Vitiligo: Causes and Treatment - Book Report/Review Example

? Vitiligo - Vitiligo Introduction Vitiligo is an acquired skin disease of unknown etiology thatis characterized by loss of pigmentation and development of white macules (Alikhan et al 2011). Melanocytes, present in the basal layer and responsible for the production of skin pigment, are destroyed leading to smooth white depigmented skin patches. It is a relatively common skin disorder that affects about 1% of the population in United States and Europe (Silverberg et al 2010). Vitiligo raises many cosmetic concerns especially in women and lot of research is underway to come up with an effective remedy. Most of the patients suffering from vitiligo experience onset of symptoms (depigmentation) before the age of 20. Although, it is possible to acquire this diseases at an advanced age it is unusual and is mostly associated with other underlying diseases such as diabetes mellitus, rheumatoid arthritis, thyroid dysfunction and alopecia areta. As the onset is at early age in more than 50% of the cases, it may be associated with severe psychological distress (Alikhan et al 2011). Further, it can severely affect the quality of life and contribute to low self esteem in affected patients. Owing to these psycho-social factors, the overall management plan should include proper counseling along with other rehabilitation processes to avoid psychiatric morbidity. Etiology The exact cause of vitilgo is not known but there are various hypotheses that have been proposed to explain the underlying mechanism. Now it is clear that loss of pigmentation occurs due to destruction of melanocytes. But what causes their destruction is the topic of debate. The best hypothesis that is widely accepted is the autoimmune hypothesis that states that the destruction of melanin producing cells is caused by the patient’s own immune system. Other theories such as autocytotoxic, neurohumoral and oxidative stress theories have also contributed in partially explaining the destruction of these cells and it is possible that all these factors can participate in the pathogenesis and development of this disease. Vitiligo has multiple complex factors that can trigger the disease. Most of the patients will give history of some kind of emotional stress such as an accident, loss of job or death of some close relative just before the onset of white patches (Abu et al 2010). According to the convergence theory many factors such as stress, mutations, autoimmunity, infection, accumulation of toxic compounds and impaired cellular migration can converge together to contribute in the pathogenesis of Vitiligo. There are evidences that vitiligo has a genetic predisposition and familial clustering is possible. About 20 % of the patients suffering from this disease also have an affected relative. Therefore, the incidence rates are high in regions where cousin marriages give rise to clustering of genetic information. The recent genetic linkage studies have identified some regions or loci on chromosome 7 and 9 that are associated with vitiligo (Alikhan et al 2011). Pathogenesis Autoimmune hypothesis: presence of antibodies against melanocytes in vitiligo patients strongly supports this hypothesis. It is proposed that antibodies are produced against autoantigens present on melanocytes and other sites can actively destroy these cells. Immunofluorescence studies have shown that IgG taken from vitiligo patients binds to cultured melanocytes. Moreover, this binding tendency increases with the progression of disease extent and activity (Abu et al 2010). Rare patients suffering from melanoma that also develops vitiligo have better prognosis (Alikhan 2011). This indicates that the same underlying mechanism is responsible for suppressing the tumor and development of vitiligo. Neurohumoral hypothesis: both nerves and melanocytes are derived from neural crest cells. It is observed that any dysfunction in the nervous system at any level can damage melanin producing cells in the skin. Studies showed that increased neurotransmitters at the neuronal junctions can be cytotoxic leading to destruction of melanocytes. This increase can be due to decrease in the acetylcholine esterase, an enzyme responsible to break down acetylcholine after it has served its purpose at the junctions of parasympathetic nerves. (Alikhan 2011). Autocytotoxic hypothesis: exposure to certain chemicals in the environment can be toxic to melanocytes and lead to their destruction. The mechanism of destruction can be direct or inhibition of some internal metabolic pathway that cause accumulation of toxic substance and indirectly cause cellular death. Oxiadative Stress hypothesis: skin cells in a vitiligo patient have very low levels of catalase enzyme. Catalase is responsible for the breakdown of hydrogen peroxide which accumulates in the absence of this enzyme. This partial deficiency is may be due to polymorphism in the gene encoding for catalase, more common in vitiligo patients indicating some form of genetic predisposition. Accumulation of hydrogen peroxide in melanocyte increase oxidative stress leading to variable cytotoxicity and melanin destruction depending on the neutralizing capability of the cell (Alikhan 2011). Melanocytorrhagy hypothesis: this is a relatively new hypothesis that explains loss of melanocytes in the affected area of the skin. The theory basically stress on the inability of melanocytes to anchor properly in the basal layer of the skin. Adhesion of melanocytes to fibronectin is inhibited by Tenascin, a molecule present in the extracellular matrix. This can partially explain the Koebner’s phenomenon, whereby, constant friction can cause melanocytes in the underlying skin to detach and migrate upwards leading to their eventual loss. These hypotheses can partially explain the destruction of melanocytes in the affected skin. Although, autoimmune hypothesis is regarded as best suitable to explain the underlying pathogenesis in vitiligo, it should be realized that perhaps all discussed phenomenon add together to give rise to a single phenotype of this disease (Alikhan 2011). Diagnosis: The diagnosis of vitiligo can be made by taking a thorough history and performing a proper physical examination. Lab tests sometimes can be done to support the findings and confirm the diagnosis. History: vitiligo has a genetic predisposition so it is crucial to ask for family history, if anyone else in the family has vitiligo or suffering from any other autoimmune disease. While taking history it is also important to ask for any stressful event prior to the onset of symptoms as stress can initiate this disease even if it is not the cause. Physical Exam: The most key feature on the physical exam is the patchy discolored areas on the skin. These patches are most commonly seen in the sun exposed areas such as face, lips and extremities but it many cases areas of trunk may also be involved. Careful examination under Wood’s lamp can help in determining the true extent of the disease. Labs: punched biopsy taken from the site of white macule or depigmented skin can be used for histopathologic evaluation to confirm the diagnosis but it is not always performed. Additional Tests: as discussed before, vitiligo is sometimes associated with other autoimmune diseases such as diabetes mellitus and thyroid problems. Therefore, it is always wise to conduct some extra lab examinations such as thyroid panel to rule out any other underlying problems. Ophthalmological and auditory exam can also be done in patients that have positive family history for such conditions (Alikhan 2011). A study demonstrated that low very levels of 25-hydroxyvitamin D levels could be associated with comorbid autoimmunity and therefore can be used as a reasonable screening tool (Silverberg et al 2010). In some cases, however, avoiding sun exposure as a precaution in vitiligo patients can lead to low levels of vitamin D (Nunes & Martins, 2010). Vitiligo and Other Autoimmune Diseases Vitiligo is considered to be an autoimmune disorder. There are other autoimmune disorders that may also be accompanied with vitiligo to form a spectrum of diseases. These include thyroid disease, diabetes mellitus, pernicious anemia, psoriasis and sometimes ophthalmic or auditory problems. Among all these associated disorders, hypothyroidism or hyperthyroidism is most commonly found in about 24% of pediatric patients suffering from vitiligo. Patients with a more generalized vitiligo are more prone to develop other autoimmune diseases as compared to those with segmental vitiligo. This is mainly because autoimmunity is a major underlying pathogenic factor in generalized vitiligo as compared to other types. Sometimes vitiligo is a part of a syndrome. Some of these syndromes include autoimmune polyendocrinopathycandidiasis ectodermal dysplasia (APECED), autoimmune polyendocrine syndrome type 1 (APS1) and polyglandular autoimmune syndrome type 1 (PGA1). Other diseases as part of these syndromes include Addison disease, hypoparathyroidsm, mucocutaneous candidiasis and ectodermal dysplasia. Kabuki, Alezzandrini and MELAS syndrome are some others with vitiligo as part of the disease spectrum (Alikhan, 2011). Epidemiology: The overall prevalence of vitiligo in general population is about 1% (Prasad & Kanwar, 2009). Studies have shown 0.093%, 0.005 and 0.38% prevalence in China, India and Denmark respectively. Gujrat, a city in India had prevalence of about 8%, highest in the world (Alikhan, 2011). Generally, the incidence is high in populations where familial clustering or consanguinity is seen. Both males and females are equally affected but owing to cosmetic effect of the disease, females seek for treatment more often than males. It is also noticeable that females are more commonly affected at an early age, normally less than 30 years of age, as compared to males who are affected in the 4th or 5th decade of life (Alikahn 2011). Quality of Life and Vitiligo Patients Vitiligo affects young population in majority of the cases that cause serious cosmetic and social problems (Yalcin et al, 2001). The fact that it manifests mostly at the exposed sites such as face, hands and other extremities make it further difficult to hide. The psychological impact on affected individual is huge and can lead to low self esteem. Therefore, this disease can seriously affect the quality of life especially in females. The disease pathology is poorly understood and in many parts of the world it is believed to be a sexually transmitted disease. The taboo and social stigma associated with this disease further ad to the psychological problems. As it is chronic and progressively worsening condition, the stress can builds up in patient severely impairing their quality of life. All patients that come for their first consultation should undergo Quality of Life (QOL) assessment. This assessment should be repeated on further visits to ensure patients satisfaction (Alikhan et al, 2011). This is important because this psycho social stress and impaired quality of life can lead the patient into some antisocial activities, whereby, patient can be a danger to own or others life. A proper counseling should be given to all patients especially with non-satisfactory Dermatology Life Quality Index to prevent any psychiatric morbidity. Reference: Abu, T. M., Pramod, K., Ali, J., & Ansari, S. H. (May 01, 2010). Current remedies for vitiligo. Autoimmunity Reviews, 9, 7, 516-520. Alikhan, A., Felsten, L. M., Daly, M., & Petronic-Rosic, V. (September 01, 2011). Vitiligo: A comprehensive overview. Journal of the American Academy of Dermatology, 65, 3, 473-491. Nunes, J. P., & Martins, C. S. (January 01, 2010). Myocardial infarction, hypovitaminosis D and vitiligo. Revista Portuguesa De Cardiologia : Orga?o Oficial Da Sociedade Portuguesa De Cardiologia = Portuguese Journal of Cardiology : an Official Journal of the Portuguese Society of Cardiology, 29, 5, 839-40. Parsad, D., & Kanwar, A. J. (August 01, 2009). Topical vitamin D3 analogues in the treatment of vitiligo. Pigment Cell and Melanoma Research, 22, 4, 487-488. Silverberg, J. I., Silverberg, A. I., Malka, E., & Silverberg, N. B. (June 01, 2010). A pilot study assessing the role of 25 hydroxy vitamin D levels in patients with vitiligo vulgaris. Journal of the American Academy of Dermatology, 62, 6, 937-941. Yalc?in, B., S?ahin, S., Bu?ku?lmez, G., Karaduman, A., Atakan, N., Akan, T., & Ko?lemen, F. (January 01, 2001). Experience with calcipotriol as adjunctive treatment for vitiligo in patients who do not respond to PUVA alone: A preliminary study. Journal of the American Academy of Dermatology, 44, 4, 634-637. Read More