Sunday, March 30

What is poliosis - Poliosis treatment

Poliosis causes, symptoms and treatment
What is poliosis?
Poliosis is a condition wherein a patch of hair is depigmented.
Poliosis may affect hair on the head, eyebrows, or eyelashes. Poliosis occurs as patches and there is substantial decrease or absence of melanin and melanocytes in the hair bulbs of the affected hair follicles. The skin beneath the poliosis patch may or may not be hypopigmented. In middle-aged persons poliosis is sometimes mistaken to aging related graying of hair. Poliosis may affect both the genders at any age. It may be congenital and be present at birth. In many cases poliosis is an acquired condition which manifest itself in the later stages of life. Diseases of the thyroid glands, some forms of malignancy, chemotherapy, irradiation, use of prostaglandin F2α analogs, cyclosporine and chloroquine have been associated with poliosis.

Melanoblasts, melanocytes and follicular melanogenesis

To understand poliosis we must know the process of pigmentation of hair. Melanin pigments, eumelanin and pheomelanin, give color to hair. Pheomelanin contributes orange and yellow colors and eumelanin subtypes contribute to black or brown hair color. The proportion and combination of these pigments give various hues of human hair color. Melanin pigment is synthesized by melanin producing cells known as melanocytes.

The precursor cells of melanocytes are formed from neural crest cells during embryonic development. The development of neural crest cells, their migration for the formation melanoblasts and the transformation of melanoblasts to melanocytes is brought about by cell protein signaling. Protein signalling is controlled by many genes. Any mutation or deletion in the concerned genes and any disturbances in these processes can manifest as congenetic or genetic poliosis disorders.

Follicular melanocytes synthesize the . The melanin granules are transferred into cortical and medulla . Finally pigmented hair shafts are formed. Any local disturbance to these processes, either physically or chemically can cause loss of hair and/or poliosis. In autoimmune conditions the follicular melanocytes may be targeted by antibodies and neutralized.

Congenital poliosis

Poliosis may be congenital and associated with several genetic disorders and conditions such as Waardenburg syndrome, piebaldism, tuberous sclerosis and giant congenital nevus.

Waardenburg syndrome is a group of genetic disorders characterized by hearing loss and hypopigmentation of skin and hair.
  • Waardenburg syndrome is caused by mutations in the EDN3, EDNRB, MITF, PAX3, SNAI2, and SOX10 genes leading to anomalies in the normal development of melanocytes. and poliosis are often associated with the disorder.

    Piebaldism is an autosomal dominant congenital disorder characterized by white forelock and patches of depigmented skin. White patches of hair on the head, eyebrows and eyelashes may be found in persons affected by piebaldism. Mutations in the KIT gene or SNAI2 are causes of this genetic disorder.

    Tuberous sclerosis is a rare genetic disease causing benign tumors to grow in many parts of the body including the skin. It is caused by the mutations in TSC1 and TSC2 genes. Patients affected by tuberous sclerosis may develop skin manifestations like white depigmented patches of hair on the head and body.

    Giant congenital nevus is sometimes associated with poliosis. G.Yosipovitch et al have reported the occurrence of this disorder in associated with a giant congenital nevus. WJ.Lee et al have described white patch of hair in association with a giant congenital melanocytic nevus on the scalp.

    Acquired poliosis

    Acquired poliosis is reported in conjunction with many benign conditions.
  • ?
  • Intradermal nevus and halo nevus have been associated with localized loss of pigment in the body hair. Kyu Mee Kay et al reported a case with the presence of white patches of hair without skin depigmentation associated with halo nevus. Whitening of eyelashes has been reported with eye conditions like blepharitis and sympathetic ophthalmia.

    Poliosis may be associated with diseases and disorders like sarcoidosis, GAPO syndrome, idiopathic uveitis, Vogt–Koyanagi–Harada syndrome, vitiligo, Marfan's syndrome, alopecia areata and herpes zoster. In Ho Kwon et al reported a case of poliosis circumscripta associated with neurofibroma.

    Marfan syndrome is an inherited autosomal dominant multisystem disorder of the connective tissue. In Marfan syndrome normal body growth is affected with characteristic overgrowth of long bones, abnormalities in skeletal bones, skin and internal organs. Skin manifestations are usually limited to striae distensae. KL. Herman et al had reported a Marfan syndrome case with acquired poliosis and white forelock.

    Poliosis and autoimmune diseases

    In autoimmune diseases, the body's immune system mistakenly attacks the body cells. In certain disorders melanocytes may be destroyed by the immune system.

    Vogt–Koyanagi–Harada syndrome is an autoimmune disease characterized by progressive uveitis with dermatologic, neurologic and auditory involvement. Poliosis of the eyelashes and eyebrows is often accompanied.
    poliosis in a person affected by vitiligo
    vitiligo and poliosis

    Vitiligo is an autoimmune disease wherein the body's immune system attacks and destroys the melanocytes.
  • The hair in the white patches of skin also turns white due to destruction of follicular melanocytes.

    Alopecia areata is considered to be an autoimmune disorder wherein the hair follicles are destroyed causing hairless patches. White hair patches is also associated with areata.

    Sarcoidosis is inflammatory disease with abnormal collection of granulomas. It can affect multiple organs. Manifestations of sarcoidosis in the eye include uveitis and retinal inflammation. K S Lett et al reported a case of eyelash poliosis in association with sarcoidosis of anterior uvea. The researchers postulated that the depigmentation is the result of an autoimmune mechanism.

    Association with malignancy and melanoma

    Alejandra G. de Alba Campomanes et al reported a case of conjunctival melanoma with eyelid poliosis. Dunn CL et al reported a case of melanoma of the scalp with white hair manifestations. Adel H. Alsuhaibani et al reported a case of primary orbital melanoma With white hair manifestations.

    Treatment for poliosis

    For treating this disorder, the causative factor has to diagnosed. Treating the cause may resolve the condition in some cases. However, if the causative factors are congenital the treatment becomes impossible. Cosmetic camouflage can help in some poliosis cases.
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    Reference:
    1.Sleiman R, Kurban M, Succaria F, Abbas O. Poliosis circumscripta: overview and underlying causes. J Am Acad Dermatol. 2013 Oct;69(4):625-33.

    Image source:
    http://en.wikipedia.org/wiki/File:Vitiligo_and_Poliosis.jpg
    Image author: Klaus D. Peter, Gummersbach, Germany | License: Cc-by-3.0-de
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    Monday, March 24

    What is piebaldism? - Piebaldism treatment

    Piebaldism causes and symptoms - Piebaldism treatment

    What is piebaldism?

    Piebaldism is a rare medical condition characterized by a white forelock and hypopigmented patches of skin.
    Piebaldism is an autosomal dominant genetic disorder of pigment producing cells (melanocytes). In this congenital disorder skin and hair are involved. Autologous cultured epidermis grafting is the best treatment for piebaldism.

    Nearly 90% of the piebaldism affected individuals have white forelocks. Apart from forelocks, eyebrows, eyelashes and the skin beneath the forelock may also lack pigmentation. In some individuals irregularly shaped white patches have been observed on the face, trunk and extremities. These hypopigmentation patches are mostly found to have symmetrical distribution. Some piebaldism affected individuals may not develop white forelocks and in some persons white forelocks are the only signs of piebaldism.

    Signs and symptoms of piebaldism

    Some of the signs and symptoms are:
    • presence of non pigmented patches of skin at birth
    • hypopigmented patches are non-progressive and do not increase in size or number
    • White forelock
    • unpigmented skin beneath the forelock
    • white eyebrows and eyelashes
    • symmetrical non pigmented patches on the face and body
    • narrow border of hyperpigmented skin surrounding the patches
    • islands of normal or hyperpigmented skin inside the hypopigmented patches

    What are the causes of piebaldism?

  • Piebaldism is caused by mutations in the KIT and SNAI2 genes. The mutations may be as deletions, nucleotide splice mutations or insertions. Individuals affected by Waardenburg syndrome may also develop the symptoms of piebaldism. The effects of mutations lead to defective melanoblasts proliferation, decreased survival and defective migration from the neural crest during development.
    KIT gene (v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog)
    The KIT gene is responsible for the synthesis of KIT proteins required for cell signaling. KIT protein signaling is important for cell proliferation, cell migration and development of hematopoietic stem cells, mast cells, interstitial cells of Cajal and reproductive cells.

    KIT protein signaling is also essential for melanocyte development. Mutations in KIT gene lead to nonfunctional KIT protein affecting the proliferation and migration of the precursor cells (melanoblasts) of the melanocytes. The location of mutation within the KIT gene correlates with phenotypic expression in piebaldism. More than 69 KIT gene mutations have been identified.
    SNAI2 gene (snail family zinc finger 2)
  • ?
  • The SNAI2 gene is involved in the production of snail 2 protein. The precursor cells of melanocytes are formed from neural crest cells during embryonic development. The development of neural crest cells and their migration and transformation is signaled by snail 2 protein. The formation melanoblasts and their transformation into melanocytes is probably brought about snail 2 protein. Any mutation in SNAI2 gene may affect the melanocyte formation and cause patches of unpigmented skin and piebaldism.

    Difference between piebaldism and Waardenburg syndrome

  • Piebaldism and Waardenburg syndrome involve mutations of genes giving rise to white patches of skin and hair. Individuals affected by piebaldism may be perfectly normal. Waardenburg syndrome is a group of genetic disorders causing hearing loss and changes in the pigmentation of hair, skin and eyes.

    A few of the piebaldism affected individuals may have normal hearing. Sometimes the eyes may be differently colored. White patches of skin and hair may be present. Waardenburg syndrome is caused by mutations in EDN3, EDNRB, MITF, PAX3, SNAI2, and SOX10 genes. There are four types of this disorder, and type II Waardenburg syndrome is caused by mutations in the MITF and SNAI2 genes.

    Differences between piebaldism, vitiligo and albinism

    • Vitiligo and piebaldism are characterized by white hypomelanosis patches of skin totally lacking skin pigment. In albinism there is total inability of skin to produce skin melanin.
    • Vitiligo is an acquired medical condition in which depigmented patches arise on normal colored skin. Vitiligo is an autoimmune disease wherein the body's immune mechanism destroys the melanocytes. Piebaldism and albinism are congenital disorders and are present at birth.
    • In albinism hair and skin are completely without skin pigment. In piebaldism, the patches are static and do not increase in size or number. Vitiligo can spreads progressively all over the body.
    • In 80-90% of cases of piebaldism, there is white forelock and triangular hypopigmentation of the skin beneath it. In vitiligo there may facial pigment loss and it may appear on the forelock also. But the typical triangular hypopigmentation is absent.
    • Albinos lack pigment in their eyes and have visual impairment. The nature and degree of their visual impairment may vary significantly. Persons with piebaldism or vitiligo usually have normal vision.

    Piebaldism treatment and management

    The unpigmented skin is unresponsive to medical treatment and light therapy. Long exposure to sunlight or UV light may cause inflammation, sunburn or cutaneous malignancy. Piebaldism affected persons are advised to use sun protective measures. If the patches are small, cosmetic camouflage makeup may be applied.

    Piebaldism treatments include dermabrasion and split-skin grafting. The split-skin grafting treatment followed by minigrafting treatment gives appreciable results. Autologous cultured epidermis graft treatment has been found to induce permanent repigmentation of large achromic lesions. In this non-invasive surgical treatment nearly 95% repigmentation is achieved. Before the treatment the non pigmented epidermis is removed with erbium:YAG laser.
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    Reference:
    Genetics Home Reference, National Institutes of Health
    1.http://ghr.nlm.nih.gov/condition/piebaldism
    2.http://ghr.nlm.nih.gov/gene/SNAI2
    3.http://ghr.nlm.nih.gov/gene/KIT
    4.Piebaldism treatment: Guerra, L., Primavera, G., Raskovic, D., Pellegrini, G., Golisano, O., Bondanza, S., Kuhn, S., Piazza, P., Luci, A., Atzori, F. and De Luca, M. (2004), Permanent repigmentation of piebaldism by erbium:YAG laser and autologous cultured epidermis. British Journal of Dermatology, 150: 715–721.

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    Friday, March 14

    Hypopigmentation on face

    Hypopigmentation on face occurs due to several skin problems. In hypopigmentation the function of melanin production by the melanocytes is reduced or lost.
    Depending upon the type of skin disorder, hypopigmentation may be total, partial or localized. Hypopigmentation on face may be harmless as in the case of pityriasis alba. However many hypopigmentation lesions may be due to severe underlying health problem. They require immediate medical attention as in the case of Alezzandrini syndrome.

    Alezzandrini syndrome

    Alezzandrini syndrome is a rare progressive unilateral degenerating syndrome in which vision and hearing on one side of the face get impaired. There is degenerative retinitis and deafness. Hypopigmentation patches of skin and patches of white hair appear on the affected side of the face.

    Idiopathic guttate hypomelanosis is an idiopathic disorder of unknown cause. It is characterized by small drop-like (guttate) hypopigmentation spots. The small lesions measuring up to 10 mm in diameter usually occur on the forearm and shin. Idiopathic guttate hypomelanosis is also found to form on other sun-exposed parts of the body such as neck, shoulders and face. The hypopigmentation spots are found to affect more women than men.

    Nevus anemicus

    Nevus anemicus is a congenital disorder with characteristic white macules appearing on the trunk. These hypopigmentation like lesions may also appear on the face. The macules do not redden on rubbing when compared to the surrounding skin. This due to permanent constriction of blood vessels in the area giving rise to blanched hypopigmentation like appearance.

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    Nevus depigmentosus is characterized by pale lesions on the body and in many cases they may be present at the time of birth. They are not progressive and grow in proportion to the body growth. The cause of nevus depigmentosus may be due to functional abnormalities of melanocytes in the lesions. The melanocytes fail to produce skin pigment. These pale hypopigmentation lesions are prone to sunburn and proper sun protection may be required.

    Piebaldism

    Piebaldism is a rare genetic disorder. It is an autosomal dominant condition affecting melanin production in patches. Piebaldism is characterized by the presence of a congenital white hypopigmentation forelock. There is also hypopigmentation patches scattered on the face and forehead. Unlike albinism, the vision of the affected person is normal. Though the cells have the ability to produce skin pigment, the function appears to have been blocked.

    Pityriasis alba is characterized by the appearance of dry scaly hypopigmentation macules, especially on the face. Young children, mostly boys are affected. The cause is unknown. No treatment is required and the patches resolve over some period of time. Moisturizers and cosmetic camouflage may be applied on the face for reassuring the youngsters.

    Poliosis

    Poliosis is due to decrease in the skin melanin in patches in head hair, eyelashes and eyebrows. The affected person is otherwise normal. however most of the patients with Waardenburg syndrome, Vogt–Koyanagi–Harada syndrome or tuberous sclerosis develop these hypopigmentation patches.

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    Like post inflammatory hyperpigmentation, post inflammatory hypopigmentation may also occur in the areas of face affected by injuries, cuts, burns and acne. Usually the normal pigmentation is restored after sometime when the damage is superficial. No specific treatment is required. If the injuries are deeper the hypopigmentation spots my acquire hyperpigmentation.

    Tinea versicolor is a fungal infection caused by the Malassezia globosa fungus and also to a lesser extent by Malassezia furfur fungus. The infection is more common in humid hot climate. The macules are differently colored. In persons with darker skin tone the patches may appear as hypopigmentation. Itching may be associated with the condition, getting aggravated by heat and sweating. Apart from the body, the macules affect the oily skin on the face. forehead, nose and cheeks.

    Vitiligo disease is characterized by the appearance of hypopigmentation patches on the extremities as well as on face. Non-segmental vitiligo is believed to be an autoimmune disorder wherein immune attacks on melanocytes cause these white patches of skin. Segmental vitiligo is associated with dorsal roots from the spine and is often unilateral. Generalized Vitiligo is the most common with widely distributed areas of depigmentation. In universal Vitiligo (vitiligo universalis) hypopigmentation is almost complete, including the face.

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    Sunday, March 9

    Dark skin pigmentation on face - Hyperpigmentation on face

    Hyperpigmentation is the medical term for dark, black or brown spots or patches on skin. Hyperpigmentation on face is quite common and it appears as lesions darker than the surrounding areas.
    Though hyperpigmentation is usually a harmless condition, it can be cosmetically disfiguring and cause great depression and psychological stress to the affected persons. Hyperpigmentation on the face may also occur due to medical conditions such as acanthosis nigricans, Addison's disease, amyloidosis and tinea versicolor which require proper medical care.

    Hyperpigmentation on face is the result of uneven, excess production and deposition melanin pigment as lesions. There are several causes for such excessive production of melanin. In some cases the cause is unknown and is idiopathic. The dark discoloration on face may be focal and well defined. It may also be diffuse with its margins gradually merging with the unaffected areas of the body.

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    Hyperpigmentation causes and types

    The quantity and type of melanin present in the skin imparts human skin color. Fair skinned individuals have lesser amounts of melanin whereas darker colored individuals have more of melanin pigment. However due to various reasons the may be concentrated as spots or patches on the face or body.
    Melasma
    In melasma symmetrical patches of hyperpigmentation appear on the face. On exposure sunlight (UV light), the lesions darken due to increased melanogenesis. Nearly 80% of the persons affected by melasma are women. The causes of melasma are, excess exposure to sunlight, hormonal imbalances, oral contraceptive pills, cosmetics, perfumes, toiletries and pregnancy. aims to inhibit tyrosinase enzyme activity. Traditional include application of epidermis bleaching agents like lemon juice and papaya juice.
    Freckles
    Freckles are concentration of melanin pigment and are more pronounced in persons with fair complexion. Apart from the face, freckles also appear on the exposed parts of the body. Freckles tend to darken on exposure to sunlight.
    Lentigo (lentigines) and age spots
    Lentigines are clusters of melanocytes. The small spots have clearly defined margin. They appear stable and are not darkened by exposure to sunlight.
    Mole (melanocytic nevus)
    Mole is a concentration of Nevus cells, a variant of melanocytes. The cause of mole formation is not clear and is believed to be caused by a defect in embryologic development. Acquired moles are formed due to excessive exposure to sunlight.
    Medication and chemicals
    Antimalarial drugs and amiodarone are known to cause hyperpigmentation. The chemicals present in the cosmetics, toiletries, perfumes are also known to cause darkened spots on face.
    UV damage
    Exposure to excessive sunlight or UV light has been found to stimulate melanocytes to produce excess melanin pigment.
    Post inflammatory hyperpigmentation
    The post inflammatory process of skin building after severe acne may result in hyperpigmentation. PIH occurs after an acne, burn, cut, abrasion and injury. The affected area turns darker than the rest of the skin.
    Smoker's melanosis
    The tar-components in the tobacco smoke stimulate melanocytes to produce more melanin pigment. Oral mucosa, lips and fingertips are found to darken with high melanin deposits. The hyperpigmentation gradually fades after quitting smoking.

    Hyperpigmentation treatment

    Tyrosinase enzyme activity mediates in the synthesis of melanin pigment. The treatment of hyperpigmentation is by applying chemical agents capable of blocking tyrosinase enzyme activity.

    Chemical peels
    Hydroquinone, kojic acid, azelaic acid, retinoic acid, trichloroacetic acid, salicylic acid, alpha hydroxy acid, beta hydroxy acid, niacinamide and croton oil are some of the chemical agents and peels used in removing hyperpigmentation on face.

    Natural hyperpigmentation remedies
    Lemon juice, honey, aloe vera gel, papaya paste, horseradish juice, apple cider vinegar, Grape seed oil, evening primerose oil, sea-buckthorn berry extract, bearberry extract and green tea extract are some of the natural remedies for removing hyperpigmentation.

    Microdermabrasion
    Microdermabrasion of the top layer of epidermis removes the old pigmented epidermis. A number of sessions may be required to get satisfactory results.

    Laser resurfacing
    Laser resurfacing removes the top layer of epidermis with hyperpigmentation and stimulates new fresh layer without the dark patches to grow out. A number of sittings may be required to get complete result.

    Hyperpigmentation can be prevented by avoiding all the triggering factors. As most of the dark spots tend to darken further on exposure to sunlight, avoiding the exposure and wearing proper sun protection can go a long way in preventing hyperpigmentation on face.


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