Report

Oxford, UK
International
IJD
Blackwell
1365-4632
45 Publishing,
Publishing
Journal Ltd,
of
Ltd.
Dermatology
2005

Scurvy: a disease almost forgotten

Olmedo et al.
Scurvy
Report

Jesse M. Olmedo, MD, James A. Yiannias, MD, Elizabeth B. Windgassen, MD, and
Michael K. Gornet, MD

From the Department of Dermatology, Abstract

Division of Regional and International
Medicine, and Division of Hematology/
Oncology, Mayo Clinic, Scottsdale, Arizona
Correspondence
James A. Yiannias, MD
Department of Dermatology
Mayo Clinic
13400 East Shea Boulevard
Scottsdale
AZ 85259
Background Although much decreased in prevalence, scurvy still exists in industrialized
societies. Few recent large studies have examined its pathogenesis, signs, and symptoms.
Methods After we diagnosed scurvy in a 77-year-old female patient in 2003, we conducted a
retrospective records review to identify patients with scurvy treated between 1976 and 2002 at
Mayo Clinic (Scottsdale, Arizona; Rochester, Minnesota; or Jacksonville, Florida). We also
searched the English-language medical literature for published reports on scurvy.
Results In addition to our patient, seven of 11 patients whose records in the institutional
database mentioned vitamin C deficiency were women. The age ranged from a neonate to
77 years (mean, 48 years). The most common associated causes were concomitant
gastrointestinal disease, poor dentition, food faddism, and alcoholism. Vitamin or mineral
deficiencies other than vitamin C deficiency were also found in our patients who had scurvy.
The most common symptoms were bruising, arthralgias, or joint swelling. The most common
signs were pedal edema, bruising, or mucosal changes. Four patients had vague symptoms of
myalgias and fatigue without classic findings, and five had concomitant nutritional deficiencies.
Follow-up available for six of 12 patients treated by vitamin C supplementation showed complete
resolution of symptoms in five.
Conclusions Patients with scurvy may present with classic symptoms and signs or with
nonspecific clinical symptoms and an absence of diagnostically suggestive physical findings.
Concomitant deficiency states occur not uncommonly. Taking a thorough dietary history and
measuring serum ascorbic acid levels should be considered for patients with classic signs and
symptoms, nonspecific musculoskeletal complaints, or other vitamin or mineral deficiencies.

identified by this method, we first describe one patient who

Introduction
Scurvy is a disease historically associated with sailors on
lengthy voyages. Although much decreased in prevalence, the
disease still exists today, even in industrialized societies.
Scurvy occurs as a result of decreased vitamin C consumption
or absorption. We report a case of profound scurvy identified
in a patient treated in 2003 at Mayo Clinic, Scottsdale, Ari-
zona. We then present a retrospective records review of all
patients with scurvy who were treated at Mayo Clinic (Scotts-
dale, Arizona; Rochester, Minnesota; or Jacksonville,
Florida) between 1976 and 2002, and review the medical
literature on scurvy.
Materials and Methods
The medical records of Mayo Clinic patients treated between 1976
and 2002 were searched electronically. Search terms were
diagnoses such as scurvy, ascorbic acid deficiency, vitamin C
deficiency, avitaminosis C, and scorbutus. In addition to patients
presented in 2003 to our clinic. This patient was also included
in our statistical analysis.
Case Report
A 77-year-old woman with a 10-year history of hives that she
attributed to all types of fruits and vegetables presented with
fatigue, bruising, gingival bleeding, and anemia. For the preceding
2 years, the patient’s diet had consisted only of bread, olive
oil, and red meat because of the perceived food allergy. In the
preceding 3–5 months, she had experienced increased fatigue
and extensive bruising on her arms and legs. She had also noticed
a grayish discoloration of her face. For weeks, she had experienced
occasional nosebleeds, bleeding of the gums while brushing
her teeth, and soreness of the tongue. On the day the patient
presented for treatment at our tertiary-care clinic, she noticed
bright red blood from the rectum during a bowel movement.
Her face and “vee” of the neck were noticeably slate gray
(Fig. 1). Her arms and legs demonstrated circumferential, 909

© 2006 The International Society of Dermatology International Journal of Dermatology 2006, 45, 909–913
910 Report Scurvy
Figure 1 Slate gray discoloration of the patient’s face and “vee”
of the neck
Figure 2 Deep, tender, ill-defined nodules (ranging in color from
flesh tones to violaceous) may accompany ecchymotic patches
with perifollicular petechiae and red nonscaling papules
ecchymotic patches with perifollicular petechiae and red
nonscaling papules. Deep, tender, ill-defined, flesh-colored to
violaceous nodules accompanied these lesions (Fig. 2). The
patient’s gums were hypertrophied and tender. The non-
International Journal of Dermatology 2006, 45, 909–913
Olmedo et al.
masticatory mucosa had dilated tortuous vessels. No joint
abnormalities were identified.
Workup revealed normocytic anemia with a hemoglobin
of 8.8 g /dL (reference range, 11.5–15.5 g /dL), hematocrit of
26.4% (reference range, 33.3–43.3%), and mean corpuscu-
lar volume of 86.1 fL (reference range, 82.7–96.8 fL). Iron
studies, prothrombin time, and international normalized
ratio were within normal ranges. A bone marrow biopsy
identified ineffective erythropoiesis. Values for vitamin B12
and folate were within normal ranges, whereas the concentra-
tion of vitamin C was undetectable. The zinc level was
0.56 µg /mL (reference range, 0.66–1.10 µg /mL).
A 6-mm punch biopsy on a violaceous nodule on the left
lower leg showed dermal and subcutaneous hemosiderin
deposition with fibrosis, suggestive of a resolving hematoma.
Findings of an external biopsy specimen from the right neck
were suggestive of ochronosis, and findings of a biopsy
specimen from the right upper alveolus indicated a pyogenic
granuloma.
A diagnosis of scurvy was established and the patient was
started on vitamin C, 100 mg three times a day for 2 weeks,
and then continued on 100 mg a day. Additional information
from the patient about her suspected food allergies revealed
that the urticarial lesions did not cease completely when she
avoided all fruits and vegetables, and so we recommended the
addition of doxepin hydrochloride, 10–20 mg once a day at
bedtime. As the urticarial lesions improved, the patient was
able to expand the types of foods she ate.
The patient was also diagnosed with a concomitant zinc
deficiency that most probably accounted for her sore tongue,
and she was started on oral zinc sulfate, 220 mg twice a day.
After only 3 days of supplementation, the patient had an
increase in the concentration of vitamin C to 0.4 mg /dL (ref-
erence range, 0.6–2 mg /dL), and signs of new bruising and
gingival bleeding resolved. On physical examination, the
ecchymoses, petechiae, and gingival tenderness were also
found to have improved.
Although, clinically, the slate gray pigmentation was
suspicious for pellagra, the patient said that she had been
applying large quantities of topical hydroquinone to her face
for years. This self-treatment seemed to account for her gray
pigmentation and for other histologic features suggestive of
ochronosis.
Results
In addition to our patient, the retrospective records review
identified 11 patients, 10 from Rochester and 1 from Scottsdale,
whose charts made reference to a vitamin C deficiency. Eight
of the overall total of 12 patients were women, and the age
range overall was from a neonate to 77 years (average, 48 years).
The causes of scurvy in the 12 patients included absorption
maladies, such as severe reflux, colitis, strictures, or nonspecific
© 2006 The International Society of Dermatology
Olmedo et al. Scurvy Report 911

Table 1 Pathogenesis of scurvy* Complete resolution of symptoms was noted as early as

Cause No. of patients
Gastrointestinal disease 4 his symptoms and the reason for his lack of response to vita-
Dentition abnormalities 4
Food faddism (avoidance) 5
Alcohol or illicit drug use 4
Concomitant deficiency (e.g. calcium, vitamin B12, iron) 5
Mental disorder 2
Prematurity 1 Scurvy was first described in the Ebers papyrus written about
*n = 12 (individual patients may have had more than one cause
of vitamin C deficiency).
malabsorption, that resulted in an inadequate intake of vita-
min C (Table 1). Poor dentition complicating mastication
also resulted in inadequate vitamin C consumption in four
patients. Alcohol abuse, illicit drug use, and severe mental dis-
orders (e.g. depression or dementia) were related to 10 cases
of vitamin C deficiency. Food faddism or avoidance of prod-
ucts containing vitamin C because of an alleged intolerance or
allergy was present in five patients.
Symptoms and signs
The most common symptoms were bruising, arthralgias, and
joint swelling (Table 2). Four patients, however, exhibited
less common symptoms that included fatigue and myalgias.
The most common signs of vitamin C deficiency were non-
specific pedal edema and bruising (11 patients; Table 2). Also
commonly present was oral mucosal involvement with
petechiae or gingival swelling. Of note, three patients demon-
strated no physical signs suggestive of scurvy, but their his-
tory suggested poor intake of vitamin C, thereby prompting
the physician to screen for its deficiency.
Response to treatment
Six patients had subsequent follow-up that mentioned their
response to vitamin C supplementation. Five patients
responded to vitamin C supplementation (500 mg daily).
1 week and as late as 1 month. One male patient did not
respond to 5 weeks of vitamin C supplementation. Because
this patient was lost to further follow-up, the pathogenesis of
min C supplementation could not be ascertained.
Discussion
1500 bc. Historically, scurvy has been known as an illness
affecting sea voyagers. Between 1500 bc and ad 1800, scurvy
killed more sailors than all other diseases and disasters com-
bined.1 In 1753, Sir James Lind, a ship’s surgeon in the British
Navy, recognized that citrus fruits could prevent and treat
scurvy on long sea voyages. Unfortunately, for many years,
“sea scurvy” was not associated with “land scurvy.”
For example, the Great Famine of Ireland was precipitated
by the failure in 1845 of the crops of potatoes, a rich source
of vitamin C that was the mainstay of the peasants’ diet.
Many deaths from scurvy also occurred during the Crimean
War, the U.S. Civil War, the California gold rush, and the
journey of settlers westward along the Mormon Trail to
Utah. It was not until 1931 that Albert Szent-Györgyi, a bio-
chemist and Nobel laureate, discovered and identified the
antiscorbutic factor in citrus fruits and potatoes. The
antiscorbutic factor was initially called hexuronic acid and
subsequently was renamed vitamin C.1
Vitamin C serves various functions in the human body. It
is responsible for the hydroxylation of collagen, the bio-
synthesis of carnitine and norepinephrine, the metabolism of
tyrosine, and the amidation of peptide hormones. Vitamin C
functions as an antioxidant and is therefore decreased in
oxidative states associated with diabetes, smoking, or myo-
cardial infarction. Vitamin C also promotes iron absorption
by reducing dietary iron from the ferric to the ferrous form.2
It is also important in disulfide bonding of hair.3
The function of vitamin C in collagen synthesis is extremely
important; the abnormality in collagen synthesis is responsible

Table 2 Symptoms and signs of scurvy*

Symptom No. of patients Sign No. of patients

Bruising 5 Pedal edema 5

Arthralgias 5 Bruising 6
Joint swelling 4 Mucosal changes (petechia /gum swelling) 5
Dysphagia 2 Normal examination 3
Nausea 2 Joint swelling 2
Fatigue 3 Alopecia 1
Depression 1 Nail clubbing 1
Myalgias 1 Emesis 1

*n = 12 (individual patients may have had more than one physical examination finding
indicative of vitamin C deficiency).

© 2006 The International Society of Dermatology International Journal of Dermatology 2006, 45, 909–913
912 Report Scurvy
for most manifestations of scurvy. Mature collagen is com-
posed of three polypeptide molecules in a triple helix. The
polypeptides are initially synthesized in the ribosome as
procollagen molecules; the lysyl and prolyl residues are then
hydroxylated using vitamin C as a cofactor. The absence
of hydroxylysyl and hydroxyprolyl residues renders the
polypeptide unstable and unable to self-assemble into rigid
triple helices. This defect in collagen results in blood vessel
fragility and poor wound healing.3
The pharmacokinetics of vitamin C have been studied
extensively. Ascorbic acid is absorbed well at lower doses, but the
percentage of absorption decreases as the dose is increased.
For a 30-mg dose, 87% is absorbed, whereas only 50% of a
1250-mg dose is absorbed. Ascorbic acid is not protein bound,
and is excreted by the kidneys. In healthy persons, vitamin C can
be reabsorbed by the kidneys, but it is lost during hemodialysis,
making patients with end-stage renal disease at particular risk
for scurvy. Circulating white blood cells contain 10 –30 times
the plasma concentration of vitamin C, which concentrates in
the brain, adrenal cortex, liver, spleen, pancreas, and kidney
tissues;2 the mechanism behind this process is not known.
Most animals require no exogenous source of vitamin C;
however, guinea pigs, fruit bats, and humans do not have the
ability to synthesize vitamin C. Humans obtain 90% of their
intake from fruits and vegetables. Cooking reduces vitamin C
content by 20–40%.3 The total body pool of vitamin C is
1500 mg, and clinical manifestations of scurvy occur when
this pool is reduced to less than 350 mg. To reach such a low
level, vitamin C must be completely eliminated from the diet
for 60–90 days. Yet, as little as 6 –10 mg of vitamin C each
day is sufficient to maintain a level of 350 mg. A single orange
contains 50 mg of vitamin C.4 The recommended dietary
allowance for vitamin C was recently increased by the Food
and Drug Administration to 75 mg per day for women and
90 mg per day for men. Notably, the vitamin C intake in 2001
was less than 60 mg in 20 –30% of US adults, a level that can
result in subclinical vitamin C deficiency.2
Scurvy occurs because of reduced intake or absorption of
vitamin C. At-risk groups include the poor (because of
reduced access to groceries), food faddists, widowers, and
individuals with purported allergies to multiple fruit and
vegetable products. Other at-risk groups include persons with
gastrointestinal disease (e.g. colitis), anatomical abnormali-
ties, or poor dentition. Cancer patients on chemotherapy who
have increased nausea and diarrhea are also at risk, as are
patients on hemodialysis. Psychiatric disorders (e.g. depres-
sion, schizophrenia, or anorexia) have also been recognized
as putting patients at risk for reduced intake of vitamin C.
Alcoholic persons represent one of the largest groups at risk
for scurvy because they may have poorly balanced diets and
because alcohol decreases the absorption of vitamin C.3
Patients with scurvy exhibit various systemic manifesta-
tions. Severe constitutional symptoms (e.g. weakness, fatigue,
International Journal of Dermatology 2006, 45, 909–913
Olmedo et al.
or myalgias) may be secondary to anemia, which develops in
75% of patients because of blood loss, concomitant folate
deficiency, or altered iron absorption. The anemia is most
commonly normochromic normocytic.5 Myalgias occur
because of the reduced production of carnitine.6
Scurvy causes changes in the skin as a result of defective
collagen synthesis. Classic changes on the legs and buttocks,
where hydrostatic pressure is greatest, are hyperkeratotic
papules with corkscrew hairs and perifollicular hemorrhage.
Petechiae becoming confluent into large ecchymoses and
even palpable purpura may occur on the lower legs because
of blood vessel fragility. The legs can become edematous
because of soft tissue hemorrhage or heart failure secondary
to anemia. The nails may develop splinter hemorrhages.
Alopecia can occur because of defective disulfide bonding.
Because of defective collagen production, wounds heal poorly
and even old scars can break down.3
Patients with scurvy may also develop oral complications.
The gingivae often bleed with minor trauma. The gums
become red, smooth, swollen, and shiny. Eventually, the
gums may recede or become necrotic. As alveolar bone
absorption occurs, tooth loss may occur.3
Rheumatologic problems, such as painful hemarthrosis
and subperiosteal hemorrhage, may develop in persons with
scurvy. Subperiosteal hemorrhage in infants may cause
Barlow syndrome, which is associated with extreme pain and
an immobilized posture (hips and knees in semiflexion).5
Scurvy can also have an impact on the heart. Cardiac
enlargement may occur because of congestive heart failure
secondary to high-output anemia. Hemopericardium result-
ing in sudden death has been reported.5
Ophthalmic manifestations include conjunctival hemor-
rhage and fundus changes, including flame-shaped hemor-
rhages and cotton-wool spots. Bleeding into the retrobulbar
space and into the optic nerve sheaths can cause papilledema
and optic nerve atrophy. Sjögren-like symptoms have also
been noted.3
The diagnosis of scurvy is generally based on clinical fea-
tures and dietary history, and there is rapid resolution of signs
and symptoms after vitamin C supplementation. Laboratory
investigations may not be necessary to diagnose scurvy, but
are useful to confirm less typical cases. The concentration of
ascorbic acid may be checked, but this value tends to reflect
recent dietary intake rather than actual vitamin C.5 A serum
level below 11 µmol/L suggests scurvy.6 A leukocyte ascor-
bate level more accurately reveals tissue stores of vitamin C,
but the test is difficult to perform and not readily available.5
An ascorbic acid tolerance test can be used to assess vitamin
C status. The test is simple to administer and suitable for
patients. It involves giving an oral load of 1 g of ascorbic acid
in water and then measuring the urinary excretion of vitamin
C during the next 6 hours.7 Biopsy of a follicular lesion
characteristically shows a dilated hair follicle with keratin
© 2006 The International Society of Dermatology
Olmedo et al.
plugging and perifollicular hemorrhage. Occasionally, a cork-
screw hair may be found;6 however, biopsy specimens of lesions,
such as the hemorrhagic cutaneous lesions of our patient, may
be nonspecific (e.g. showing only hemorrhage and fibrosis).
The treatment of scurvy involves increased vitamin C
intake. Correcting the deficit and repleting body stores
requires 100 mg three times daily. Subjective improvement in
fatigue, pain, and anorexia typically occurs within 24 hours.
Joint swelling resolves in days. The ecchymoses resolve in 1–
2 weeks. By 4 weeks, the corkscrew hairs regain normal
growth. The gums heal within 1–2 weeks, and complete
recovery occurs after about 3 months of treatment.3
Our study clearly shows that scurvy continues to exist,
even in industrialized nations such as the USA. Our findings
also indicate that decreased vitamin C consumption can be
associated with gastrointestinal disease, poor dentition, food
faddism, alcoholism, or mental disorders such as major
depression. Thus, a thorough dietary review to detect both
clinical and subclinical cases of scurvy should be part of every
review of systems.
The patients in our study reported the classic symptoms of
scurvy, including bruising, arthralgias, and joint swelling.
They also demonstrated the classic signs of vitamin C defi-
ciency (e.g. pedal edema, ecchymoses, friability of the gums,
and occasional joint swelling). Our study also identified
several nonspecific findings, including the absence of classic
physical examination findings of scurvy and the presence of
concomitant deficiency states.
Of these 12 patients, three (25%) had normal physical
examinations, yet described symptoms of vitamin C defi-
ciency (e.g. arthralgias, myalgias, or fatigue). These non-
specific musculoskeletal symptoms can be explained by the
importance of vitamin C, not only in the hydroxylation of
collagen but also in many other functions, such as carnitine
synthesis and iron absorption. Our findings suggest that
© 2006 The International Society of Dermatology
Scurvy Report 913
screening for vitamin C deficiency by dietary history and,
possibly, by evaluating serum ascorbic acid levels should be
considered for patients with classic signs and symptoms of
scurvy, as well as for those with common, nonspecific,
chronic musculoskeletal complaints.
Concomitant nutritional deficiencies were also identified
in this study population. Five (42%) of the 12 patients had
concomitant deficiencies in calcium, vitamin B12, or iron. We
therefore recommend screening broadly for other nutritional
deficiencies in patients identified with vitamin C deficiency.
Specifically, screening should include vitamin B12, folate, iron,
and zinc levels. The corollary of this concept is that clinicians
should be aware of possible vitamin C deficiency when defi-
ciencies in other minerals or vitamins are identified.
All physicians should be aware of the clinical presentations
of vitamin C deficiency, because the presentation of the patient
with scurvy may be subtle. Recognizing the disease requires
heightened vigilance; however, when patients with scurvy are
diagnosed early, the condition can be readily treated.
References
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2 Padayatty SJ, Levine M. New insights into the physiology and
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3 Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad
Dermatol 1999; 41: 895–906.
4 Ghorbani AJ, Eichler C. Scurvy. J Am Acad Dermatol 1994;
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5 Wong JJ, Laumann A. Scurvy. Emedicine 2002.
6 Nguyen RT, Cowley DM, Muir JB. Scurvy: a cutaneous
clinical diagnosis. Australas J Dermatol 2003; 44: 48–51.
7 Neale RJ, Lim H, Turner J, et al. The excretion of large
vitamin C loads in young and elderly subjects: an ascorbic
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International Journal of Dermatology 2006, 45, 909–913