Table 1.

Functional types of telogen effluvium with clinical correlations

In immediate anagen release, follicles that would normally complete a longer cycle by remaining in anagen prematurely enter telogen; it is a very common form of telogen effluvium, typically occurring after periods of physiologic stress.

Because the shedding is dependent on transition from anagen through catagen and telogen with a subsequent release of telogen hairs, hair loss occurs 3–4 months after the inciting event; a host of different triggers has been implicated and identifies the clinical species of the genus, e.g. postfebrile, posttraumatic, postinterventional, psychogenic effluvium, and others; febrile illness, accidental trauma, or surgical operations with a large hemorrhage, a crash diet, or severe emotional distress are among the most common causes; most are self-limiting and will undergo normal reversal; a careful patient history with respect to the chronology of events usually reveals the diagnosis and the cause.

In delayed anagen release, hair follicles remain in prolonged anagen rather than cycling into telogen; when finally released from anagen, the clinical sign of increased shedding of telogen hair will be found.

This type of telogen effluvium underlies postpartum hair loss; during the second half of pregnancy, the percentage of anagen hairs increases from the normal 85 to 95%; after parturition, the follicles, in which anagen has been prolonged, rapidly enter catagen and then telogen, with an increased shedding of hair evident after 3–4 months; most women will return to their usual hair growth cycle and prepregnancy thickness of hair between 6 and 12 months after birth; in case of persistent postpartum effluvium (>12 months), excessive hair loss may be caused by common conditions, such as female androgenetic alopecia, iron deficiency, or hypothyroidism; less common conditions include persistent hyperprolactinemia (Chiari-Frommel syndrome) and postpartum hypopituitarism (Sheehan syndrome) caused by pituitary necrosis due to blood loss and hypovolemic shock during childbirth.

In immediate telogen release, hair follicles normally programmed for release of telogen hairs after an interval of usually 100 days after the end of anagen are prematurely stimulated to cycle into anagen; there is premature teloptosis.

This type of telogen effluvium underlies the seemingly ironic increased shedding of hair upon initiation of therapy with the topical hair growth-promoting agent minoxidil (shedding phase); patients should be prepared and informed that this represents a physiological response to treatment, since minoxidil not only increases the duration of anagen, but triggers an immediate telogen release.

In delayed telogen release, hair follicles remain in prolonged telogen rather than being shed and recycling into anagen; when finally teloptosis sets in, again the clinical sign of increased shedding of telogen hair is observed. This process underlies moulting in mammals and probably also seasonal shedding of hairs in humans or mild telogen effluvia following travel from low- to high-daylight conditions; it is likely that environmental factors, such as the photoperiod, mediate through the optic pathway and the neuroendocrine system hair coat phenotype and function to photoperiod-dependent environmental changes; we published a study of 823 otherwise healthy women with telogen effluvium observed over a period of 6 years and demonstrated the existence of overall annual periodicity in the growth and shedding of hair, manifested by a maximal proportion of telogen hairs in July; a second peak seemed to exist, although less pronounced, in April; the telogen rate was lowest towards the beginning of February [20]; the fact that human hair follicles, just as those of other mammals, undergo cyclical activity and are influenced by hormones, implies that human hair is not unaffected by these phenomena; from an evolutionary point of view, the maintenance of the low winter level of hair shedding and the postponement of hair fall until the end of summer might, perhaps, be postulated as having a selective advantage with respect to isolation of the head against the cold in winter, and protection of the scalp against the midday sun in summer, respectively.

Finally, existence of a short anagen phase was proposed by Headington [19], resulting in a mild form of persistent telogen effluvium in association with decreased hair length.

Later, we confirmed the existence of short anagen hair as an isolated disorder in otherwise healthy children in an original report of two children with a peculiar type of isolated congenital hypotrichosis [21]; both presented with persistent short, fine hair since birth; shortening of the anagen phase of the scalp hair cycle leads to a decrease in the maximal hair length and an increase in the number of hairs in telogen, resulting in an increase in hair shedding; far more frequent is the acquired progressive shortening of anagen due to androgenetic alopecia (and probably senescent alopecia).

Modified from Headington [19].