L E T TE R S
Scurvy and stroke — is there
an association?
Emily Y-J He, Louis W Wang and
Matthew C Kiernan
TO THE EDITOR : We report a case of
ischaemic stroke in a 34-year-old man with
severe vitamin C deficiency caused by poor
nutrition. The patient was a lifelong nonsmoker with no history of hypertension or
hypercholesterolaemia, and no family history
of stroke, although he had recently been
diagnosed with type 2 diabetes mellitus.
At presentation, neurological examination
showed profound left-sided hemiparesis,
with normal sensory examination and visual
fields. Cardiovascular examination was normal, and there were no carotid bruits. The
patient’s body mass index was 25.5 kg/m2.
Magnetic resonance imaging of of his brain
showed acute infarction in the right posterior corona radiata (Box, A).
Coagulation and lipid profiles were normal. Glycosylated haemoglobin was 7.1%.
Comprehensive testing for underlying
thrombophilia, vasculitides and Fabry disease all returned negative results. Computed
tomography angiography and carotid ultrasonography confirmed normal carotid and
v ertebral arteries. Transoesop hageal
echocardiography showed a structurally
normal heart without a source of embolus.
The patient had poor dentition, with calculus deposition, scorbutic gums and gingival inflammation (Box, B), and reported easy
bruising in recent months. Suspecting a
diagnosis of scurvy, we conducted a nutritional assessment of the patient. His diet
consisted mainly of fast food, with negligible
vegetable and fruit intake, and no vitamin
supplementation. For the week before
admission, we determined that his average
vitamin C intake was 4 mg/day. This corresponded to a > 99% probability of inadequate intake when compared with the
estimated average requirement of 30 mg/day
for adults1 (z = − 4.33; P = 0.0015). Laboratory testing confirmed the presence of severe
vitamin C deficiency (< 5 μmol/L; reference
range, 40–100 μmol/L).
The patient was admitted to a stroke
unit, commenced on aspirin, ramipril and
atorvastatin, and received dietary counselling. Vitamin C 1000 mg daily was prescribed for one month. Subsequent testing
confirmed normalisation of his plasma vitamin C. Following inpatient rehabilitation,
he regained motor function and returned to
independent living.
There is growing evidence that vitamin C
deficiency is an important, but largely
unrecognised, risk factor for modification in
patients with cerebrovascular disease.2 Vitamin C is a water-soluble antioxidant that
inhibits oxidation of low-density lipoprotein
and protects against endothelial dysfunction. Primate models have confirmed that
cerebral infarct size is inversely related to
cerebral vitamin C content. 3 Although
scurvy is now relatively rare, subclinical
vitamin C deficiency is not uncommon,
being present in about 10% of the general
population.4 Alcoholics, institutionalised
and elderly people are particularly at risk.
In this case, we hypothesise that an
unhealthy diet resulted in deficiencies in
antioxidants (including vitamin C), and that
this contributed to stroke pathogenesis. The
marked prematurity of disease onset may
have resulted from effect modification of
antioxidant deficiency on conventional
atherosclerotic risk factors (such as diabe-
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L E T TE R S
A: Diffusion-weighted magnetic resonance image of the patient’s brain showing an acute
infarction in the posterior limb of the right corona radiata. B: The patient’s mouth showing
scorbutic gums consistent with scurvy.
tes). A cohort study previously observed the
modifying effect of vitamin C deficiency on
the association between stroke and hypertension.5 However, it is unlikely that a direct
causal link will ever be established. Since
malnutrition and unhealthy eating practices
continue to be serious public health problems, we suggest attention to nutritional
status should be incorporated into the new
standard of stroke care. Perhaps a new adage
should be considered: an orange a day keeps
stroke away?
Acknowledgements: We thank Karen Tokutake,
the stroke unit dietitian at Prince of Wales Hospital,
for her assistance in managing this patient during
his inpatient stay and calculating the patient’s
intake of essential nutrients.
Emily Y-J He, Medical Registrar1
Louis W Wang, Medical Registrar1
Matthew C Kiernan, Professor of Medicine and
Consultant Neurologist1,2
556
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1 Prince of Wales Hospital and Prince of Wales
Clinical School, University of New South
Wales, Sydney, NSW.
2 NeuroScience Research Australia, Sydney,
NSW.
[email protected]
1 Australian Government National Health and Medical Research Council; New Zealand Ministry of
Health. Nutrient reference values for Australia and
New Zealand including recommended dietary
intakes. Canberra: NHMRC, 2006; 119-125.
2 Frikke-Schmidt H, Lykkesfeldt J. Role of marginal
vitamin C deficiency in atherogenesis: in vivo models and clinical studies. Basic Clin Pharmacol Toxicol
2009; 104: 419-443.
3 Ranjan A, Theodore D, Haran P, Chandy MJ. Ascorbic acid and focal cerebral ischaemia in a primate
model. Acta Neurochir (Wien) 1993; 123: 87-91.
4 Hampl JS, Taylor CA, Johnston CS. Vitamin C deficiency and depletion in the United States: the Third
National Health and Nutrition Examination Survey,
1988 to 1994. Am J Public Health 2004; 94: 870-875.
5 Kurl S, Tuomainen TP, Laukkanen JA, et al. Plasma
vitamin C modifies the association between hypertension and risk of stroke. Stroke 2002; 33: 15681573.
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MJA • Volume 193 Number 9 • 1 November 2010