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Diffuse hair loss or hair thinning; most often an acute self-limited process
Telogen effluvium (TE) is a transient condition in which there is a premature conversion of a significant proportion of anagen (growth phase) hairs into telogen (resting phase) hairs, resulting in increased shedding of these resting hair follicles and the clinical appearance of moderate to severe hair thinning.
- Five proposed types of TE
- Immediate anagen release: a highly common form, lasting 3 to 4 weeks, in which follicles meant to remain in anagen phase enter telogen prematurely due to a signal, including high fever, drug induced, or stress
- Delayed anagen release: occurs most often postpartum, in which a large group of hair follicles that have remained in the anagen phase for an extended period all together enter the telogen phase, resulting in hair loss
- Short anagen: a somewhat speculative type, in which at least 50% of the hair follicles have an idiopathic shortening of the anagen phase, resulting in a corresponding doubling of the follicles in the telogen phase
- Immediate telogen release: Normal resting club hairs remain within the hair follicle until an unknown signal causes their release, initiating the anagen stage to begin. In this type, the resting club hairs are prematurely released, ending the telogen phase abruptly and causing diffuse shedding.
- Delayed telogen release: In this type, the presence of increased visible light, whether it be a seasonal or environmental change, is thought to end a prolonged telogen phase and initiate the anagen phase, resulting in diffuse shedding of hair follicles.
Second most common cause of alopecia
Etiology and Pathophysiology
- The hair cycle consists of two predominant phases. The anagen (growth phase) and the telogen (resting phase), lasting ~3 years and 3 months, respectively. On the scalp, ~10–15% of hairs are in the telogen phase normally. Due to the presence of some types of external/internal stress, there may be an increase in the percentage of telogen hairs. As new anagen hairs emerge, these telogen hair follicles are forced out. The preceding event usually occurs 2 to 3 months prior to the appearance of hair loss.
- It is hypothesized that substance P plays a key role in the pathogenesis of TE through various mechanisms (1). Studies have been conducted on human hair follicles in vitro and mice hair follicles in vivo, which support this theory.
- Role of substance P includes the following (2):
- Upregulation of substance P receptor, NK1, at the gene and protein level, leading to premature catagen development and hair growth inhibition
- Upregulation of nerve growth factor (NGF) and subsequently its hair apoptosis–producing receptor, p75NTR
- Downregulation of hair growth–promoting receptor, TrkA
- Upregulation of major histocompatibility class (MHC) I and β2-microglobulin, resulting in loss of hair follicle immune-privilege
- Increase in tumor necrosis factor-α release by mast cells resulting in hair keratinocyte apoptosis
- Decreased cortisol levels in chronic stress states may also enhance the effects of substance P.
- Major surgery
- Thyroid disorder
- Febrile illness
- Allergic contact dermatitis (3)
- Iron deficiency anemia (4)
- Excess vitamin A
- Protein-calorie restriction
- End-stage liver or renal disease
- Hormonal changes (including pregnancy, delivery, and estrogen-containing medications)
- Chronic stress
- Drug induced (β-blockers, anticonvulsants, antidepressants, anticoagulants, retinoids, ACE-inhibitors, etc.)