Dermatology: Practical and Conceptual Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 1 Antinuclear Antibody Positivity in Patients With Hair Loss After COVID-19 Infection Vildan Manav1,2, Duygu Erdil1, Ayşe Esra Koku Aksu1 1 Department of Dermatology, University of Health Sciences, İstanbul Training and Research Hospital, İstanbul, Turkey 2 Cosmetology, İstanbul University Graduate School of Medicine, İstanbul, Turkey Key words: SARS-CoV-19, hair loss, antinuclear antibody positivity, trichodynia Citation: Manav V, Erdil D, Koku Aksu A. Antinuclear Antibody Positivity in Patients with Hair Loss after COVID-19 Infection. Dermatol Pract Concept. 2023;13(2):e2023081. DOI: https://doi.org/10.5826/dpc.1302a81 Accepted: August 29, 2022; Published: April 2023 Copyright: ©2023 Manav et al. This is an open-access article distributed under the terms of the Creative Commons Attribution- NonCommercial License (BY-NC-4.0), https://creativecommons.org/licenses/by-nc/4.0/, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original authors and source are credited. Funding: None. Competing interests: None. Authorship: All authors have contributed significantly to this publication. Corresponding author: Vildan Manav, MD, Istanbul Training and Research Hospital, Department of Dermatology, Kasap İlyas Mah. Org. Abdurrahman Nafiz Gürman Cd. PK: 34098, Istanbul, Turkey. Phone: +905334323524. Fax: +9002126320060, E-mail: drvildanmanav@gmail.com Introduction: Hair loss is one of the most common disorders after coronavirus disease 2019 (COVID-19) infection. This study aimed to investigate the relationship between COVID-19-related hair loss and antinuclear antibody (ANA) positivity and patterns. Methods: ANA positivity and patterns were analyzed in 30 female COVID-19 patients with hair loss complaints and compared in terms of the presence of autoimmunity between patients with and without COVID-19 exhibiting hair loss. Results: ANA positivity and cytoplasmic patterns were detected in 40% of the patients with COVID-19 infection and hair loss. Trichodynia and diffuse hair loss were observed in 63.3% and 53.3%, respectively. Conclusions: In patients with COVID-19-related hair loss, diffuse hair loss and ANA positivity may be related to the high antibody levels triggered by COVID-19 infection. ABSTRACT Introduction More than 175 million people were infected with coronavirus disease 2019 (COVID-19) within one year of the first COVID-19 infection reported in China in early December 2019 [1]. It has been reported that 80% of patients with COVID-19 infection develop one or more long-term symp- toms. The most common symptoms are fatigue (58%), head- ache (44%), attention deficit (24%), and hair loss (25%) [2]. Skin findings have received increasing attention for the early 2 Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 diagnosis of COVID-19. COVID-19-related skin findings in- clude vascular eruptions, maculopapular eruptions (atypical forms of pityriasis rosea) [3], urticarial rash, vesicular, petechiae/purpuric eruptions, erythema multiforme–like rash, palmar erythema, perifollicular eruption, pruritus, mucosal rash, and androgenetic alopecia [4]. Autoimmune diseases that develop or worsen after COVID-19 infection have also been increasingly reported. These include connective tissue diseases (rheumatoid arthri- tis, systemic lupus erythematosus vasculitis, myositis, sys- temic sclerosis, and psoriatic arthritis) [5], multiple sclerosis, and autoimmune hepatitis [6] in adults, as well as rheumatic diseases [7,8] and type 1 diabetes in children [9]. Antinuclear antibody (ANA) tests were mainly developed for systemic lupus erythematosus screening. However, ANA positivity has also been detected in many rheumatic diseases and is an indicator of autoimmunity [10]. ANA positivity is not expected in non-scarring hair loss. In only one study, the rate of ANA positivity was reported in patients with pattern hair loss (30.4%) [11]. Objectives Since COVID-19 can trigger autoimmunity, and as hair loss is one of the most common symptoms after COVID-19 infec- tion, this study aimed to evaluate the relationship between the two and investigate the differences between autoimmunity- and non-autoimmunity-related hair loss. Methods This cross-sectional case-control study was performed between June and September 2021. The case group con- sisted of 30 patients who had contracted COVID-19 up to 12 weeks previously and had hair loss complaints. The con- trol group consisted of 60 patients who complained about hair loss but did not have COVID-19. For the control group, each patient consisted of 2 consecutive patients who came to the dermatology outpatient clinic immediately after the patient selected for COVID-19- related hair loss. Patients under the age of 18 years, patients with autoimmune or inflammatory diseases or acute or chronic infections, pa- tients receiving any medications (corticosteroids, biological agents, antibiotics, or vitamin or mineral supplements), and pregnant or lactating women were excluded from the study. COVID-19 infection was confirmed using nasopharyngeal swabs and polymerase chain reaction tests. Demographic characteristics (age and gender) and clinical findings (date of COVID-19 infection, duration of hair loss after COVID-19 infection (time from hair loss onset to pre- sentation to the clinic), severity of hair loss, and presence of trichodynia, oily scalp, dandruff, and diffuse hair loss) were collected. Hair loss was recorded using the hair-shedding visual scale [12] as follows: < 50, 50–100, 100–150, and > 150 hairs/day. Additionally, a pull test was performed at four locations on the scalp. The pull test was considered posi- tive when more than 10% of the hair at each location was removed after applying steady traction. Chemiluminescence enzyme immunoassays were per- formed to measure vitamin B12 and ferritin levels using an Im- munity 2000 device (Diagnostic Products Corporation). TSH (thyroid stimulating hormone) and anti-TPO (anti-thyroid peroxidase) levels were measured using an ARCHITECT ci16200 Integrated System (Abbot Diagnostics). Antinuclear antibody titers and patterns were studied using enzyme-linked immunosorbent assays and immunoflu- orescence, with human epithelioma type 2 (HEp-2) cells used as the substrate. The ANA tests were first run at titers of 1:100 with both kits, and positive samples were reanalyzed with further serial dilutions (1:160, 1:320, 1:640, 1:1280, 1:2560, and 1:5120). C3 and C4 levels were measured using a Behring nephelometer and Beckman Reagent kits. This study was approved by the tertiary hospital ethics committee (No. 2939; October 8, 2021). Written informed consent was obtained from all participants. Statistical Analysis Statistical analyses were performed using SPSS version 25.0 (IBM). Histograms and the Kolmogorov–Smirnov test were used to assess data normality. In descriptive analyses, means ± standard deviations and medians were used. Categorical variables were compared using Pearson chi-squared test. The Mann–Whitney U test was used to evaluate non-normally distributed (nonparametric) variables between the case and control groups, and the Kruskal–Wallis test was used for comparisons between more than two variables. Spearman correlation coefficient was used to investigate correlations between variables. The ability of C3 and C4 values to predict ANA positivity was investigated using receiver operating characteristic (ROC) curves. Values of P < 0.05 were consid- ered statistically significant. Results The mean ages of the patients in the case and control groups were 30.0 ± 11.2 and 29.2 ± 8.3 years, respectively. The difference was not statistically significant (P = 0.952). All patients were female. There were no statistically significant differences in standard laboratory test values between the two groups (Table  1). Conversely, the duration of hair loss was signifi- cantly longer in the control group than in the case group (P < 0.001). In the case group, hair loss started 5.2 ± 3.4 weeks after COVID-19 infection. Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 3 The rate of patients in the case group losing more than 100 hairs per day was 86%, whereas the corresponding rate in the control group was only 26% (P < 0.001). Trichodynia, oily scalp, and diffuse hair loss were significantly more com- mon in the case group than in the control group (Table 2). Moreover, the case group had a significantly higher number of ANA-positive patients (40.0%) than the control group (11.6%) (P = 0.002). The rate of cytoplasmic ANA patterns in the case group was 83%, which was significantly higher than that in the control group (P = 0.001). In the control group, granular ANA patterns represented 71.4% of the patients. There was no significant relationship between ANA patterns and the severity of hair loss in the case group (Table 3). The relationships between ANA positivity and clinical findings are shown in Table 4. In the covid-related hair loss group, the relationship between ANA positivity and trichodynia, duration of hair loss (week), oilyscalp, dan- druff, diffuse loss of hair volume, pull test was investigated. Accordingly, in the covid-related hair loss group, all ANA positive patients had diffuse hair loss (12/12) whereas only %22 of ANA negative patients (4/18) had diffuse hair loss and pull test positivity were statistically significantly higher in patients with ANA positivity.In the case group, there were no significant relationships between ANA positivity and pattern or trichodynia (P = 0.279 and P = 0.670, re- spectively). Likewise, there was no significant correlation between hair loss duration and ANA positivity (r = −0.012, P = 0.949). No significant relationships were observed between ANA positivity and C3 or C4 levels in the case group (P = 0.735 and P = 0.566, respectively). Furthermore, the ROC analysis indicated no significant cut-off values. Conclusions ANA positivity is detected in many viral and autoimmune diseases. However, studies on antibody responses after COVID-19 infection have not produced definitive results [13,14]. It remains unclear whether hair loss after COVID-19 infection is caused by the infection itself, the autoimmune re- sponse to the infection, or stress triggered by the COVID-19 pandemic. To our knowledge, the relationship between COVID-19-related ANA positivity and hair loss developing after the infection has not been previously investigated. In this study, we detected ANA positivity in 40% of pa- tients exhibiting hair loss after COVID-19 infection. This is consistent with previous studies reporting rates ranging from 21% to 64% [15-20]. Nevertheless, it is important to note that all COVID-19 patients in those studies had severe or moderate COVID-19, whereas the patients in- cluded in our study had mild COVID-19 and did not require hospitalization. The rate of ANA positivity observed in this study is also in line with studies on hair diseases triggering stronger au- toimmunity. Such studies have reported rates of 21.2% in telogen effluvium [21], 30.4% in pattern hair loss [11], and 46% in lichen planopilaris [22]. Surprisingly, in this study, cytoplasmic ANA patterns were observed in 83.3% of the patients with hair loss af- ter COVID-19 infection. Trachtenberg et al., who reported 64% ANA positivity, found a highly dense and fine-speckled cytoplasmic pattern associated with COVID-19 worsening clinical severity scores [20]. However, as previously noted, all patients with hair loss in our study had mild COVID-19. Chang et al detected cytoplasmic patterns at titers higher than 1:160 [23], whereas in this study, we observed Table 1. Comparison of standard laboratory test values of patients with covid-related hair loss and without covid-related hair loss. Covid-related hair loss group Control Total PaMean SD Medin Mean SD Median Mean SD Median Age (years) 30.03 ±11.22 27.00 29.15 ±8.32 27.00 29.44 ±9.33 27.00 0.952 Duration of hair loss (weeks) 13.87 ±7.54 12.00 20.50 ±6.47 20.00 18.29 ±7.49 20.00 <0.001 Vitamin B12(ng/L) 295.83 ±125.18 280.50 300.13 ±117.86 279.00 298.70 ±119.66 279.50 0.911 Ferritin (μgr/L) 36.35 ±28.63 32.60 33.33 ±32.62 25.47 34.34 ±31.22 26.38 0.419 C3(g/L) 1.27 ±0.27 1.26 1.23 ±0.30 1.26 1.24 ±0.29 1.26 0.945 C4(g/L) 0.64 ±2,20 0.25 0.29 ±0.19 0.26 0.41 ±1.28 0.25 0.566 TSH (mU/L) 2.65 ±2.36 1.98 2.12 ±0.97 2.04 2.30 ±1.58 2.04 0.939 SD = standard deviation. aMann Whitney U Test 4 Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 Table 2. Comparison of clinical examination and laboratory findings of patients with covid-related hair loss and without covid-related hair loss. Covid-related hair loss group Control Total PaN (%) N (%) N (%) Pre-exisiting TE No 20 (66.67) 41 (68.33) 61 (67.78) 0.873 Yes 10 (33.33) 19 (31.67) 29 (32.22) Amount of hair loss 50hairs/day 0 (0.00) 5 (8.33) 5 (5.56) <0.001 50-100hairs/day 4 (13.33) 39 (65.00) 43 (47.78) 100-150hairs/day 24 (80.00) 16 (26.67) 40 (44.44) >150hairs/day 2 (6.67) 0 (0.00) 2 (2.22) Trichodynia No 11 (36.67) 42 (70.00) 53 (58.89) 0.002 Yes 19 (63.33) 18 (30.00) 37 (41.11) Oilyscalp No 15 (50.00) 44 (73.33) 59 (65.56) 0.028 Yes 15 (50.00) 16 (26.67) 31 (34.44) Dandruff No 11 (36.67) 35 (58.33) 46 (51.11) 0.053 Yes 19 (63.33) 25 (41.67) 44 (48.89) Diffuse loss of hair volume No 14 (46.67) 45 (75.00) 59 (65.56) 0.008 Yes 16 (53.33) 15 (25.00) 31 (34.44) Pull test Negative 9 (30.00) 15 (25.00) 24 (26.67) 0.613 Positive 21 (70.00) 45 (75.00) 66 (73.33) ANA positivity Negative 18 (60.00) 53 (88.33) 71 (78.89) 0.002 Positive 12 (40.00) 7 (11.67) 19 (21.11) ANA pattern Cytoplasmic 10 (83.33) 0 (0.00) 10 (52.63) 0.001 Granular 0 (0.00) 5 (71.43) 5 (26.32) Nucleolar 1 (8.33) 0 (0.00) 1 (5.26) Nuclear/Granular 1 (8.33) 2 (28.57) 3 (15.79) AntiTPO μL <9 29 (96.67) 57 (95.00) 86 (95.56) 0.718 >9 1 (3.33) 3 (5.00) 4 (4.44) ANA = antinuclear antibody; Anti-TPO = anti-thyroid peroxidase; TE = Telogen Effluvium aChi-Square Test Table 3. The relationship between the antinuclear antibody pattern and the amount of hair loss in patients in the covid-related hair loss group. Covid- related hair loss group Amount of hair loss P 50 hairs/day 50-100 hairs/day 100-150 hairs/day > 150 hairs/day N (%) N (%) N (%) N (%) ANA positivity Negative 0(.00) 3(75.00) 14(58.33) 1(50.00) 0.784 Positive 0(00) 1(25.00) 10(41.67) 1(50.00) ANA pattern Cytoplasmic 0(00) 1(10.00) 9(90.00) 0(.00) 0.016 Granular 0(00) 0(.00) 0(.00) 0(.00) Nucleolar 0(00) 0(.00) 1(10.00) 0(.00) Nuclear/Granular 0(00) 0(.00) 0(.00) 1(100.00) ANA = antinuclear antibody Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 5 ANA positivity and trichodynia or between trichodynia and autoimmunity. Since no financial support is received, ENA (extractable nu- clear antigen) (anti-RNP, anti-Scl70, anti-Sm, anti-SS-A/Ro52, anti-SS-A/Ro60, or anti-SS-B/La), p-ANCA (perinuclear anti-neutrophil cytoplasmic antibodies), anticardiolipin IGM, and IGG, which are frequently measured in COVID-19 antibody studies, were not measured and were performed. scalp biopsies. Moreover, we did not evaluate patients stress levels using an anxiety scale to investigate the relationship between hair loss and stress. In conclusion, hair loss after COVID-19 infection may be triggered by the release of autoantibodies in response to the infection. Cytoplasmic ANA patterns may be essential clinical markers for elucidating the pathogenesis of hair loss after COVID-19 infection. References 1. Harapan H, Itoh N, Yufika A, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020;13(5):667-673. DOI: 10.1016/j.jiph.2020.03.019. PMID: 32340833. PMCID: PMC7142680. 2. Galeotti C, Bayry J. Autoimmune and inflammatory diseases following COVID-19. Nat Rev Rheumatol. 2020;16(8):413-414. DOI: 10.1038/s41584-020-0448-7. PMID: 32499548. PMCID: PMC7271827. 3. Martora F, Picone V, Fornaro L, Fabbrocini G, Marasca C. Can COVID-19 cause atypical forms of pityriasis rosea refractory to conventional therapies? J Med Virol. 2022;94(4):1292-1293. DOI: 10.1002/jmv.27535. PMID: 34931329. 4. Wollina U, Karadağ AS, Rowland-Payne C, Chiriac A, Lotti T. Cutaneous signs in COVID-19 patients: A review. Dermatol cytoplasmic patterns even at a titer of 1:100. Further- more, nucleolar patterns have been shown to be dominant in COVID-19 [15,17,18,23]. Thus, our results differ from those of previous studies in this respect. Massabki et al [24] and Eystathioy et al [25] suggested that cytoplasmic patterns at low and moderate titers had low clinical relevance. Con- versely, Pazini et al reported that they were associated with autoimmune diseases even at low titers [26]. In our study, the cytoplasmic pattern of ANA was positive even at low titer, but it was also clinically significant. Trichodynia is a symptom of local paresthesia often associated with telogen effluvium, androgenetic alopecia, and alopecia areata [27,28]. It is a crucial dermatological marker of the severity of hair disease and the response to treatment [29]. The pathophysiology of trichodynia is un- clear, although substance P, a stress-related neuronal peptide, has been suggested to elicit the sensation [28]. According to previous studies, the rates of coexistence between telogen ef- fluvium and trichodynia range from 34% to 73.6%, while the rates of coexistence between AGA (androgenetic alo- pecia) and trichodynia range from 26.4% to 36% [30-32]. Starace et al reported that telogen effluvium coexisted with trichodynia in 58.4% of COVID-19 patients [33], which is comparable to our findings. Di Landro et al. suggested that severity of trichodynia might be directly related to the severity and intensity of hair loss [34]. In this study, diffuse hair loss after COVID infection was observed in 53.3% of the patients. The sig- nificant relationship between trichodynia and diffuse hair loss supports Di Landro et al.’s hypothesis. However, our results did not show a significant relationship between Table 4. The relationship between antinuclear antibody positivity and clinical findings in patients in the covid-related hair loss group. ANA Pa Negative Positive N (%) N (%) Trichodynia No 8 (44.44) 3 (25.00) 0.279 Yes 10 (55.56) 9 (75.00) Duration of hair loss (weeks), mean ± SD 12.89±6.48 15.33±9.00 0.520b Oilyscalp No 9 (50.00) 6 (50.00) 1.000 Yes 9 (50.00) 6 (50.00) Dandruff No 5 (27.78) 6 (50.00) 0.216 Yes 13 (72.22) 6 (50.00) Diffuse loss of hair volume No 14 (77.78) 0 (0.00) <0.001 Yes 4 (22.22) 12 (100.00) Pull test Negative 8 (44.44) 1 (8.33) 0.034 Positive 10 (55.56) 11 (91.67) a Chi-Square Test; bMann Whitney U Test ANA = antinuclear antibody. 6 Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 2020;3:100073. DOI: 10.1016/j.jtauto.2020.100073. PMID: 33263103. PMCID: PMC7691817. 18. Pascolini S, Vannini A, Deleonardi G, et al. COVID-19 and Im- munological Dysregulation: Can Autoantibodies be Useful? Clin Transl Sci. 2021;14(2):502-508. DOI: 10.1111/cts.12908. PMID: 32989903. PMCID: PMC7536986. 19. Sacchi MC, Tamiazzo S, Stobbione P, et al. SARS-CoV-2 in- fection as a trigger of autoimmune response. Clin Transl Sci. 2021;14(3):898-907. DOI: 10.1111/cts.12953. PMID: 33306235. PMCID: PMC8212749. 20. Trahtemberg U, Fritzler MJ; On behalf of the COVID-19 chapter of the “Longitudinal Biomarkers in Lung Injury” study group. COVID-19-associated autoimmunity as a feature of acute respi- ratory failure. Intensive Care Med. 2021;47(7):801-804. DOI: 10.1007/s00134-021-06408-z. PMID: 33928414. PMCID: PMC8084710. 21. Yorulmaz A, Hayran Y, Ozdemir AK, et al. Telogen effluvium in daily practice: Patient characteristics, laboratory parameters, and treatment modalities of 3028 patients with telogen effluvium. J Cosmet Dermatol. 2022;21(6):2610-2617. DOI: 10.1111 /jocd.14413. PMID: 34449961. 22. Kłosowicz A, Englert K, Pełka K, Pastuszczak M, Pastuszczak A. Autoimmunity in lichen planopilaris patients. Pol Merkur Lekar- ski. 2019;46(271):32-35. PMID: 30810113. 23. Chang SE, Feng A, Meng W, et al. New-onset IgG autoanti- bodies in hospitalized patients with COVID-19. Nat Commun. 2021;12(1):5417. DOI: 10.1038/s41467-021-25509-3. PMID: 34521836. PMCID: PMC8440763. 24. Massabki PS, Accetturi C, Nishie IA, da Silva NP, Sato EI, Andrade LE. Clinical implications of autoantibodies in HIV infection. AIDS. 1997;11(15):1845-1850. DOI: 10.1097/00002030-199715000 -00009. PMID: 9412703. 25. Eystathioy T, Chan EK, Tenenbaum SA, Keene JD, Griffith K, Fritzler MJ. A phosphorylated cytoplasmic autoantigen, GW182, associates with a unique population of human mRNAs within novel cytoplasmic speckles. Mol Biol Cell. 2002;13(4): 1338-1351. DOI: 10.1091/mbc.01-11-0544. PMID: 11950943. PMCID: PMC102273. 26. Pazini AM, Fleck J, dos Santos RS, Beck ST. Clinical relevance and frequency of cytoplasmic and nuclear dense fine speck- led patterns observed in ANA-HEp-2. Rev Bras Reumatol. 2010;50(6):655-660. PMID: 21243306. 27. Xerfan EMS, Andersen ML, Facina AS, Tufik S, Tomimori J. The role of sleep in telogen effluvium and trichodynia: A commen- tary in the context of the current pandemic. J Cosmet Derma- tol. 2021;20(4):1088-1090. DOI: 10.1111/jocd.13929. PMID: 33387387. 28. Rebora A. Trichodynia: a review of the literature. Int J Der- matol. 2016;55(4):382-384. DOI: 10.1111/ijd.13204. PMID: 26696219. 29. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: part I. History and clinical examination. J Am Acad Dermatol. 2014;71(3):415.e1-415.e15. DOI: 10.1016/j.jaad.2014.04.070. PMID: 25128118. 30. Baldari M, Montinari M, Guarrera M, Rebora A. Trichodynia is a distinguishing symptom of telogen effluvium. J Eur Acad Dermatol Venereol. 2009;23(6):733-734. DOI: 10.1111/j. 1468-3083.2009.03201.x. PMID: 19281607. Ther. 2020;33(5):e13549. DOI: 10.1111/dth.13549. PMID: 32390279. PMCID: PMC7273098. 5. Wollina U, Karadağ AS, Rowland-Payne C, Chiriac A, Lotti T. Cutaneous signs in COVID-19 patients: A review. Dermatol Ther. 2020;33(5):e13549. DOI: 10.1111/dth.13549. PMID: 32390279. PMCID: PMC7273098. 6. Hong JK, Chopra S, Kahn JA, Kim B, Khemichian S. Autoimmune hepatitis triggered by COVID-19. Intern Med J. 2021;51(7): 1182-1183. DOI: 10.1111/imj.15420. PMID: 34278694. PM- CID: PMC8447478. 7. Nikiphorou E, Alpizar-Rodriguez D, Gastelum-Strozzi A, Buch M, Peláez-Ballestas I. Syndemics & syndemogenesis in COVID-19 and rheumatic and musculoskeletal diseases: old challenges, new era. Rheumatology (Oxford). 2021;60(5): 2040- 2045. DOI: 10.1093/rheumatology/keaa840. PMID: 33496334. PMCID: PMC7928641. 8. Walters HM, Mian Z, Thomas L, et al. Seroprevalence and clinical outcomes of SARS-CoV-2 in paediatric patients with rheumatic disease. Rheumatology (Oxford). 2022;61(SI2):SI112-SI119. DOI: 10.1093/rheumatology/keab730. PMID: 34599820. 9. Vlad A, Serban V, Timar R, et al. Increased Incidence of Type 1 Diabe- tes during the COVID-19 Pandemic in Romanian Children. Medicina (Kaunas). 2021;57(9):973. DOI: 10.3390/ medicina57090973. PMID: 34577896. PMCID: PMC8470921. 10. Aringer M, Johnson SR. Systemic Lupus Erythematosus Classi- fication and Diagnosis. Rheum Dis Clin North Am. 2021;47(3): 501-511. DOI: 10.1016/j.rdc.2021.04.011. PMID: 34215376. 11. Choi WJ, Kim JE, Kang H. Frequency of antinuclear antibody positivity in patients with pattern hair loss. Ann Dermatol. 2015;27(2):210-212. DOI: 10.5021/ad.2015.27.2.210. PMID: 25834364. PMCID: PMC4377414. 12. Martínez-Velasco MA, Vázquez-Herrera NE, Maddy AJ, Asz-Sigall D, Tosti A. The Hair Shedding Visual Scale: A Quick Tool to Assess Hair Loss in Women. Dermatol Ther (Heidelb). 2017;7(1):155-165. DOI: 10.1007/s13555-017-0171-8. PMID: 28220468. PMCID: PMC5336434. 13. Peker BO, Şener AG, Kaptan Aydoğmuş F. Antinuclear antibodies (ANAs) detected by indirect immunofluorescence (IIF) method in acute COVID-19 infection; future roadmap for laboratory diag- nosis. J Immunol Methods. 2021;499:113174. DOI: 10.1016/j .jim.2021.113174. PMID: 34737165. PMCID: PMC8556075. 14. Ruggiero A, Martora F, Picone V, et al. The impact of COVID-19 infection on patients with psoriasis treated with bi- ologics: an Italian experience. Clin Exp Dermatol. 2022;47(12): 2280-2282. DOI: 10.1111/ced.15336. PMID: 35867020. PMCID: PMC9349949. 15. Chang SH, Minn D, Kim YK. Autoantibodies in moderate and critical cases of COVID-19. Clin Transl Sci. 2021;14(5): 1625-1626. DOI: 10.1111/cts.13036. PMID: 33934534. PMCID: PMC8239866. 16. Gazzaruso C, Carlo Stella N, Mariani G, et al. High prevalence of antinuclear antibodies and lupus anticoagulant in patients hospitalized for SARS-CoV2 pneumonia. Clin Rheumatol. 2020;39(7):2095-2097. DOI: 10.1007/s10067-020-05180-7. PMID: 32462425. PMCID: PMC7251560. 17. Lerma LA, Chaudhary A, Bryan A, Morishima C, Wener MH, Fink SL. Prevalence of autoantibody responses in acute coro- navirus disease 2019 (COVID-19). J Transl Autoimmun. Original Article | Dermatol Pract Concept. 2023;13(2):e2023081 7 33. Starace M, Iorizzo M, Sechi A, et al. Trichodynia and telogen effluvium in COVID-19 patients: Results of an international expert opinion survey on diagnosis and management. JAAD Int. 2021;5:11-18. DOI: 10.1016/j.jdin.2021.07.006. PMID: 34368790. PMCID: PMC8328568. 34. Di Landro A, Naldi L, Glaser E, Paus R, Tosti A. Pathobiol- ogy questions raised by telogen effluvium and trichodynia in COVID-19 patients. Exp Dermatol. 2021;30(7):999-1000. DOI: 10.1111/exd.14352. PMID: 33838048. PMCID: PMC8250761. 31. Kivanç-Altunay I, Savaş C, Gökdemir G, Köşlü A, Ayaydin EB. The presence of trichodynia in patients with telogen effluvium and androgenetic alopecia. Int J Dermatol. 2003;42(9):691-693. DOI: 10.1046/j.1365-4362.2003.01847.x. PMID: 12956679. 32. Durusoy C, Ozenli Y, Adiguzel A, et al. The role of psychological factors and serum zinc, folate and vitamin B12 levels in the ae- tiology of trichodynia: a case-control study. Clin Exp Dermatol. 2009;34(7):789-792. DOI: 10.1111/j.1365-2230.2008.03165.x. PMID: 19508569.