Clinical Studies

Telogen effluvium (TE) is a type of non-scarring alopecia characterized by diffuse shedding of telogen hairs in response to metabolic or psychological stresses. The role of nutritional deficiencies in this disorder is a well-known but controversial topic. At a molecular level, certain vitamins and minerals such as vitamin D, ferritin, vitamin B12, folate, and zinc have been shown to play some role in hair follicle cycling or growth. From a mechanistic view, iron is a cofactor for ribonucleotide reductase, a rate-limiting enzyme for DNA synthesis, and its levels are higher in rapidly proliferating hair matrix cells.1 Zinc is an enzymatic cofactor required for maintaining homeostasis in the body and also plays a role in hair follicle cycling.2 The vitamin D receptor is also involved in Wnt and Hedgehog signaling pathways in hair follicle cycling.3 While past literature has suggested that low serum levels of these vitamins and minerals may be associated with TE, some studies have refuted these claims. was performed an Institutional Review Board-approved, retrospective cross-sectional study of 413 patients diagnosed with TE (both acute and chronic) at the University of Pittsburgh Medical Center hair clinic from June 2012 to December 2014. All patients were evaluated by a dermatologist investigator (JE) and diagnosed based on both clinical history of diffuse shedding and physical examination. Regardless of past medical history, patients had to obtain ordered serum levels of 25-hydroxyvitamin D, ferritin, vitamin B12, folate, and zinc. No control population was included. A total of 115 patients (110 females, 5 male), aged 16 to 89, completed the required bloodwork. Our primary outcome was to determine the rate of deficiency of the aforementioned vitamins and minerals. The study revealed that the largest proportion of patients had deficiencies in ferritin at 45.2%, followed by vitamin D at 33.9% and zinc at 9.6%. Vitamin B12 deficiency was scarce at 2.6% and no one had folate deficiency. These findings corroborate previous published studies that suggest TE is associated with these deficiencies. However, a proper control population could not be obtained for this retrospective study since these laboratory values are not routinely obtained in normal patients without hair loss, unless clinically suspected to be low for other reasons, and therefore inclusion of such a population would bias the data. While the retrospective nature and lack of a control population preclude our ability to draw conclusions about the association between nutritional deficiencies and TE, our data nonetheless demonstrate how common these deficiencies are in this population. A recent study showed that the prevalence of vitamin D deficiency in the US from 2001 to 2004 was 77%,5 which may suggest that our TE population has vitamin D levels higher than those of the average US population. However, these observed nutritional levels could reflect seasonal variations, sun practices, or diet choices among residents.

Telogen effluvium is a form of diffuse, nonscarring hair loss that presents as a transient or chronic loss of hair. Hair loss in telogen effluvium occurs as a result of an abnormal shift in follicular cycling that leads to the premature shedding of hair.A wide variety of endogenous and exogenous factors have been linked to the induction of telogen effluvium. Examples include major surgery, serious illness, childbirth, protein or caloric malnutrition, drugs, and severe emotional distress. In some cases, the inciting cause is unclear or multiple inciting triggers are identified. The clinical features, diagnosis, and management of telogen effluvium will be reviewed here. An overview of the evaluation of patients with scalp hair loss is provided separately. Data on the epidemiology of telogen effluvium are limited. The disorder is one of the most common forms of nonscarring hair loss for which patients present for clinical evaluation. Telogen effluvium does not appear to have a predilection for particular racial or ethnic groups. Most experts divide telogen effluvium into acute and chronic variants. Acute telogen effluvium may occur at any age, including infants and children. For unclear reasons, women are more likely to present for evaluation of acute telogen effluvium than men. Chronic telogen effluvium is much less common than the acute variant, and is most frequently diagnosed in women between the ages of 30 and 60 years. Chronic telogen effluvium can further be subdivided into chronic and chronic-repetitive clinical presentations. The excessive hair shedding that characterizes telogen effluvium occurs as a result of altered regulation of the hair follicle growth cycle. Normally, each follicle on the human scalp cycles independently through three major phases: anagen (growth), catagen (transformation), and telogen (rest). The end of the four to six-week telogen phase is marked by the shedding of hair from the follicle. The asynchronous cycling of scalp hair follicles in humans prevents periodic episodes of mass shedding of hair. Rather, shedding of hair occurs on a continuous basis. In the absence of scalp or hair disorders, 50 to 150 hairs typically are shed each day. Telogen effluvium occurs when the proportion of hair follicles in the telogen phase increases significantly, resulting in subsequent prominent shedding of hair. On the normal human scalp, only about 10 percent of follicles are in the telogen phase at any given time, while anagen and catagen follicles account for approximately 90 and <1 percent of follicles, respectively. In telogen effluvium, it is estimated that 7 to 35 percent of the follicles that normally would have remained in the anagen phase shift into the telogen phase. The mechanism of hair loss in telogen effluvium is not completely understood. It is generally accepted that an identifiable or occult, physiologic event stimulates a change in follicular cycling due to an insult to the anagen bulb (one of the two hair growth centres). Several theories of the mechanism of hair loss have been proposed, some of which have been associated with specific stimuli for telogen effluvium. Immediate anagen release and delayed anagen release are the most commonly cited theories: Immediate anagen release – Immediate anagen release may be a common mechanism for telogen effluvium. According to this theory, a significant proportion of anagen follicles are stimulated to enter telogen prematurely. Immediate anagen release may be the primary mechanism for telogen effluvium related to physiologic stress (eg, high fever) or drugs. Delayed anagen release – The theory of delayed anagen release describes prolongation of the duration of anagen, thereby delaying the onset of telogen. Hair loss is noted once the stimulus for sustaining anagen ends and the affected follicles enter telogen and subsequently shed. Delayed anagen release may be the primary mechanism for postpartum telogen effluvium. Additional theories for the mechanism of telogen effluvium have been proposed. Abnormal shortening of the anagen phase could contribute to an increase in hair shedding by augmenting the proportion of follicles in the telogen phase. In addition, shortening of the telogen phase could lead to the simultaneous release of hair from a large proportion of telogen follicles (immediate telogen release). Reduced variance in the duration of anagen has been proposed as a mechanism of chronic telogen effluvium. Last, a delay in telogen release could lead to an increase in hair shedding due to the sudden release of hairs from follicles that were stimulated to remain in the telogen phase for an extended period. Delayed telogen release may account for seasonal fur shedding in mammals. Inciting factors — A wide variety of factors have been associated with the induction of telogen effluvium based upon clinical observations. However, data to confirm and define the level of risk for telogen effluvium related to these factors are lacking. It is estimated that in approximately one-third of patients with acute telogen effluvium, an inciting factor cannot be identified. The cause of chronic telogen effluvium usually is more difficult to identify, but careful history taking can be helpful. The relationship between serum levels of ferritin or vitamin D and telogen effluvium is controversial. Studies evaluating the relationship between serum ferritin levels and telogen effluvium have yielded conflicting results, contributing to continued uncertainty about a relationship between these conditions as well as the value of iron supplementation in non-anaemic patients. However, doing these labs and prescribing multivitamin rich of elements can aid the treatment.