The primary symptom of hypertrichosis is excessive growth of hair. There are several forms of hypertrichosis with characteristic symptoms. Hypertrichosis may be present at birth or acquired at a later stage of life.
Hypertrichosis symptoms
Congenital hypertrichosis (CH) forms are present at birth and are caused due genetic mutations. CH may be hereditary, passed on by the parents. There are instances wherein spontaneous mutation during embryonic growth causes the excessive growth. The parents and family members may be symptom-free.Congenital hypertrichosis lanuginosa
CH lanuginosa is present at the time of birth. The characteristic symptom is the presence of lanugo hair. The newborn is covered with excessive growth of hair. In normal circumstances, the lanugo is shed by the fetus at about eighth month of pregnancy to be gradually replaced by vellus hair. The persisting lanugo hair may somewhat get thinner as the child grows.Generalized congenital hypertrichosis
In generalized CH, the affected patient present excessive hair growth all over the body. Only the palms, soles and mucous membranes are spared.Ambras syndrome
Ambras syndrome is a type of generalized CH. The typical symptom of Ambras syndrome are silky, long, light-colored hair, prominent on face, ears and shoulders. The vellus hair uniformly covers the eyelids, nose, cheeks, ears and shoulder. Only the palms, soles and mucous membranes are spared.In Congenital hypertrichosis universalis the differentiating symptoms from Ambras syndrome are the presence of dense hair on the nose, preauricular regions, external ears and external auditory canal. In congenital terminal hypertrichosis also, the entire body is covered with hair. The differentiating symptoms are the growth of terminal type of hair as well as the occurrence of gingival hyperplasia. The patients appear like "werewolf".
Circumscribed (localized) congenital hypertrichosis
Circumscribed CH is the characteristic symptoms of congenital melanocytic nevus, congenital Becker nevus, Hypertrichosis cubiti, smooth muscle hamartoma and nevoid hypertrichosis. Congenital melanocytic nevus is found in some newborns. The melanin filled lesions are quite often have thick black terminal hair growth. Becker's nevus is present at birth in some cases and is characterized by an overgrowth of the epidermis, melanocytes and hair follicles.Congenital smooth muscle hamartoma is due to bundling of smooth muscles within the dermis with associated excessive growth of vellus hair at the lesion. Nevoid Hypertrichosis is a solitary patch of terminal hair. In most cases it is symptom-free. If the patch of excess hair is present in lumbosacral area it has to be diagnosed to rule out faun tail deformity and associated spina bifida occulta and diastematomyelia disorders.
In hairy elbow syndrome, both the elbows of the patient have long vellus hair. The condition may be associated with physical abnormalities such as dysmorphic facial features, microcephaly, joint hyperlaxity and mental retardation. In rare cases patients may have congenital, symmetric patches of vellus hypertrichosis on the palms or soles of the feet. Anterior cervical hypertrichosis is an autosomal recessive or X-linked chromosomal mutation with characteristic symptom of excessive hair growth on the neck.
Acquired hypertrichosis (AH) appears after birth. It is associated with side effects of drugs, porphyria cutanea tarda, cancers and eating disorders (anorexia nervosa). Some of the culprit medications are, iodine, psoralens, acetazolamide, minoxidil, phenytoin and cyclosporin. AH lanuginosa is characterized by rapid growth of lanugo hair. Generalized AH usually affects the cheeks, upper lip, and chin. Oral minoxidil treatments for hypertension is known to cause this condition. One of the symptoms of internal malignancy is the appearance of patterned hypertrichosis.
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Reference: 1.Trüeb RM. Causes and management of hypertrichosis. Am J Clin Dermatol. 2002;3(9):617-27. 2.Goel N, Rajaram S, Gupta B, Gupta K. Familial congenital generalized hypertrichosis. Indian J Dermatol Venereol Leprol 2013;79:849. |
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