deficiencies because of an inadequate intake, impaired
vitamin synthesis or malabsorption in disease states such as
cysticfibrosis and Crohn’s disease.
The use of vitamins as general‘pick-me-ups’is of
unproven value and, the‘fad’for mega-vitamin therapy with
water-soluble vitamins, such as ascorbic acid p. 629 and
pyridoxine hydrochloride p. 627 , is unscientific and can be
harmful. Many vitamin supplements are described as
‘multivitamin’but few contain the whole range of essential
vitamins and many contain relatively high amounts of
vitamins A and D. Care should be taken to ensure the correct
dose is not exceeded.
Dietary reference values for vitamins are available in the
Department of Health publication:
Dietary Reference Values for Food Energy and Nutrients
for the United Kingdom: Report of the Panel on Dietary
Reference Values of the Committee on Medical Aspects of
Food Policy.Report on Health and Social Subjects 41. London:
HMSO, 1991.
Dental patients
It is unjustifiable to treat stomatitis or glossitis with
mixtures of vitamin preparations; this delays diagnosis and
correct treatment.
Most patients who develop a nutritional deficiency despite
an adequate intake of vitamins have malabsorption and if
this is suspected the patient should be referred to a medical
practitioner.Vitamin A
Deficiency of vitamin A (retinol) p. 626 is associated with
ocular defects (particularly xerophthalmia) and an increased
susceptibility to infections, but deficiency is rare in the UK
(even in disorders of fat absorption).
Vitamin A supplementation may be required in children
with liver disease, particularly cholestatic liver disease, due
to the malabsorption of fat soluble vitamins. In those with
complete biliary obstruction an intramuscular dose once a
month may be appropriate.
Preterm neonates have low plasma concentrations of
vitamin A and are usually given vitamin A supplements,
often as part of an oral multivitamin preparation once
enteral feeding has been established.Vitamin B group
Deficiency of the B vitamins, other than vitamin B 12 ,israre
in the UK and is usually treated by preparations containing
thiamine (B 1 )p. 628 , and riboflavin (B 2 ). Other members (or
substances traditionally classified as members) of the
vitamin B complex such as aminobenzoic acid, biotin,
choline, inositol nicotinate, and pantothenic acid or
panthenol may be included in vitamin B preparations, but
there is no evidence of their value as supplements; however,
they can be used in the management of certain metabolic
disorders. Anaphylaxis has been reported with parenteral B
vitamins.
As with other vitamins of the B group, pyridoxine
hydrochloride (B 6 )deficiency is rare, but it may occur during
isoniazid p. 367 therapy or penicillamine p. 616 treatment in
Wilson’s disease and is characterised by peripheral neuritis.
High doses of pyridoxine hydrochloride are given in some
metabolic disorders, such as hyperoxaluria, cystathioninuria
and homocystinuria; folic acid p. 574 supplementation may
also be beneficial in these disorders. Pyridoxine
hydrochloride is also used in sideroblastic anaemia. Rarely,
seizures in the neonatal period or during infancy respond to
pyridoxine hydrochloride treatment; pyridoxine
hydrochloride should be tried in all cases of early-onset
intractable seizures and status epilepticus. Pyridoxine
hydrochloride has been tried for a wide variety of other
disorders, but there is little sound evidence to support the
claims of efficacy.A number of mitochondrial disorders may respond to
treatment with certain B vitamins but these disorders require
specialist management. Thiamine is used in the treatment of
maple syrup urine disease, mitochondrial respiratory chain
defects and, together with riboflavin, in the treatment of
congenital lactic acidosis; riboflavin is also used in glutaric
acidaemias and cytochrome oxidase deficiencies; biotin is
used in carboxylase defects.
Folic acid and vitamin B 12 are used in the treatment of
megaloblastic anaemia. Folinic acid p. 555 (available as
calcium folinate) is used in association with cytotoxic
therapy.Vitamin C
Vitamin C (ascorbic acid) therapy is essential in scurvy, but
lessflorid manifestations of vitamin C deficiency have been
reported. Vitamin C is used to enhance the excretion of iron
one month after starting desferrioxamine mesilate p. 578
therapy; it is given separately from food as it also enhances
iron absorption. Vitamin C is also used in the treatment of
some inherited metabolic disorders, particularly
mitochondrial disorders; specialist management of these
conditions is required.
Severe scurvy causes gingival swelling and bleeding
margins as well as petechiae on the skin. This is, however,
exceedingly rare and a child with these signs is more likely to
have leukaemia. Investigation should not be delayed by a
trial period of vitamin treatment.
Claims that vitamin C ameliorates colds or promotes
wound healing have not been proved.Vitamin D
The term Vitamin D is used for a range of compounds
including ergocalciferol (calciferol, vitamin D 2 )p. 634 ,
colecalciferol (vitamin D 3 )p. 631 , dihydrotachysterol,
alfacalcidol ( 1 a-hydroxycholecalciferol) p. 630 , and calcitriol
( 1 , 25 - dihydroxycholecalciferol) p. 631.
Asymptomatic vitamin D deficiency is common in the
United Kingdom; symptomatic deficiency may occur in
certain ethnic groups, particularly as rickets or
hypocalcaemia, and rarely in association with
malabsorption. The amount of vitamin D required in infancy
is related to the stores built upin-uteroand subsequent
exposure to sunlight. The amount of vitamin D in breast milk
varies and some breast-fed babies, particularly if preterm or
born to vitamin D deficient mothers, may become deficient.
Most formula milk and supplement feeds contain adequate
vitamin D to prevent deficiency.
Simple, nutritional vitamin D deficiency can be prevented
by oral supplementation of ergocalciferol (calciferol, vitamin
D 2 ) or colecalciferol (vitamin D 3 ) daily, using multi-vitamin
drops, preparations of vitamins A and D, manufactured
‘special’solutions, or as calcium and ergocalciferol tablets
(although the calcium and other vitamins in supplements are
unnecessary); excessive supplementation may cause
hypercalcaemia.
Inadequate bone mineralisation can be caused by a
deficiency, or a lack of action of vitamin D or its active
metabolite. In childhood this causes bowing and distortion
of bones (rickets). In nutritional vitamin D deficiency rickets,
initial high doses of ergocalciferol or colecalciferol should be
reduced to supplemental doses after 8 – 12 weeks, as there is
a significant risk of hypercalcaemia. However, calcium
supplements are recommended if there is hypocalcaemia or
evidence of a poor dietary calcium intake. A single large dose
of ergocalciferol p. 634 or colecalciferol p. 631 can also be
effective for the treatment of nutritional vitamin D
deficiency rickets.
Poor bone mineralisation in neonates and young children
may also be due to inadequate intake of phosphate or
calcium particularly during long-term parenteral nutrition—624 Vitamin deficiency BNFC 2018 – 2019
Blood and nutrition9