Alopecia areata: Clinical presentation, diagnosis, and unusual cases

Alopecia areata (AA) is a nonscarring hair loss disorder with a 2% lifetime risk. Most patients are below 30 years old. Clinical types include patchy AA, AA reticularis, diffuse AA, AA ophiasis, AA sisiapho, and perinevoid AA. Besides scalp and body hair, the eyebrows, eyelashes, and nails can be affected. The disorder may be circumscribed, total (scalp hair loss), and universal (loss of all hairs). Atopy, autoimmune thyroid disease, and vitiligo are more commonly associated. The course of the disease is unpredictable. However, early, long‐lasting, and severe cases have a less favorable prognosis. The clinical diagnosis is made by the aspect of hairless patches with a normal skin and preserved follicular ostia. Exclamations mark hairs and a positive pull test signal activity. Dermoscopy may reveal yellow dots. White hairs may be spared; initial regrowth may also be nonpigmented. The differential diagnosis includes trichotillomania, scarring alopecia, and other nonscarring hair loss disorders such as tinea capitis and syphilis.     

斑秃的外用药物治疗

外用药物在斑秃治疗中具有重要作用,本文就外用糖皮质激素、致敏剂二苯基环丙烯酮和斯夸酸二丁酯、蒽林、米诺地尔、比马前列素、维A酸、贝沙罗汀、卡泊三醇、辣椒碱、壬二酸、大蒜凝胶和洋葱汁治疗斑秃的在斑秃中的应用进行综述。     

Investigative guidelines for alopecia areata

The reported efficacy of various treatments for alopecia is difficult to compare based on a general lack of consideration in case reports/series and clinical trials of the spontaneous regrowth or baseline prognostic factors seen in alopecia areata and a general lack of quantification of hair growth. This report will give both the investigator and clinician guidelines for clinical trial design that will take into account variables known to effect efficacy results such as baseline severity, pattern, and duration of hair loss, age of the subject, and concomitant conditions that may impact on potential regrowth. Reliable methods of assessment of efficacy and response criteria that will enable direct comparison of results between agents will also be discussed.     

Circumscribed alopecia areata incognita

The characteristic lesion of alopecia areata is a smooth bald patch on the scalp. When there is no bald surface it is called alopecia areata incognita. To date, all cases of alopecia areata reported as so‐called ‘incognito’ have shown a diffuse involvement of the scalp as in acute telogen effluvium. Recently, we have observed two patients who showed localised hair thinning of the scalp without bald spots. Histopathologically, the lesions were typical of alopecia areata with peribulbar lymphocytic infiltrates. The response to corticosteroid treatment and its clinical course were also compatible with alopecia areata.     

光疗法在斑秃中的应用

近年来,光疗治疗斑秃取得较好疗效。本文对PUVA疗法、长波紫外线A1、308nm单频准分子光和准分子激光、红外线,低能量激光疗法及点阵二氧化碳激光在斑秃治疗中的应用进行综述。     

痣周围性斑秃一例

患者女,20岁,因左枕部脱发2个月,颈部脱发1个月于2008年7月7日就诊.患者2个月前发现左枕部一脱发斑,中间一黑色丘疹,曾于当地医院行头皮内注射(具体不详)后无好转.1个月前发现颈部一脱发斑,脱发斑中间有一增生物,无疼痛、瘙痒.     

Prominent follicular mucinosis with diffuse scalp alopecia resembling alopecia areata

A 56‐year‐old Caucasian female presented with a 2‐month history of alopecia. On examination, she had diffuse hair loss of her scalp with some discrete patches of nonscarring alopecia. Histopathology revealed an inflammatory nonscarring alopecia with prominent follicular mucinosis and findings suggestive of alopecia areata. The patient's alopecia completely resolved with oral prednisone. The histopathologic findings and clinical presentation are most consistent with a diagnosis of alopecia areata with follicular mucinosis, although the differential diagnosis is broad. As follicular mucinosis may be associated with both benign and malignant conditions, it is important to be cautious regarding the clinical diagnosis when this reaction pattern is observed histopathologically.     

Clinical observations in alopecia areata: Implications and hypotheses

Alopecia areata (AA) is a T‐cell‐mediated hair loss disorder but the exact cause is unknown. In this report we describe patterns of onset, regrowth and relapse in AA and propose potential underlying mechanisms. We believe that these aspects of AA require integration into modern theories of AA pathogenesis.