INTRODUCTION
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. One of the major limitations of these studies is the small sample population size, often fewer than 45 patients.
METHODS
We 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 female, 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. Deficiency was defined as 4
RESULTS
Our 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% (Table 1). 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.
DISCUSSION
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 in western
