How Do You Get Vitiligo?
To Summarize:
- Vitiligo is a depigmentation disorder, where white patches appear on the skin
- Vitiligo is a multifactorial condition - with multiple theories, all of which are likely to contribute to varying amounts
- The theories of vitiligo include autoimmune, neural driven, biochemical (inflammatory and oxidative)
- Treatment must be comprehensive and involve all of the above theories
What is Vitiligo
Vitiligo is an acquired depigmentation disorder. It presents with white macules on the skin. Although relatively rare, it still affects 1% of the population [1]. More and more research is emerging on the underlying causes of vitiligo. It's important to understand how you get vitiligo, this concept is known as pathophysiology - understanding how pathology (or disease) affects our physiology. We need to understand the contributing factors before we can properly tailor treatment.
There are several types of vitiligo, based on the distribution of the lesions. We have segmental, focal, and generalized types of vitiligo. The course of disease is unpredictable but there may be some patterns noticed with close observation.
More on the basics of vitiligo can be found here.
Vitiligo Is Multifactorial
A single dominant pathway is UNLIKELY to account for all cases of vitiligo. Rather, it's a complex interaction of biochemical, environmental and immunological events [1]. The why and how of vitiligo is not fully understood [2].
We Know for Certain the Melanocyte is Involved
The melanocyte is the cell that makes melanin. Melanin is what makes our skin pigmented (or darker). A loss of melanoctyes or melanin will result in de-pigmentation. Depigmentation is when the skin turns white. A huge part of treating vitiligo will be focused on the melanocyte. More info on the basics of the melanocyte can be found here.
The Theories of Vitiligo
The following theories are individually known to contribute in one way or another to vitiligo. I approach each case differently but assume all the following are playing a role.
Furthermore, there is a believe that different pathways could be involved in the various clinical types of vitiligo. The neural hypothesis may be involved in segmental vitiligo. The Autoimmune etiology is commonly related to generalized or focal non-dermatomal vitiligo.
Theory 1: Autoimmune Etiology [2]
Autoreactive T cells: these are a special class of immune cells known to be key players in autoimmune diseases (not just vitiligo). Patients with vitiligo have been found to have abnormal T-cells and Natural Killer cells [2].
Humoral Immune Response: this is another aspect of the immune system which can also contribute to autoimmunity. This involves antibody molecules that are secreted by special cells called plasma cells. Antibodies contribute to immunity through various mechanisms. Some patients with vitiligo have been found to have specific autoantibodies that otherwise healthy individuals do not have [2]. Furthermore, people suffering from other certain autoimmune diseases are more likely to suffer from vitiligo - another common trend found in autoimmune disease [3].
Theory 2: The Neural Hypothesis [2]
Accumulation of neurochemical substances decreases melanin production. Melanocytes can be damaged by a toxin released by the nerve endings or that they produce [2].
In one study, researchers too blood samples of 60 patients with vitiligo. They divided the patients into two groups, those with active vitiligo were in one group and those with inactive vitiligo put into another group. The objective was to determine if various neural and endocrine chemicals varied between those with vitiligo versus those who didn't.
It was found patients with vitiligo (both active and stable) had increased levels of [4]:
- Epinephrine
- Norepinephrine
- Dopamine
- Homo-vanillic acid (HVA)
- Serotonin
- 5-HIAA
- Melatonin
- TSH
- prolactin
It was found patients with vitiligo (both active and stable) had decreased levels of [4]:
- Free T3
- free T4
Higher estrogen found in women with active vitiligo [4] (compared to those with stable vitiligo or healthy controls) [4].
Higher levels of cortisol in the blood in men and women with active vitiligo (compared to those with stable vitiligo or healthy controls) [4].
Disturbed levels of any of these can contribute to melanocyte destruction and/or depigmentation [4]
Theory 3: The Biochemical Hypothesis [2]
The large part of this theory involves an imbalance of antioxidants and immune cells in and around the melanocytes (the cells being destroyed in vitiligo).
Our immune system has multiple ways of working. One of those ways is managing inflammation and oxidation. Reactive oxygen species and H2O2 (both bad things) can damage biological processes and it's known that these things are excess in active vitiligo skin [1].
It's been found that people with vitiligo have disturbed cytokine activity at the level of the skin [5]. This goes to show topical, localized anti-inflammatory herbs may be helpful in the management of vitiligo.
Convergence Theory of Vitiligo
Research agrees on one thing: many factors contribute into the pathogenesis of vitiligo. Not only do the above theories play a role, but other factors at are likely at play. These other factors include:
- Deficiency of unidentified melanocyte growth factors
- Intrinsic defect of structure and function of melanocytes
- Genetic factors
All of these have convincing evidence but none of them explain on its own the cause of disease [2]. The idea is they all contribute in variable proportions to the destruction of melanocytes as proposed in the 'convergence theory' [2].
Summary
Vitiligo is a complicated disease. There are multiple proposed theories of how and why vitiligo may occur. To manage any vitiligo patient, all theories must be well understood and considered.
We must consider systemic factors (like the immune system, inflammation) but also focus on the skin and melanocytes too.