87: Alopecia Areata Flashcards
What is alopecia areata and how does it present clinically?
Alopecia areata is a nonscarring hair disorder that can affect both genders and all age groups, with a higher incidence in younger individuals. Clinically, it presents with well-demarcated round or oval bald spots on the scalp or other parts of the body.
What are the characteristic hallmarks of alopecia areata?
The characteristic hallmarks of alopecia areata include: 1. Black dots (cadaver hairs, point noir): Hair that breaks off by the time it reaches the skin surface. 2. Exclamation point hairs: Hairs with a blunt distal end that taper proximally, appearing when broken hairs are pushed out of the follicle.
What is the etiology and pathogenesis of alopecia areata?
Alopecia areata is considered a chronic, organ-specific autoimmune disease. Key points include: - Autoactive, cytotoxic CD8 T cells affect hair follicles and nails, driven by an interferon gamma immune response. - IFN γ and induced chemokines are main drivers of disease pathogenesis. - NK cells may play a regulatory role in the condition.
What diagnostic features are used to identify alopecia areata?
The diagnosis of alopecia areata is supported by: 1. Clinical features leading to diagnosis. 2. Positive family history. 3. Presence of associated diseases (e.g., thyroid disease). 4. Dermatoscopic evaluation showing: - Follicular ostia - Exclamation point hair - Cadaver hair (black dots in follicular ostia) - Yellow dots 5. Biopsy for sudden diffuse AA showing generalized miniaturization and immune infiltrate around hair bulbs.
What is the significance of stress perception in alopecia areata?
Stress perception may influence the onset and exacerbation of alopecia areata, indicating a potential link between psychological factors and the autoimmune response in this condition.
A 10-year-old child presents with well-demarcated round bald spots on the scalp. What is the most likely diagnosis, and what clinical features would confirm it?
The most likely diagnosis is alopecia areata. Clinical features include black dots (cadaver hairs), exclamation point hairs, and possibly nail changes like pitting or sandpaper nails. Dermatoscopic evaluation may show follicular ostia, cadaver hairs, and yellow dots.
A patient with alopecia areata has a family history of autoimmune diseases. What is the likely etiology and pathogenesis of their condition?
Alopecia areata is a chronic, organ-specific autoimmune disease. Cytotoxic CD8 T cells attack hair follicles, driven by an interferon-gamma immune response. A positive family history is common, occurring in 10-42% of cases.
A patient with alopecia areata reports sudden whitening of their hair. What is this phenomenon called, and what causes it?
This phenomenon is called canities subita. It occurs because white hairs are spared by the disease, creating the illusion of sudden whitening.
A patient presents with alopecia areata and thyroid disease. What other associated disorders should be considered?
Other associated disorders include vitiligo, atopic dermatitis, psoriasis, cataracts, Cronkhite-Canada syndrome, and Down syndrome.
A biopsy of a patient with alopecia areata shows a ‘swarm of bees’ pattern. What does this indicate?
The ‘swarm of bees’ pattern indicates peribulbar immune infiltrate (CD8, CD4, NK cells) centered around the hair bulb, which is characteristic of the acute phase of alopecia areata.
A patient with alopecia areata has a positive family history and reports stress as a trigger. How do these factors influence the condition?
A positive family history indicates a hereditary component, and stress perception can influence the onset and exacerbation of alopecia areata.
A patient with alopecia areata has black dots visible on dermatoscopic evaluation. What do these black dots represent?
Black dots represent cadaver hairs or residual hair shafts visible in follicular ostia.
A patient with alopecia areata has exclamation point hairs. What do these hairs indicate?
Exclamation point hairs have a blunt distal end and taper proximally, indicating broken hairs being pushed out of the follicle.
A patient with alopecia areata has yellow dots on dermatoscopic evaluation. What do these dots signify?
Yellow dots signify follicular ostia filled with keratin and sebum, which are characteristic of alopecia areata.
How does the presence of associated diseases influence the diagnosis of Alopecia Areata?
The presence of associated diseases, such as thyroid disease, can support the diagnosis of Alopecia Areata (AA). A positive family history and clinical features are also critical in diagnosing AA. Dermatoscopic evaluation can reveal: 1. Follicular ostia 2. Exclamation point hairs 3. Cadaver hair (residual hair shafts visible as black dots in follicular ostia) 4. Yellow dots.
What role do CD8+ NKG2D T cells play in the pathogenesis of Alopecia Areata?
CD8+ NKG2D (natural killer group 2 member D positive) T cells are involved in the inflammatory infiltrate in Alopecia Areata (AA). They contribute to the autoimmune response affecting hair follicles.
What is the significance of stress perception in the onset and exacerbation of Alopecia Areata?
Stress perception may influence both the onset and exacerbation of Alopecia Areata (AA). Individuals with a high perception of stress may experience a higher incidence of AA, particularly in early onset cases.
In what scenarios should Alopecia Areata be included in the differential diagnosis (DDx)?
Alopecia Areata (AA) should be included in the differential diagnosis (DDx) whenever there are high percentages of telogen hairs or miniaturized hairs present, even in the absence of peribulbar inflammation.
What are the complications associated with alopecia areata?
- Relapsing course - Progression to alopecia totalis or universalis - Increased incidence of sunburns and skin cancers, nasopharyngeal and ophthalmologic inflammation - Diminished sense of personal well-being and self-esteem, leading to severe depressive mood and withdrawal from social situations.
What is the prognosis for patients with alopecia areata?
- Variable course of disease with irregular relapsing course: 40% relapse within the 1st year - Larger percentage relapses within 5 years - 25% experience a solitary episode - Spontaneous regrowth of hair is common but often followed by repeated episodes of hair loss.
What are the treatment options available for alopecia areata?
- There is no single therapy that can alter the natural course of the disease; all treatments are palliative. A. Conservative Management B. Topical Corticosteroids: Superpotent (Class I) corticosteroids C. Intralesional Corticosteroids: Triamcinolone acetonide D. Platelet Rich Plasma: Superior to low dose triamcinolone acetonide E. Systemic Corticosteroids: Prednisone 20 to 40 mg F. Topical Minoxidil 5% solution G. Prostaglandin Analogs.
A patient with alopecia areata has a relapsing course. What is the likelihood of relapse within the first year and within five years?
40% of patients relapse within the first year, and a larger percentage relapse within five years.
A patient with alopecia areata has nail changes and childhood onset. What is the prognosis?
The prognosis is poor due to the presence of nail changes and childhood onset, which are associated with a chronic relapsing course.
A patient with alopecia areata is treated with intralesional corticosteroids. What is the expected timeline for response, and what are the potential side effects?
Response is typically seen after 4 to 8 weeks. Side effects include atrophy of subcutaneous fat.
A patient with alopecia areata is considering systemic corticosteroids. What are the risks and limitations of this treatment?
Systemic corticosteroids do not alter the long-term prognosis and frequently result in relapse after discontinuation. Adverse effects include striae, acne, obesity, cataracts, and hypertension.
A patient with alopecia areata totalis is prescribed topical minoxidil. What is the expected efficacy of this treatment?
Topical minoxidil has little efficacy in treating alopecia areata totalis and universalis.
A patient with alopecia areata has a solitary episode of hair loss. What is the likelihood of spontaneous regrowth?
Spontaneous regrowth of hair is common, with 60% of patients experiencing partial regrowth within one year.
A patient with alopecia areata has occipital involvement. How does this affect the prognosis?
Occipital involvement is associated with a poor prognosis.
A patient with alopecia areata is treated with platelet-rich plasma (PRP). How does PRP compare to other treatments?
In a double-blind trial, PRP was found to be superior to low-dose triamcinolone acetonide and placebo injections.
A patient with alopecia areata is treated with prostaglandin analogs. What areas are these treatments most effective for?
Prostaglandin analogs like latanoprost and bimatoprost are effective for treating alopecia areata of the eyelashes and eyebrows.
A patient with alopecia areata is diagnosed with telogen effluvium. How can this condition be differentiated from alopecia areata?
Telogen effluvium is characterized by diffuse hair shedding without the well-demarcated bald spots seen in alopecia areata.
A patient with alopecia areata is diagnosed with trichotillomania. How can this condition be differentiated from alopecia areata?
Trichotillomania involves irregularly shaped patches of hair loss with broken hairs of varying lengths, unlike the well-demarcated bald spots of alopecia areata.
A patient with alopecia areata is diagnosed with tinea capitis. How can this condition be differentiated from alopecia areata?
Tinea capitis often presents with scaling, inflammation, and broken hairs, which are not typical of alopecia areata.
A patient with alopecia areata is diagnosed with androgenetic alopecia. How can this condition be differentiated from alopecia areata?
Androgenetic alopecia involves gradual thinning and miniaturization of hair, typically in a patterned distribution, unlike the patchy hair loss of alopecia areata.
A patient with alopecia areata is diagnosed with secondary syphilis. How can this condition be differentiated from alopecia areata?
Secondary syphilis may present with a ‘moth-eaten’ appearance of hair loss, which is distinct from the well-demarcated patches of alopecia areata.
A patient with alopecia areata is diagnosed with early scarring alopecia. How can this condition be differentiated from alopecia areata?
Early scarring alopecia involves permanent destruction of hair follicles, leading to scarring, which is not seen in alopecia areata.
A patient with alopecia areata is diagnosed with anagen effluvium. How can this condition be differentiated from alopecia areata?
Anagen effluvium involves rapid hair loss due to disruption of the anagen phase, often caused by chemotherapy, unlike the autoimmune etiology of alopecia areata.
A patient with alopecia areata is diagnosed with temporal triangular alopecia. How can this condition be differentiated from alopecia areata?
Temporal triangular alopecia is a congenital condition with hair loss confined to the temporal region, unlike the autoimmune and variable presentation of alopecia areata.
What are the potential complications associated with alopecia areata, particularly regarding its progression and psychological impact?
- Relapsing course: Progression to alopecia totalis or universalis is common, especially in younger patients with hair loss from trunk and extremities. - Increased incidence of: Sunburns, skin cancers, nasopharyngeal and ophthalmologic inflammation. - Psychological effects: Diminished sense of personal well-being, leading to severe depressive mood and withdrawal from social situations.
What factors contribute to a poor prognosis in patients with alopecia areata?
- Occipital involvement and/or hairline 2. Chronic relapsing course 3. Presence of nail changes 4. Childhood onset.
What are the treatment options available for alopecia areata, and what is the general effectiveness of these treatments?
- No single therapy can alter the natural course of the disease; all treatments are palliative. - Topical Corticosteroids: Superpotent (Class I) and potent (Class II) corticosteroids with minoxidil. - Intralesional Corticosteroids: Triamcinolone acetonide or Hexacetonide, with a response seen after 4 to 8 weeks.
What is the general effectiveness of treatments for alopecia areata?
No single therapy can alter the natural course of the disease; all treatments are palliative.
What are the types of corticosteroids used in alopecia areata treatment?
Topical Corticosteroids: Superpotent (Class I) and potent (Class II) corticosteroids with minoxidil.
Intralesional Corticosteroids: Triamcinolone acetonide or Hexacetonide, with a response seen after 4 to 8 weeks.
What is the role of Platelet Rich Plasma in alopecia areata treatment?
Platelet Rich Plasma has been shown to be superior to low dose triamcinolone acetonide in trials.
Why are systemic corticosteroids not recommended for alopecia areata?
Systemic Corticosteroids are not recommended as routine treatment due to lack of long-term prognosis alteration.
What is the efficacy of topical minoxidil 5% in alopecia areata?
Topical Minoxidil 5% is used in combination with corticosteroids, but has little efficacy in AA totalis and universalis.
What are the prostaglandin analogs used for in alopecia areata?
Prostaglandin Analogs, such as Latanoprost and Bimatoprost, are used for the treatment of AA of eyelashes and eyebrows.
What is the mechanism of action (MOA) of Diphenylcyclopropenone (DPCP) in alopecia areata?
The MOA of DPCP involves a decrease in the peribulbar CD4/CD8 lymphocyte ratio and a shift of T lymphocytes from the perifollicular area to the interfollicular area and dermis.
What are the side effects associated with the use of Anthralin in alopecia areata treatment?
Side effects of Anthralin include irritation, scaling, folliculitis, regional lymphadenopathy, and brown discoloration of the skin.
What is the desired effect of using DPCP in alopecia areata treatment?
The desired effect of using DPCP is the creation of contact dermatitis.
What are the advantages and disadvantages of using cyclosporine for alopecia areata?
Advantages: Effective in some cases. Disadvantages: High recurrence rate and side effect profile, including elevation of serum transaminases, headaches, and myalgia, render it impractical as a treatment for alopecia areata.
What is the role of Janus Kinase inhibitors in the treatment of alopecia areata?
Janus Kinase inhibitors, such as Baricitinib and Tofacitinib, play a significant role in maintaining autoreactive CD8+ infiltrate in alopecia areata and can lead to full regrowth of scalp hair in widespread cases.
What is the relapse rate associated with photo(chemo)therapy for alopecia areata?
Photo(chemo)therapy has a very high relapse rate in the treatment of alopecia areata.
What is the mechanism of action of Anthralin in alopecia areata treatment?
Anthralin has a nonspecific immunomodulating effect (anti-Langerhans cell).
What are the adverse effects of topical immunotherapy with DPCP?
Adverse effects include lymphadenopathy, severe contact eczema, and discoloration of the skin.
What are the limitations of phototherapy in alopecia areata?
Phototherapy has a very high relapse rate and is therefore not a long-term solution.
What are the potential side effects of cyclosporine in alopecia areata treatment?
Side effects include elevation of serum transaminases and cholesterol levels, headaches, dysesthesia, fatigue, diarrhea, gingival hyperplasia, flushing, and myalgia.
What is the mechanism of action of UVB phototherapy in alopecia areata?
UVB phototherapy affects T-cell function and antigen presentation, inhibiting the local immunologic attack against hair follicles by depleting Langerhans cells.
What is the expected outcome of treatment with baricitinib for alopecia areata?
Baricitinib, a Janus kinase inhibitor, can lead to full regrowth of scalp hair in widespread cases of alopecia areata.
What is the expected outcome of treatment with tofacitinib citrate for alopecia areata?
Tofacitinib citrate, a Janus kinase inhibitor, can lead to full regrowth of scalp hair in widespread cases of alopecia areata.
What is the expected outcome of treatment with ruxolitinib for alopecia areata?
Ruxolitinib, a Janus kinase inhibitor, can lead to full regrowth of scalp hair in widespread cases of alopecia areata.
What precautions should be taken when using anthralin for alopecia areata?
Precautions include avoiding application near the eyebrows and beard, using cool or lukewarm water for rinsing, and being cautious of potential irritation to the eyes.
What is the significance of Janus Kinase inhibitors in the treatment of alopecia areata?
Janus Kinase inhibitors, such as Baricitinib and Tofacitinib, play a significant role in maintaining autoreactive CD8+ infiltrate in alopecia areata and have shown potential for full regrowth of scalp hair in widespread cases.
What is the initial treatment for alopecia areata in patients under age 10?
The initial treatment for alopecia areata in patients under age 10 includes topical corticosteroids (mometasone) with or without topical 5% minoxidil.
How does the treatment approach differ for patients over age 10 with less than 50% scalp involvement?
For patients over age 10 with less than 50% scalp involvement, the treatment approach includes topical corticosteroids with or without intralesional corticosteroids and topical 5% minoxidil.
What treatment options are available for patients over age 10 with greater than 50% scalp involvement?
For patients over age 10 with greater than 50% scalp involvement, treatment options include JAK inhibitors with or without intralesional corticosteroids and scalp prosthesis.
What is the next step if a patient responds successfully to topical immunotherapy (DPCP)?
If a patient responds successfully to topical immunotherapy (DPCP), the next step is to continue DPCP as needed.
What should be done if there is no successful response to JAK inhibitor therapy in patients over age 10?
If there is no successful response to JAK inhibitor therapy in patients over age 10, the next step is to continue JAK inhibitor therapy with or without intralesional corticosteroids and consider topical immunotherapy.
What treatment options are available for patients with alopecia areata under age 10 with less than 50% scalp involvement?
For patients under age 10 with less than 50% scalp involvement, the treatment options include:
1. Topical corticosteroids (mometasone)
2. Topical 5% minoxidil (optional)
3. Intralesional corticosteroids (optional)
What is the next step if a patient over age 10 with greater than 50% scalp involvement does not respond to JAK inhibitor therapy?
If a patient over age 10 with greater than 50% scalp involvement does not respond to JAK inhibitor therapy, the next step is to consider:
1. Topical immunotherapy
2. Scalp prosthesis (if needed)
What is the role of topical immunotherapy (DPCP) in the treatment of alopecia areata for patients over age 10 with less than 50% scalp involvement?
Topical immunotherapy (DPCP) is used for patients over age 10 with less than 50% scalp involvement as follows:
- If there is a successful response to topical immunotherapy, it should be continued as needed.
- If there is no successful response, the treatment may progress to SADBE (squaric acid dibutylester) as needed.
