Re: Alopecia long post

[Guest guest]

Great information Nik glad to know some of this stuff. I was wondering how

your doing? Is the stuff your new Derm has been treating you with helping

and are you seeing improvement? I hope so, hope you had a nice Chrsitmas,

and New Year.

Love,

----- Original Message -----

From: " nikkipep " <GP369@...>

< >

Sent: Sunday, January 06, 2002 11:10 PM

Subject: Alopecia long post

> Alopecia means hair loss, so not all alopecia is autoimmunie. There

> are many, many reasons for hair loss. A good website to learn about

> hair loss is, WWW.Keratin.com. Alopecia areata, universalis and

> totalis, are believed to be autoimmune. They really have no clue what

> causes it. I just wanted to clear this up as not all hair loss is

> autoimmune.

> Alopecia areata is a common, unpredictable, non-scarring form of

> hair loss. This disorder affects all age groups, with a higher

> prevalence in children and adolescents. Limited scalp involvement is

> the most common presentation but more severe forms of the disorder,

> involving the entire scalp or body, also exist. Research has linked

> alopecia areata with certain HLA-Class II alleles, implicating an

> autoimmune etiology. Various therapeutic modalities have been

> employed to gain clinically acceptable hair regrowth.

>

> Alopecia areata is a common disorder, hypothesized to be autoimmune

> in etiology, and estimated to affect almost 2% of the US population

> (1). This non-scarring alopecia affects both sexes equally and is

> seen in all age groups. A higher incidence is found in children and

> young adults, with common presentation before the age of five years

> (2-4). The unpredictable severity and course of the disorder exacts a

> high emotional cost from the affected patient and may result in

> psychiatric comorbidity (5).

> Etiology

> The etiology of alopecia areata is as of yet unclear, but is presumed

> to be due to an autoimmune reaction. Consistent evidence of

> autoantibodies directed against anagen stage hair follicle structures

> are found in both affected humans and in mouse models (6,7). Though

> autoantibodies are postulated to play an integral role in the disease

> process, current research implicates a cell-mediated autoimmune

> mechanism as the underlying pathogenic etiology (8). Supporting this

> theory is that activated CD4 and CD8 T lymphocytes have been found in

> a characteristic peri- and intrafollicular inflammatory infiltrate of

> anagen hair follicles of affected individuals (9-11). The transfer of

> alopecia areata by T lymphocytes cultivated from affected scalp and

> transferred to human scalp explants on a severe combined

> immunodeficiency mouse model has been demonstrated (12). Recent

> investigations on mouse models reported that transplanted alopecia

> areata tissue to normal mice would not induce alopecia areata if a

> specific monoclonal antibody, anti-CD44v10, was injected into the

> mice shortly after transplant surgery (8). CD44v10 is believed to be

> involved in the activation mechanism of CD4 and CD8 lymphocyte

> migration into tissue and the initiation of the subsequent defense

> response against antigenic stimuli (8). Similar research has

> demonstrated that invivo depletion of CD4+ cells using CD4+ cell-

> depleting OX-35/OX-38 monoclonal antibody (MoAb) partially restores

> hair growth in rats affected with alopecia areata (11). Current

> investigative efforts strongly implicate CD4 and CD8 T-cell

> lymphocytes in the pathogenic autoimmune etiology of this disorder.

> Alopecia areata, similar to many other autoimmune diseases, is linked

> with certain HLA-Class II alleles. The HLA antigen DQ3 (DQB1*03) has

> been identified as a general susceptibility marker for alopecia

> areata (13-15). Patients with the more severe forms of the disorder,

> alopecia totalis and alopecia universalis, were found to express the

> HLA alleles DQB1*0301, DRB1*0401 and DRB1*1104 in a significantly

> higher frequency (8). Milder, patchy forms of alopecia areata were

> also found to be associated with a significantly higher frequency of

> DRB1*1104, but no association was reported with the other two

> aforementioned alleles (8).

>

> Clinical description

> Alopecia areata usually appears abruptly as a patch of clearing on

> the scalp with no evidence of scarring. Scalp involvement is the most

> clinically distinguishing characteristic, but axillae, eyebrows and

> eyelashes may also be involved (16). Mild, limited involvement of the

> scalp is the most common presentation; multiple patches may become

> confluent over time. Regression may occur, with new hair growth

> taking place; recurrences in different locations occur unpredictably.

> Severe involvement may produce a loss of all scalp hair (alopecia

> totalis) or all hair on the body (alopecia universalis). Patients

> with alopecia areata that have a history of atopy may have a less

> favorable prognosis (17).

> Clinical variants of alopecia areata exist (16). Ophiasis alopecia

> areata describes band-like hair loss affecting the temporal and

> occipital regions of the scalp. Reticular alopecia areata describes a

> type that clinically shows patches of hair loss in various stages of

> disease activity. Diffuse alopecia areata has been attributed to a

> short anagen phase and subsequent inability of hair to grow. Alopecia

> areata has also been linked with a number of autoimmune diseases

> (18).

>

> Alopecia areata produces nail changes in 3-30% of affected patients

> (3,18-20). In one study of 201 affected children under 16 years nail

> changes were clinically evident in 60 (3). Of these 60 children, nail

> changes were more common in severely affected children (18 out of 34)

> than in children with localized disease (42 out of 167). In another

> study, 21 patients had clinical evidence of nail changes out of a

> total of 136 patients (103 adults, 33 children) affected with

> alopecia areata. Nail changes were found to be more common in

> children, especially in children with severe, long-standing disease

> (19). The nail changes associated with alopecia areata usually

> accompany hair loss, but may occasionally precede or follow the onset

> of hair loss by months or years (16). The main patterns of nail

> changes are: diffuse fine pitting (most common), thin and brittle

> fingernails and toenails, longitudinal ridging and rough surface

> trachyonychia (3,20-22).

>

> Systemic associations

> Atopy, vitiligo and autoimmune thyroid disease, namely Hashimoto's

> thyroiditis and Graves' disease, are more prevalent in patients with

> alopecia areata ????. Serum thyrotropin measurement has been

> recommended for all children with this disorder. (23) Although

> children are frequently screened for thyroid disease, the presence of

> disease in these patients is only 10% (3). A recent study on the

> evaluation of thyroid function in northern Indian patients with

> alopecia areata revealed that thyroid disease was clinically evident

> in only 16 (0.85%) of the 1700 affected patients evaluated over the

> interval of 1983-1997 (24). The incidence of thyroid structural and

> functional abnormalities is much higher in affected patients (78

> percent) than in controls (33 percent) (21). One study of 45 affected

> children, 16 years of age and younger, reported thyroid function

> abnormalities in 24 percent of these children (25). Thyroid function

> abnormalities include abnormal thyroid hormone (T3,T4) and thyroid

> stimulating hormone (TSH) values and the presence of antithyroid and

> antimicrosomal antibodies (25). Celiac disease, systemic lupus

> erythematosus and diabetes mellitus may also possibly be increased in

> incidence in patients with alopecia areata (2,3,26-29).

> Differential diagnosis

> Mild forms of alopecia areata are seen as solitary areas of non-

> scarring hair loss on the scalp and should be distinguished from

> trichotillomania and tinea capitis. Other forms of non-scarring

> alopecia, including traumatic alopecia and congenital hair loss

> syndromes such as congenital triangular alopecia, must also be

> considered in the differential diagnosis (30-33). Alopecia

> neoplastica, a rare form of alopecia, is associated most commonly

> with breast cancer; it may resemble localized alopecia areata

> (34,35). Systemic lupus erythematosus, syphilis and post-febrile

> alopecia may also at times resemble alopecia areata (16).

> Alopecia areata may be first evident in young patients as the sudden

> onset of diffuse alopecia (16,17). Telogen effluvium, believed to be

> associated with high fever, severe emotional stress, sudden

> starvation and certain medications, must also be considered in the

> differential diagnosis of diffuse alopecia. Other conditions

> associated with diffuse alopecia include acrodermatitis

> enteropathica, arsenicism and thallium poisoning, though these

> conditions usually have systemic symptoms (16). Recent research has

> identified the human hairless gene, equivalent to a gene studied in

> mouse models (hairless IRS/3 mouse), and has confirmed its

> association with a disease called atrichia or atrichia with papules

> (8,36). This condition was previously named alopecia universalis

> congenita. These patients are born with hair, but the hair matrix

> cells progressively undergo apoptosis by the third month, culminating

> in permanent hair loss (8,36).

>

> A skin biopsy specimen is diagnostic of alopecia areata, and is

> sometimes necessary to make a diagnosis (37,38). On histological

> examination a peribulbar lymphocytic infiltrate resembles a " swarm of

> bees. " (39). Scarring is characteristically absent.

>

> Treatment

> Treatment of alopecia areata may be divided into four different

> categories of widely accepted therapeutic modalities (9,18,23,40-55):

> immune inhibitors such as steroids or psoralen and UV-A light (PUVA);

> topical sensitizers such as squaric acid dibutylester (SADBE) and

> diphenylcyclopropenone (DPCP); non-specific irritants (anthralin) and

> the vasodilator minoxidil. Treatment goals are hair regrowth that is

> cosmetically acceptable to the patient; hair loss is not prevented

> with these treatments (23,53,56).

> Mild forms of alopecia areata are mostly treated by intralesional

> injection of a glucocorticoid, usually triamcinolone, every four to

> six weeks (16,23). Steroid injection may produce minimal transient

> atrophy or, less commonly, severe atrophy of the targeted skin; the

> most common side effect of steroid injection is pain, which is a

> complicating factor in treatment of children (53). Topical steroid

> application to areas of hair loss, usually applied twice daily, has

> also been found to be efficacious clinically, although combination

> treatment with minoxidil, anthralin or injected steroids is probably

> more therapeutic (23,53,57). Systemic steroids are reserved for use

> in rapidly progressive or extensive alopecia areata (53).

>

> Anthralin, the only non-specific irritant widely used for hair growth

> in alopecia areata, is applied topically as a 0.5 or 1% cream to

> affected areas once per day for 20-45 minutes; overnight application

> can also be used in certain patients who can tolerate the side

> effects (23,53). Application of topical anthralin may cause pruritus,

> erythema, scaling and folliculitis, necessitating the short

> application time (53). The combination therapy of anthralin and

> minoxidil has also shown favorable results in a group of treatment-

> resistant patients (58,59).

>

> Minoxidil (5% topical solution) is applied twice daily to areas of

> hair loss. Side effects are limited to mild local irritation and,

> less frequently, allergic contact dermatitis (60-62). Topical

> sensitizers induce an allergic contact dermatitis in applied areas of

> hair loss; weekly re-stimulation with the potent allergen is needed.

> Topical sensitizers have proven efficacy in patients with long-

> standing alopecia areata involving more than 50 percent of the scalp

> (23,57,63). Squaric acid dibutylester (SADBE) has shown good

> tolerability and mild side effects. In one study of 144 patients with

> varying degrees of alopecia areata, an 80% rate of regrowth was

> demonstrated in patients with mild alopecia areata and a 49% rate of

> regrowth was demonstrated in more severely affected patients (52). A

> study of squaric acid dibutylester in a pediatric population of

> twenty-eight children under the age of 13 with severe, long-standing,

> refractory alopecia areata reported nine patients achieving

> cosmetically acceptable or complete regrowth, and six patients

> achieving significant regrowth (64). Diphenylcyclopropenone (DPCP) is

> also an accepted modality for treatment of severe alopecia areata.

> One study demonstrated a 70% response rate in DPCP-treated patients

> with severe alopecia areata affecting more than 40% of the scalp

> (65). Of these patients, 30.9% demonstrated complete remission, while

> 39.7% underwent partial remission (65). Pruritus, dermatitis,

> urticaria, face and scalp edema and the development of vitiligo are

> known side effects of DPCP use (66).

>

> Cyclosporine is a potent immunomudulatory agent whose mechanism

> involves inhibition of T4 lymphocyte activation (67). A known side

> effect of cyclosporine is hypertrichosis, which has been attributed

> to prolongation of the anagen phase of hair growth (68). In one study

> of 15 alopecia areata patients treated with systemic cyclosporine,

> seven patients obtained cosmetically acceptable hair regrowth (67).

> Teshima et al describe a 24 week regimen containing cyclosporine (2.5

> mg/kg daily) and prednisolone (5mg/day) which produced a 100%

> response rate in six patients with persistence of hair regrowth six

> months after cyclosporine was discontinued (69,70). A similar study

> combining cyclosporine with prednisone reported two out of eight

> patients developing cosmetically acceptable hair regrowth (71). Gupta

> et al report cosmetically acceptable hair regrowth in three of six

> patients treated with 6 mg/kg cyclosporine daily for 12 weeks; hair

> loss occurred in all patients within 3 months of discontinuation of

> cyclosporine (72). Larger studies need to be performed to determine

> the efficacy of systemcic cyclosporine in the treatment of alopecia

> areata. The significant side-effect profile of cyclosporine deters

> long-term treatment (73).

>

> Cryotherapy has also been employed to stimulate hair growth in

> alopecia areata (49,50). One study, utilizing both children and

> adults, revealed hair regrowth in greater than 60% of affected areas

> in 70 of 72 patients (49).

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