Consumer involvement in clinical trials has become a requirement of NHMRC and other funders, so that the consumer perspective is taken into account. Our poster has two aims:
This poster sets out to generate an hypothesis rather than to answer one.
There are scattered but significant clinical reports of association between iron deficiency and PN, one from oxaliplatin-induced PN1, others from anaemia alone2,3, and in diabetics4, the latter supported by good animal evidence5,6.
Also there are numerous in-vitro studies describing mechanisms where ID interferes with the peripheral nervous system (PNS) directly; e.g. via myelination, a process that requires iron, or by interfering with DNA replication and repair, which is also iron dependent7,8. Finally platinum in oxaliplatin has an oxidative state of +2, as does ferrous iron. Oxaliplatin is not transported by the same enzyme as iron, but possibly the iron-transporting enzyme is impacted by oxaliplatin without itself being transported.
In summary there is both clinical and biological evidence for ID (not just anaemia) to play a role in PN which can only worsen the PN from oxaliplatin.
As consumers, we feel the potential impacts of ID on the PNS demands consideration of iron status when treating anyone with cytotoxic drugs that are associated with peripheral neuropathy. Prospective studies are needed to correlate iron status with PN severity, and explore benefit of correcting ID.
Recommendation: Clinicians conducting clinical trials involving oxaliplatin consider iron deficiency as a possible risk factor for PN, and add iron studies to trials involving oxaliplatin. This should establish whether iron deficiency (not just anaemia) worsens the PN from platinum-based agents.