DEXA. We found no significant difference in bilirubin or alkaline phosphatase (AlkP) between those with/without bone disease, although there was a clear trend towards higher AlkP in longer-term, advanced disease.

Conclusion The majority of the cohort had bone disease, and we found a higher than expected rate of fracture. We found a high prevalence of bone disease even in those with no evidence of advanced liver disease, a group previously considered low risk. This was accompanied by poor adherence to guidelines for DEXA and use of Ca/vit D. This suggests there are many undiagnosed patients with bone disease not receiving appropriate therapy, with subsequent implications for long-term health. We have developed a PBC management policy, highlighting the importance of bone health assessment and management.

Disclosure of interest None Declared.


  1. Collier JD, et al. Guidelines on the management of osteoporosis associated with chronic liver disease. Gut. 2002;50(Suppl I):i1–i9

  2. EASL clinical practice guidelines: management of cholestatic liver diseases. J Hepatol. 2009;51:237–267

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