Kaiser Epilation

[Lucy Ginsburg]

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Background: Photoepilation has been an essential field of application of dermatologic laser therapy for many years. The present article evaluates whether the use of a new operation mode of a long-pulsed diode laser can be effective, nearly painless, with few side effects and independent of the skin type. To this aim, its use has been compared to an established method of photoepilation.

Results: The alexandrite laser is slightly more effective with fair skin types; the SHR mode is clearly more effective with dark skin types. Regarding painfulness, the SHR mode is clearly superior. In terms of speed, the two systems are comparable. The alexandrite laser is more user-friendly because of its light and small handpiece.

Conclusion: The major advantages of the SHR mode are its effectiveness in dark skin types and its lack of pain. The alexandrite laser is slightly more effective with fair skin types, slightly faster and its handling is considerably more comfortable. None of the two systems has yet brought about a breakthrough with fair hair.

Hypertrichosis is defined as excessive hair growth anywhere on the body in either males or females. It is important to distinguish hypertrichosis from hirsutism, which is a term reserved for females who grow an excessive amount of terminal hairs in androgen-dependent sites. This activity explains when this condition should be considered on a differential diagnosis, articulates how to properly evaluate for this condition, and highlights the role of the interprofessional team in caring for patients with this condition.

Objectives:Review the etiology of hypertrichosis.Describe the presentation of a patient with hypertrichosis.Summarize the treatment options for hypertrichosis.Outline the importance of enhancing care coordination among the interprofessional team to ensure proper evaluation and management of hypertrichosis.Access free multiple choice questions on this topic.

Hypertrichosis is defined as excessive hair growth anywhere on the body in either males or females. It is important to distinguish hypertrichosis from hirsutism, which is a term reserved for females who grow an excessive amount of terminal hairs in androgen-dependent sites.[1][2][3]

There are several ways of classifying hypertrichosis. These are based on the distribution (generalized vs. localized), the age of onset (congenital versus acquired), and the type of hair (vellus versus terminal).

Forms of generalized hypertrichosis include, but are not limited to, congenital generalized hypertrichosis (which is further divided into congenital hypertrichosis lanuginosa, universal hypertrichosis, and hypertrichosis universalis congenita), prepubertal hypertrichosis, acquired generalized hypertrichosis, and acquired hypertrichosis lanuginosa. They each differ in their etiology and clinical findings.[4][5][6][7][8]

Forms of localized hypertrichosis include, but are not limited to, congenital localized hypertrichosis (congenital nevi, plexiform neurofibromas, Becker melanosis/nevus, nevoid hypertrichosis, spinal dysraphism, and the hair collar sign), localized hypertrichosis in hereditary and acquired systemic disease, and acquired localized hypertrichosis.[9][10][11][12][13]

Congenital generalized hypertrichosis is a feature of several rare inherited syndromes in which genetic errors result in the dysfunction of proteins involved in the development of the hair follicle.[10] There is some evidence to support that exposure to medications such as minoxidil in utero may predispose to congenital generalized hypertrichosis.[14]

Although drugs are usually the culprit, acquired generalized hypertrichosis can also be seen in traumatic brain injuries, juvenile hypothyroidism, juvenile dermatomyositis, acromegaly, malnutrition, and advanced HIV infection.[16][17][16]

Acquired hypertrichosis lanuginosa is considered to be a paraneoplastic phenomenon, and in certain instances precedes the diagnosis of cancer.[18][19] The most common malignancies that it is associated with include lung, colon, and breast cancers. It is sometimes seen in concert with other paraneoplastic dermatoses such as acanthosis nigricans, palmoplantar keratoderma, Leser-Trelat sign, and acquired ichthyosis.

Several forms of congenital localized hypertrichosis including hypertrichosis cubiti (hairy elbow syndrome), hairy palms and soles, hypertrichosis of the auricle, hypertrichosis of the nasal tip, and anterior or posterior cervical hypertrichosis are inherited in an autosomal dominant fashion.[20] Trichomegaly of the eyelashes is the exception, as it is an autosomal-recessive disorder.[21][22]

Congenital melanocytic nevi are often associated with hypertrichosis that becomes apparent during the infantile period of childhood. Plexiform neurofibromas, lesions pathognomonic for neurofibromatosis type I, also have associated hypertrichosis.[23]

There are several hereditary and acquired systemic diseases that present with localized hypertrichosis. Cornelia de Lange syndrome, caused by autosomal dominant or X-linked dominant mutations can present with synophrys (unibrow), as well as hypertrichosis over the forehead, lateral face, shoulders, and back.[26] Rubinstein-Taybi syndrome is due to autosomal-dominant mutations and leads to hypertrichosis over the lateral face, shoulders, and back.[27] Porphyria cutanea tarda is a cause of hypertrichosis in sun-exposed areas.[28][29] Lipodystrophy syndromes, such as Berardinelli-Seip syndrome caused by AGPAT2, BSCL2, CAV1, CAVIN1/PTRF gene mutations, can present with hypertrichosis as well.[30]

Acquired localized hypertrichosis is caused by repetitive trauma, friction, irritation, or inflammation. For example, localized hypertrichosis is often observed on the back of sack carriers, over a fractured limb after plaster casting, and over the posterior neck in weightlifters. It can also be seen within vaccination sites and varicella scars.[10] Hypertrichosis at sites of wart removal and laser epilation has also been reported in the literature. Acquired localized hypertrichosis can also be iatrogenic; it has been described following PUVA therapy, topical corticosteroids, tacrolimus, creams containing mercury or iodine, anthralin, and prostaglandin F-2 alpha analogs (latanoprost, bimatoprost).[31]

In the majority of hypertrichosis cases, men and women are equally affected, with a few exceptions. Prepubertal hypertrichosis is common in healthy, Mediterranean, or South Asian infants and children. Hypertrichosis of the auricle and hypertrichosis of the nasal tip, types of hereditary hypertrichosis, primarily affect males.[32][33]

History and physical exam findings for hypertrichosis differ between types of hypertrichosis. In generalized forms of hypertrichosis, the patient will present with lanugo hair, vellus hair, or terminal hair covering a majority of their body. Transformation of terminal hair to lanugo hair can be seen.[34]

There are several disorders characterized by congenital generalized hypertrichosis. Congenital hypertrichosis lanuginosa presents rather dramatically; the entire body surface, except for the palms, soles, dorsal hands and feet, and prepuce are covered with fine, silver-gray to blond lanugo hair. Hair may grow up to 10 centimeters in length, giving a "werewolf" appearance. Congenital hypertrichosis lanuginosa may present with dental anomalies, glaucoma, pyloric stenosis, and photophobia.[35]

Universal hypertrichosis, another form of congenital generalized hypertrichosis, presents with thick, long hair on the back, proximal extremities, and preauricular areas. It is often thought of as "exaggerated normal hairiness."[36]

Hypertrichosis universalis congenita sometimes referred to as Ambras syndrome, presents with fine, silky, light-colored long hair primarily involving the face, ears, shoulders, and nose. It is associated with minor facial dysmorphism, supernumerary nipples, and dental anomalies.[37][38]

Patients with prepubertal hypertrichosis typically present with widespread, diffuse involvement that becomes obvious and bothersome during childhood. Hair growth favors the face (especially the forehead, temples, and preauricular area), proximal extremities, and back. It is described as having an "inverted fir tree" pattern. It also features thick, bushy eyebrows and a low anterior hairline.[7]

Acquired generalized hypertrichosis presents with the reversible, slow growth of terminal hairs over the forehead, temples, flexors, and trunk. Patients will report a history of frequently implicated medications traumatic brain injury, or systemic disease (see etiology section for a complete list).

Several forms of congenital localized hypertrichosis exist. Hypertrichosis cubiti (hairy elbow syndrome) presents anywhere from birth to early childhood with hypertrichosis over the forearms and antecubital fossa. It is occasionally associated with short stature. Hairy palms and soles syndrome presents at birth. Hypertrichosis of the auricle presents during childhood or adolescence and favors males. Hypertrichosis of the eyebrows and nasal tip appear in adolescence. Anterior cervical hypertrichosis presents from birth to early childhood and is associated with sensory and motor neuropathy, mental retardation, and hallux valgus. Posterior cervical hypertrichosis appears at birth and is associated with kyphoscoliosis.[39]

Becker melanosis (nevus) presents as a patch of hyperpigmentation with irregular borders on the upper trunk. Typically, hyperpigmentation appears during childhood, with hypertrichosis developing later in the second decade of life. Patients with Becker melanosis may have associated asymmetry of the extremities and hyperplasia or hypoplasia underlying the affected areas; ipsilateral mammary hypoplasia is a common finding in women). There are reports of Becker melanosis arising in the context of genitourinary abnormalities (SNUB syndrome; supernumerary nipples, uropathies, and Becker melanosis). Becker melanosis can also be associated with hemimaxillofacial dysplasia, which presents as unilateral maxillary enlargement manifesting as facial asymmetry, gingival hyperplasia, and hypoplastic teeth.[40]

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