VITILIGO

VITAMINS
Folic Acid, Vitamin B12 and Vitamin C Combined supplementation may be beneficial. Experimental Study: In a gp. of 15 consecutive Argentinian pts., serum folate was below normal in 11, serum vitamin B12 was below normal in 5, and serum vitamin C was below normal in 4. They were treated with folic acid 2 mg twice daily, vitamin B12 100-1000 mcg IM every 2 wks. and vitamin C 500 mg twice daily. 8/15 noted that depigmentation stopped shortly after treatment began. It took about 3 mo. for repigmentation to become clinically visible. After 2 yrs., 6/15 pts. had 100% repigmentation, and 2/15 had 80% repigmentation. In some cases, an initial response was obtained by using folic acid 2 mg/d alone; however, the speed of repigmentation increased when vitamins B12 and C were added (Montes LF, Diaz ML, Lajous J, Garcia NJ. Folic acid and vitamin B12 in vitiligo: a nutritional approach. Cutis 50:39-42, 1992).

MINERALS
Copper Necessary for the activation of tyrosinase. Decreased tyrosinase activity will impede the conversion of tyrosine to the melanins, resulting in albinism and vitiligo (Chorazak T, Rzempoluch E. Etiopathogenesis of vitiligo in the light of our studies. Pol Med J 7(2):494-500, 1968; Genov D et al. Copper pathochemistry in vitiligo. Clin Chim Acta 37:207-11, 1972; Lal S et al.

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Serum caeruloplasmin in vitiligo. Indian J Med Sci 24(10):678-9, 1970; Sen S. Caeruloplasmin, copper and disease. J Indian Med Assoc 52(4):182-4, 1969). Supplementation may be beneficial (Bagaeva MI. [Treatment of vitiligo in children with copper sulfate.] Vestn Dermatol Vernerol (3):48-50, 1979 (in Russian).

OTHER NUTRITIONAL FACTORS

Para Amino Benzoic Acid (PABA) Supplementation may be beneficial. WARNING: Vitiligo has been reported as being caused by PABA (Hughes CG. Oral PABA and vitiligo. Letter. J Am Acad Dermatol 9(5):770, 1983). Other potential side-effects (of the potassium salt) include skin rash, anorexia, nausea and fever (Physicians Desk Reference. Oradell, NJ, Med. Economics, 1986) as well as liver toxicity (Kantor GR, Ratz JL. Liver toxicity from potassium para-aminobenzoate. Letter. J Am Acad Dermatol 13(4):671-2, 1985). Note: The acid compound is far more difficult for patients to tolerate than the potassium salt (Potaba; Glenwood) (Grace WJ et al. Therapy of scleroderma and dermatomyositis. N Y State J Med 63(1):140-44, 1963). Experimental Study: Pts. received PABA 100 mg 3 times daily. After 5-20 wk. there was a return of color to the depigmented areas (Sieve BF. The clinical effects of a new B complex factor, paraaminobenzoic acid, on pigmentation and fertility. South Med Surg 104:135-9, 1942).

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- with Vitamin B complex Experimental Study: 48 pts. (25 females, 23 males) were studied over 10 months. Most had a history of inadequate diet and symptoms of fatigue, irritability, emotional instability, constipation, headaches and joint pains were common. Pts. received PABA 100 mg 3-4 times daily in addition to vitamin B complex. Later, due to the slowness of the effect, parenteral monoethanolamine PABA 100 mg was added twice daily in order to maintain adequate blood levels. Results were slow, but were striking by 6-7 mo. of treatment (Sieve BF. Further investigations in the treatment of vitiligo. Virginia Med Monthly January 1945, pp. 6-17). L-Phenylalanine Precursor to tyrosine. Vitiligo is frequently associated with the presence of tyrosinase autoantibodies (Song Y-H, Connor E, Li Y, et al. The role of tyrosinase in autoimmune vitiligo. Lancet 344:1049-52, 1994). - and ultraviolet-A radiation Experimental Double-blind Study: 32 pts. with vitiligo over 10-40% of their body surface received either L-phenylalanine 100 mg/kg daily or placebo, either alone or combined with long-wave ultraviolet light (UVA) treatment. Phenylalanine was ingested with a low-protein breakfast with nothing ingested afterwards for at least one hour. UVA exposure was usually twice weekly 30-45 min. after phenylalanine ingestion, and was later reduced to once weekly in most cases. After 6 mo., 75% of pts. receiving phenylalanine and UVA had 30-60% repigmentation; the other gps. did less well (Siddiqui AH, Stolk LM, Bhaggoe R, et al. L-phenylalanine and UVA irradiation in the treatment of vitiligo. Dermatology 188(3):215-18, 1994).

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Experimental Controlled Study: 149 pts. with vitiligo over 10-40% of their body surface received either L-phenylalanine 50-100 mg/kg daily plus long-wave ultraviolet light (UVA) treatment, phenylalanine alone, or no treatment. Phenylalanine was ingested with a low-protein breakfast with nothing ingested afterwards for at least one hour. UVA exposure was usually twice weekly 30-45 min. after phenylalanine ingestion, and was later reduced to once weekly in most cases. After 18 mo., 71.2% of pts. in the combined treatment had repigmentation ranging from 25-80% of the affected area; 22% had >60% repigmentation. 83% of pts. receiving phenylalanine alone remained stable, while 17% deteriorated and none improved. 64% of those who received no treatment remained stable, 36% deteriorated and none improved. There was no advantage to the higher dosages of phenylalanine (Siddiqui AH, Stolk LM, Bhaggoe R, et al. Lphenylalanine and UVA irradiation in the treatment of vitiligo. Dermatology 188(3):215-18, 1994). Experimental Study: 21 pts. were treated with oral L-phenylalanine 100 mg/kg and UVA exposure. In addition, 10 of these pts. also applied a cream containing 10% phenylalanine to the vitiliginous areas, and this gp. had the best results. Neither gp. had side effects (Antoniou C et al. Vitiligo therapy with oral and topical phenylalanine with UVA exposure. Int J Dermatol 28(8):545-7, 1989). Experimental Study: 13 children were supplemented with Lphenylalanine and treated with ultraviolet light (UVA) radiation. 3 experienced repigmentation of all vitiliginous areas, 6 showed 50-90% improvement, and 4 failed to respond. None experienced side effects (Schulpis CH et al. Phenylalanine plus ultraviolet light: preliminary report of a promising treatment for childhood vitiligo. Pediatr Dermatol 6(4):332-5, 1989).

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Experimental Study: 20 pts. were treated with L-phenylalanine 50 mg/kg and UVA radiation. 85% had a follicular and partially confluent repigmentation, which did not exceed 50% of the vitiliginous area (Thiele B, Steigleder GK. [Repigmentation treatment of vitiligo with L-phenylalanine and UVA radiation. Z Hautkr 62(7):519-23, 1987) (in German). Experimental Study: Pts. were treated thrice weekly with Lphenylalanine 50 mg/kg and exposed to sunlight as a source of UVA. 81% responded; 43% responded within 3 months. One pt. was overirradiated. The repigmentation was predominantly of the follicular pattern (Kuiters GR et al. Oral phenylalanine loading and sunlight as source of UVA irradiation in vitiligo on the Caribbean island of Curacao NA. J Trop Med Hyg 89(3):149-55, 1986). Experimental Study: Pts. received phenylalanine 50 mg/kg along with exposure to UVA light 30-45 min. after ingestion (the time of peak blood concentrations). After 4 mo. (32 treatments), reasonable repigmentation occurred. Apart from the repigmentation of hypopigmented macules, pts. became able to tolerate more sun than usual, especially at the vitiliginous lesion (Cormane RH et al. Phenylalanine and UVA light for the treatment of vitiligo. Arch Dermatol Res 277(2):126-30, 1985). See Also: Biella U, Haustein UF. [Treatment of vitiligo using phenylalanine and UVA radiation.] Hautarzt 41(11):636, 1990 (in German)

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OTHER RELATED FACTORS

Rule out arsenic toxicity. Chronic arsenicism may be associated with vitiligo (Binkley LK, Papa CM. Chronic arsenicism with vitiligo, hyperthyroidism, and cancer. N J Med 86(5):377-80, 1989). Rule out nickel toxicity. Chronic skin contact may be associated with vitiligo. Case Reports: 2 pts. showed vitiligo-like depigmentations where their skin had been in close contact with a metal spectacle frame made of nickel alloy. Both had nickel hypersensitivity; however, they showed clinical and histologic findings indicating that the depigmentation did not result from postinflammatory hypopigmentation but from chemical hypomelanosis. The mechanism is unexplained (Kim HI et al. Two cases of nickel dermatitis showing vitiligo-like depigmentations. Yonsei Med J 32(1):79-81, 1991). Rule out hydrochloric acid deficiency. Observational Study: Gastric acid secretion was assessed in 102 consecutive pts. by means of the augmented histamine test. 20/102 (19.6%) were achlorhydric, and 19 of the 20 were female. 8 of the 20 (all females) were found to have pernicious anemia (Howitz J, Schwartz M. Vitiligo, achlorhydria, and pernicious anemia. Lancet i:1331-5, 1971). Observational Study: In a survey of 801,670 hospital admissions, the combination diagnoses of vitiligo and pernicious anemia should have occurred once, but actually occurred 22 times, suggesting that pernicious anemia, and thus hydrochloric acid deficiency, is not uncommon in pts. with vertigo (Allison JR, Curtis AC. Vitiligo and pernicious anemia. Arch Dermatol 72:407-8, 1955).

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Experimental and Observational Study: Of 29 pts., 10 (35%) had no hydrochloric acid and only 3 (10%) had normal levels. The severity of the condition seemed to correlate with the extent of the hydrochloric acid deficiency and also seemed to be associated with signs of vitamin B complex deficiency. Good results were obtained following hydrochloric acid and vitamin B complex supplementation where a definite hypochlorhydria was found (Allison JR. The relation of HCl and vitamin B complex deficiency in certain skin diseases. South Med J 38:235-41, 1945). Experimental Study: 4 pts. with vitiligo and achlorhydria experienced disappearance of the vitiligo by 2 yrs. after starting hydrochloric acid 15 cc with each meal (Francis HW. Achlorhydria as an etiological factor in vitiligo, with report of four cases. Nebraska Med J 16:25-6, 1931). See Also: Ishida K. Jpn J Dermatol Venerol 64:155, 1954