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653 vity in building up the hair shaft. The common pathogenesis which unites the different aetiologies of dystrophic anagen effluvium is a direct insult to the rapidly dividing bulb matrix cells. Telogen effluvium results from lateonset increased shedding of hairs from the telogen phase of the hair cycle and represents by far the commonest cause of hair loss. An increase in the percentage of follicles in telogen by >20% leads to increased shedding of hairs in telogen. This can either be due to synchronization phenomena of hair cycling, with shedding of hairs in the hundreds (in telogen effluvium), or to a decrease of anagen duration with variable shedding of hair and increasing diversity of hair shaft diameters (in androgenetic alopecia). Post-infectious hair loss has traditionally been categorized as telogen effluvium, yet it may present with different pathomechanisms and clinical patterns. Evidence exists that the hair follicle may respond to infection with both shedding patterns, dystrophic anagen effluvium and telogen effluvium, depending on the type and intensity of the insult. Accordingly, the hair may fall out very quickly in clumps or gradually. Savil originally reported that for post-febrile effluvium, the critical temperature should be 39-39.5◦C [8], however, circulating pyrogenic cytokines appear to be the important determinant rather than body temperature. The immune system is involved in both the regulation of hair follicle cycling and the pathogenesis of some immunemediated hair pathologies. Immunomodulatory cytokines not only act as mediators of immunity and inflammation, but also regulate cell proliferation and differentiation and, as such, play a role in hair growth and shedding. Philpott et al. reported ILs and TNF to be potent inhibitors of hair follicle growth in vitro in a dose-dependent manner [9]. In addition, IFNhas been shown to be a potent inducer of catagen-like changes in cultured human anagen hair follicles [10]. The cytokine profiles generated by SARS-CoV-2 vaccination, particularly in those with febrile vaccine reactions, are yet to be established. We observed sixteen patients who developed a similar pattern of hair loss following vaccination against SARSCoV-2. All patients had a reduced density of hair and a positive hair-pull test. One patient, in whom a trichogram was performed, showed mixed telogen and dystrophic anagen effluvium. The demographic data, symptoms, and hair manifestations of the indicator cases with SARS-CoV-2 vaccine related to effluvium and sixteen control vaccinees without a febrile reaction are summarized in table 1. The age difference between the two groups may be explained by a reduced febrile response to infections with increasing age. The observation and analogies related to effluvium following febrile SARS-CoV-2 vaccination reaction are in favour of COVID-19-related effluvium being due to the systemic inflammatory reaction rather than to a direct infection of the hair follicle with SARS-CoV-2. As yet, histopathological and ultrastructural evidence for a direct infection of the hair follicle with SARS-CoV-2 is lacking.