Biochemical effects of moderate dose vitamin A supplementation – How do we monitor vitamin A status?

The paper by Farhangi et al. ¹ demonstrated the potential for moderate doses of vitamin A to produce changes in biochemical markers in otherwise well subjects over a four-month period. It would have been of interest to have seen the effect of the supplementation on serum concentrations of the vitamin, although measurement of serum retinol alone may not have demonstrated the potential for increased hepatic reserves of the vitamin.

Although many will be aware of the dangers of eating polar bear liver as experienced by early arctic explorers, ² acute intoxication is still reported, often secondary to the ingestion of carnivorous fish livers. ³

Perhaps less well appreciated is the potential for harm by relatively low doses of vitamin A. The first reported case of chronic hypervitaminosis A was reported in 1944 by Josephs, ⁴ in a patient who had ingested in excess of 25,000 IU vitamin A daily over a period of years. There are reports of toxic effects or biochemical abnormalities occurring in patients ingesting only modest quantities [10,000 IU/day].^5,6

Serum retinol measurements do not reflect increasing hepatic stores of vitamin A, with little relationship between hepatic and serum concentrations of the vitamin apart from at the extreme of hepatic concentration. ⁷ Consistently, the importance of measuring serum retinyl esters in the assessment of hepatic vitamin A status is recommended in the literature, both where hypervitaminosis A is suspected either due to ingestion of vitamin A,^6,8 excessive ingestion of carotene ⁹ or even in conditions where malabsorption may be seen as more likely. ¹⁰

Where vitamin A toxicity is being considered as a possible cause for symptoms/laboratory findings, as ever, it is important that the correct analyses are performed including retinyl ester determination.