Figure 5.1
Depigmented macules of vitiligo
Chemical Leukoderma: Chemical leukoderma, or occupational vitiligo, is caused by exposure to agents such as phenolic germicides, thiols, catechols, mercatoamines, and several quinines. Typically depigmented patches will only occur in areas where skin has contact with chemical agents [5].
Postinflammatory hypomelanosis: Postinflammatory hypomelanosis is a very common skin disorder that occurs more often in dark skinned individuals. Psoriasis, seborrheic dermatitis, atopic dermatitis, sarcoidosis, lichen sclerosis, pityriasis versicolor, and lupus can all produce this secondary hypomelanosis. Decreased pigmentation most often occurs following inflammation but complete depigmentation can occur after severe atopic dermatitis or discoid lupus [5].
Pityriasis (tinea) versicolor: Pityriasis (tinea) versicolor normally presents with multiple oval to round patches or thin plaques with mild, fine scale. Patients can be hyper or hypopigmented. Hypopigmentation is secondary to inhibitory effects of dicarboxylic acids on melanocytes as well as decreased tanning secondary to the ability of the malassezia yeast to filter sunlight [5].
Tuberous Sclerosis: Tuberous Sclerosis Complex is an autosomal dominant disorder that can present with a white macule most often on the trunk in addition to hamartomas in multiple organs. Hypomelanotic macules can be lance-ovate and confetti shaped. This is usually due to decreased size and poor development of melanosomes [5].
Piebaldism: Piebaldism is rare autosomal dominant disorder due to abnormal migration of melanoblasts. Clinically there are patches of depigmented skin with hyperpigmented borders most often on the mid-forehead, neck, anterior trunk, and mid-extremities. A white forelock is a common finding. The disorder is stable and permanent but patients generally have a normal lifespan [5].
Further Workup
Wood’s lamp examination is useful for lightly pigmented patients. Skin biopsy for histopathology and melanin stains can be used to confirm the diagnosis in difficult cases [5]. On further history, the patient denies any occupational hazards or exposure to chemicals. She does not give a family history of similar symptoms. The patient endorses constipation. There is a documented weight gain of 25 lb over 2 years. A serum level of thyroid stimulating hormone is found to be above the upper limit of normal.
Diagnosis
Vitiligo
Discussion
Vitiligo comes in multiple forms. The most common form is described as discrete amelanotic milky-white macules and patches ranging from 5 mm to 5 cm or greater surrounded by normal skin. Trichrome vitiligo is a variant that has three colors (white, light brown, dark brown). Inflammatory vitiligo is a variant with an elevated erythematous potentially pruritic margin. Vitiligo ponctue is characterized by multiple small confetti-like discrete amelanotic macules occurring on normal or hyperpigmented skin [6].
Most patients with vitiligo are otherwise healthy, although associated autoimmune endocrinopathies can occur in some individuals. The strongest association is thyroid disease, therefore a screening with review of systems and possible TSH is indicated. There are also studies showing association of vitiligo with diabetes mellitus and cases of vitiligo associated with Addison’s disease, gonadal failure, and pernicious anemia [5, 7].
In our patient, above, we see an association with hypothyroidism. She has the most common form of vitiligo, which is progressive. The components of the diseases seem to be associative rather than causative. Therefore each issue should be dealt with separately.
There is no cure for vitiligo. A conventional treatment algorithm would include:
Two month trial of mid-high potency steroids for focal/limited disease
Topical calcipotriene daily to help increase efficacy of steroids
Tacrolimus (0.1 %) ointment to cosmetically sensitive areas or genital skin, twice daily
PUVA (phototherapy): topical application of 8-methoxypsoralen to affected areas followed by controlled ultraviolet A (UVA) exposure for focal disease, and methoxsalen capsules 2 h before UVA in systemic disease.
Surgical therapy such as minigrafting for limited, stable disease unresponsive to therapies [10]
An integrative treatment algorithm can include substances which are applied topically, ingested, or available commercially. They can be used alone or as supplements to conventional therapies.
Topical integrative approaches are as follows.
Coconut oil for the strong antioxidant activity [13].
Black cumin or the seeds of Nigella sativa—efficacy is due to its immunomodulatory effect [13]
Bavachi (Psoralia carylifolia), a psoralen derivative, to help induce pigmentation [14].
Polypodium leucotomos, a type of fern native to the tropical and subtropical regions of the Americas when combined with PUVA [15]
Piperine, the major alkaloid of black pepper, stimulates melanocyte proliferation when combined with UV radiation [16].
Amino acid l-phenylalanine reduces Langerhans cells present in lesional skin [17].
Chinese cupping: providing suction over the skin to induce blisters on the thigh whose roofs are subsequently used for epithelial grafts [18]
Oral therapies which have showed benefit are as follows.
Ginkgo biloba 40 mg PO three times a day or 60 mg PO twice a day [21]
Anti-inflammatory, immunomodulatory, antioxidant, and anxiolytic effects [22]
Cheap, relatively few side effects
Vitamin E (antioxidant) 900 IU/day in combination with PUVA [23]
Antioxidants: Vit B12, Vit C, Folic Acid, Vit A 20,000 IU, Vit C 1,000 mg, Zinc 15 mg, Selenium 50 μg, Magnesium 2 mg, CoQ10 75 mcg, and pygnogenol 1 mg [24]
Herbs: Liquid extract of Acacia catechu bark, Psoralea corylifolia leaves with psorlanes [25]
Hyperemia caused by psoralen increases melanin producing activity in skin
Monitor for hepatotoxicity
Chinese mixture of “Xiaobai” 160 mL, orally daily [26]
Contains 30 g walnut, 10 g red flower, 30 g black sesame, 30 g black beans, 10 g zhi bei fu ping, 10 g lu lu tong, 5 plums
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