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Exploration of "Alternative" and "Natural" Drugs in Dermatology
Cheryl Levin, BA;
Howard Maibach, MD
Arch Dermatol. 2002;138:207-211.
ABSTRACT
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Objective To review some of the promising natural remedies within dermatology
to explore their potential clinical benefit in supplementing conventional
drugs.
Data Sources MEDLINE searches from January 1966 through October 2000 and Science
Citation Index searches from January 1974 through October 2000 were conducted.
Study Selection Primary importance was given to in vivo and in vitro controlled studies,
the results of which encourage further exploration.
Data Extraction The controls used, the statistical approach to analysis, and the validity
of the experimental method analyzed were considered particularly important.
Data were independently extracted by multiple observers.
Data Synthesis Natural remedies seem promising in treating a wide variety of dermatologic
disorders, including inflammation, phototoxicity, psoriasis, atopic dermatitis,
alopecia areata, and poison oak.
Conclusions The alternative medications presented seem promising, although their
true effects are unknown. Many of the presented studies do not allow deduction
of clinical effects. Further experimentation must be performed to assess clinical
benefit.
INTRODUCTION
RECENTLY, ALTERNATIVE remedies have been investigated to supplement
traditional drugs. We performed a literature search to highlight recently
reported medicaments. Emphasis was placed on studies that followed the evidence-based
dermatology guidelines.1-2
METHODS
MEDLINE searches from January 1966 through October 2000 and Science
Citation Index searches from January 1974 through October 2000 were conducted.
Boolean searches relating to skin, allopathic remedies, herbal extracts, glycolic
acid, and vitamins were conducted. Specific diseases and therapies were searched
as title words or key words.
RESULTS
Alternative medications and their potential clinical uses from human
studies and animal and in vitro studies3-24
are summarized in Table 1.
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Alternative Medications and Their Potential Clinical Uses*
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TEA EXTRACTS
Ultraviolet solar radiation may induce a variety of adverse effects
in humans, including melanoma,25 photoaging
of the skin,26-27 sunburn,28 and immunosuppression.29-30
Protection against UV-induced skin damage includes avoidance of sun exposure,
application of sunscreens, low-fat diets,31-32
and pharmacologic intervention with retinoids.33
More recently, green tea extracts have been reported to be beneficial in treating
UV-induced photodamage.
In a study by Elmets et al,6 1% to 10%
green tea polyphenolic (GTP) fractionsin ethanol and water vehicle were applied
onto the backs of 6 volunteers. Thirty minutes after GTP application, patients
were exposed to twice the minimal erythema dose of UV radiation from a solar
simulator. The minimal erythema dose was determined for each patient by exposing
skin to graded doses of UV radiation from the solar simulator. Green tea extracts
resulted in a dose-dependent reduction of UV-induced erythema as measured
by chromatometry and visual evaluation. The (-)-epigallocatechin-3-gallate
and (-)-epicatechin-3-gallate polphenolic fractions were most effective, while
the (-)-epigallocatechin (EGC) and (-)-epicatechin fractions had little effect.
Histologic examination showed a decrease in sunburn cells in GTP-treated skin.
Epidermal Langerhans cells, the antigen-presenting cells involved in the skin
immune response, were significantly protected against UV damage. Finally,
GTP fractions reduced UV-induced mutations in DNA, as detected by means of
a phosphorus 32 postlabeling technique. Spectrophotometric analysis indicated
that GTP fractions did not absorb UV-B light, implying a mechanism of action
different from that of sunscreens. This study demonstrates the potential benefit
of GTP extracts in preventing UV-induced immunosuppression and erythema.
The use of GTP extracts was also found to be beneficial in treating
UV-induced immunosuppression in mice. The GTP extracts, fruits and vegetables,
and quercetin and chrysin significantly prevented the UV-induced suppression
of contact hypersensitivity to picryl chloride when compared with irradiated,
untreated control (P<.05). Increased ear thickness
measurements were used to evaluate the response. The GTP was administered
in concentrations of 0.1% and 0.01%.17 Green
tea extracts have been beneficial in preventing early signs of photochemical
damage to mouse and human skin treated with psoralen–UV-A therapy. Psoralen–UV-A,
a treatment for psoriasis, increases the patient's risk of developing melanoma
and squamous cell carcinoma. Pretreatment and posttreatment with the green
tea extracts in mouse and human skin significantly decreased markers of this
photochemical damage, namely hyperplasia and hyperkeratosis, c-fos and p53,
and erythema, (P<.05), when compared with vehicle
controls (water given before and after treatment).34
The effects of green tea on skin are further discussed by Katiyar et al.35
Oral and topical standardized black tea extracts also decreased photochemical
damage to the skin. In one study, standardized black tea extracts significantly
reduced erythema and skinfold thickness associated with UV-B–induced
carcinogenesis in cultured keratinocytes and mouse and human skin (P<.05). In topically treated mice, a 64% reduction in severity of
erythema and a 50% decrease in skinfold thickness were observed when compared
with vehicle control. A decrease in the expression of c-fos, c-jun, and p53
in mouse skin and keratinocytes pretreated with standardized black tea extracts
was also noted. This study indicates that when green tea is oxidized to black
tea, the extracts remain beneficial in preventing the early signs of UV-B–induced
phototoxic effects, namely, sunburn and skin thickness.18
OTHER HERBS
Tea produced from the leaves of the Eucommia ulmoides OLIVER tree (EUOL) is commonly consumed in China, Korea, and Japan.
Geniposidic acid, a main component of EUOL, seems beneficial in improving
some of the signs of aging in model rats. Falsely aged model rats fed a diet
consisting of a 2.4% water-soluble methanol extract of EUOL had a statistically
significant increased stratum corneum turnover rate compared with rats fed
a comparable diet without the EUOL. In a similar experiment, rats fed geniposidic
acid also had improved stratum corneum turnover. With aging, the stratum corneum
turnover rate decreases, suggesting that EUOL and, specifically, geniposidic
acid may alter the aging process.22
Benzoyl peroxide (BPO) is a free radical–generating compound and
strong oxidizer. It is commonly used as a polymerization initiator,36 an additive in cosmetics,37
and a bleaching agent for flour and cheese.38
Spearmint may abrogate the effects of BPO-induced tumor promotion.
In a recent study, pretreatment with spearmint (Mentha
spicata) induced a statistically significant decrease in the BPO oxidative
damage, toxic effects, and cellular hyperproliferation in adult female albino
mice when compared with the BPO-treated control group. Topical spearmint extracts
salvaged the levels of antioxidant enzymes glutathione peroxidase, glutathione
reductase, glutathione S-transferase, and catalase
that are reduced by BPO treatment alone. The BPO-elevated microsomal lipid
peroxidation and hydrogen peroxide generation were significantly reduced with
spearmint pretreatment. Furthermore, spearmint significantly decreased markers
for cellular DNA synthesis, namely ornithine decarboxylase activity and thymidine
uptake, as compared with BPO treatment alone. Analysis was performed on excised
mouse skin.20
HYDROXYACIDS
Topical  -lipohydroxyacid (-LHA), a derivative of salicylic
acid, improved some of the manifestations of aging in women by inducing a
statistically significant epidermal thickening and dendrocytic hyperplasia.
Both the younger and elder populations exhibited improvement, but the changes
were more diverse in the older women. When compared with placebo, 6% of the
young and 16% of the elderly population experienced increased filaggrin layer
thickness. Further studies are needed to understand the mechanism of hydroxyacid
action and, thereby, their full effect on aging skin.7
ESSENTIAL FATTY ACIDS
Patients with atopic dermatitis (AD) are thought to have a reduced rate
of conversion from linoleic acid to  -linolenic acid (GLA), dihomo--linolenic
acid, or arachidonic acid as compared with healthy subjects.39-42
Replacement of GLA, in the form of primrose oil or borage oil, may therefore
benefit in the treatment of these patients.
In fact, more than 20 randomized controlled studies assessing the effects
of GLA have been performed, with most studies indicating an improved epidermal
barrier on GLA application.8-9,40, 43-49
In one recent study, topical application of 20% evening primrose oil caused
a statistically significant stabilizing effect on the epidermal barrier in
patients with AD as evaluated by transepidermal water loss and stratum corneum
hydration. When compared with placebo, the water-in-oil emulsion of primrose
oil proved effective, whereas the amphiphilic emulsion did not, emphasizing
the importance of the vehicle.9 In addition,
borage oil, which contains a large quantity of GLA, improved pruritus, erythema,
vesiculation, and oozing in atopic patients when compared with placebo-treated
patients (P<.05). Patients were given 40 drops
of borage oil twice daily for 12 weeks; dermatologists and patients visually
assessed the signs.8
In contrast, 2 important studies did not observe a significant clinical
effect of GLA on AD compared with placebo. In studies by Bamford et al10 and Berth-Jones and Graham-Brown,11
evening primrose oil capsules did not improve erythema, excoriation, and lichenification
clinical scores, as evaluated by dermatologists and patients.
Meta-analysis of all previous randomized placebo-controlled studies
indicated a significant difference between treatment and placebo groups.12-13 Critics of the meta-analysis claim
that it included unpublished trials and inadequate baseline data in terms
of disease severity.11 Apparent differences
in response between placebo and treatment groups may result from a greater
severity at baseline in subjects receiving active treatment.11, 50
Treatment of AD with GLA remains controversial.
ESSENTIAL OILS
Other essential oils have been investigated in treating IgE-mediated
allergic reactions as well as alopecia areata. Mice and rats pretreated with
lavender oil inhibited mast cell degranulation, indicating that the oil could
inhibit immediate-type allergic reactions. Topical and intradermal lavender
oil inhibited the ear swelling response in mice and passive cutaneous anaphylaxis
in rats when compared with isotonic sodium chloride solution control treatment
(P<.05). Peritoneal mast cells were also inhibited
from releasing histamine or tumor necrosis factor  in vitro when lavender
oil was applied.24
Alopecia areata was treated with 7 months of aromatherapy. A mixture
of thyme, rosemary, lavender, and cedarwood essential oils in jojoba and grape
seed carrier oils massaged into patients' scalps significantly improved the
alopecia when compared with the carrier oils alone. The efficacy of the treatment
was evaluated at initial assessment and 3 and 7 months after treatment by
dermatologists' visual scoring of photographs and a computerized analysis
of traced areas of alopecia.14 This study did
not mention disease duration before aromatherapy treatment. Half of patients
with recent-onset alopecia areata have remission within 1 year, which could
account for the aromatherapy's putatively beneficial results.51
ASCORBIC ACID AND VITAMIN E
The hydrophobic ascorbic acid and lipophilic vitamin E have found increasing
use in dermatologic treatment. Several studies investigated the effects of
both ascorbic acid and vitamin E against oxidative stress. In mice, acute
and chronic UV-B–induced photodamage was significantly decreased with
intraperitoneal postadministration of magnesium-L-ascorbyl phosphate (MAP),
a precursor to ascorbic acid (P<.05). Compared
with irradiated, untreated mice, MAP-treated mice had a 60% decrease in UV-B–induced
tumor formation, a 50% decrease in skin thickness, and a 55% decrease in ornithine
decarboxylase, a marker for DNA synthesis. In addition, on acute exposure
to UV-B irradiation, MAP prevented increases of lipid peroxidation in skin
and sialic acid in serum. The MAP produced an immediate and transient increase
in vitamin C in the serum, skin, and liver, indicating its conversion in those
tissues.19 The effect of topical application
of MAP in reducing UV-B photodamage is unknown. The clinical significance
of this study remains uncertain.
Oral ingestion of ascorbic acid (2000 mg/d) and vitamin E (1000 IU/d)
reduced the sunburn reaction in human subjects. The volunteers' threshold
dose for eliciting sunburn and their cutaneous blood flow of skin irradiated
with incremental UV doses were determined before and after 8 days of treatment.
A statistically significant difference was observed in the median minimal
erythema dose of ascorbic acid– and vitamin E–treated patients
as compared with placebo-treated patients. The former minimal erythema dose
increased 17%; the latter declined 14%.4
Topical pretreatment in humans with a combination of ascorbic acid,
vitamin E, and melatonin provided a statistically significant enhanced photoprotection
against UV-induced erythema. Dermal blood flow, visual grade, and chromatometry
measures decreased with the combined treatment, as well as with each treatment
alone, when compared with placebo-treated skin. The effect of the combined
treatment was more pronounced.5
Ascorbic acid and vitamin E have also proved beneficial in treating
other conditions. Nitrate tolerance describes a developed tolerance to the
vasodilatory effects of nitrate, due to both neurohormonal counterregulation
and enhanced response to vasoconstrictor agonists.52
Oral administration of two 500-mg ascorbic acid capsules daily along with
glycerol trinitrate for 3 days prevented nitrate tolerance in healthy volunteers
taking transdermal glycerol trinitrate. With those taking ascorbic acid, the
vasodilatory and conductivity responses evoked by glycerol trinitrate were
potentiated throughout the 3-day period (24.5% increase vs control), while
in those taking glycerol trinitrate alone, the responses slowly declined (8.2%
increase vs control).3 This observed effect
was statistically significant.
A combination of vitamin E, sodium pyruvate, and membrane-stabilizing
fatty acids induced a statistically significant decrease in the lesion development,
duration, and severity of genital herpes simplex virus when applied after
infection to guinea pigs and mice. The combined treatment yielded a 36% decrease
in lesion severity score in guinea pigs and a 33% decrease in lesion size
in hairless mice when compared with no treatment.21
MISCELLANEOUS
Quaternium-18 bentonite, an organoclay used in cosmetics to thicken
or stabilize the products, has been investigated for its ability to prevent
poison ivy or poison oak contact dermatitis reactions in humans. Pretreatment
with 5% quaternium-18 bentonite lotion on the forearm of patients with allergic
contact dermatitis to poison oak or poison ivy significantly reduced or prevented
a severe reaction to urushiol, the allergenic resin of both plants. Trained
technicians blinded to the treated area visually evaluated the reactions.
Statistical significance was found when treated test sites were compared with
untreated controls.15
Pretreatment with diluted homeopathic gels effectively decreased the
inflammation caused by methyl nicotinate in humans. The vasodilatory response
to methyl nicotinate was measured by laser Doppler velocimetry. This measure
was significantly reduced when the skin was pretreated with Urtica urens, Apis mellifica, Belladonna, or Pulsatilla aqueous gels as
compared with vehicle control.16 It is important
to note that methyl nicotinate inflammation is primarily a pharmacologic effect
and has few immunologic implications, thereby minimizing the clinical significance
of this study.
Capsular polysaccharides from various strains of cyanobacteria were
found to have anti-inflammatory effects on adult albino male mice. Six-hour
application of hydrophilic extracts of capsular polysaccharides subsequent
to croton oil–induced dermatitis caused a statistically significant
reduction in the mouse ear edema when compared with croton oil inflammation
without treatment. Some strains were not effective, and at least 1 other strain
of capsular polysaccharides significantly increased the edema after croton
oil application by about 29%. The most effective inflammation-reducing strains
decreased the edema by as much as 56%, were dose-dependent, and were composed
primarily of neutral sugars, uronic acids, and proteins. The inflammation-increasing
extract contained a monosaccharide composition (glucose and mannose) similar
to those of extracts that most significantly decreased dermatitis.23
COMMENT
The sampling of investigative medications presented by this review seems
promising, although their true effects are unknown. Caution must be used when
animal studies are interpreted. In addition, experimental design, such as
sample size, drug concentration, method of exposure to the medicine, and analytic
techniques, may greatly influence a study's outcome. Further exploration of
these medications under different experimental conditions would better estimate
their true clinical benefit. Certainly, the lower cost, wide accessibility,
and possible clinical improvement with many of these newer unconventional
remedies has encouraged their continued research. It remains to be seen which,
if any, provide a more advantageous therapeutic ratio than standard agents.
These observations presumably are valid, thoughtful, and correct; as in the
case of most pharmacologic arenas, the final arbiter is the patient. Alas,
these patient truths are unfortunately not as hard a science as most physicians
would like.
AUTHOR INFORMATION
Accepted for publication July 31, 2001.
Corresponding author: Howard Maibach, MD, Department of Dermatology,
UCSF Medical Center, 90 Medical Center Way, Room 110, San Francisco, CA 94143
(e-mail: himjlm{at}itsa.ucsf.edu).
From the University of California–San Francisco Medical Center.
REFERENCES
| |
1. Bigby M. Evidence-based medicine in dermatology. Dermatol Clin. 2000;18:261-276.
FULL TEXT
|
ISI
| PUBMED
2. Bashir S, Maibach H. Evidence Based Dermatology. Toronto, Ontario: BC Dekker. In press.
3. Bassenge E, Fink N, Skatchkov M, Fink B. Dietary supplement with vitamin C prevents nitrate tolerance. J Clin Invest. 1998;102:67-71.
ISI
| PUBMED
4. Eberlein-Konig B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid
(vitamin C) and d--tocopherol (vitamin E). J Am Acad Dermatol. 1998;38:45-48.
FULL TEXT
|
ISI
| PUBMED
5. Dreher F, Gabard B, Schwindt D, Maibach H. Topical melatonin in combination with vitamins E and C protects skin
from ultraviolet-induced erythema: a human study in vivo. Br J Dermatol. 1998;139:332-339.
FULL TEXT
|
ISI
| PUBMED
6. Elmets C, Singh D, Tubesing K, Matsui M, Katiyar S, Mukhtar H. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. J Am Acad Dermatol. 2001;44:425-432.
FULL TEXT
|
ISI
| PUBMED
7. Avila-Camacho M, Montastier C, Perard GE. Histometric assessment of the age-related skin response to 2-hydroxy-5-octanoyl
benzoic acid. Skin Pharmacol Appl Skin Physiol. 1998;11:52-56.
FULL TEXT
|
ISI
| PUBMED
8. Andreassi M, Forleo P, Lorio AD, Masci S, Abate G, Amerio P. Efficacy of -linolenic acid in the treatment of patients with
atopic dermatitis. J Int Med Res. 1997;25:266-274.
ISI
| PUBMED
9. Gehring W, Bopp R, Rippke F, Gloor M. Effect of topically applied evening primrose oil on epidermal barrier
function in atopic dermatitis as a function of vehicle. Arzneimittelforschung. 1999;49:635-642.
PUBMED
10. Bamford J, Gibson R, Reiner C. Atopic eczema unresponsive to evening primrose oil (linoleic and -linolenic
acids). J Am Acad Dermatol. 1985;13:959-965.
ISI
| PUBMED
11. Berth-Jones J, Graham-Brown R. Placebo-controlled trial of essential fatty acid supplementation in
atopic dermatitis. Lancet. 1993;341:1557-1560.
FULL TEXT
|
ISI
| PUBMED
12. Morse PH, Horrobin DF, Manku MS, et al. Meta-analysis of placebo-controlled studies of the efficacy of Epogam
in the treatment of atopic eczema. Br J Dermatol. 1989;121:75-90.
ISI
| PUBMED
13. Stewart J, Morse P, Moss M, et al. Treatment of severe and moderately severe atopic dermatitis with evening
primrose oil (Epogam). J Nutr Med. 1991;2:9-15.
14. Hay I, Jamieson M, Ormerod A. Randomized trial of aromatherapy: successful treatment for alopecia
areata. Arch Dermatol. 1998;134:1349-1352.
FREE FULL TEXT
15. Marks J, Fowler J, Sherertz E, Rietschel R. Prevention of poison ivy and poison oak allergic contact dermatitis
by quaternium-18 bentonite. J Am Acad Dermatol. 1995;33:212-216.
FULL TEXT
|
ISI
| PUBMED
16. Handschuh J, Debray M. Modification of cutaneous blood flow by skin application of homeopathic
anti-inflammatory gels. STP Pharma Sci. 1999;9:219-222.
17. Steerenberg P, Garseen J, Dortant P, et al. Protection of UV-induced suppression of skin contact hypersensitivity. Photochem Photobiol. 1998;67:456-461.
FULL TEXT
|
ISI
| PUBMED
18. Zhao J, Jin X, Yaping E, Zheng ZS, Zhang YJ, Athar M. Photoprotective effect of black tea extracts against UVB-induced phototoxicity
in skin. Photochem Photobiol. 1999;70:637-644.
FULL TEXT
|
ISI
| PUBMED
19. Kobayashi S, Takehana M, Kanke M, Itoh S, Ogata E. Postadministration protective effect of magnesium-L-ascorbyl-phosphate
on the development of UVB-induced cutaneous damage in mice. Photochem Photobiol. 1998;67:669-675.
FULL TEXT
|
ISI
| PUBMED
20. Saleem M, Alam A, Sultana S. Attenuation of benzoyl peroxide–mediated cutaneous oxidative
stress and hyperproliferative response by the prophylactic treatment of mice
with spearmint (Mentha spicata). Food Chem Toxicol. 2000;38:939-948.
FULL TEXT
|
ISI
| PUBMED
21. Sheridan J, Kern E, Martin A, Booth A. Evaluation of antioxidant healing formulations in topical therapy of
experimental cutaneous and genital herpes simplex virus infections. Antiviral Res. 1997;36:157-166.
FULL TEXT
|
ISI
| PUBMED
22. Li Y, Metori K, Koike K, Che Q-M, Takahashi S. Improvement in the turnover rate of the stratum corneum in false aged
model rats by the administration of geniposidic acid in Eucommia ulmoides OLIVER leaf. Biol Pharm Bull. 1999;22:582-585.
ISI
| PUBMED
23. Garbacki N, Gloaguen V, Damas J, Hoffmann L, Tits M, Angenot L. Inhibition of croton-oil induced oedema in mice ear skin by capsular
polysaccharides from cyanobacteria. Naunyn Schmiedebergs Arch Pharmacol. 2000;361:460-464.
FULL TEXT
|
ISI
| PUBMED
24. Kim H-M, Cho S-H. Lavender oil inhibits immediate-type allergic reaction in mice and
rats. J Pharm Pharmacol. 1999;51:221-226.
FULL TEXT
|
ISI
| PUBMED
25. Koh H, Kligler B, Lew P. Sunlight and cutaneous malignant melanoma: evidence for and against
causation. Photochem Photobiol. 1990;51:765-779.
ISI
| PUBMED
26. Wenk J, Brenneisen P, Meewes C, et al. UV-induced oxidative stress and photoaging. Curr Probl Dermatol. 2001;29:83-94.
PUBMED
27. Krutmann J. Ultraviolet A radiation–induced biological effects in human skin. J Dermatol Sci. 2000;23(suppl 1):S22-S26.
28. Biesalski H, Obermueller-Jevic U. UV light, beta-carotene and human skin—beneficial and potentially
harmful effects. Arch Biochem Biophys. 2001;389:1-6.
FULL TEXT
|
ISI
| PUBMED
29. Hart P, Grimbaldeston M, Finlay-Jones J. Sunlight, immunosuppression and skin cancer: role of histamine and
mast cells. Clin Exp Pharmacol Physiol. 2001;28:1-8.
FULL TEXT
|
ISI
| PUBMED
30. Gil E, Kim T. UV-induced immune suppression and sunscreen. Photodermatol Photoimmunol Photomed. 2000;16:101-110.
FULL TEXT
|
ISI
| PUBMED
31. Hakim I, Harris R, Ritenbaugh C. Fat intake and risk of squamous cell carcinoma of the skin. Nutr Cancer. 2000;36:155-162.
FULL TEXT
|
ISI
| PUBMED
32. Black H. Influence of dietary factors on actinically-induced skin cancer. Mutat Res. 1998;422:185-190.
ISI
| PUBMED
33. DiGiovanna J. Retinoid chemoprevention in patients at high risk for skin cancer. Med Pediatr Oncol. 2001;36:564-567.
FULL TEXT
|
ISI
| PUBMED
34. Zhao JF, Zhang YJ, Jin XH, et al. Green tea protects against psoralen plus ultraviolet A–induced
photochemical damage to skin. J Invest Dermatol. 1999;113:1070-1075.
FULL TEXT
|
ISI
| PUBMED
35. Katiyar S, Ahmad N, Muhktar H. Green tea and skin. Arch Dermatol. 2000;136:989-994.
FREE FULL TEXT
36. Kadoma Y, Fujisawa S. Kinetic evaluation of reactivity of bisphenol A derivatives as radical
scavengers for methacrylate polymerization. Biomaterials. 2000;21:2125-2130.
FULL TEXT
|
ISI
| PUBMED
37. Piérard G, Piérard-Franchimont C, Goffin V. Digital image analysis of microcomedones. Dermatology. 1995;190:99-103.
ISI
| PUBMED
38. Karasz A, Decocco F, Maxstadt J. Gas chromatographic measurements of benzoyl peroxide in (as benzoic
acid) cheese. J Assoc Anal Chem. 1974;57:706-709.
39. Biagi P, Hrelia S, Celadon M, et al. Erythrocyte membrane fatty acid composition in children with atopic
dermatitis compared to age-matched controls. Acta Paediatr. 1993;82:789-790.
ISI
| PUBMED
40. Schalin-Karrila M, Mattila L, Jansen C, Uotila P. Evening primrose oil in the treatment of atopic eczema: effect of clinical
status, plasma phospholipid fatty acids and circulating blood prostaglandins. Br J Dermatol. 1987;117:11-19.
PUBMED
41. Oliwiecki S, Burton J, Elles K, Horrobin D. Levels of essential and other fatty acids in plasma and red cell phospholipids
from normal controls and patients with atopic eczema. Acta Derm Venereol. 1991;71:224-228.
ISI
| PUBMED
42. Wright S, Sanders T. Adipose tissue essential fatty acids in the plasma phospholipids of
patients with atopic eczema. Br J Dermatol. 1991;110:643-648.
FULL TEXT
43. Lovell C, Burton J, Horrobin D. Treatment of atopic eczema with evening primrose oil [letter]. Lancet. 1981;1:278.
44. Wright S, Burton J. Oral evening-primrose-seed oil improves atopic eczema. Lancet. 1982;2:1120-1122.
ISI
| PUBMED
45. Bordoni A, Biagi P, Masi M, et al. Evening primrose oil (Efamol) in the treatment of children with atopic
eczema. Drugs Exp Clin Res. 1988;14:291-297.
ISI
| PUBMED
46. Biagi P, Bordoni A, Hrelia S, et al. The effect of -linolenic acid on clinical status, red cell fatty
acid composition and membrane microviscosity in infants with atopic dermatitis. Drugs Exp Clin Res. 1994;20:77-84.
ISI
| PUBMED
47. Biagi PL, Bordoni A, Masi M, Ricci G, Fanelli C, Patrizi A, Ceccolini E. A long-term study on the use of evening primrose oil (Efamol) in atopic
children. Drugs Exp Clin Res. 1988;14:285-290.
ISI
| PUBMED
48. Guenther L, Wexler D. Efamol in the treatment of atopic dermatitis [letter]. J Am Acad Dematol. 1987;17:860.
49. Humphreys F, Symons H, Brown H, Duff G, Hunter J. The effects of -linolenic acid on adult atopic eczema and premenstrual
exacerbation of eczema. Eur J Dermatol. 1994;4:598-603.
50. Horrobin D, Stewart C. Evening primrose oil and eczema. Lancet. 1990;335:864-865.
51. Kalish R. Randomized trial of aromatherapy: successful treatment for alopecia
areata. Arch Dermatol. 1999;135:602-603.
FREE FULL TEXT
52. Munzel T, Giaid A, Kurz S, Stewart D, Harrison D. Evidence for a role of endothelin 1 and protein kinase C in nitroglycerin
tolerance. Proc Natl Acad Sci U S A. 1995;92:5244-5248.
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