Friday, January 30

Does diabetes cause hair loss?

  ›     ›   Can diabetes cause hair loss?
Does diabetes cause hair loss?
Yes! Diabetes can cause hair loss.
There are two types of diabetes and one of the common symptom for both the types is hair loss. Diabetes is a disease in which the body does not properly control the levels of sugar in the blood. Diabetes occurs when the body does not produce enough insulin or does not use it properly. Insulin is a peptide hormone produced by beta cells in the pancreas.

Type I diabetes

Type I diabetes is insulin dependent and is usually caused by an autoimmune destruction and loss of insulin producing beta cells in the pancreas. Alopecia areata, a disease of hair loss, is again an autoimmune disorder in which the functional hair follicles are targeted by the autoimmune response. The loss is only of functional follicles and the follicle stem cells are not affected. The autoimmune responses though appear to be an specific action on target cells, diffused autoimmune activity on other cell types cannot be ruled out.

Type II diabetes

Type II diabetes is non insulin-dependent disease. It is caused by several physiological factors.
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In Type II diabetes there is loss in sensitivity as well as development of resistance to insulin in the body cells. The physio-hormonal changes brought about by the level of sugar in the blood can impact the health of follicles and disrupt their genetically programmed function.

It is also pertinent to discuss here, even if briefly, the factors responsible for androgenic alopecia, the male-pattern hair loss. Though AR gene is associated with androgenic alopecia, a variety of hormonal, genetic and environmental factors are likely causes of this disorder. Several medical conditions are associated with this type of loss, including disorders of insulin resistance, such as diabetes and obesity.

The diabetes disorder causes several negative physiological conditions such as, endocrine abnormalities, inadequate blood circulation, high blood sugar levels, weakened immune system and physical and mental stress.

Endocrine abnormalities

Diabetes affected are likely to have issues with thyroid glands. Malfunctioning thyroid can lead to alopecia. The androgenic hormone dihydrotestosterone is important for regulating follicular function and growth. The androgenic alopecia is related to increased activity of androgen receptors in hair follicles. The increased blood sugar levels affects the production of dihydrotestosterone, the activity of androgen receptors proteins and the loss of function of follicles.

Inadequate blood circulation

Diabetes compromises blood circulation and reduces blood supply to skin. The tissues get starved of nutrients and oxygen. In such circumstances anagen growth phase of the follicles gets interrupted and they enter into resting telogen phase. The increase in the number of follicles in the resting phase causes excessive hair loss.

Weakened immune system

Individuals suffering from diabetes have compromised immune system and poor circulation is one of the causes. Further patients with diabetes are prone to bacterial and fungal infections. These infections can inhibit normal follicular processes leading to excessive hair loss.

Physical and mental stress

Diabetics may experience stress and anxiety while making the disorder a part of their life. Diabetes is a lifestyle changing disease. Its treatment requires many restrictions in the type and quantity of food consumed. Further, continuous medication and rigid daily routine can be very stressful for the mind and body. Mental and physical stress is known to cause hair loss.

Diabetics must closely monitor their health to keep the sugar levels under control. Taking prescribed medications followed by diet control and sufficient exercise can stall many health complications, including alopecia. Certain diabetes medications are known to cause hair loss in some people.
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Reference:
1.Diabetes Research in Children Network (DirecNet) Study Group, Buckingham B, Beck RW, Tamborlane WV, et al. Continuous glucose monitoring in children with type 1 diabetes. J Pediatr. 2007;151(4):388-93, 393.e1-2.
2.Lee HJ, Chapa D, Kao CW, Jones D, Kapustin J, Smith J, Krichten C, Donner T, Thomas SA, Friedmann E. Depression, quality of life, and glycemic control in individuals with type 2 diabetes. J Am Acad Nurse Pract. 2009;21(4):214-24.
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Current topic in natural skin care: Hair loss can be caused by diabetes.
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Wednesday, January 28

What is telogen effluvium? - Telogen effluvium definition

  ›     ›     ›   What is telogen effluvium? - Telogen effluvium definition.

What is telogen effluvium?

Telogen effluvium is excessive shedding of hair during the resting or telogen phase.
In normal circumstances, at any given time, 80% to 90% of hairs of a person are in the growth (anagen) phase. The rest are in the transitional (catagen) and the resting (telogen) phases. The length of hair depends upon the duration of follicular growth phase, which in turn is genetically defined and determined.

The length of anagen phase differs in different areas of the body and in the same area under different conditions. When the follicular growth phase reaches the defined duration, the hair follicle, passing through the transitional stage, is transformed into telogen stage with the associated cellular changes. The resting may last up to two months.

In many mammals, the hair growth phases are synchronous and the coat shedding is apparent. In humans, the follicular growth phases are asynchronous.
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Each follicle is independently switches from growth phase to resting phase and vice versa. At the end of telogen, the follicle is reactivated and goes through cellular changes. The new hair pushes out the hair in the resting stage, leading to its detachment and shedding.

Typically a person sheds 50 to 100 hairs per day. When the loss of hair is greater than hundred strands and is very apparent on the comb and pillow, we may consider the loss as telogen hair loss. There will be thinning of the hair. The typical symptom of telogen effluvium is the presence of barely perceptible hair bulb on the end of the hair.

Due to many causative factors, the initiation of and the growth of new hair is delayed, leading to increase in the percentage of telogen hair and increase in shedding and generalized thinning. There may be abrupt shift of an increased number of growing hairs into resting stage.
Related topics: Causes - Treatment
Definition of telogen effluvium
Definition: considering what is telogen effluvium, it can be defined and summarize as "increased loss of hair, abrupt shift in growth phase to resting stage and delay in onset of fresh growth."
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Reference:
1.Whiting, DA. Chronic telogen effluvium: Increased scalp hair shedding in middle-aged women. Journal of the American Academy of Dermatology 35(6): 899-906 ,1996.
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Current topic in natural skin care: What is telogen effluvium definition.
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Saturday, January 24

Vitamin D deficiency and hair loss

  ›     ›     ›   Vitamin D deficiency and hair loss.
Can vitamin d deficiency cause hair loss?
Yes! Vitamin D deficiency can cause hair loss. Alopecia is the medical term for hair loss from the head or body.
Hair loss may have many causes including, nutritional deficiency, androgenic hormonal effects, infections, side effect of medications, trauma, sudden onset of telogen effluvium, rapid weight loss, radiotherapy and chemotherapy.

Certain health conditions like, postpartum effluvium, alopecia areata, lupus erythematosus, inflammatory diseases and diabetes can also cause hair loss. Vitamin D deficiency is linked to many inflammatory and autoimmune diseases such as asthma, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, type 1 (juvenile) diabetes, Crohn's disease, autoimmune thyroiditis, multiple sclerosis and alopecia areata.

The role of calcitriol

The biologically active form of vitamin D is known as calcitriol, which circulates as a hormone in the blood. The calcitriol hormone activates the calcitriol receptor (NR1I1). The calcitriol receptor plays an important role in regulating the hair cycle. The insufficiency of calcitriol can disturb and affect the hair cycle.

Vitamin D in the form of cholecalciferol is available in fish and fish oil, milk, fortified fruit juices and cereals. The human skin can synthesize this nutrient in the form of cholecalciferol with the help of sunlight. Lack of exposure to the sunlight or living in higher latitudes can cause vitamin D deficiency and related hair problems. At the sametime it is to be noted that megadoses of this nutrient can be toxic for the body.

Vitamin D deficiency and hair loss - Research evidence

There is compelling research evidence linking deficiency of calcitriol to hair fall. The very common form of autoimmune hair hypotrichosis, alopecia areata, as well as telogen effluvium or female pattern hair loss have been associated with vitamin D deficiency.

Mahmud Mahamid et al studied the possible association between serum 25-hydroxyvitamin D levels and alopecia areata ( autoimmune hair loss). They have published their research report in the Israel Medical Association Journal (June 2014). The pathogenesis of AA is considered to be autoimmune and inflammatory.
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In their clinical studies they followed up 23 patients with alopecia areata (AA) as well as a control group matched for age and gender. They collected blood samples and tested blood count, C-reactive protein (CRP), and 25-hydroxyvitamin D levels of the group. The C-reactive protein, a marker of inflammation, is released by the liver in response to inflammation.

They found that the patients with hair loss had significantly higher values for CRP than the control group. Further the AA group had deficiency in 25-hydroxyvitamin D serum levels (less than 30 ng/ml) lower than the control group. They concluded that,
We found a significant correlation between AA and vitamin D deficiency. Vitamin D deficiency can be a significant risk factor for AA occurrence.
Rasheed H et al in their study published in Skin pharmacology and physiology (2013), have reported that deficiency in serum ferritin and 25-hydroxyvitamin D levels can causes chronic telogen effluvium (TE) or female pattern hair loss (FPHL). They concluded that,
Low serum ferritin and vitamin D2 are associated with hair loss in females with TE and FPHL. Screening to establish these levels in cases of hair loss and supplementing with them when there is deficiency may be beneficial in the treatment of disease.
Aksu Cerman A et al reporting in British Journal of Dermatology (June, 2014) concluded that screening patients with alopecia areata hair loss for 25-hydroxyvitamin D deficiency seems to be of value for the possibility of supplementing these patients with vitamin D.
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Reference:
1.Aksu Cerman A, Sarikaya Solak S, Kivanc Altunay I. Vitamin D deficiency in alopecia areata. Br J Dermatol. 2014 Jun;170(6):1299-304.
2.Rasheed H, Mahgoub D, Hegazy R, El-Komy M, Abdel Hay R, Hamid MA, Hamdy E. Serum ferritin and vitamin d in female hair loss: do they play a role? Skin Pharmacol Physiol. 2013;26(2):101-7.
3.Roberto d’Ovidio, Margherita Vessio, Francesco Domenico d’Ovidio. Reduced level of 25-hydroxyvitamin D in chronic/relapsing Alopecia Areata. Dermatoendocrinol. Apr 1, 2013; 5(2): 271–273.
4.Mahamid M, Abu-Elhija O, Samamra M, Mahamid A, Nseir W. Association between vitamin D levels and alopecia areata. Isr Med Assoc J. 2014 Jun;16(6):367-70.
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Current topic in natural skin care: Does vitamin D deficiency cause hair loss.
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Sunday, January 18

Melanocytic nevus

   ›      ›      ›   Melanocytic nevus.
what is melanocytic nevus?
Melanocytic nevus is the medical term for mole, a pigmented lesion on the body.
Melanocytic nevus is also known as nevocytic nevus. It is the benign proliferation of a variant of melanocytes known as nevus cells. The nevus cells are larger than the typical melanocytes. They lack dendrites and have copious cytoplasm with coarse granules.

The melanocytes are pigment producing cells, having dendrites for transferring melanosomes containing melanin pigment to keratinocytes (cells forming outer layer of skin). These variant melanocytes are the primary component of a melanocytic nevus. They may occupy the junction between epidermis and dermis or the dermis of the skin. They may migrate towards epidermis or move deeper down into dermis.

Types of melanocytic nevi

Depending upon the location, the nevi are variously classified as junctional, intramucosal, compound, Ota, simplex, intradermal, Spitz or blue nuvi. The atypical (dysplastic) mole appear different from other moles and most of the melanoma arise from them. Further the mole may be present at birth (congenital) or acquired later in life.
congenital mole
melanocytic nevus on the nose

Junctional melanocytic nevus

The junctional mole is located along the junction of epidermal and dermal skin layers. These moles usually appear flat or slightly raised. They are usually acquired lesions. As they age they may become compound moles and become increasingly papular. Depending upon the depth and density and number of cells involved they may range in color from brown to black. There is slight risk of these moles turning into melanoma. Junctional intramucosal lesions are found usually in the mouth or genital area.

Intradermal melanocytic nevus

The intradermal moles are extremely common type of moles and are located in the dermis. They are flesh colored. Though there is proliferations of melanocytes, because of their depth from skin surface, the skin does not appear colored. These intradermal lesions appear usually as small, raised, round, dome-shaped or wart-like growths on the skin. If they are of recent origin or appear to grow fast, differential diagnosis is required to rule out basal cell carcinoma.

Compound melanocytic nevus

The compound mole represents the melanocyte proliferation of junctional as well as intradermal origins. These compound nevi are slightly raised and appear light brown to dark brown. They may be present at birth or appear later in life. If there is enlargement or symptomatic changes in compound lesion medical examination is required.

Congenital moles are present at birth or appear soon after birth.
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They are anomaly in embryogenesis and are considered as malformations or hamartomas. These lesions can be small or very large. Giant pigmented nevi are large dark colored lesions. Nearly 10 to 15% of these giant moles can develop into melanoma. The risk of melanoma increases with the increase in the size of the congenital mole.

Nevus of Ito or Ota are congenital moles appearing on the face and shoulder. Blue nevus and mongolian spots are also deep hyperpigmentation patches which are congenital. Congenital moles are sometimes associated with halo or vitiligo. Nath AK. et al reported a case where the congenital mole started regressing when the patient developed hypopigmentation at a different site. Lymphocytic infiltration and loss of pigment production was observed in the area of mole regression.

Acquired melanocytic nevus

Acquired moles appear later in life and are considered as benign neoplasms. Acquired moles may of junctional, compound or intradermal types. They are believed to be caused by sun exposure. In fair persons the sunburn areas can develop into these lesions.

Dysplastic (atypical) melanocytic nevus

Dysplastic moles are atypical and tend to have irregular borders and irregular coloration. These atypical moles may be flat or raised. When a number of atypical lesions are present, medical help must be sought to rule out melanoma, a virulent form of skin cancer. Atypical mole syndrome is an hereditary condition.

Causes
The cause of congenital moles is considered to be a defect in embryological development or hereditary condition. Sun damage, overexposure to sunlight and the resultant premature aging of skin are believed to be the causes of acquired moles.

Management
The melanocytic nevi may be left alone. If there is cosmetic or other concern they may be removed either by surgery or by medical lasers. A raised mole may also interfere with daily life chores like shaving or dressing. If there are any remnants of the lesion after the removal, it may regrow. If the mole is growing fast, if it is crusting and oozing, if there is any familial incidence of skin cancer or a number of atypical melanocytic nevi are present, immediate medical help is to be sought to rule out melanoma.
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Reference:
1.Arpaia N, Cassano N, Filotico R, Laricchia F, Vena GA. Unusual clinical presentation of regression in a congenital melanocytic nevus. Dermatol Surg 2005;31:471-3.
2.Martín JM, Jordá E, Calduch L, Alonso V, Revert A. Progressive depigmentation of a palmar congenital melanocytic nevus without an associated halo phenomenon. Dermatology 2006;212:198-9.
3. Nath AK, Thappa DM, Rajesh NG. Spontaneous regression of a congenital melanocytic nevus. Indian J Dermatol Venereol Leprol 2011;77:507-10
4.Gass JK, Grant JW, Hall PN, Atherton DJ, Burrows NP. Clinical resolution of a neonatally eroded giant congenital melanocytic nevus. Pediatr Dermatol 2006;23:567-70.
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Image source: en.wikipedia.org/wiki/File:Congenital_melanocytic_nevus_01.jpg
Author: M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara.
License: CC BY 2.0
Current topic in natural skin care: Melanocytic nevus.
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Tuesday, January 13

Hypertrichosis symptoms

   ›      ›   Hypertrichosis symptoms.
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 may be localized to a few spots or extensively cover a major portion of body. Hypertrichosis may involve one of the three types of hairs, viz., terminal, vellus and lanugo hairs. The symptoms are specific to each form of excessive growth of hair.

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.
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Congenital hypertrichosis universalis is a type of generalized CH. It is a rare familial disorder. The hairiness increased progressively. The patient's face, trunk and limbs get covered with long hair. In one case the patient's father and paternal grandfather were also noted to have the typical symptoms.

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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Current topic: Hypertrichosis symptoms.
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Monday, January 5

Werewolf syndrome

   ›      ›   Werewolf syndrome.
Werewolf syndrome is the informal term for hypertrichosis. The werewolf syndrome is characterized by abnormal growth of hair all over the body.
The affected patient being covered with hair on the face, appears like a werewolf. The werewolf syndrome may be present at birth (congenital) or acquired later on. The hypertrichosis syndrome is categorized into generalized or localized hypertrichosis.

The term werewolf syndrome is more commonly used to denote generalized hypertrichosis. In generalized hypertrichosis the whole body is covered by abnormal growth of hair. Ambras syndrome is a type of congenital generalized hypertrichosis wherein hair growth is also present on the face including forehead, nose, preauricular regions, external ears and external auditory canals, eyelids, cheeks, ears and shoulders. Ambras syndrome may aptly suit the term werewolf syndrome.

What is 'werewolf'?

This word has origin in late Old English word wer(e)wulf, were meaning "adult male human" and wulf meaning "wolf".
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Werewolf refers to a man changing into a wolf. In ancient Greek literature and mythology there are many references to men changing into wolves or other animals. In Europe, there are folklores of men transforming into wolves once every year for several days, and then changed back to their human shape.

These stories give bizarre reasons for the transformation, such as curse, sin, impiety, cannibalism, bite or scratch from wolf, sleeping under full moon, sorcery etc. These supposed werewolves were persecuted and involved in witchcraft trials. By the end of 18th century these beliefs subsided and the wolf-like character has become a subject of fictions and movies.

To know more about hypertrichosis and related information you may follow the links given alongside. Please note that CGH or werewolf syndrome is entirely different from hirsutism. Hirsutism is caused due high levels of androgen hormone in children and women, manifesting as excessive hair growth on the beard, axillary and pubic areas.
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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.
3.Baumeister FA, Egger J, Schildhauer MT, Stengel-Rutkowski S. Ambras syndrome: delineation of a unique hypertrichosis universalis congenita and association with a balanced pericentric inversion (8) (p11.2; q22). Clin Genet. 1993 Sep;44(3):121-8.
4.Rashid M Rashid, Lucile E White. A hairy development in hypertrichosis: a brief review of Ambras syndrome. Dermatology Online Journal 13 (3): 8.
5.Tadin M, Braverman E, Cianfarani S, Sobrino AJ, Levy B, Christiano AM, Warburton D. Complex cytogenetic rearrangement of chromosome 8q in a case of Ambras syndrome. Am J Med Genet. 2001 Jul 22;102(1):100-4.
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Current topic in natural skin care: Werewolf syndrome.
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Thursday, January 1

Ambras syndrome

   ›      ›   Ambras syndrome.
What is Ambras syndrome?
Ambras syndrome (AS) is a type of congenital generalized hypertrichosis (CGH).
Ambras disorder is an extremely rare type of excessive growth of hair. The condition is androgen-independent. Ambras syndrome is characterized by the extensive presence of hair on the body, including face, ears and shoulders. In Ambras hypertrichosis the type of hair involved is vellus, whereas in congenital hypertrichosis lanuginosa, lanugo hair is involved and ears are usually spared.

The ambras disorder is usually associated with several deformities such as dental anomalies, enlarged nose tip, triangular coarse face. This type of congenital hypertrichosis was first described by Baumeister et al (1993) and the name Ambras syndrome was proposed by them. They reviewed nine other cases of CGH from literature and argued for the naming of the particular type of CGH as Ambras syndrome.

History of Ambras syndrome

The ambras disorder was well-documented as the 'family of Ambras'. This was documented by Altrovandus in his book Monstrorum Historia cum Paralipomenis historiae omnium animalium published in 1642. He had mentioned of two daughters, a son, and a grandchild in Gonzales family having hypertrichosis and named them as Ambras family.
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Petrus Gonsalvus (c.1537–1618) was born in Tenerife, the largest and most populous island of the seven Canary Islands. The family of Ambras, Petrus Gonsalvus, three of his daughters Maddalena, Francesca and Antonietta and two of his sons Enrico and Orazio had generalized . Petrus Gonzales moved to France and resided at the court of Henri II of France. He was sent to the court of Margaret of Parma, regent of the Netherlands and later he moved into the court of Alexander Farnese, Duke of Parma.

The Chamber of Art and Curiosities located in Ambras Castle near Innsbruck in Austria, has a painting of Petrus Gonsalvus. Presently, the painting is exhibited in the Kunsthistorisches museum in Vienna. Baumeister et al coined the term Ambras syndrome for CGH with symptoms similar to Gonzales family.

Causes of Ambras syndrome

As reported by Baumeister et al, a genetic alteration is believed to play a central role. A pericentric inversion (8)(q12q22) is cited as the cause. Balducci et al (1998) reported a similar case with paracentric inversion, at (8)(q12q22). Baumeister et al disputed the claim of Balducci et al and suggested that the condition could be hypertrichosis universalis and not AS. The typical symptom of the hypertrichosis disorder,like the presence of dense hair on the nose, preauricular regions, external ears and external auditory canal were absent. Fantauzzo et al. (2008) reported that the positional change and the resultant downregulation of TRPS1 expression as the possible cause of Ambras hypertrichosis.

Diagnosis

The AS patients have vellus hair hypertrichosis. The hair is silky. long, light-colored and is prominent on face, ears and shoulders. The trichosis uniformly covers the eyelids, nose, cheeks, ears and shoulder. There are no metabolic and endocrine defects and the hormonal levels are normal.

There no cure for this congenital disorder and frequent shaving of the face may relieve some of the miseries.
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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.
3.Baumeister FA, Egger J, Schildhauer MT, Stengel-Rutkowski S. Ambras syndrome: delineation of a unique hypertrichosis universalis congenita and association with a balanced pericentric inversion (8) (p11.2; q22). Clin Genet. 1993 Sep;44(3):121-8.
4.Rashid M Rashid, Lucile E White. A hairy development in hypertrichosis: a brief review of Ambras syndrome. Dermatology Online Journal 13 (3): 8.
5.Tadin M, Braverman E, Cianfarani S, Sobrino AJ, Levy B, Christiano AM, Warburton D. Complex cytogenetic rearrangement of chromosome 8q in a case of Ambras syndrome. Am J Med Genet. 2001 Jul 22;102(1):100-4.
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Current topic in natural skin care: Ambras syndrome.
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