OBJECTIVE: To review clinical and pathologic features and the long-term follow-up of patients with loose anagen hair (LAH). DESIGN: Clinical evaluation and long-term follow-up. SETTING: A university medical center. PATIENTS: Beginning in January 1990, 14 children and 5 adults (age range, 8 months to 47 years) were diagnosed as having LAH. Associated diseases included alopecia areata in a 3-year-old boy and Noonan syndrome in a 5-year-old boy. Two adult patients were parents of 2 affected children; the other 3 adults were the only members of their families with LAH. These 3 patients presented with a diffuse hair shedding that had suddenly developed 1 to 3 years before our observation. In all cases, findings of a trichogram showed a predominance of anagen hairs (80% to 100%) devoid of sheaths. INTERVENTION: None. RESULTS: In 4 children and 1 adult the condition remained stable; in 2 children and 1 adult, a considerable improvement in hair density was noticed. The pathologic study of hair from 5 patients did not reveal morphological abnormalities of the hair follicles except for a high incidence of fragmentations of the inner root sheath. CONCLUSIONS: Analysis of our patients with LAH reveals that the condition does not develop exclusively during childhood but can occasionally manifest itself later in life. The development of LAH may be sporadic, occur in association with developmental or acquired conditions, or, less commonly, be a familial disorder. While adult-onset LAH may not be exceptional, it can be easily misdiagnosed as telogen hair loss. The pathologic findings of LAH do not demonstrate any specific features and are of little value in the diagnosis of this condition.
OBJECTIVE: To review clinical and pathologic features and the long-term follow-up of patients with loose anagen hair (LAH). DESIGN: Clinical evaluation and long-term follow-up. SETTING: A university medical center. PATIENTS: Beginning in January 1990, 14 children and 5 adults (age range, 8 months to 47 years) were diagnosed as having LAH. Associated diseases included alopecia areata in a 3-year-old boy and Noonan syndrome in a 5-year-old boy. Two adult patients were parents of 2 affected children; the other 3 adults were the only members of their families with LAH. These 3 patients presented with a diffuse hair shedding that had suddenly developed 1 to 3 years before our observation. In all cases, findings of a trichogram showed a predominance of anagen hairs (80% to 100%) devoid of sheaths. INTERVENTION: None. RESULTS: In 4 children and 1 adult the condition remained stable; in 2 children and 1 adult, a considerable improvement in hair density was noticed. The pathologic study of hair from 5 patients did not reveal morphological abnormalities of the hair follicles except for a high incidence of fragmentations of the inner root sheath. CONCLUSIONS: Analysis of our patients with LAH reveals that the condition does not develop exclusively during childhood but can occasionally manifest itself later in life. The development of LAH may be sporadic, occur in association with developmental or acquired conditions, or, less commonly, be a familial disorder. While adult-onset LAH may not be exceptional, it can be easily misdiagnosed as telogen hair loss. The pathologic findings of LAH do not demonstrate any specific features and are of little value in the diagnosis of this condition.