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Hypercarotenaemia is clinically diagnosed by yellowing of the dermal tissue
particularly of the palms and soles but not the sclera of the eye. It is reported in Sri
Lanka particularly, but not exclusively in infants and young children. This study
excludes hypercarotenaemia caused by liver and thyroid pathology and is confined to
the feeding of carotenoid rich foods. In this case there are relatively few subjects who
develop hypercarotenaemia. In Sri Lanka the carotenoid rich foods fed to infants and
children are boiled, carrot, pumpkin and ripe papaw. In the present study an attempt
was made to study hypercarotenaemic serum profiles, time course on serum carotenoid
profiles on cessation of feeding carotenoids, proportion of hypercarotenaemics in the
Westernprovince and the aetiology using animal models.
Hypercarotenaemic subjects (n=36) were tested for carotenes III their serum. The
carotenoids were classified as a and ~ carotenes, monohydroxy metabolites and
polyhydroxy metabolites which varied from 119 ug/dl, to trace amounts, 148.7 ug/dl.
to trace amounts, 214 ug/dl. to non detectable or less than 0.5 ug/dl., 822.7 ug/dl. to
7.0 ug/dl. respectively. It was possible to predict the contribution of carotenoid rich
foodsto the condition by the presence of a-carotene (carrot), ~-cryptoxanthin (papaw).
Therewas no hypervitaminosis due to vitamin A.
Longitudinal studies following withdrawal of carotenoid rich food indicated serum
carotenoid levels declining at slightly varying rates in each individual, while vitamin A levels were more or less maintained, probably due to the liver 15-15' -dioxygenase
activity.
Classically hypercarotenaemia is termed to be genetic or metabolic. However, in types
of hypercarotenaemia studied it can be predicted to be in some way or another due to
genetics. In the present study, identical hypercarotenaemic twins had similar serum
carotenoid profiles which may be due to genetics. However, this needs further studies
with statistically significant number of such twins before it can be confirmed.
Preliminary tests on faeces to study the effect of absorption of carotenoids in the
development of hypercarotenaemia with 08 hypercarotenaemic and 10 nonhypercarotenaemic subjects showed that no a and B carotenes were present (LOD = 0.5
ug/dl.) in hypercarotenaemic patient's faeces while the faeces of the 10 non
hypercarotenaemics showed 1.53 ug/dl. and 0.7Ilg/dL, 1.74 ug/dl. and 1.0 ug/dl., 1.0
ug/dl. and trace amounts, 1.8 ug/dl, and 1.4 ug/dl., 1.2 ug/dl. and 1.0 ug/dl., 1.6
ug/dl. and 0.9 ug/dl., 1.0 ug/dl. and 1.3 ug/dl, and trace amount and 0.7 ug/dl, of B
and a carotenes respectively per one gram of freeze dried faeces. This indicated that
the mechanism responsible for controlling absorption of carotenoids III
hypercarotenaemics to be deranged which again could be due to a genetic factor.
A study in determining the proportion of hypercarotenaemics among pre-school
children aged below 5 years in the Western Province showed that the proportion was
1.5%. However, the proportion of hypercarotenaemiaamong subjects fed carotenoid
rich food was approximately 2%. This observation was made irrespective of vitamin A
mega dosing.
Animal studies were designed originally to determine the bilary excretion product(s) of
carotenoids in hypercarotenaemia induced Wistar rats and ICR mice with the intention of studying the carotenoid metabolism. This was unsuccessful as neither breed, despite
being fed on high carotenoid rich diet, developed hypercarotenaemia. The serum, liver,
adipose tissue around the kidneys, bile (in mice), digesta (in rats) did not show
carotenoids. However both types of rodents had high levels of a and ~ carotenes in the
faeces similar to the human fecal study. This indicates that one natural way of
preventing hypercarotenaemia is by controlling the absorption of carotenoids.
This study proves that the genes responsible for synthesis of proteins which are
responsible for metabolism and/or absorption of carotenoids are not common in the
group studied.
