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Zinc is an essential trace element in health and disease. It chiefly functions as a cofactor to various metalloproteins and enzymes and is involved in transcription and gene expression. In contrast to Western countries, acquired zinc deficiency is common in South Asian countries principally in infants and young children due to poor diet and malnutrition. Herein we describe an infant with canities due to acquired zinc deficiency, which to our knowledge has not been described previously, and also briefly discuss the role of zinc in melanogenesis.
A 5-month-old boy born to a nonconsanguineously wed couple presented to the dermatology outpatient clinic with erythematous, eczematous scaly plaques and erosions involving the perioral, perianal, and acral sites and diarrhea of 7 days’ duration. The infant had an uneventful birth history, a birth weight of 2.3 kg, and was exclusively breast-fed. The child’s weight at the time of presentation was 7 kg. His scalp hair was sparse and depigmented (Figure, A). The serum zinc level was 40 µg/dL, and serum alkaline phosphatase level was 120 IU/L.
A, Pretreatment clinical photograph shows sparse, fine, and depigmented hair over the parieto-occipital area. B, A 3-month posttreatment clinical photograph after zinc supplementation shows complete regrowth of pigmented hair.
Based on these findings, a diagnosis of acquired zinc deficiency was made, and treatment was started with 3 mg/kg/d of oral elemental zinc. The mother was also given oral zinc supplements. One week after starting treatment, there was marked improvement in skin lesions, and perioral and perianal lesions had subsided with postinflammatory hypopigmentation. Zinc supplementation was continued, and 3 months after initiation of treatment, there was complete regrowth of darkly pigmented hair over the scalp (Figure, B).
Zinc plays a vital role in health and disease of skin and its appendages. Its deficiency characteristically presents with eczematous, crusted plaques in perioral, perianal, and acral sites. Hair involvement is common and can present as total alopecia, alternative light and dark bands on polarized microscopy, and structural hair changes.1 Diarrhea, photosensitivity, lethargy and poor growth are usual associated features. Premature canities is rarely seen in infants, usually in association with autoimmune diseases like pernicious anemia, premature aging syndromes, protein-energy malnutrition, and micronutrient deficiencies.2 These were excluded by relevant history, physical examination, and laboratory investigations. Furthermore, regrowth of darkly pigmented hair after zinc supplementation suggested zinc deficiency as the probable cause of canities in our patient.
Skin contains approximately 6% of total body zinc.3 At the subcellular level, melanosomes act as a storehouse for zinc, and its concentration in human hair melanosomes is the highest zinc concentration attained in a structural element of the human body.4 Zinc plays a major role in melanogenesis by virtue of its catalytic function in the synthesis of 5,6-dihydroxindole derivatives and increasing its incorporation into the pigment polymer.4 Zinc inhibits the activity of tyrosinase and glutathione reductase in vitro, enhances the activity of dopachrome tautomerase, and has agonistic effects on melanocortin receptor signaling.5 In addition, because of its antioxidative property, zinc protects the melanocytes from free-radical damage.4 Hence, zinc deficiency may adversely affect melanogenesis.
Inamadar and Palit6 reported in 2 siblings with acrodermatitis enteropathica vitiligolike depigmented lesions over the acral parts of the body. The patients had thin, lusterless scalp hair broken at the distal ends, but depigmentation was not noted. Paradoxically Plonka et al5 in their mouse experiments found that high-dose zinc supplementation induced a bright brown lightening of new hair shafts due to potent downregulation of eumelanin content. It is possible that zinc is essential for melanogenesis because of its antioxidant action and regulatory function of metalloproteins, and its deficiency may lead to pigment lightening or complete loss of pigment as seen in our case. Zinc excess can also downregulate melanogenesis because of the inhibitory action of zinc on tyrosinase. Thus zinc homeostasis is essential for optimal melanogenesis.
Corresponding Author: Savita Yadav, MD, Department of Dermatology, Venereology, and Leprology, Postgraduate Institute of Medical Education and Research, Sector 12, Chandigarh 160012, India (firstname.lastname@example.org).
Published Online: July 9, 2014. doi:10.1001/jamadermatol.2014.368.
Conflict of Interest Disclosures: None reported.
Vinay K, Yadav S, Handa S. Zinc Deficiency and Canities: An Unusual Manifestation. JAMA Dermatol. 2014;150(10):1116–1117. doi:10.1001/jamadermatol.2014.368
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