Loose hair - Loose anagen syndrome

Home › Anagen effluvium › Loose hair - Loose anagen hair syndrome.

What is loose anagen hair syndrome?
Loose anagen syndrome aka loose hair syndrome is an underdiagnosed and underreported disorder of abnormal anagen hair anchorage.

This anagen hair abnormality is characterized by easily detachable hairs mostly in the growth phase. There is also reduction in density and reduction in length of the shaft. Mostly the anagen hair of the scalp are affected by the syndrome. The diffuse baldness in more pronounced in the back of the head due pillow contact and rubbing. Though of esthetic concern, there is normal spontaneous recovery in adolescence.

This anagen hair abnormality was first described in 1984 by Zaun. The anomaly being a recently noticed and described anagen condition, its level of prevalence in the population is not known. Most of the cases are predominantly reported in young girls in between two and six years with light complexion and blond or light-brown hair. It is possible that the anagen anchorage abnormality may be equally present in boys but may go unnoticed due to their short hairstyles. A few cases of the syndrome is also reported in adults, perhaps with different etiology. Though earlier it was rarely described in children of African or Asian descent, in the recent years many cases are being described among these ethnic groups.

Causes of loose anagen hair syndrome

The exact cause of this abnormality is not known.

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Loose anagen syndrome is considered to be defective keratinization of the inner root sheath. The inner root sheath is posited to play an important role in anchoring the hair shaft within the follicle. The premature keratinization of inner root sheath impairs the adhesion of its cuticle to that of the growing shaft. In a clinical and molecular study, Valerie Chapalain et al considered loose anagen hair syndrome to be an autosomal dominant inheritance with mutation E337K in the gene K6HF. K6HF gene is one among the genes responsible for the production of keratin.

Diagnosis

In clinical observation, the presence of loose detachable hair of anagen phase helps in the diagnosis of the syndrome.

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Under microscopic examination, the strands appear devoid of inner and outer root sheaths. They are present with irregularly shaped bulbs and ruffled cuticle. Irregular longitudinal grooves are observed on the strands. Mild traction test results in clumps of anagen hair getting detached. In differential diagnosis, alopecia caused by nutritional deficiency must be ruled out. Other forms of alopecia as well as medical conditions causing alopecia such as anemia, abnormal function of thyroid glands or use of cytotoxic medication must be ruled out.

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Treatment

There is no standard treatment for this defective anchoring of shaft within the follicle. As the children grow old, progressively the anagen phase tends to be longer. Though the intensity is lesser in adulthood, the anchorage abnormality persists. Gentle handling during washing, shampooing and combing can reduce the shedding of strands. The affected child may suffer from psychological impact. In some severe cases of loose anagen hair syndrome, application of minoxidil on the scalp appears to improve the condition.

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Reference: 1.Rachita P Dhurat, Deepal J Deshpande. Loose Anagen Hair Syndrome. Int J Trichology. 2010; Jul-Dec; 2(2): 96–100.

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Anagen effluvium causes - Anagen effluvium treatment

Home › Anagen phase › Anagen effluvium treatment - Anagen effluvium causes.

What is anagen effluvium?
Anagen effluvium (AE) is a dystrophic disorder of extensive and sudden loss of hair in its growth phase.

Anagen effluvium is caused when factors antagonistic to metabolic and mitotic activity of the hair matrix suppress, interrupt or arrest the cell division. The anagen hair loss starts occurring even before the transition of the follicle to the telogen phase. It can affect both the genders at any age. For appropriate treatment, the triggers must be identified by thorough examination of patient's history of ailments, nutritional status and hair shedding episodes.

As at any time, about 90% of the hair is in anagen phase, its loss is very apparent, especially on the scalp. However, hairs of the beard, eyebrows, eyelashes, armpits and pubic regions may also be lost. Generally the anagen arrest is reversible and the regrowth of hair is possible when the suppressing antimitotic factor is withdrawn. However it may take up to three months for the recovery to become apparent, as the hair follicle, which was abruptly forced into regression and rest, has to recover and spring back into growth phase. Hair loss during the growth phase can be categorized into anagen effluvium and the loose anagen syndrome. The loose anagen syndrome has an entirely different etiopathogenesis.

Causes of anagen effluvium

Anagen effluvium is generally considered as the side effect of cancer treatment regimens such as chemotherapy and radiation.

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In patients undergoing chemotherapy, hair may fall out in large clumps. Cytostatic cancer chemotherapy is to block rapid cell proliferation. These medications, apart from blocking the rapid proliferation of cancer cells also block proliferation of hair matrix cells.

However, many cytotoxic medications and toxic chemicals, including bismuth, copper, cadmium, mercury, boron and thallium, may also induce termination of rapid hair growth phase. These antagonistic factors of mitosis and metabolism interrupt or arrest the cell division in the hair matrix. Consequently the hair shaft gets, partially keratinized, narrowed and weakened at the root and becomes vulnerable to fracture and break at minimal stress like combing, wearing head covers or friction during sleep.

Hair growth phases Follicular mucinosis Alopecia barbae Alopecia totalis Alopecia universalis Types of alopecia

Certain conditions like extreme malnutrition, protein energy malnutrition, extensive seborrhoeic dermatitis and dermatoses, extreme iron and zinc deficiency, excess of vitamin A, oral contraceptives caused hormonal imbalances, secondary syphilis, use of tyrosine kinase inhibitors, severe debilitating diseases also can cause anagen effluvium. In some cases autoimmune and inflammatory conditions like alopecia areata and pemphigus can affect the anagen phase and cause sudden alopecia.

Diagnosis

Hair-pull test with gentle traction and trichogram are usually done to diagnose the type of hair loss. The shed hair are observed under light microscope to differentiate the anagen and telogen phases. The anagen effluvium hair shaft can easily be differentiated from telogen hair. The telogen hair shows depigmentation at the root end with bulb at the root. The anagen effluvium hairs are fully pigmented and have tapered or feathered root ends. In the differential diagnosis of anagen hair loss, alopecia areata must be ruled out.

Treatment of anagen effluvium

Covering the scalp during chemotherapy with cooling pads or caps is found to temporarily slow down and suspend the blood circulation to the hair follicles as well as the hair matrix cell division. Scalp hypothermia stops the hair matrix cells from taking up the cytostatic medicine and getting damaged.

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However, any cancer cell in the cooled scalp area may also escape from damage. Hence any effort to protect the hair matrix from damage may also protect the cancer cells in the scalp. Scalp tourniquet is also used to apply pressure on the scalp to get the same results as in cool pad.

As anagen effluvium is almost certain to follow chemotherapy or radiation therapy, patient must be mentally prepared to face the situation. Cutting the hair short or shaving the scalp is a better option for the patient than having hair as patches on the head. The cancer patient will already be in a state of great mental stress due to the ailment. To reduce the stress from the balding appearance practical medical-aesthetic advice is needed. The patient may be encouraged to wear wigs or to cover the head with hat or scarf to disguise anagen effluvium.

Every cloud has a silver lining. With the completion of the cancer treatment, the hair loss may reverse and anagen phase may resume. In other cases removing or curing the triggering condition will help.

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Reference: 1.Kanwar AJ, Narang T. Anagen effluvium. Indian J Dermatol Venereol Leprol. 2013; Sep-Oct;79(5):604-12.

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Anagen phase - Anagen hair follicle growth

Home › Stages of hair growth › Anagen phase - Anagen hair follicle growth.

What is anagen?
Anagen phase is the active stage of hair follicle growth.

During anagen, there is vigorous mitotic activity in the germinal matrix of the follicle and the hair shaft is formed. Addition of new cells and pigmentation takes place at the base of the hair shaft. The anagen period extends from termination of the telogen to beginning of the catagen. The hair shaft keeps growing long till the termination of this phase by some unknown biological or chemical signals.

Anagen phase may last anywhere between 2-7 years and it is considered that the length of the period is predetermined genetically. People of Asian origin are found to have long follicle growth phase and have long strands, sometimes even reaching up to one meter. At any one time, approximately 80-90% of all follicles in a healthy individual are in the anagen growth phase. Different body regions have different anagen periods. The growth period may be short and last up to one or two months in case of follicles on the arms, legs, eyelashes and eyebrows.

It is estimated that on the entire surface of the human body, there are about 5 million hair strands.

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Approximately 50 to 100 of them are shed daily by a healthy individual. Not having long hair of desired length and its regression and balding are distressing concerns. Can we stimulate or prolong the anagen phase? The possibilities are discussed at the end of this post.

Anagen phases

Anagen phase comprises of follicular regeneration and active generation of pigmented hair shaft. Considering the cytohistological aspects, this period is further divided into six sub-phases.

Anagen subphase-I
Before this substage, follicles are in a mode of mitotic and transcriptional inactivity. In subphase-I, transcriptional activation of dermal papilla as well as the secondary hair germ occurs. The dermal papilla increases in size and there is proliferation of epithelial cells of secondary hair germ and their growth.

Anagen subphase-II
The bulb matrix cells, with the advent of vigorous mitotic activity grow down and envelop the dermal papilla. Dermal papilla differentiates into components of hair shaft and inner root sheath.

Anagen subphase-III

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There is continued proliferation and growth of bulb matrix cells and the precursors of follicular components are formed. The follicle reaches its maximum size and the bulb is fully formed. There is proliferation of follicle melanocytes and melanin granules are produced for incorporation of pigment into the hair shaft. The internal sheath attains a conical shape and the papillary cavity of the follicle is constricted at its base.

Anagen subphase-IV
In this phase, the melanin pigment is incorporated into the growing shaft, still within the cone of the internal root sheath. It now reaches the level of sebaceous glands.

Anagen subphase-V
The bulb and follicle reach their final shape and the shaft emerges from the inner root sheath to be in level with epidermis. The telogen shaft is dislodged and shed in this phase.

Anagen subphase-VI
The hair shaft emerges from the cone of external root sheath and transcends the skin surface. The fully formed anagen follicle keeps producing the strand till the activity is switched off.

Stimulating and prolonging the anagen phase

There are some compounds and hormones that can stimulate and prolong the anagen phase.

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Methylsulfonylmethane, a supplement intended for joint pain, is found to lengthen anagen phase of follicle growth which helps to grow long hair. Melatonin (N-acetyl-5- methoxytryptamine) is a hormone produced by the pineal gland which controls sleep regulation, circadian rhythms and follicle growth among many other functions. Application of topical melatonin induces and prolongs the anagen phase.

There are also hormones like androgens, regulating or restricting the follicle growth. Autoimmune and inflammatory factors can target and regress the follicles as in the case of many types of alopecia. Androgen inhibitors, anti inflammatory agents, antioxidants and immunosuppressants are prescribed to deal with the above problems. Hwang et al reported in the International Journal of Molecular Medicine that "adenosine promoted the expression of several growth factors that are responsible for hair growth, including fibroblast growth factors (FGF)-7, FGF-2, insulin-like growth factor (IGF)-1, and vascular endothelial growth factor (VEGF)."

However it advised to consult a physician or a trichologist for treating the follicle problems and rejuvenating anagen phase.

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Reference: 1.Hwang, Hwang, Lee, Kim, Roh, Lee, Kim, Lee, and Kyung-Chul Choi. "Adenosine stimulates growth of dermal papilla and lengthens the anagen phase by increasing the cysteine level via fibroblast growth factors 2 and 7 in an organ culture of mouse vibrissae hair follicles." International Journal of Molecular Medicine International Journal of Molecular Medicine 29 no. 2 (2012): 195-201. 2.Rachita P Dhurat. Deepal J Deshpan. Anagen Hair Syndrome. Int J Trichology. 2010; Jul-Dec; 2(2): 96–100.

Current topic on natural skin care: Anagen phase hair follicle growth.

Human hair growth cycle - Stages of hair growth

Home › Hair loss (alopecia) › Hair growth cycle - Human hair growth phases.

Human hair follicles, deceptively simple structures, with the most obvious function of producing hair shafts, have different growth phases.

Depending upon their location, the human hair follicles individually differ in their regenerative functions to produce shafts varying in length, thickness, shape, color, curl and growth phases. Hair growth passes through anagen (rapid growth), catagen (regression), telogen (resting) and finally exogen (shedding) phases.

In humans the hair cycling is asynchronous, intrinsic and autonomous. Though all the body hair goes through this cycling, the follicles have varying duration of growth phases at different body regions and also within the same site. The human follicular growth phases are independent of seasons and circannual rhythms. However, what initiates the stimulus for hair growth phases and the origin of the stimulus remains to be clarified.

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Akin to human skin turnover, hair growth cycling in phases is an unique inherent evolutionary process. Perhaps the process had evolved to 1) keep pace with the body growth; 2) adapt to periodic changes in the environmental conditions; 3) meet certain biological needs such as reproduction; 4) protect from malformations and malignancy; or 5) adapt to social, ethnic and regional evolutionary pressures.

Follicular morphogenesis and regeneration

Prenatal follicles form from primitive epidermis and there is follicular cell differentiation to form sheath and shaft. Follicle formation occurs once in a person's lifetime. Normally a person is born with a fixed number of hair follicles. Thereafter there is only follicular cycling.

The human skin has approximately five million follicles. The follicular cells have regenerative properties. In anagen there is complete regeneration of the lower portion of the follicle. The stem cells are present at the base of the follicle bulb and in catagen, during the regression of the follicle, these primitive epithelial stem cells remain behind.

Anagen phase in hair growth

Anagen phase is the shaft growth period and approximately 80 percent to 90 percent of healthy follicles are in anagen at any given time. Anagen of each strand on the human scalp may last between two to seven years depending on the individual. Longer anagen period contributes to long hair. However, in arms, legs, eyebrows and eyelashes have shorter strands because the anagen period lasts only for a few months.

In anagen period the follicles are very sensitive and prolonged diseases, nutritional deficiencies, extreme physical stress or mental stress may end the growth phase and trigger telogen effluvium leading to massive shedding of strands. The duration of anagen appears to have genetic influence in humans as generally Asians have longer anagen and long hair.

Follicular mucinosis Alopecia barbae Alopecia totalis Alopecia universalis Alopecia areata Alopecia types

The anagen has six subphases. Substage-I is primarily regrowth of papilla and onset of cell division. Substage-II involves descent of evolving bulb and differentiation of cells. In substage-III, the follicle attains its full size and cells differentiate into follicular components. In substage-IV, melanocytes are reactivated and produce melanin pigment. Substage-V involves dislodging of club hair and emergence of shaft through the tip of the internal sheath. In substage-VI hair shaft emerges through the skin surface.

Catagen Phase in human hair growth

Catagen phase in humans is a short transition period between anagen and telogen and lasts for about three weeks. The outer hair root sheath shrinks during this period and at any time about 5% of the shafts are in this mode. An unknown signal brings about catagen. There is stoppage of follicular cell growth and pigment deposit. The papilla is released from the bulb. There is cessation in differentiation of the lower follicular cells. In the follicle there is apoptosis of the distal region and vertical shrinkage.

Telogen phase in human hair

Telogen phase is the resting period and may last approximately for two or three months. After telogen, anagen returns.

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About 10 to 15% of the scalp follicles will be going through this phase at any time in a healthy individual. The ratio of between the anagen and telogen decides the density of hair present in the human scalp. Telogen is prolonged in case of strands on the eyebrows, eyelashes, arms and legs.

Exogen (shedding) phase in human hair

Humans shed 50-100 strands of hair daily. When the anagen resumes, the cells in the root region start dividing rapidly and push out the earlier telogen strand (club hair) which had stopped growing. This leads to loosening of the telogen strand and its shedding.

Further research may throw light on the following areas of importance in human follicular phases. The genetic aspects of anagen, catagen, telogen and exogen have to be further investigated. The triggers of anagen, catagen, telogen, and exogen phases of hair growth in humans have to be studied. The effects of extraneous factors including endocrine and immune functions on the human pilosebaceous apparatus have to be further understood. The factors behind vellus-to-terminal follicle switch as well as the inverse terminal-to-vellus switch have to be have to be further investigated. We further need to elucidate the dynamics of cellular division as well as apoptosis in the follicles. Better understanding of the human hair growth phases may help us in dealing with alopecia, a worldwide problem of great esthetic concern.

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Reference: 1.K. S. Stenn , R. Paus. Controls of Hair Follicle Cycling. Physiol Rev. 2001; Jan;81(1):449-494. 2.Krause K1, Foitzik K. Biology of the hair follicle: the basics. Semin Cutan Med Surg. 2006; Mar;25(1):2-10.

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Scleromyxedema - Papular mucinosis - Lichen myxedematosus

Home › Nevus simplex › Papular mucinosis - Lichen myxedematosus - Scleromyxedema.

Lichen myxedematosus (aka papular mucinosis or scleromyxedema) are heterogenous spectrum of rare idiopathic cutaneous disorders characterized by excess deposits of mucin (mucinosis).

Scleromyxedema, a generalized lichen myxedematosus, presents generalized mucinosis with papules, sclerosis and paraproteinemia. Scleromyxedema is associated with several systemic involvements that can result in impaired functions.

Papular mucinosis, a localized form of lichen myxedematosus, is characterized by papules, nodules and plaques. Unlike scleromyxedema, papular mucinosis does not present monoclonal gammopathy, sclerosis or systemic manifestations. Scleromyxedema form of lichen myxedematosus is not reported in children. Scleromyxedema usually affects adults above thirty years of age. There is no gender predilection in scleromyxedema affliction.

Causes of scleromyxedema and papular mucinosis

The cause of primary lichen myxedematosus disorder is idiopathic and unknown.

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Lichen myxedematosus is believed to be a fibroblast disorder inducing excess mucinosis. The cytokines interleukin (IL)–1, tumor necrosis factor (TNF)–alpha, and TNF-beta are also believed to cause mucinosis. Some of these papular mucinosis disorders are found to be associated with bone marrow cancers, HIV infection and hepatitis C.

Signs and symptoms of papular mucinosis

The localized form of lichen myxedematosus disorder involves mucinosis of limited areas on hands, face and extremities and appears as waxy solid bumps, nodules, papules and plaques. The papules in papular mucinosis contain mucin and on injury the papular wound may exude mucin.

Signs and symptoms of scleromyxedema

The generalized lichen myxedematosus disorder covers larger parts of the body with scleroderma-like induration and skin stiffening.

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The mobility of the mouth, lips, hands, arms, joints and legs may be hampered by scleromyxedema. The hair on the eyebrows, armpits and pubic area may be sparse in the scleromyxedema affected persons. The generalized mucinosis involved areas may be erythematous and edematous with pinkish-brownish discoloration.

Systemic manifestations of scleromyxedema

Scleromyxedema presents systemic manifestations. Systemic involvements of generalized scleromyxedema include neurologic complications, rheumatologic manifestations, respiratory problems, gastrointestinal abnormalities, renal problems and cardiac abnormalities. Some of the systemic manifestations of scleromyxedema are listed below.

• Difficulty in swallowing
• Proximal muscle weakness
• Reduced oxygen intake
• Dyspnea
• Arthritis of the joints
• Renal failure
• Inflammatory myopathy
• Raynaud syndrome
• Ectropion eyelid
• corneal opacities
• Acute neurologic complications
• Encephalopathy
• Peripheral neuropathy
• Cardiovascular abnormalities
• Myocardial ischemia
• Valvular mucin deposition
• Nasal regurgitation
• Decreased epiglottis mobility
• Decreased vocal cord mobility
• Paraproteinemia - typical symptom of Scleromyxedema

Diagnosis of scleromyxedema and papular mucinosis

In scleromyxedema histologic examination may reveal mucinosis, fibroblast proliferation, and fibrosis.

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There is monoclonal gammopathy. However thyroid disease is absent. In papular mucinosis, though certain amount of fibroblast proliferation is seen, both paraproteinemia and thyroid disease are absent.

Atypical forms of lichen myxedematosus disorder do not meet the criteria for either papular mucinosis or scleromyxedema. Peng Wang et al have described case of an atypical localized lichenoid plaque form in a patient appearing like papular mucinosis. The patient had lichenoid plaque eruptions restricted to neck region. There were no paraproteinemia or thyroid dysfunction in the patient. The patient also suffered from the systemic involvement of kidney with immunoglobulin A nephropathy (IgA nephropathy). There was proliferation of fibroblasts and mucin deposition in the renal interstitium and glomeruli.

Myxedema of thyroid disease, scleroderma (systemic sclerosis), scleredema, and nephrogenic systemic fibrosis may have to be ruled out by differential diagnosis lichen myxedematosus.

Treatment options for lichen myxedematosus

Treatment of both mucinosis and scleromyxedema include use of topical tacrolimus, retinoids, isotretinoin, thalidomide, corticosteroids, high-dose dexamethasone, methotrexate, psoralen UV-A (PUVA), plasmapheresis, UV phototherapy, intravenous immunoglobulin, dermabrasion, carbon dioxide laser excision, electrocoagulation, autologous stem cell transplantation and lenalidomide. These treatments shows various degrees of success.

M. Dolenc-Voljc et al reported successfully treating scleromyxedema having subcutaneous nodules with thalidomide and intravenous immunoglobulin. Biopsies of the scleromyxedema lesions showed fibroblasts proliferation and mucinosis between collagen bundles. Treatment with thalidomide and intravenous immunoglobulin lead to complete scleromyxedema remission. Dilip K Sa et al reported a case of localized papular mucinosis. Treatment with oral cyclophosphamide showed excellent response and papular mucinosis lesions had disappeared.

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Interesting topics in the natural skin care: Follicular mucinosis. Skin discoloration pictures. Types of skin discoloration. Brown skin discoloration. White skin discoloration. Reddish skin discoloration. Bluish skin discoloration. Yellow skin discoloration. Orange skin discoloration. Reddened skin.

References: 1.M. Dolenc-Voljc, V. Jurcic, A. Hocevar, M. Tomsic. Scleromyxedema with Subcutaneous Nodules: Successful Treatment with Thalidomide and Intravenous Immunoglobulin. Case Rep Dermatol. 2013;Sep-Dec; 5(3): 309–315. 2.Rongioletti F, Rebora A. Updated classification of papular mucinosis, lichen myxedematosus, and scleromyxedema. J Am Acad Dermatol. 2001; Feb;44(2):273-81. 3.Dilip K, Aparajita Ghosh, Piyush Kumar, Ramesh C Gharami. A Case of Localized Papular Mucinosis Showing Excellent Response to Cyclophosphamide. Indian J Dermatol. 2014 Mar-Apr; 59(2): 202–204. doi: 10.4103/0019-5154.127697.

Current topic in the dynamic natural skin care: What is Papular mucinosis - Lichen myxedematosus - Scleromyxedema.

Follicular mucinosis - Alopecia mucinosa - Mucinosis follicularis

Home › Alopecia barbae › Mucinosis follicularis - Alopecia mucinosa - Follicular mucinosis.

What is Alopecia mucinosa?
Follicular mucinosis is also known as alopecia mucinosa or mucinosis follicularis.

Alopecia mucinosa is a rare disorder characterized by mucin deposition (mucinosis) in pilosebaceous follicles and with much less frequency in sebaceous glands. Alopecia mucinosa commonly affects the face, neck and scalp, but any hairy part of the body may be involved. It is usually associated with the loss of hair at the affected follicular sites. Though many treatment options are available, there is no specific standard treatment for mucinosis follicularis.

Causes of follicular mucinosis

There are two forms of the follicular disorder. The primary form is idiopathic with unknown cause. The idiopathic form may undergo spontaneous regression and remission within two months to two years. Idiopathic follicularis is usually encountered in children or adolescents and rarely in adults. The secondary mucinosis follicularis form is usually associated with inflammatory skin diseases such as lupus erythematosus and lichen simplex and neoplastic conditions such cutaneous T-cell lymphoma, Hodgkin's disease and mycosis fungoides. The secondary form usually manifests in the adults.

Differential diagnosis of alopecia mucinosa

Differential diagnosis of follicularis condition is necessary to rule out hives, leprosy, eczema, acne, folliculitis, scarring alopecia and other forms of dermatosis.

Interesting reading: Definition of alopecia | What is alopecia areata | Alopecia areata totalis | Alopecia areata universalis

There is typical accumulation of mucin at the follicular areas and the presence of infiltrates of lymphocytes surrounding and involving follicular epithelium. Histological evaluation is necessary for the confirmation of the mucinosis follicularis. Colloidal iron stains may demonstrate the presence of mucin. Immunohistochemical staining may be used to diagnose the presence of abnormal cells associated with alopecia mucinosa.

Treatment of follicular mucinosis

There are no specific standard treatment for primary alopecia mucinosa. Mucinosis follicularis Treatment with topical, intralesional and systemic corticosteroids show mixed results.

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In some mucinosis follicularis patients photodynamic therapy had been effective. Rajiv Joshi et al reported complete cure of A. mucinosa with standard multidrug therapy (MDT) for leprosy. They treated two patients with a single mucinosis follicularis lesion with MDT for six months. The alopecia mucinosa had completely cleared and follicular growth resumed.

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The authors infer that dapsone in MDT may have cured alopecia mucinosa. Minocycline had cured a few cases of follicular, mucinosis follicularis. Treating the causative disorder may resolve the secondary follicularis.

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References: 1.Marie Lewars, Josh Levin, Stephen Purcell. Follicular mucinosis. Indian Dermatol Online J. 2013;Oct-Dec; 4(4): 333–335. doi: 10.4103/2229-5178.120667 2.Rajiv Joshi, Vinay Gopalani. Alopecia Mucinosa Responding to Antileprosy Treatment: Are we Missing Something?. Indian J Dermatol. 2013;May-Jun; 58(3): 227–231. doi: 10.4103/0019-5154.110834. 3.Paola C. Vieira da Rosa Passos, Manuela Ferrasso Zuchi, Andréa Buosi Fabre, and Luis Eduardo A. Machado Martins. Follicular mucinosis - Case report. An Bras Dermatol. 2014;Mar-Apr; 89(2): 337–339. doi: 10.1590/abd1806-4841.20142968

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Alopecia areata barbae causes - Alopecia barbae treatments

Home › Alopecia areata totalis › Alopecia areata barbae causes - Treatments for alopecia areata barbae.

What is alopecia areata barbae?
Alopecia areata barbae is hair loss as patches in the beard area.

Alopecia areata barbae is a non contagious condition affecting a very small percentage of men. It has no specific cause and there is no standard treatment. It is considered to be an autoimmune disorder. The immune mechanism mistakenly identifies the hair follicle as an antigen and attacks it. This autoimmune activity leads to inflammation of the hair follicles and the detachment of the affected hair. Hereditary predisposition is also a major contributing factor for developing Alopecia areata barbae.

Those men suffering from spotted hair loss on the scalp may or may not develop A. areata barbae. The disorder can also affect apparently perfectly healthy men having no problem on the scalp. In some cases the disorder may resolve by itself and disappear. In some men AA. barbae may recur. The affected area may remain as a patch or progress to cover the entire beard. In rare cases there may be involvement of nails like pitting, thinning or detachment from the nail bed. In rare cases burning, itching or tingling sensation is experienced in the affected skin.

Causes of alopecia areata barbae

Though it known that autoimmune reactions are the cause of hair loss, it is not still clearly understood why the hair loss appears as patches on the scalp and/or beard area and why particularly certain areas are only being targeted.

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It also not clear why perifollicular accumulation of antigen-presenting cells occurs at the site of AA. barbae. Hormonal imbalances, extreme mental or physical stress, environmental stress, allergic reactions, chemicals and presence of autoimmune diseases may contribute or trigger AA. barbae disorder.

Diagnosis and differential diagnosis

Differential diagnosis has to be done to rule out certain conditions wherein hair loss occurs in the beard area. Infection or inflammation of the follicles as in tinea barbae and folliculitis barbae may sometimes cause temporary or permanent damage to hair follicles and the affected area may appear as hairless patch after resolution of the condition.

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Pseudofolliculitis barbae (shave bumps) affected skin may also show patches of hair loss in the affected area after the resolution. In such conditions the observed hair loss on the beard area is not alopecia areata barbae.

Treatment options

Early diagnosis and treatment can prevent aggravation and mental stress. Shaving daily is the immediate treatment. Immunosuppression of cytokines responsible for the inflammatory reactions is the best treatment option. Immunosuppression causes inhibitory effect on the autoimmunity at the site of AA. barbae.

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Intralesional corticosteroid injections or topical corticosteroids shows good results but prolonged use can lead to thickening or thinning of the skin. Minoxidil, an antihypertensive vasodilator medication is found to promote regrowth of hair. Anthralin, a synthetic anti-psoriatic medication controls progress of alopecia areata barbae and promotes hair growth.

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Current topic in dynamic natural skin care: Causes of alopecia areata barbae and its treatment.