We found that in the case of our patient, there was an unusually low placental weight and a low infant birth weight when compared with data recorded from three control patients and from previous studies of our population . These previous studies also recorded an association of low birth weight infants with low haemoglobin concentrations, especially during the first trimester. However, this was not a factor in this case, as the patient maintained normal plasma concentrations of haemoglobin throughout the pregnancy.
Low weight gain during pregnancy is another risk factor that contributes to low infant birth weight ; however, the control patients that experienced similar weight gain did not give birth to low birth weight infants. Although our comparisons are limited by the lack of dietary intake information, previous reports have confirmed that mood stabilizers can contribute to low birth weight outcome .
On further comparison of this patient with controls, it appeared that there was a decrease in plasma choline and phosphatidylcholine concentrations in this patient. Both nutrients are especially important during pregnancy and are actively transported to the foetus [1, 11]. The decreases in plasma concentrations of these nutrients in our patient were unexpected, as plasma concentrations of both are increased during pregnancy [12, 13], possibly to ensure adequate supply to the foetus. Phosphatidylcholine, for example, supplies important long chain polyunsaturated fatty acids, and deficiency of polyunsaturated fatty acids to the foetus is a known risk factor for negative foetal outcomes such as low birth weight . Furthermore, animal studies have demonstrated that inadequate maternal supply of these nutrients impairs cognitive and memory functions of pups and that dietary supplementation with these nutrients during pregnancy can prevent these effects [1, 15].
Our data analysis was limited by the lack of information on the actual amounts of choline and phosphatidylcholine that were consumed by this patient during pregnancy and therefore whether inadequate dietary intake contributed to the unexpected depletions. However, previously documented evidence supports negative influences of at least one of the drugs involved (lithium) on these nutrients. We therefore conclude that there is need for further studies to clarify the causal associations between drug therapy, maternal outcomes, foetal outcomes and the availability of these nutrients in patients being treated for bipolar affective disorder. Whether benefits could be derived from dietary supplementation with choline and phosphatidylcholine should also be considered.