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12 of 63 (19%) were quite certain that exposure to the sun
was the cause of their melanoma, seven (11%) blamed
sunbed use and 10 more (16%) did not exclude the
possibility that exposure to UV radiation was the cause of
their melanoma (Table 1). Males attributed their melanoma
directly to the sun or sunbeds more often (32%) than
females (22%).
Patients who were more susceptible to the sun (fairskinned, blue eyes, blond hair) and had been sunburned
frequently during childhood and adulthood were more likely
to hold UV radiation responsible for their melanoma. Of
those with skin type 1 and 2, 42% attributed their
melanoma directly to the sun or sunbeds, whereas 43% of
those with skin type 3 and 4 assumed the opposite, with an
odds ratio of 3Æ3 (0Æ9–12Æ1). Comparing patients with a
high level of education and patients with a lower level of
education, 60% vs. 40%, respectively, mentioned UV radiation as a possible cause of their melanoma. Only two of
five patients with melanomas on the most exposed areas of
the body (head and neck) blamed exposure to the sun for
their melanomas. In the category other, one patient
mentioned the Chernobyl incident and two patients mentioned swimming in polluted water as a cause. The latter
received a lot of attention in the media after it was listed as
a risk factor for melanoma in a 1994 Dutch study.4 Four
people assumed that they had a greater risk of developing
melanomas because a relative had had (skin) cancer: a
father with non-melanoma skin cancer, a grandmother with
melanoma, two relatives with cancer of unknown type.
Patient perception of the cause of their melanoma did not
correlate with the reported number of sessions on sunbeds,
tanning habits, or wearing protective clothing when in the
sun. Although most scientists, health educators and physicians assume that melanomas are usually caused by
exposure to the sun, only one-third of patients say that
such exposure could have caused their melanomas; only in
the group with a higher level of education was this
percentage higher (60%). Most patients who blamed exposure to the sun for their melanoma had a sun-sensitive skin
(skin type 1 abd 2) and had suffered more sunburns, during
both childhood and adulthood. In an earlier case–control
study cancer patients held less firm convictions about
causative factors in the aetiology of cancer than did
non-cancer patients and cancer patients listed Gods
will’ and Inherited more often as one of the top four
causes of cancer.5 How can this discrepancy between real
risks and risk perception be explained? Patients may not
like the idea that their behaviour could have caused the
melanoma. By endorsing other explanations that are beyond
their control, they avoid blaming themselves. However,
patients who easily get sunburnt were more familiar with
the harmful effects of the sun and more likely to mention
the sun as a risk factor. People with a less sensitive skin
type may be less familiar with the adverse effects of
UV radiation and therefore assume that exposure to the
sun is harmless, despite the fact that the dangers of
389
exposure to the sun have been reported extensively in the
media.
*Department of Public Health,
Erasmus University Rotterdam,
PO Box 1738, 3000 DR Rotterdam,
the Netherlands
INSERM Unit 453, 28 Rue
Laennec, F-69373 Lyon Cedex 08,
France
CRP Santé, Rue Dicks 18, L-1417,
Luxembourg, Luxembourg
§Department of Surgical Oncology,
Daniël den Hoed Cancer Clinic,
Rotterdam, the Netherlands
–Eindhoven Cancer Registry,
Comprehensive Cancer Centre South,
Eindhoven, the Netherlands
Correspondence: Esther de Vries
E-mail: devries@mgz.fgg.eur.nl
E.DE VRIES*
J . F . D O R É P.AUTIER
A.M.M.EGGERMONT§
J.W.W.COEBERGH*–
FOR THE EORTC
MELANOMA
COOPERATIVE GROUP
References
1 Elwood JM, Jopson J. Melanoma and sun exposure: an overview of
published studies. Int J Cancer 1997; 73: 198–203.
2 Armstrong BK, Kricker A. How much melanoma is caused by sun
exposure? Melanoma Res 1993; 3: 395–401.
3 Autier P, Dore JF. Influence of sun exposures during childhood and
during adulthood on melanoma risk. EPIMEL and EORTC Melanoma Cooperative Group. European Organisation for Research and
Treatment of Cancer. Int J Cancer 1998; 77: 533–7.
4 Nelemans PJ, Rampen FH, Groenendal H et al. Swimming and the
risk of cutaneous melanoma. Melanoma Res 1994; 4: 281–6.
5 Linn MW, Linn BS, Stein SR. Beliefs about causes of cancer in
cancer patients. Soc Sci Med 1982; 16: 835–9.
Chronic onycholysis dramatically responds to
enhanced intake of carotene-rich food
SIR, Onycholysis refers to the detachment of the nail from its
bed at its distal end and ⁄ or its lateral attachments. It may be
associated with a variety of conditions such as psoriasis,
onychomycosis, hyperthyroidism, drug photosensitivity, etc.
Among them, contact and irritant and ⁄ or moisture and
trauma are the most common.1 However, chronic idiopathic
onycholysis is often seen without associated conditions and
there are no reliable therapeutic modalities. Here, we report
two patients with prolonged history of chronic idiopathic
onycholysis that improved dramatically after 12 weeks of
ingestion of carotene-rich food.
A 44-year-old waitress presented with distal separation of
nail plates on all fingers that started 8 years ago and became
more severe in the past 3 years (Fig. 1a). Topical treatment
including clotrimazole, clobetasol propionate, and salicylic
acid ointment produced little effect. There was no known
2002 British Association of Dermatologists, British Journal of Dermatology, 147, 385–410
390
CORRESPONDENCE
Figure 1. (a) A 44-year-old waitress presented with distal nail
separation of different severity in all fingernails; (b) 3 months after
carotene-rich diet, the onycholysis improved dramatically in all
fingernails.
history of psoriasis, autoimmune disorders, anaemia or other
familial nail diseases except for a nodular goitre in euthyroid
status. She denied excessive wet work, use of nail cosmetics or
taking medicine. Examination revealed distal separation of
nail plate of different severity in all fingers. The nail plates
were clean and thin without pitting. The toenails were all
normal. No suspicious psoriatic skin lesions were found on
her scalp or trunk. She was encouraged to ingest a glass of
papaya milk juice, a popular beverage in Taiwan, daily, and
carrots every other day. No other medication was given.
Onycholysis started to improve from the first month. Three
months later, the onycholysis had improved strikingly in all
fingernails (Fig. 1b). Carotenosis could be observed from the
marked yellow skin colour of both palms and all her skin
diffusely. No intolerance was observed during the food
supplement except that the yellowish skin discoloration
aroused the concern of her family and friends. She is now
still on carotene-rich diet but at a lesser dose.
Another patient, a 71-year-old housewife, complained of
distal separation of her fingernails for 1 year. She had
diabetes mellitus and hypertension, under regular medical
control for 4 years. On examination, distal nail onycholysis
was noted in all fingernails. Nail thickening with yellowish
(oil-spot like) colour distally was found in several fingernails
of this patient (Fig 2a,b). Psoriatic nails, although suspected,
could not be further supported owing to the absence of nail
pitting and psoriatic plaques on the trunk and scalp. Her
toenails were also thick but without pitting or onycholysis.
Previous treatment with topical clobetasol dipropionate and
calcipotriol for 6 months had produced little improvement.
Three months after encouraging carotene-rich food intake,
the onycholysis improved visibly in all her fingernails
(Fig 2c,d). She could barely tolerate the taste of carrot and
papaya, so thereafter she continued on a very small amount
of the food additives.
Onycholysis is a disease of heterogeneous aetiology. The
administration of rational treatment strategies for onycholysis relies on the discovery and verification of its causes. Quite
often, however, treatment is not satisfactory, and sometimes
patients have no possibly relevant causes or precipitating
factors. The most important treatment principles proposed for
onycholysis are all passive and preventive.1 They include
elimination of the predisposing causes; strict irritant ⁄ contact
moisture avoidance; keeping the nail short; avoiding trauma
to the nail; and informing the patient in advance that the
healing process is slow, and that all therapy must be followed.
Frequently, the longer the onycholysis is present, the less
likely it is to resolve.2 From our experience, these principles
do little help to patients with onycholysis owing to poor
compliance. To date, an active reliable treatment modality
with consistent effect on onycholysis is lacking.
In our clinic, a patient told us that her prolonged
separation of distal nail plates disappeared since she had
been on a carotene-rich diet several years ago. Although we
were not able to examine her nails to confirm the diagnosis of
onycholysis, we tried carotene-rich food in our two patients
because of its simple feasibility without obvious harmful
effects. These two patients showed dramatic improvement of
onycholysis in 3 months without adhering to the preventive
principles described above. The possibility of spontaneous
healing, while it could not be excluded, may be remote as the
improvement correlated significantly with the encouraged
intake of carotene-rich food. Such a dramatic improvement
had never occurred spontaneously nor been achieved by any
previous treatment measures. The nail improvement in these
two patients in parallel with the food supplements may
suggest a beneficial effect of carotene, presumably the major
component in carrot or papaya.
Carotenoids are natural pigments that are synthesized by
plants and are responsible for the bright colours of various
fruits and vegetables. b-carotene has been best studied as, in
most countries, it is the most common carotenoid in fruits and
vegetables.3 A lower risk of lung cancer has been observed
in individuals who eat more fruits and vegetables that are rich
in carotenoids, and in people who have higher serum
b-carotene. However, high-dose b-carotene supplements associated with an increased risk for lung cancer among smokers
was observed in two human intervention studies.4 Inconsistent results in chemoprevention of skin cancer,5 or decrease
in the risk of coronary heart diseases6 were also observed. The
2002 British Association of Dermatologists, British Journal of Dermatology, 147, 385–410
CORRESPONDENCE
391
Figure 2. (a,b) A 71-year-old housewife
presented with distal nail onycholysis in all
fingernails and subungual thickening with
yellowish colour (oil spot-like) distally in
several fingernails; (c,d) 3 months later, the
onycholysis was strikingly improved in all
fingernails.
puzzle may be explained in that b-carotene itself may act as
an anticarcinogen or antiatherosclerosis agent (both by
reducing free radicals through antioxidation), but its oxidized
products (increased in smokers) may facilitate carcinogenesis.4,6 The benefit reported in some observational studies may
be related to consumption of foods rich in b-carotene rather
than b-carotene itself, as foods rich in b-carotene are usually
also rich in other antioxidant vitamins and micronutrients.6
Regarding the effect on other skin diseases, b-carotene has
been successfully used against photosensitivity in patients
with erythropoietic protoporphyria,7 but it only slightly
increases the sunburn threshold in normal humans. The
photoprotection must therefore work through an alternative
mechanism other than a direct sunscreen effect.8 Actions on
lipid peroxidation pathways may be an important element of
any protection activities it exerts.9 To date, a specific effect
on nail disorders has not been reported. The obvious effect
on onycholysis in these two patients may imply a role of
carotene in sunlight protection of the nail bed or alternatively a role in normal epithelial differentiation or keratinization of the nail plate. Nutritional imbalance or
photosensitivity in the pathogenesis of onycholysis may
therefore be proposed. Both speculations need further studies
for verification.
Carotenaemia after ingestion of carotene-rich food is a
benign condition. It has been proven that hypervitaminosis A
does not occur despite massive doses of carotene because the
conversion of carotene to vitamin A is slow.10 This simple
and practicable fruit intake or additive of carotene-rich food
without significant side-effect seems to be promising for
patients with chronic idiopathic onycholysis. A rough
estimation of the carotene intake in patient 1, who ingested
the recommended food more regularly in the first 6 weeks,
was around 10 mg daily, a level easily obtainable by a
change in diet. A larger scale trial with carotene-rich food
supplement or quantitative intake of specific carotene in nonsmokers to verify its effect on onycholysis is warranted.
Department of Dermatology, College
of Medicine, National Cheng-Kung
University, Tainan, Taiwan
*Department of Dermatology, Tainan
Municipal Hospital, Tainan, Taiwan
Correspondence: Mark Ming-Long
Hsu, MD
E-mail: a441224@mail.ncku.edu.tw
M.M-L.HSU
Y-R.HUANG*
References
1 Daniel CR. Onycholysis: an overview. Semin Dermatol 1991; 10:
34–40.
2 Daniel CR, Daniel MP, Daniel CM et al. Chronic paronychia and
onycholysis: a thirteen-year experience. Cutis 1996; 58: 397–401.
3 Paiva SA, Russell RM. b-carotene and other carotenoids as antioxidants. J Am Coll Nutr 1999; 18: 426–33.
4 Wang XD, Russell RM. Procarcinogenic and anticarcinogenic
effects of b-carotene. Nutr Rev 1999; 57: 263–72.
5 Frieling UM, Schamberg DA, Kupper TS et al. A randomized,
12-year primary-prevention trial of beta-carotene supplementation for nonmelanoma skin cancer in the physician’s health
study. Arch Dermatol 2000; 136: 179–84.
6 Tavani A, La Vecchia C. b-carotene and risk of coronary heart
disease. A review of observational and intervention studies. Biomed Pharmacother 1999; 53: 409–16.
7 Marsden RA, Dawber RP. Erythropoietic protoporphyria with
onycholysis. Proc Roy Soc Med 1977; 70: 572–4.
8 Sayre RM, Black HS. Beta-carotene does not act as an optical filter
in skin. J Photochem Photobiol 1992; 12: 83–90.
9 Bar-Natan R, Lomnitski L, Sofer Y et al. Interaction between betacarotene and lipoxygenase in human skin. Int J Biol Cell Biol
1996; 28: 935–41.
10 Lascari AD. Carotenemia. A review. Clin Pediatr 1981; 20: 25–9.
2002 British Association of Dermatologists, British Journal of Dermatology, 147, 385–410