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Year : 2021  |  Volume : 22  |  Issue : 3  |  Page : 286-287

Changing hair color

Department of Pediatrics, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Date of Submission29-May-2020
Date of Decision10-Sep-2020
Date of Acceptance21-Mar-2021
Date of Web Publication30-Jun-2021

Correspondence Address:
Meenakshi Bhatt
Department of Pediatrics, Safdarjung Hospital, Ward 21, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpd.IJPD_96_20

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How to cite this article:
Sehgal R, Gupta R, Bhatt M. Changing hair color. Indian J Paediatr Dermatol 2021;22:286-7

How to cite this URL:
Sehgal R, Gupta R, Bhatt M. Changing hair color. Indian J Paediatr Dermatol [serial online] 2021 [cited 2021 Oct 22];22:286-7. Available from: https://www.ijpd.in/text.asp?2021/22/3/286/319957


A 12-year-old boy presented to the pediatric outpatient department with progressive decrease in vision noticed since the age of 1 year. The problem was greater in near vision. He underwent right eye lensectomy for anterior dislocation of the lens and pars plana lensectomy of the left eye for posterior dislocation, and on presentation, he was wearing aphakic glasses with thick lenses.

He also had poor scholastic performance which was noticed since he started attending school. He had intellectual disability with a development quotient of <40. There was no history of seizures or focal neurological deficit. He was born out of a third-degree consanguineous marriage. There was no history of intellectual disability or visual deficits in any of his four siblings.

On examination, he had light-colored fine hair [Figure 1]a, marfanoid habitus, kyphosis, and hyperextensibility of the wrist. His systemic examination was normal. The possibility of homocystinuria was considered, and tests were performed accordingly. The serum homocysteine level was elevated (50 μmol/L; normal 5–15 μmol/L), the Vitamin B12 level was normal, and methylmalonic acid and methionine levels were normal. With a diagnosis of possible methylenetetrahydrofolate reductase deficiency, the child was started on oral pyridoxine, folic acid, and methylcobalamin. On this treatment, his hair color normalized after 3 months [Figure 1]b.
Figure 1: (a) Light-colored hair at presentation. (b) Darkening of hair after therapy

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Homocystinuria is a defect in the metabolism of methionine that is inherited in an autosomal recessive manner. There is accumulation of homocysteine and metabolites in urine and in blood. Some of the presenting features of homocystinuria include chest deformities such as pectus carinatum, marfanoid habitus, ectopia lentis, intellectual disability, and stroke.

There is very scant literature on changed hair color in patients with hyperhomocystinemia. One of the earliest reports of change in hair color with supplementation with pyridoxine was described by Shelley et al.[1] They treated an 18-year-old girl with homocystinuria with oral pyridoxine and noticed blackening of the growing scalp hair. There were an increased number of melanin granules on microscopic examination of the hair cortex.

These changes are different from the hair changes seen in some cases of systemic lupus erythematosus where hair is sometimes found to be scanty and brittle. The scanty and ragged look of hair may be a form of telogen effluvium.

Reish et al. treated a 23-year-old woman with homocystinuria.[2] She was treated with pyridoxine, and there was darkening of her blond hair 6 weeks after initiation of therapy. She had self-administered vitamins in each of her previous pregnancies and had noticed the same darkening of hair, and there was return of blond hair after discontinuing the vitamins.

They demonstrated that homocysteine inhibited the activity of tyrosinase in human cultured melanocytes in vitro.[3] They postulated that normalization of homocysteine level after therapy reversed this inhibition and caused hair color to darken.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Shelley WB, Rawnsley HM, Morrow G 3rd. Pyridoxine-dependent hair pigmentation in association with homocystinuria. The induction of melanotrichia. Arch Dermatol 1972;106:228-30.  Back to cited text no. 1
Reish O, Berry SA, King RA. Spontaneous hair hyperpigmentation in response to vitamin intake in pregnancy -A clue for homocystinuria. Am J Obstet Gynecol 1995;173:1640-1.  Back to cited text no. 2
Reish O, Townsend D, Berry SA, Tsai MY, King RA. Tyrosinase inhibition due to interaction of homocyst(e)ine with copper: The mechanism for reversible hypopigmentation in homocystinuria due to cystathionine beta-synthase deficiency. Am J Hum Genet 1995;57:127-32.  Back to cited text no. 3


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