Dear Editor,
Initially described in 1961, Telogen Effluvium (TE) and its variants are still unclear with respect to classification, diagnosis and treatment. A new phase of the hair cycle was described by Stenn in 2002, when recognizing a proteolytic phase at the end of telogen, when shaft release occurs: the “exogen” phase.1 Hypoxia was recognized—among other several well-documented factors, such as cytokines, hormones and nutrients — as impacting the follicle’s reentry into a new hair cycle, which was termed by Rathman-Josserand et al. as the “neogen” phase.2 In further development, a 2010 study by Gilmore and Sinclair suggested that chronic (TE) may be secondary to a reduction in anagen-phase variance, which would represent a new functional type of recurrent hair loss.3
Between 2015 and 2018, 42 women were treated for recent onset diffuse thinning (6 to 12 weeks) associated with a certain history event with a shedding of more than 100 shafts a day. Follow-up showed a reduction in fall with or without treatment in 6 to 12 weeks in all cases. These cases were initially considered as acute telogen effluvium, since they did not present previous complaints. The most frequent causes identified in the patients’ history were divided into three groups: postpartum (n = 16); initiation of new drugs (n = 12), especially antidepressants and anticonvulsants (7 out of these 12); and recent medical events (n = 14) such as a diagnosis of other diseases (11 out of 14), specially thyroid diseases (6 out of 14) and surgical procedures (4 out of 14). Interestingly, 28 of the patients re-evaluated 12 to 18 weeks after diagnosis had dermatoscopic criteria for female pattern hair loss (FPHL). Reduction in density, variation in shaft diameter, and increase of perifollicular dyschromia or yellow dots in the central region (when compared to occipital region) were identified in this group. One year after diagnosis, 19 of them continued with follow-up and remained with clinical and dermatoscopic (n = 13) or histopathological (n = 6) diagnosis of FPHL.
Complete blood count, thyroid stimulating hormone (TSH) and ferritin were evaluated in all patients. Three had microcytic hypochromic anemia, four showed abnormalities in TSH (two others had started treatment and had normal levels), and 31 had ferritin below 40mg/L. Low levels of ferritin have been associated with telogen effluvium. However it may be a confounding factor in this group, since only cases with obvious causes were included and some were postpartum (nine other cases of clinical diagnosis with no obvious cause were discarded).
Of the 16 postpartum patients identified in our group, 12 were in the group that remained with a diagnosis of FPHL after one year of follow-up, which may suggest postpartum effluvium as a sign of possible FPHL. In addition, these findings are consistent with the lack of evidence for a postpartum physiological telogen effluvium already discussed in the literature.4
Knowledge about TE has progressed, but questions remain to be answered through studies with reliable methodologies. In addition, as suggested in this sample of patients, TE may be the initial manifestation in patients with FPHL. Rebora5 emphasized that alopecia areata incognita occurs more frequently in patients with FPHL. Alopecia areata incognita is a diffuse loss of telogen hairs, usually without glabrous areas, that mimics severe TE; moreover, this entity involves a loss of more than 350 strands per day, with rare dystrophic anagen strands. Perhaps some of our cases were misdiagnosed, and dystrophic anagen bulbs may not have been identified among the fallen hair. ☐
