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Examination of the hair shafts with a microscope may reveal changes of trichorrhexis nodosa.
Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits.
There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.
Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.
Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair. The laser targets the melanin color in the lower 1/3 of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able treat all colors of hair.
Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.
Trichorrhexis invaginata (also known as "Bamboo hair" ) is a distinctive hair shaft abnormality that may occur sporadically, either in normal hair or with other hair shaft abnormalities, or regularly as a marker for Netherton's syndrome. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing for intussusception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft.
In 1937, Touraine and Solente first noted the association between hair-shaft defects (bamboo node) and ichthyosiform erythroderma. Còme first coined the term ichthyosis linearis circumflexa in 1949, although Rille had previously recorded the distinctive features of ichthyosis linearis circumflexa by 1922. In 1958, Netherton described a young girl with generalized scaly dermatitis and fragile nodular hair-shaft deformities, which he termed trichorrhexis nodosa. Later, this was more appropriately renamed as trichorrhexis invaginata (bamboo hair) for a ball-and-socket–type hair-shaft deformity at the suggestion of Wilkinson et al.
In 1974, Mevorah et al. established the clinical relationship between ichthyosis linearis circumflexa and Netherton syndrome, and an atopic diathesis was found to occur in approximately 75% of patients with Netherton syndrome.
There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.
Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.
Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.
Hypertrichosis is diagnosed clinically by the occurrence of hair in excess of what is expected for age, sex, and ethnicity in areas that are not androgen-sensitive. The excess can be in the form of excessive length or density and may consist of any hair type (lanugo, vellus, or terminal).
Hypotrichosis ("" + "" + "") is a condition of abnormal hair patterns, predominantly loss or reduction. It occurs, most frequently, by the growth of vellus hair in areas of the body that normally produce terminal hair. Typically, the individual's hair growth is normal after birth, but shortly thereafter the hair is shed and replaced with sparse, abnormal hair growth. The new hair is typically fine, short and brittle, and may lack pigmentation. Baldness may be present by the time the subject is 25 years old.
Hypotrichosis is a common feature of Hallermann–Streiff syndrome as well as others. It can also be used to describe the lack of hair growth due to chemotherapy.
The opposite of hypotrichosis is hypertrichosis, where terminal hair (thick) grows in areas that would otherwise normally have vellus hair (thin), for example abnormally thick facial hair growth in women.
Fordyce spots are completely benign and require no treatment. Often their presence is considered normal anatomic variance rather than a true medical condition.
The main diagnosis technique is observing the area. Then blood tests can be done to determine if there is a pre-existing condition. Family history can be considered because some of the related causes/conditions can be inherited.
Genetic forms of localized autosomal recessive hypotrichosis include:
CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be a female-pattern hair loss.
Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.
Bubble hair deformity is an abnormality of the hair shaft.
It is characterized by rows of bubbles seen microscopically within localized areas of brittle hair.
There is currently researching being done to find more treatments dependent on the different pre-existing conditions.
Studies are being conducted in which madarosis can be related to malignancy. A study by Groehler and Rose found that there was a statistical significance between these two. They concluded that patients malignancy lesions on the eyelid have a higher chance of having madarosis than a patient with a benign lesion. They stated that despite the fact that it is significant, the absence of madarosis does not mean the lesion cannot be malignant.
In many leprosy cases, madarosis is a symptom or a quality after diagnosis. However, in India, leprosy is common and researchers report a case of madarosis before diagnosis of leprosy with no skin lesions, only madarosis. This allowed for quicker treatment.
A main reason many people have madarosis is due to the chemotherapy drugs. There was a clinical trial in 2011 that tested an eyelash gel called bimatoprost. This gel enhanced the eyelashes in quantity and thickness. They tested this on 20 breast cancer patients who were undergoing chemotherapy. Results seemed positive, in that the group of people who used the gel had growth of eyelashes after the chemotherapy drugs.
In general, children with a small isolated nevus and a normal physical exam do not need further testing; treatment may include potential surgical removal of the nevus. If syndrome issues are suspected, neurological, ocular, and skeletal exams are important. Laboratory investigations may include serum and urine calcium and phosphate, and possibly liver and renal function tests. The choice of imaging studies depends on the suspected abnormalities and might include skeletal survey, CT scan of the head, MRI, and/or EEG.
Depending on the systems involved, an individual with Schimmelpenning syndrome may need to see an interdisciplinary team of specialists: dermatologist, neurologist, ophthalmologist, orthopedic surgeon, oral surgeon, plastic surgeon, psychologist.
Latanoprost and bimatoprost are specific PGF2a analogues applied topically, and have been found to lengthen eyelashes, darken hair pigmentation and elongate hair. Bimatoprost is available as treatment for eyelash growth. Latanoprost has shown ability to promote scalp hair density and pigmentation, and is theorized to function at the dermal papilla. A study found latanoprost ineffective on eyelashes in a patient with alopecia areata. It has also been found ineffective in treatment of eyebrow hair loss.
Physicians can often diagnose keratosis pilaris simply by examining the skin; tests are usually not needed. However, a dermatologist can use dermoscopy to confirm the diagnosis and assess if a person with KP is responding to treatment. Physicians will often consider family history and the presence of symptoms when making the diagnosis. Those with this condition are generally encouraged to contact a physician if the bumps are bothersome and do not improve with over the counter lotions.
A May 2013 review on the use of platelet-rich plasma (PRP) to regrow hair concluded more evidence is needed to verify the efficacy of PRP.
There are several different types of keratosis pilaris, including "keratosis pilaris rubra" (red, inflamed bumps which can be on arms, head, legs), "keratosis pilaris alba" (rough, bumpy skin with no irritation), "keratosis pilaris rubra faceii" (reddish rash on the cheeks), and related disorders. Keratosis pilaris is commonly described in association with other dry skin conditions, such as ichthyosis vulgaris, xerosis and atopic dermatitis, including those of asthma and allergies.
Keratosis pilaris does not bear any known, long-term health implications, nor is it associated with increased mortality or morbidity. It is not related to goose bumps, which results from muscle contractions, except that both occur in the area where the hair shaft exits the skin.
Intermittent hair–follicle dystrophy is a disorder of the hair follicle leading to increased fragility of the shaft, with no identifiable biochemical disturbance, also with an unknown prevalence.
Most doctors consider this a normal physiological phenomenon and advise against treatment.
The hair is normal in quantity and is usually silvery-blond or straw-colored. It is disorderly, it stands out from the scalp, and cannot be combed flat. The underlying structural anomaly is longitudinal grooving of the hair shaft, which appears triangular in cross section. This is caused by mutations in one of three possible genes; "PADI3", "TGM" or "TCHH3." The characteristic hair shaft anomaly can be demonstrated in asymptomatic family members by scanning electron microscopy. To be noticeable, 50% of hairs must be affected by the structural abnormality. Improvement often occurs in later childhood. An autosomal dominant mode of inheritance has been suggested though an autosomal recessive pattern with varying degrees of penetrance has also been noted. The stiffness of the uncombable hair has been reasoned to be due to the triangular form of the hair shaft in cross section. It has been suggested that the condition may result from premature keratinization of the inner root sheath.
Other syndromes with hair abnormalities may also show features of uncombable hair syndrome such as Rapp–Hodgkin ectodermal dysplasia syndrome, loose anagen syndrome, EEC syndrome (ectodermal dysplasia, ectrodactyly and cleft lip/palate) and familial tricho-odonto-onychial ectodermal dysplasia with syndactyly. However, unlike these conditions, uncombable hair syndrome alone is not associated with physical, neurologic, or mental abnormalities.
The most effective prevention is to grow a beard. For men who are required to; or simply prefer to shave, studies show the optimal length to be about 0.5 mm to 1 mm to prevent their hair growing back into the skin. Using a beard trimmer at the lowest setting (0.5mm or 1mm) instead of shaving is an effective alternative. The resulting faint stubble can be shaped using a standard electric razor on non-problematic areas (cheeks, lower neck).
For most cases, completely avoiding shaving for three to four weeks allows all lesions to subside, and most extrafollicular hairs will resolve themselves in about ten days.
Permanent removal of the hair follicle is the only definitive treatment for PFB. Electrolysis is effective but limited by its slow pace, pain and expense. Laser-assisted hair removal is effective. There is a risk of skin discoloration and a very small risk of scarring.
Exfoliation with various tools such as brushes and loofahs also helps prevent bumps.
Some men use electric razors to control PFB. Those who use a razor, should use a single blade or special wire-wrapped blade to avoid shaving too closely, with a new blade each shave. Shaving in the direction of hair growth every other day, rather than daily, may improve pseudofolliculitis barbae. If one must use a blade, softening the beard first with a hot, wet washcloth for five minutes or shave while showering in hot water can be helpful. Some use shaving powders (a kind of chemical depilatory) to avoid the irritation of using a blade. Barium sulfide-based depilatories are most effective, but produce an unpleasant smell.