Gray hair in children

Can a child have gray hair? Yes, they can.

Why do they appear and what does it mean? It means that the hair follicles have reduced levels or a complete absence of the hair coloring pigment melanin.

Polyosis is also a medical term for patches of discolored hair on the hairline in the forehead, eyebrows, and/or eyelashes, as well as patches of gray hair elsewhere on the scalp. Polyosis can even occur in newborns.

Reasons why a child has gray hair

Causes of such a symptom as gray hair in a child - focal or diffuse hypopigmentation (depigmentation) of the hair or hypomelanosis.

This condition may be caused by:

• vitiligo; [1]
• Albinism in children or piebaldism (incomplete albinism); [2]
• hypomelanosis Ito, a rare neurodermatologic disease associated with X-chromosomal abnormalities that manifest themselves in skeletal deformities, ophthalmologic abnormalities (nystagmus, strabismus, cataracts), and CNS abnormalities (intellectual and motor retardation); [3]
• Recklinghausen's disease or hereditary neurofibromatosis type I; [4], [5]
• tuberous sclerosis - a genetic disorder with autosomal dominant inheritance in which a child has strands of gray hair and hypopigmented patches of skin at birth; [6]
• Chediak-Higashi syndrome (Chediak-Higashi); [7]
• Vogt-Koyanagi syndrome (or Vogt-Koyanagi-Harada disease) with inflammation of the iris and vasculature of the eye, hearing problems, and marked neurologic clinic; [8]
• associated with inherited gene mutations, Griscelli syndrome, which has three forms and various nonpigmentary, neurologic, and immune symptoms; [9]
• Graves' disease or hyperthyroidism in children, [10] and Hashimoto's disease or autoimmune thyroiditis.

In Waardenburg syndrome, gray hair in a newborn child (along the forehead) is not the only sign of pathology, and children may have iris heterochromia (eyes of different colors); hypertelorism (wide nose bridge) and sinophrysis (fused eyebrows); sensorineural hearing loss, seizures, tumor masses. The prevalence of this syndrome in the population is estimated at one case per 42-50 thousand people, and in schools for the deaf, according to some data, one child out of 30 has Waardenburg syndrome. [11] At the same time, if a newborn is diagnosed with intestinal obstruction or constipation from birth (congenital agangliosis of the colon or Hirschprung's disease), then Waardenburg-Shah syndrome is diagnosed. [12] And when combined with hypoplasia of limb muscles and joint contractures - Kline-Waardenburg syndrome. [13]

Risk factors

Among the risk factors for impaired melanin synthesis, experts note:

• insufficiency and/or protein-energy malnutrition;
• deficiency of cyanocobalamin - vitamin B12 - with the development of pernicious anemia (quite common in veganism), as well as deficiency of this vitamin and folic acid (vitamin B9) during pregnancy in the mother, leading to megaloblastic anemia in the child;
• copper deficiency in the body;
• thyroid problems;
• adrenal insufficiency;
• chronic exposure to heavy metals (lead).

Pathogenesis

Melanin-producing cells, melanocytes, are formed from the neuroectoderm cells of the neural crest of the embryo (melanoblasts), which spread in tissues and are further transformed. Melanocytes are present not only in the skin and hair follicles, but also in other tissues of the body (in the brain membrane and heart, in the vasculature of the eyes and inner ear).

Production of hair shaft melanin (follicular melanogenesis) by oxidation of L-tyrosine does not occur continuously, as in the epidermis, but cyclically, depending on the phase of hair growth. At the beginning of anagen, melanocytes multiply, mature by the end of this stage, and then - in the catagen period - undergo apoptosis (death). And this whole process depends on a variety of factors and is regulated by a multitude of enzymes, structural and regulatory proteins, etc.

Melanin production and its transport from melanocytes to keratinocytes in hair follicles depends not only on the presence of its precursors (5,6-dihydroxyindoles, L-dopaquinone, DOPA-chromium), but also on many auto- and endocrine factors. The researchers concluded that follicle melanocytes - compared to skin melanocytes - are more sensitive to the effects of peroxides and free radicals, that is, they are more easily damaged by oxidative stress.

For example, mutations in the tyrosinase gene (TYR), a copper-containing enzyme that catalyzes the synthesis of melanin from the amino acid tyrosine, lead to minimal or no melanin formation in all forms of albinism. As well as mutations in the genes of TYRP1 and TYRP2 enzymes - important participants of melanogenesis, regulating the activity of tyrosinase, proliferation of melanocytes and stability of the structure of their melanosomes.

In tuberous sclerosis (which occurs in one child per 6,000 children), the pathogenesis is associated with inherited or sporadic mutation of the genes for the gamartin and tuberin proteins (TSC1 and TSC2), which regulate the growth and proliferation of cells (including melanocytes).

Multisystem Vogt-Koyanagi syndrome is thought to be the result of an abnormal autoimmune reaction to melanin-containing cells in any tissues of the body.

And in such an orhan disease as Waardenburg syndrome, the mechanism of development of the pathological condition is rooted in mutations of the genes EDN3, EDNRB, MITF, PAX3, SNAI2 and SOX10, which are directly related to the formation of melanocytes.

Read also: Anatomo-physiologic features of the skin and its appendages.

Consequences and complications

By itself, gray hair in children may not produce complications or cause negative health effects.

However, the appearance of such a symptom as discolored hair in a child may be combined with other signs of certain diseases and pathological conditions (listed above) that pose serious risks.

Diagnosis

A complete history (including family history) is needed to determine the cause of hair depigmentation.

General blood tests and thyroid hormones are taken.

An area of skin with depigmented hair is examined using a Wood's lamp and also by dermatoscopy.

Based on the evaluation and correlation of all clinical signs, a differential diagnosis is made.

What to do, treatment

If PUVA therapy is used in the therapy of vitiligo, hypomelanosis Ito try to treat with glucocorticosteroid injections, since etiotropic agents for the treatment of pathologies of this type or albinism simply do not exist.

In syndromes with ophthalmologic or neurologic lesions, appropriate symptomatic agents are used. But what to do when melanin synthesis is impaired?

If vitamin B12 deficiency is detected, supplements with this vitamin are prescribed. In case of copper deficiency, it is recommended to introduce whole grain products, legumes, beef liver, sea fish, eggs, tomatoes, bananas, apricots, walnuts, sunflower seeds and pumpkin seeds into the child's diet.

Doctors also recommend taking ginkgo biloba preparations for two to three months, which are claimed to promote repigmentation.

You can use a hair tonic consisting of carrot juice, sesame oil and fenugreek seed powder; make hair masks of aloe vera gel (which contains antioxidants, vitamins B12 and B9, zinc and copper).

Prevention

Specific ways to regulate melanogenesis have not yet been found, so there are no measures to prevent congenital abnormalities of melanin synthesis in hair follicles.

Although researchers say that antioxidants: vitamins A, C and E, as well as bioactive compounds found in greens, berries and dark-colored fruits and brightly colored vegetables contribute to increased melanin synthesis.

Forecast

Most likely, gray hair in a child will be his "mark" for life: this is the medical prognosis for genetically determined focal or diffuse pigmentation disorders and orphan syndromes.