COVID-19 infection can cause a variety of hair loss disorder. A systematic review by Czech et al. found that acute and chronic TE, anagen effluvium, alopecia areata, and androgenetic alopecia are all related to COVID-19 infection, with TE being the most common (74,1%) [11]. In our study, all cases found were TE. We found that post-COVID-19 hair loss occurred in the age range of 31.58 ± 9.49 years. According to Moreno-Arrones et al., hair loss post-COVID-19, notably acute TE, occurred at an average age of 47.4 years (range 15–88 years) [12]. Our study indicated 90% post-COVID-19 hair loss in women. According to a systematic review by Czech et al., post-COVID-19 hair loss was more common in women (82.8%) than men. Acute viral infections that lower systemic estrogen and progesterone levels may result in predominant post-COVID-19 hair loss in women. Meanwhile, estrogen and progesterone are known to function as hair follicle protectors [11].
Hussain et al. found that in COVID-19 subjects with TE, hypertension (27%), diabetes (17%), and dyslipidemia (17%) were the most prevalent comorbidities. These comorbidities may increase the risk of COVID-19-related acute TE [11]. Our findings were in line with Hussain et al., where 5% of subjects had hypertension and 10% had dyslipidemia. Other comorbidities we found were hyperuricemia, osteoarthritis, kidney cysts, sleep apnea, allergic rhinitis, psoriasis vulgaris, asthma, GERD, and eczema.
The presence of post-COVID-19 hair loss was found in all severity of COVID-19. A theory related to post-COVID-19 hair loss shows the involvement of interleukin-6 (IL-6), which inhibits hair shaft elongation and hair follicle proliferation [11]. We found that 10% of our subjects had a history of hospitalization, 65% had antiviral medications, 15% had antibiotics, and 5% had antithrombotic therapy. Moreno-Arrones et al., suggested that TE can also be triggered by drugs such as heparin (antithrombotic) [12]. Thus, the possibility of TE caused by the use of these drugs cannot be ignored. On the contrary, Monari et al., has shown no significant correlation between TE and COVID-19 symptoms and severity (hospitalization duration, duration of fever), treatment, and laboratory findings [13].
We found that the onset of hair loss in post-COVID-19 subjects was around 5.48 ± 7.65 weeks (1 to 128 days) after being infected with COVID-19. This result was in line with Moreno-Arrones et al., who found the onset of TE around 57.1 days (SD of 18.3) [12]. Herein, we also found the duration of hair loss occurred around 33.35 ± 23.41 weeks (40 to 227 days). In accordance with Morioka S et al., hair loss can remain for over a year after a positive PCR test for COVID-19 infection [14]. This proves that although TE is self-limiting, the process requires a long time. Hypoxic factors, inflammation, metabolic abnormalities, drugs, nutrition and mechanical ventilation can influence the onset, severity, and duration of hair loss in TE [9].
Among all subjects, 92.5% had impaired levels of vitamin D-25 OH. The Demay MB study demonstrated that hair follicles contain vitamin D receptors and can modulate keratinocyte proliferation and the hair growth cycle [15]. Disorders of vitamin D levels were found to be more common in subjects with excessive hair shedding, especially on hair-washing day. Interestingly, a subject with significant hair loss (Sinclair Hair Shedding Scale of six on hair-washing days and five on non-hair-washing days) had the highest vitamin D-25-OH level (65 ng/dL). We did not find a significant correlation (p > 0.05) between vitamin D levels with hair loss severity. Until now, we have not found a study that mentions the correlation of vitamin D with post-covid hair loss disorders.
Several theories explained that vitamin D can reduce the risk of COVID-19 infection, including the inactivation of viruses by inducing cathelicidins, regulating effector differentiation processes in CD 8 and CD4 cells and regulating T cell proliferation, thus initiating adaptive immunity [16–19]. However, this state of acute infection can also reduce vitamin D-25-OH [20]. We assumed that low vitamin D levels may increase the risk of COVID-19 infection. COVID-19 infection may stimulate inflammation, resulting in lower vitamin D levels in subjects, hence triggering TE.
We discovered five (12.5%) subjects had positive hair pull test results. Low findings may be due to recalcitrant subjects who had their hair washed before the examination, leading hair to fall prior to the examination. In a study by Shairquie KE, a positive hair pull test was found on 39 subjects with TE (> 10–50% with a mean number of 35%) [4].
Of the 40 subjects, the majority had excessive hair loss (72.5% Hair Washing Day, 50% Non-Hair Washing Day) compared to those with normal hair loss. There were 36 subjects (90%) who had a poor quality of life (mild to severe effect), with the highest percentage of subjects experiencing moderate effect (42.5%). Hair loss affected self-confidence and made subjects uncomfortable with their appearance, according to Williamson et al. (mean DLQI score 8.3) [10]. In addition, a systematic review by Schielein MC et al. found that from three studies, the quality of life of subjects who experienced hair loss was lower than the control group (p = 0.025) [21]. In our study, there was no significant difference (p > 0.05) between quality of life and hair loss severity, but subjects with excessive hair loss (67.5% on hair washing days and 47.5% on non-hairwashing days) had a higher quality of life decrease than those with normal hair loss.
Trichoscopic features determined in our study were empty follicles, vellus hair, and canities. Empty follicles were found in all of our subjects; all diagnosed with TE. Hussain et al. suggested that TE's most common trichoscopic features were decreased hair density and empty follicles [22]. We concluded that there was no difference in trichoscopic features in post-COVID-19 TE subjects compared to other types of TE. To the best of our knowledge, no other studies have investigated trichoscopic appearance in post-COVID-19 hair loss subjects, making our study novel.
In subjects with low vitamin D levels, vellus hair was found in 13 (32.5%) subjects, while 24 (60%) subjects had no vellus hair. The presence of canities was more common in subjects with excessive hair loss (60% on hair-washing days and 50% on non-hair-washing days) than in the group with normal hair loss (22.5% on hair-washing days and 32.5% on non-hair washing days). A significant difference is seen in the incidence of canities and excessive hair loss on non-hair washing days (p < 0.05). Of the six subjects who experienced canities, the age range was between 42 to 58 years. All subjects had canities prior to COVID-19 infection. However, five out of six subjects felt rapid growth of canities post COVID-19 infection. It was unclear if the rapid rise of canities was caused by heredity, ageing, or COVID-19. Post-COVID-19 hair loss and canities have not been addressed in studies. From what we found, COVID-19 infection could trigger the production of reactive oxygen species (ROS) in both mild and severe COVID-19 [23]. ROS is also known to be a trigger factor for canities [24]. In addition, psychological stress on subjects with COVID-19 can also contribute to the emergence of canities [25]. Further investigation is needed to confirm the theory.