A thorough history is very important, as there is generally an inciting trigger such as psychological stress, childbirth, weight loss, or medications (eg, interferons, antihyperlipidemic medications, derivatives of retinol, anticoagulants) that precedes telogen effluvium by a few months. Telogen effluvium, a condition of noninflammatory, diffuse hair loss, is often difficult to distinguish from female pattern hair loss. Nail involvement (eg, pitting, trachyonychia, and longitudinal ridging) and patchy hair loss in nonscalp regions (eg, the eyebrows) are inconsistent with the diagnosis of male or female pattern hair loss. Seborrheic dermatitis is often associated with seborrhea (oily scalp) which is a result of androgen stimulation of the sebaceous glands. Nevertheless, seborrheic dermatitis is more prevalent in people with pattern hair loss, 12 so male and female pattern hair loss can present with another scalp condition. Inflammation, scarring, or scaling of the scalp suggests a different diagnosis, as pattern hair loss is usually unaccompanied by these signs. Hair miniaturization can be seen better using a sheet of paper as a backdrop and comparing the caliber of adjacent hair shafts. Hair loss can be assessed by comparing the hair part of the central scalp with that of the occipital scalp, which is generally spared. In women, the vertex and midfrontal scalp are commonly affected, as described above. Male pattern hair loss typically presents as a receding hairline and hair miniaturization on the frontal and vertex scalp. When examining the scalp, note the distribution of hair loss, the caliber of hairs, and other clinical features. This review focuses on clinical presentation, diagnosis, and treatment of pattern hair loss.Ī complete skin evaluation should be conducted, including the face, scalp, and nails. It is the most common form of hair loss in both men and women and has psychosocial effects, including stress and diminished quality of life. Pattern hair loss is a progressive, nonscarring form of hair loss characterized by gradual loss of terminal hair and follicular miniaturization to vellus hair fibers on the scalp in a characteristic distribution. Topical minoxidil and oral finasteride are first-line treatments for male pattern hair loss and topical minoxidil is the first-line therapy for female pattern hair loss, but there are a number of other off-label pharmacologic and nonpharmacologic treatments. A hair biopsy may be of value for clinically challenging cases. Pattern hair loss is commonly diagnosed with a thorough history physical examination of the face, scalp, and nails the hair-pull test dermoscopy and laboratory testing. The process can begin soon after puberty, and the resulting hair loss negatively affects quality of life and self-image. Higher AAT dosing than currently recommended may lead to enhanced clinical benefits and should be explored further.Ĭlinical trial registered with (NCT 01669421).Male and female pattern hair loss is a nonscarring, progressive form of alopecia that typically affects the temporal, frontal, and vertex scalp in men and central scalp in women. On restarting SD after DD treatment, a possible carryover effect was seen for several biological markers.Ĭonclusions: Subjects with AATD on SD augmentation therapy still exhibit inflammation, protease activity, and elastin degradation that can be further improved by normalizing AAT levels. DD therapy also further downregulated BALF ILs and cytokines including Jak-STAT (Janus kinases–signal transducer and activator of transcription proteins), TNFα (tumor necrosis factor-α), and T-cell receptor signaling pathways, cytokines involved in macrophage migration, eosinophil recruitment, humoral and adaptive immunity, neutrophil activation, and cachexia. Measurements and Main Results: DD therapy increased trough AAT levels to normal and, compared with SD therapy, reduced serine protease activity in BALF (elastase and cathepsin G), plasma elastase footprint (Aα-Val 360), and markers of elastin degradation (desmosine/isodesmosine) in BALF. At the end of each phase, BAL fluid (BALF) and plasma samples were obtained. Methods: Clinically stable subjects were evaluated after 4 weeks of SD therapy, followed by 4 weeks of DD therapy, and 4 weeks after return to SD therapy. Objectives: To evaluate the biological effects of normalizing AAT trough levels with double-dose (DD) therapy (120 mg/kg/wk) in subjects with AATD already receiving SD therapy. The recommended standard dose (SD 60 mg/kg/wk) elevates AAT trough serum levels to around 50% of normal however, outside of slowing emphysema progression, its effects in other clinical outcomes have not been rigorously proven. Rationale: Augmentation therapy with intravenous AAT (alpha-1 antitrypsin) is the only specific therapy for individuals with pulmonary disease from AAT deficiency (AATD).
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