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average of 4.6 years apart, still did have significantly greater rates of loss (0.53%/year vs
0.35%/year in non-users. Thus as a potentially remedial iatrogenic cause the overall message
should be cause for concern.

Case finding, treatment and prevention

On this background of confusing information, what then should we advise our patients, while
awaiting the outcome of much needed further research? Much of the literature debate on this
topic considers AED bone disease as a type of osteoporosis. As discussed above, this may not
be strictly accurate, but given that BMD (as a measure of osteopenia/osteoporosis) is clearly
related to fracture risk, and that we do have effective treatments to slow declining BMD, from
a pragmatic/treatment point of view this is probably reasonable, at least until further
information is available.

Published consensus guidelines12 on the treatment and prevention of osteoporosis continue to
argue, as they have done since the late 1990s, against primary prevention on the grounds that
most osteoporotic fractures do not occur in the small groups at very high risk, but in the larger
numbers at moderate risk. Thus population-wide interventions would be required for good
effect. The problem then is that, although the population attributable risk is high, absolute
individual risk for most is low, and the safety, feasibility and cost of any intervention are
especially crucial and, as yet, largely not established. Instead it is recommended that the major
thrust of osteoporosis prevention should be directed towards selective case-finding.

DEXA case-finding/screening of at-risk populations
In line with this, population screening with for example DEXA scans is also not recommended,
but should be used only as a case-finding strategy for individuals already considered at risk12.
Biochemical markers are considered as having ‘the potential to aid risk assessment’ (and
treatment monitoring), but their utility in clinical practice still in need of further evaluation.
Thus despite recommendations from some that DEXA and biochemical markers of bone
turnover should be routinely studied in patients on AEDs59, the evidence to support anything
beyond the standard bone profile every 25 years79 (unchanged since 2004) is lacking.

Current NICE osteoporosis guidelines (http://pathways.nice.org.uk/pathways/osteoporosis)
caution against DEXA in all but very high risk individuals under 40, and for older patients
recommend the use of additional now readily available web-based algorithms to better identify
individuals at risk, culminating in various web-based tools. These ask for basic demographics
and additional clinical information on proven risks (low body mass index; prior characteristic
fracture; parental hip fracture; alcohol intake; smoking; rheumatoid arthritis, glucocorticoid
treatment; other known cause secondary osteoporosis), leading to a 10-year probability of hip
or major osteoporotic fracture estimate for any individual over 40 to guide future management.

Both the FRAX (http://www.shef.ac.uk/FRAX) and the more recent Qfracture
(http://www.qfracture.org/) have been externally validated in independent cohorts, and guide
the clinician as to fracture risk and/or whether DEXA is indicated (or in some instances not
required, if BMD is already known or the clinical picture already points to the need for
treatment). Both are applicable only for adults (FRAX >40 years, Qfracture >30), reflecting
that the biggest risk factor for fracture, independent of BMD or anything else, is age. Both
include long-accepted secondary causes such as type I (insulin dependent) diabetes,
osteogenesis imperfecta in adults, untreated long-standing hyperthyroidism, hypogonadism or
premature menopause (<45 years), chronic malnutrition, or malabsorption and chronic liver
disease management and, probably most significant in our patient population, prolonged
immobility. However, only since 2012 has Qfracture80 included ‘epilepsy or taking
anticonvulsants’ as a selectable option, inferring that after some years of accumulating