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Wayne T. McCormack, Ph.D.
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Wayne T. McCormack, Ph.D.
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For on-line support groups and chat rooms, see VitiligoSupport.org, the Yahoo vitiligo support group, and the Vitiligo Support and Information Group (VSIG, which you can also link to from the National Vitiligo Foundation's website).
To search the web yourself, here are a few search engines: http://www.google.com/ http://www.metacrawler.com http://www.hotbot.com/
To
search the medical and scientific literature, use PubMed, a service of the
National Library of Medicine at the National Institutes of Health:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
Below is a collection of information items about vitiligo, treatments, cosmetics, etc.
Guidelines for Care for Vitiligo, from the American Academy of Dermatology Association
Janet Haslam on the Skin Disease Which Causes Gradual Loss of Colour
Over ten years of research by Dr. Karin Schallreuter and colleagues has demonstrated that the skin of vitiligo patients has elevated levels of hydrogen peroxide and low activity of the enzyme catalase, which breaks down hydrogen peroxide. This research has led to the epidermal oxidative stress model for vitiligo pathogenesis. Based on this basic science research, her research team has developed a treatment called "pseudocatalase", referred to as PC-KUS. (This research also led to my laboratory's investigation of the possible role of the catalase gene in vitiligo susceptibility.)
Detailed information about the mechanism of action and photos illustrating successful treatment are available at Dr. Schallreuter's website, from which the following description was copied: "Pseudocatalase cream plus calcium has been originally developed by Schallreuter et al and was used as a substitution for low catalase levels in the treatment of vitiligo (KU Schallreuter et al. Treatment of vitiligo with a topical application of pseudocatalase and calcium in combination with short term UVB exposure, Dermatology (1995) 190:223-229). The word pseudocatalase has been introduced by these authors to differentiate between the natural enzyme catalase and a chemical complex which does the same job, i.e. degrading hydrogen peroxide. In this context, it is noteworthy that catalase cannot penetrate the top layer of the skin. Therefore, it is important to note that any products containing natural catalase in a cream are basically ineffective, and any product advertised as catalase in the treatment of vitiligo should be used with caution."
Individually tailored treatment for vitiligo using PC-KUS is offered in the Institute for Pigmentary Disorders in Association with the University of Greifswald in Germany and the University of Bradford in the United Kingdom.
For further information please contact:
Mrs. Angela Panske
Institute for Pigmentary Disorders e.V. in
Association with the Ernst-Moritz-Arndt University Greifswald Biotechnikum
Walter-Rathenau-Str. 49a
D-17489 Greifswald
Germany
Fax: +49 (0)3834 515573
email: vitiligo@biotechnikum.de
or
Mrs. Susan Shergill
Other versions of pseudocatalase (P-CAT) have been manufactured in the United States at Northwestern University in Chicago, IL and Community Drug in Pittsburgh, PA, however, no clinical trials about the safety or efficacy of these P-CAT copies have been published yet in medical journals. Information about the Northwestern version of P-CAT is available at the National Vitiligo Foundation website. Please note Dr. Schallreuter's cautions about the efficacy and safety of using P-CAT copies (see pages 9-10).
Guidelines for Care for Vitiligo
from the American Academy of Dermatology Association: http://www.aadassociation.org/Guidelines/vitiligo.html
by Dr. R. Su, from the Hong Kong Medical Association: http://www.hkmj.org.hk/skin/vitiligo.htm
THE TREATMENT OF CHILDREN WITH VITILIGO
by Aaron B. Lerner, M.D.
Department of Dermatology
Yale University School of Medicine
Vitiligo is common in children. Of the one percent of the population who have vitiligo, approximately 50 percent develop it by the age of 18. Only a few infants are born with vitiligo. The diagnosis is usually easy to make. Sometimes, the relatively rare disorder, piebaldism, which is always present at birth and which remains stationary for life, may be confused with vitiligo. My definition of vitiligo is fairly broad because I include early graying of hair, halo nevi, and segmental vitiligo (that is, unilateral loss of pigment) as part of or related to ordinary (or bilateral) vitiligo. My reasons for having this broad definition is that it is common to see overlaps in these conditions. A 10-year-old boy may have both regular vitiligo plus halo nevi, or an 8-year-old girl may have vitiligo and 50 percent gray hair. I may see a 5-year-old child who recently developed white spots on his/her hands and face. The parents who would be in their early 30's will say that there is absolutely no family history of vitiligo. However, I will notice that one of the parents has marked early graying of hair. For me, the family history is positive. A child with white spots on the skin and a parent with early graying have related disorders.
People with vitiligo have lost most, but not necessarily all, pigment cells, or melanocytes, in a patch of skin. The goals in treatment are to stop further loss of cells and to get new melanocytes from the division of pigment cells in the follicles of pigmented hairs; from the few remaining cells in the white patch; and from cells at the edges of the lesions.
For the treatment of children with vitiligo, I must emphasize four points. Do not overtreat. Never use oral steroids. Potent topical steroids should not be used. Do not use PUVA (oral psoralens plus ultraviolet light) before the age of 10. The treatment for repigmentation consists of carefully controlled exposure to sunlight and the application of weak steroid creams or ointments. The child should be exposed to as much sunlight as possible without getting a sunburn. Ultraviolet light is a mitogen for pigment cells. That is, light stimulates pigments cells to divide so that new cells can be made. Whether this action of light on pigment cells is direct or indirect is not known. We are walking a tightrope here because a sunburn is trauma to the skin, and the normal pigmented skin in a person with vitiligo is easily depigmented when traumatized. In fact, it is common for a patient to state that his/her vitiligo first appeared after a sunburn. Following a 15- to 60-minute stay in sunlight, a light protective preparation or sunscreen cream or lotion of SPF 8 or higher should then be applied to the skin to stop the further action of light. This controlled, limited exposure to light will most likely avoid predisposing the child to significant photoaging of skin.
Steroids applied to the skin sometimes have a dramatic effect in bringing about repigmentation. These agents do not act as mitogens as does ultraviolet light. Instead, they may reduce the microscopic level of mild, largely imperceptible inflammation present in the skin surrounding the patches of vitiligo. The combination of light acting as a mitogen and steroids suppressing inflammation can stop vitiligo from spreading and for new pigment cells to form. However, topically applied steroids have their own set of side effects. The most important one is thinning of skin, which in turn can lead to formation of stretch marks. Areas where the skin comes together, such as the axillae and the groin, are especially sensitive and in most cases should not be treated. Hydrocortisone, available as Lanacort or Cortaid in 0.5 to 1.0 percent strength, can be used. The superpotent steroids, Temovate and Diprolene, useful in the treatment of vitiligo in adults, must be avoided in children. The mid-potent steroids should be used with care.
Most people with vitiligo, children and adults, are in good physical health, even when they are being treated for another disorder such as a thyroid problem or diabetes. However, when a disorder that makes one especially reactive to sunlight is present - lupus erythematosus, porphyria, xeroderma pigmentosum - no form of light therapy can be used. Also, emotional or physical stress -- a divorce or death in the family or an automobile accident can be a major factor in the onset and spread of vitiligo and may be difficult to compensate for.
Many patients want to know if a special diet can help. Should one take vitamin C or some of the B vitamins, folic acid, B-12, PABA? For most children, I do not believe that diet or vitamins help but if parents want to add them, fine. However, if someone is going to take folic acid for several years, his/her physician should know about that.
I have not used the phenylalanine-ultraviolet light treatment because I did not believe it would help. If some good studies show that it helps, I can begin to use it.
I do not recommend any treatment in which the medication has ingredients that are kept secret. That is, I would not use the herbal treatment from South American and Hong Kong, the topical treatment from Thailand, or the unknown treatment from the Ukraine.
PUVA Therapy. PUVA therapy consists of taking one of the psoralen drugs Oxsoralen or Trisoralen and two hours later exposing oneself to sunlight or the ultraviolet A lamps. The psoralens increase dramatically the response of cells in the skin to light, including the proliferation of pigment cells. This action increases the proliferation of pigment cells to get repigmentation. The treatment gives satisfactory results in approximately 20 percent of patients with vitiligo. I do not recommend the use of this therapy in children because it will increase the photoaging of skin. In addition, the treatment takes a fair amount of dedication and is boring. One has to be motivated to undertake PUVA therapy. It takes 2-4 months of treatment just to find out whether or not one is a good candidate for this therapy. Self-motivation usually comes after ten years of age. For a few it becomes before ten; for many it doesn't come until the teens. It does not help for a parent to push a child into therapy.
When a patient has a few small spots, some physicians like using psoralen solutions topically. When this is done the stock solution must be diluted from 1 percent to 0.01 percent because severe burns can result from not being careful. The physician should have experience in using this treatment.
Depigmentation. Nearly all patients with vitiligo want to be repigmented so that they have on color, preferably their original color. However, when vitiligo is extensive, more than 50 percent of exposed areas, hands, arms, face - repigmentation is unrealistic. Another approach is to depigment the skin completely so that the individual is totally white. On occasion depigmentation can be tried in a child. That therapy consists of applying a cream containing monobenzylether of hydroquinone, previously sold under the trade name Benoquin. But Benoquin goes on and off the market. There are problems of patients developing a contact dermatitis to the medication. However, when everything works properly and the patients end up with perfect results, they are always happy in spite of the fact the skin is now very light in color, does not tan, and has to be rigorously protected from exposure to sun to prevent sunburn and photo damage.
In Summary: Children should be exposed to sunlight but not enough to
get a burn. Weak topical steroids should be applied to the skin. Do not
give steroids by mouth; do not use superpotent topical steroids; and do
not use PUVA. Do not overtreat.
SECTION: The Guardian Features Page; Pg. 16
HEADLINE: Health: Losing face; JANET HASLAM ON THE SKIN DISEASE
WHICH CAUSES GRADUAL LOSS OF COLOUR
BYLINE: JANET HASLAM
Imagine something very personal and precious being taken away from you a little at a time. You're not in control of when it goes and you can't argue about the amount removed. This is the predicament faced by people with vitiligo - a common skin disease that causes areas of the body to progressively lose colour, leaving white, sunburn-vulnerable patches. The condition is indiscriminate and affects up to 4 per cent of the population worldwide.
Yet although more than half a million people in Britain suffer from it, vitiligo receives little recognition from health professionals, because it is neither painful nor infectious. Its attack on the largest organ of the body is mainly cosmetic: darker skins suffer greatly from its disfiguring signature. The depigmented areas usually affect both sides of the body in a symmetrical pattern. And as it creeps across the skin, often taking years to spread, it can be socially and psychologically devastating.
There is no outright cure but there are treatments that sometimes re-awaken dormant melanocytes - the pigment cells that tan the skin. Why they self -destruct in the first place is a mystery. It is thought to be triggered by genetic, immune and stress-related factors. No one in Maxine Whitton's immediate family has it. She has lived with her 'spotted calf' appearance - the medical name comes from the Latin word vitellus, which aptly describes the patchy condition on her black skin - for more than 40 years and it covers nearly half of her body. She wears make-up on her face, but to cover her hands and arms would take hours.
She says the loss of pigment is like a 'constant bereavement'. White patches first appeared on her knees when she was a child in Jamaica. Her face was soon affected. 'It became a problem in my teens because I didn't think anyone would find me attractive,' she remembers. 'I resigned myself to a life of celibacy.' In fact she has been married for nearly 30 years and has two grown-up children. She has just stepped down as chair of the Vitiligo Society, a self -help group with 2,500 members. The organisation has produced the first comprehensive book on the condition, Understanding The Loss Of Skin Colour - promoted as essential reading for health professionals.
Although Whitton gives the impression of coping easily, she has been close to a nervous breakdown. 'While it was on my face I could pretend I didn't have it,' she admits. 'But when it became rampant and started on my body, I became depressed and panicky. By the time I got to my forties, I needed counseling. My self-esteem was very low, I was crying all the time.' Nearly 50 per cent of Jane Mitchell's white skin has succumbed to vitiligo. It's on her face, neck, arms and legs. Even though the patches only show when she tans, she says it has had a devastating effect on her life. It started 10 years ago, when her father died. 'I wouldn't go swimming. I always wore a fake tan which ruined all my underwear, and I never went on holiday.' Today she wears short sleeves. Her confidence comes from her 13-year-old-son, Lee, who inherited the complaint. Earlier this year he spoke candidly on television about the condition, which is rapidly denying him his mixed-race identity.
He says he's not bothered by it and doesn't camouflage the patches. 'My school friends accept me. I had some problems with name calling, like 'panda' and 'jigsaw' but I just fought back or made a joke,' he says. 'It's just hard when you go somewhere new and people stare and say horrible things about me and my mum.' But Lee's self-assurance was shaken last year when he took part in a year-long clinical trial at Great Ormond Street Hospital which involved rubbing a cream on the affected areas then exposing it to short bursts of ultra-violet B light. He was 'gutted' by the lack of improvement.
The trial follows research in Germany showing that the skin of people
with vitiligo appeared to lack an enzyme called catalase. A cream containing
the enzyme was tested on volunteers in London hospitals. The results of
the trial will not be ready until next year, but consultant dermatologist
Dr John Hawk, heading the research in London, predicts the outcome. 'We're
very disappointed that the cream didn't work. There are good theoretical
reasons why it should. We hope to do further studies over the next six
months to a year with a reformulated preparation.' Jane Mitchell isn't
sure she wants to put Lee through the process again. Unlike Maxine Whitton,
she's never had any treatment. 'I've changed my doctors four times,' she
reveals. 'None of them seemed to appreciate that it isn't just a cosmetic
problem.' When Dr Gina Agarwal, an academic general practitioner at Imperial
College School of Medicine, recently completed an extensive survey of vitiligo
sufferers, she discovered that many felt rejected and abandoned by their
doctor's indifference: 'I found that GPs were not really addressing the
psychological problems, and had not offered any treatment to the sufferers.
If the GP had offered treatment, perhaps patients wouldn't have been so
depressed or isolated.'
Spot check:
Treatments available on the NHS: n Steroid creams applied aggressively to the affected areas can sometimes halt the condition.
PUVA ( Psoralen + UVA) Patients given the drug psoralen, which makes the skin sensitive to light, are then exposed to ultra-violet A light to encourage the natural colour to return.
Other remedies: Special creams can help to disguise the patches. The Red Cross offers a free cosmetic camouflage advice service. Many of the cosmetics are available on prescription.
The Vitiligo Society is at 19 Fitzroy Square, London W1T 5HQ.
Endocrine autoimmunity
deals with autoimmune disorders that affect specific endocrine glands.
Hashimoto's thyroiditis (low thyroid function) and Graves' disease (overactive
thyroid function), are among the most commonly occurring endocrine autoimmune
diseases.
The endocrine
system co-ordinates the body's physiology and assists in responses to internal
or external stimuli. Endocrine cells produce hormones that are secreted
into the bloodstream, and act at distant sites throughout the body. Endocrine
cells may be grouped into glands (e.g., pituitary, thyroid, pancreas, adrenal,
ovary, etc) or reside within other organs (e.g., gastric cells in the stomach).
Many endocrine organs are regulated by the hypothalamus, an area in the
brain that synthesizes "releasing hormones". The "releasing hormones" in
turn stimulate hormone release from the pituitary gland (situated at the
base of the brain). The pituitary gland secretes a variety of hormones
that regulate different target endocrine glands. An example of a hormone
is estrogen, produced by the ovary. Cyclic secretion of pituitary FSH (follicle
stimulating hormone) and LH (luteinizing hormone) regulates the ovary.
During each cycle, growing follicles produce estrogen. Estrogen modifies
the metabolism of many tissues such as muscle, bone, nerve cells, etc.
Thus at menopause, as the function of the ovary declines and estrogen decreases,
there are multiple effects on the cardiovascular system, skeletal and nervous
system.
The action of
hormones on cells is specific. Although hormones circulate through the
body, only specific cells respond. The cells that respond have specific
receptors that recognize the correct hormone. The receptors perform two
functions, they recognize and bind the appropriate hormone, and then translate
the recognition event into a cellular signal that alters the cell function.
This article
from a recent InFocus Newsletter provides information about Endocrine autoimmunity,
the Endocrine System, Graves' disease, Addison's disease, Hashimoto's disease
and the risk factors associated with endocrine autoimmunity. Also discussed are the advances made in treating this disorder. InFocus Newsletter has
many articles dealing with autoimmunity and autoimmune related diseases.
The general features
of endocrine autoimmune disorders are similar to those for all autoimmunity.
The disorders develop gradually, and may take several years to show clinically
recognizable symptoms. Autoimmunity seems to arise from multiple factors
that includes a genetic predisposition combined with specific triggers.
The diagnosis of endocrine autoimmunity by a physician involves assessing
symptoms and measurement of a relevant hormone to determine if it is within
normal levels. Antibody tests to specific cellular components often are
performed to confirm autoimmunity. Treatment for endocrine autoimmunity
usually consists of hormone replacement or agents to suppress overactive
glands.
Family history
and genetics: Autoimmunity tends to run in families. However, different
family members can have any type of autoimmune disease, not necessarily
just endocrine autoimmunity.
Age: Although
autoimmune diseases can occur at any age, there is a general tendency for
autoimmune disease to increase with age.
Sex: Women are
more likely to develop many of the autoimmune disorders, with different
probabilities for different disorders. Overall, autoimmune disease is 5
times more common in women. Diabetes (IDDM) is one exception and occurs
at similar rates in men and women.
Ethnicity: The
incidence of autoimmune diseases is different in different ethnic groups.
The specific differences depend on the disease. For example, (IDDM) is
higher in Caucasians while non-autoimmune diabetes (NIDDM) is more frequent
in African Americans, Hispanic and Native Americans.
Life events:
Although the exact mechanisms that trigger an autoimmune disease in susceptible
individuals are not well understood, there is an association with some
life events. For example, childhood neck irradiation is associated with
later development of thyroid disease. Pregnancy may trigger thyroid autoimmunity
(postpartum thyroiditis) in susceptible individuals.
Environmental
and dietary influence: The incidence of some autoimmune diseases varies
by geographic location. Dietary components may be another factor in development
of autoimmune diseases. An example of a dietary and environmental factor
is the relationship of iodine and thyroid autoimmunity. Iodine was introduced
into the diet (iodized salt) in the US to reduce goiter. In western Europe,
which has not added iodine to food, there is a lower prevalence of Hashimoto's
disease, but a higher prevalence of nodular goiter and thyroid cancer.
Although these observations are intriguing, the exact mechanism of how
dietary and environmental factors influence autoimmune diseases remains
to be determined.
Thyroid: Pituitary
TSH (thyroid stimulating hormone) stimulates the thyroid to produce T4
(thyroxine) and T3. Synthesis of thyroid hormones is accompanied by the
uptake of iodine from the blood and its incorporation into thyroglobulin,
the precursor of T4 and T3. T4 and T3 regulate metabolic functions by co-operating
with other factors throughout the body. Low thyroid function (Hashimoto's
disease) is associated with elevated TSH and decreased T3 and T4 compared
to normal, and antibodies to thyroid cell components [TPO (thyroid peroxidase)
and/or TG (thyroglobulin)]. Hypothyroidism affects about 5 million Americans,
and affects women about 10 times more often than men. Symptoms commonly
associated with Hashimoto's are fatigue, depression, weight gain (fluid
retention), cold intolerance, hair loss, altered menstrual cycles, infertility,
constipation, dry skin, etc. Hormone replacement in the form of thyroxine
is usually given for hypothyroidism. Graves' disease, or overactive thyroid,
is associated with decreased pituitary secretion of TSH, but increased
T3 and T4. The overstimulation of the thyroid is related to auto-antibodies
that bind to the TSH receptor and act like hormone, but with more prolonged
effects. Graves' disease occurs 5-10 times more often in women (or about
2% of women in the United States). Symptoms of Graves' include nervousness,
heart palpitations, weight loss, insomnia, increased sweating, premature
graying of hair, muscle weakness, heat intolerance, altered menstrual cycles,
and in some cases goiter (enlarged thyroid) and exophthalmos. Exophthalmos
is an independent autoimmune disease that results in protrusion of the
eyes. Graves' disease is diagnosed by measurement of TSH, T4 and T3 and
TSH receptor antibody. TPO and TG antibodies may also be present. There
are several treatments for Graves', all directed at reducing thyroid function:
radioactive iodine to shrink the thyroid or anti-thyroid drugs such as
propylthiouracil or methimazole. Graves' disease may switch to Hashimoto's
over time, since treatments directed at suppressing an over-active thyroid
may eventually reduce thyroid function below normal. These individuals
may then be treated with thyroxine replacement. Individuals with other
autoimmune diseases such as lupus, rheumatoid arthritis, vitiligo, myasthenia
gravis, IDDM, etc. are more likely to also develop thyroid autoimmunity.
Adrenal: The
adrenal secretes cortisol in response to pituitary ACTH (adrenocorticotropic
hormone). Cortisol has many functions, but the most significant are to
control immune inflammatory reactions, balance insulin effects, assist
in the maintenance of blood pressure and cardiovascular function, and
modification of general metabolism. The adrenal also produces aldosterone,
which helps maintain blood pressure and acts on the kidney to promote water
and salt balance. Addison's disease is characterized by inadequate levels
of cortisol and sometimes aldosterone (adrenal insufficiency or hypocortisolism).
Addison's disease is relatively rare, affects about 1/20,000 individuals,
and
occurs in men and women at about equal rates. Symptoms may include weight
loss, salt craving, fatigue, muscle weakness, hyperpigmentation and low
blood pressure. When Addison's is suspected, it may be confirmed by a poor
cortisol (measured in blood or urine) response to ACTH stimulation. Treatment
is usually by oral cortisol replacement.
Pancreas: The
autoimmune target of IDDM (insulin dependent diabetes mellitus) is the
pancreas. IDDM (type 1 diabetes) represents about 5-10% of all diabetes
(overall diabetes affects about 8% of women and 8% of men). IDDM often,
but not always, develops in children and young adults. Symptoms include
increased thirst and urination, blurred vision, constant hunger, weight
loss and tiredness. IDDM is diagnosed by measurement of abnormally elevated
fasting glucose. Tests for antibody to pancreatic beta cells are not well
correlated with disease progression and thus are not standardly used in
diagnosis. IDDM is treated with insulin replacement and glucose monitoring.
Ovary: As mentioned
above, ovarian production of estrogen is controlled by cyclic secretion
of the pituitary hormones, FSH and LH. In turn, estrogen controls the pituitary
production of FSH and LH. Thus as the ovary fails, and estrogen declines,
FSH increases dramatically. Premature menopause (i.e. ovarian failure before
age 40) occurs in about 1% of women. There is no similar disorder documented
for the testes. Recent evidence has shown that a majority of premature
menopause is autoimmune. FSH becomes elevated, and estrogen declines, similar
to natural menopause. The usual treatment is estrogen replacement to protect
cardiovascular, skeletal and nervous systems.
Polyglandular:
There is a tendency for some disorders to occur together. For descriptive
purposes these are termed polyendocrine type I and type II and type III
(see "InFocus" vol 4, #5, Dec 1997). Type I tends to begin in early childhood
with skin infection (Candidiasis) and is commonly associated with hypoparathyroidism
as well as Addison's and is often associated with gonadal failure. Type
II usually involves diabetes or thyroid disease and Addison's disease and
sometimes ovarian failure and non-endocrine autoimmune diseases. Type III
involves thyroid autoimmune disease and at least two other autoimmune diseases,
but not Addison's disease.
The current advances
related to endocrine autoimmunity involve improved hormone preparations
for therapy, and greater awareness leading to earlier detection and treatment.
The advances related to autoimmunity in general include understanding the
genetics, triggering influences, and the relationship of stress (and the
hypothalamic-adrenal axis) to development of autoimmunity.
Judy Luborsky, Ph.D. is an associate professor of Obstetrics and
Gynecology and Director, Endocrine Immunology at Rush Medical College (of
Rush- Presbyterian-St. Luke's Medical Center) in Chicago, Illinois
USE OF COSMETICS TO COVER VITILIGO SPOTS
Suggestions from vitiligo patients:
(This listing is for information only, may not be up-to-date,
is not meant to be all inclusive, and does not represent an endorsement
by me or the University of Florida of any particular product.) Product: Dermablend
Product: Dy-O-Derm
Product: Natural Cover
Product:
Melasyn
For information about UV light units for at-home use:
(This listing is for information only, may not be up-to-date,
is not meant to be all inclusive, and does not represent an endorsement
by me or the University of Florida of any particular product.)
PhotoTherapeutiX: http://www.photothrx.com/
Amjo Corporation -
Daavlin line: http://www.uv-light.com/dv-nb-uvb.htm
National Biological Corporation: http://www.natbiocorp.com/
What is the Endocrine System?
General Features
Risk factors
Specific Disorders: symptoms, diagnosis and treatment
New Directions
Copyright 1998 American Autoimmune Related Diseases Association,
Inc.
Where to find it: http://www.aarda.org/endocrine_art2.html
(1) Experiment with these products until they
achieve the desired appearance.
(2) Seek advice from cosmetics sales representatives
about application methods. Applying too much is a common problem.
(3) You may need to blend different shades
of some products to achieve the results you desire.
(4) If you are testing these products in the
store, go outside into natural sunlight to see which shade looks best.
Never buy a shade using only fluorescent light, because what looks good
in the store may not look good in natural light.
Phone: (877) 900-6700
Web site: http://www.dermablend.com/
Other: available at
J.C. Penneys, Sears, and many other major department stores
Company: Delasco
Phone: (800) 831-6273, (712)
323-3269
E-mail: questions@delasco.com
Web site: http://www.delasco.com
Company: Linda Seidel
Phone: (800) 752-0066
Web site: http://www.lindaseidel.com/natural_cover.html
Company: Vitiligo Solution, Inc.
Phone: (888) 322-1335
Web site: http://vitiligosolution.com
Last updated:
5/25/05
wtm
Vitiligo Information & Links