- 1Vitiligo Society, London SE11 6SF
- 2Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2JF
- Correspondence to: J Viles , D J Gawkrodger
- Accepted 9 June 2010
My vitiligo started in 1978, when I was 40. It first appeared on my left hand as small white lines around my cuticles; I was diagnosed with “leucoderma” and told that “it would go away.” However, more white patches appeared, and a friend told me that in America this is called vitiligo. Six months later, spots appeared on the right hand, and the loss of pigment spread rapidly over the next 12-18 months.
I went to my GP, who referred me to a specialist dermatologist, who in the first instance gave me steroid cream to use “lightly” for 12 months. About the same time the vitiligo started on my face, as a patch on the right side near my mouth, and subsequently spots occurred and replicated themselves on my hands and body. My GP decided on a different approach and referred me to the homoeopathic hospital for the vitiligo to be treated holistically, because at that time she had no other treatment to suggest. Over the years I had tried various homoeopathic treatments for vitiligo on visits to India with different dermatologists and homoeopaths; none of the treatments they had suggested had any success. I saw a psychologist because I had a very stressful job and she advised meditation as stress was believed to be a contributing factor. I didn’t get any repigmentation, but the patches didn’t get any worse for two years.
Then with a new job, with increased stress levels, the loss of pigment started to get much worse, and my GP referred me to a research programme at St Thomas’ Hospital, London, during the late 1980s. By that time I had two large patches on my face, around the mouth and forehead and around my eyes, in addition to areas on the rest of my body. I was given psoralen and ultraviolet A (PUVA) twice a week, and the repigmentation was quite rapid and noticeable. Within one month I started to repigment on the face. It was a darker shade than my normal skin, and I was lucky because I didn’t have any side effects. I continued the treatment for a year and repigmented on the legs and calves, but with a lighter shade than my normal pigment. About this time, narrowband ultraviolet B (UVB) was just becoming available. I noticed that the PUVA treatment seemed to be increasing my white patches, which was evident on my calves and shins. The consultant changed the treatment to narrow band UVB and there was a noticeable improvement with re-pigmentation (figure⇓), but not on the hands or feet.
I felt that the visual effect my depigmented skin had on other people was the main effect of the disease. The psychological impact was quite painful, and took some time to overcome. In the early 1990s I became an advocate for younger people seeing GPs to get treatment, and I was selected to be a test case for skin diseases on various training seminars for GPs. It was during these sessions I discovered, to my surprise, how little dermatological training medical students and GPs were given. GPs’ attitude and responses, and minimal patient support, must have been rather disconcerting to patients.
Vitiligo was my first autoimmune condition. In 1995 I was diagnosed with diabetes, almost by accident: I was waiting for an underground train and read an advertisement by the British Diabetic Association and realised I had all the symptoms. I went to a diabetes clinic and took tablets for a year with no control of the condition. I was then given insulin, which had an immediate response—I felt quite normal again and was able to continue to play sport. That was my second autoimmune condition. Then in the late 1990s I started to get pains in my left knee; this was initially diagnosed as osteoarthritis but later was rediagnosed as rheumatoid arthritis. This was my third autoimmune condition. The Vitiligo Society has asked if my thyroid has been tested. I have not had this done yet, but I suspect I should.
Throughout this time I continued to have narrowband UVB treatment and continued to repigment, but when I had completed 250 sessions it was decided that I should stop treatment (the maximum is 300 sessions, depending on other medical factors and the dermatologist’s judgment). Repigmentation seemed to have stalled. The area of skin that had white patches is thinner, particularly on the hands, and I am careful to use a high sun protection factor. I have been given tacrolimus ointment to use on the remaining spots on my face, as anecdotal evidence on other patients has shown good results.
During this time my rheumatoid arthritis got much worse; when my condition reached an extremely debilitating level I was prescribed etanercept. I was fortunate that it had no side effects. I noticed a dramatic improvement within four hours of starting the treatment. That morning I had struggled to get out of a chair due to the high level of pain, which severely restricted my mobility and required me to walk with a walking stick; by teatime I was able to walk freely with a minimum of pain. I am now virtually pain-free.
A doctor’s perspective
Vitiligo causes a lot of psychological distress, but this is only one of many facets of the disease that are illustrated by Darryl’s case. Darryl’s vitiligo came on rather late in life, as the most common time of onset is the second or third decade. The onset on the hands is common in the symmetrical types of vitiligo that are usual in adults (as opposed to the segmental type found mostly in children, which is seen in a unilateral and dermatome-like pattern). Darryl’s vitiligo spread rapidly. This would have been unpredictable to his doctors, as the rate of progress of vitiligo varies. Vitiligo is usually a progressive disease that shows periods of activity interspersed with times of inactivity. Spontaneous repigmentation can occur but is rare.
The initial treatment in Darryl’s case was a topical steroid. This is a reasonable initial approach for limited area vitiligo (according to the published guidelines), and about a half of patients show some pigment gain with a highly potent topical steroid. Vitiligo on the face is currently treated with a topical calcineurin inhibitor (pimecrolimus or tacrolimus) because of the concern about steroid induced skin atrophy on the face. The reaction of Darryl’s doctors in referring him for homoeopathic treatment illustrates the feeling of powerlessness that doctors may experience and the desperation of patients when faced with a disease like vitiligo, for which there is little effective treatment.
When Darryl’s vitiligo became extensive he was correctly prescribed phototherapy. PUVA (psoralen and ultraviolet A) has mostly been superseded by narrow band ultraviolet B (NB-UVB), which is safer and more effective than PUVA. One study indicates that about 60% of patients achieve 50% or more repigmentation with NB-UVB, but a prolonged course (6-12 months) is often required. The number of treatments should be limited to 200 for patients with lighter skin colour but can be higher for those with a darker skin. Darryl lost pigment after the phototherapy: unfortunately this is not uncommon. Twelve months after completion of a course of PUVA, about a quarter of patients have less pigmentation than they did before starting the treatment (the proportion with pigment loss is less with NB-UVB).
The spread of vitiligo to the face produced psychological trauma in Darryl, underlining the extreme emotional effect vitiligo has. Darryl’s experience as an expert patient, observing the level of knowledge of doctors and medical students, underlines inadequacies in the curriculum of some medical schools and GP courses. In many medical schools, only one or two weeks of dermatology is taught; in some it is absent altogether.
Vitiligo shows many characteristics of an autoimmune disease, and Darryl’s experience bears this out. Up to 30% of vitiligo patients have autoimmune thyroid disease, and a personal or family history of thyroid problems, diabetes, or other endocrine disorder is common. Patients with vitiligo are shown to have circulating autoantibodies and T lymphocyte activity against melanocyte antigens, resulting in the loss of functioning melanocytes within the depigmented macules of vitiligo (the histological feature of the disease). Darryl developed rheumatoid arthritis, but this is not a common association with vitiligo.
Interestingly, the biological drug etanercept given for Darryl’s rheumatoid arthritis did not improve his vitiligo. There is still no really effective treatment for vitiligo. Scientific studies that give a better understanding of the causative mechanisms and the genetics of vitiligo offer the hope of developing a properly effective treatment.
David J Gawkrodger
The Vitiligo Society (www.vitiligosociety.org.uk) is a charity offering support and reliable information to people with vitiligo and their families. It promotes and funds research to establish the causes of vitiligo and to find safe and effective treatments.
Cite this as: BMJ 2010;341:c3780
This is one of a series of occasional articles by patients about their experiences that offer lessons to doctors. The BMJ welcomes contributions to the series. Please contact Peter Lapsley () for guidance.
Contributors: JV runs the Vitiligo Society and helped to pull thisarticle together. DM wrote the main part of the article; JV helped with editing. DJG wrote the medical perspective.
Competing interests: All authors have completed the unified competing interest form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare no support from any organisation for the submitted work; no financial relationships with any organisation that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work.
Provenance and peer review: Not commissioned; externally peer reviewed.