Hair Loss and Telogen Effluvium Related to COVID-19: The Potential Implication of Adipose-Derived Mesenchymal Stem Cells and Platelet-Rich Plasma as Regenerative Strategies.

The diffusion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) inducing coronavirus disease 2019 (COVID-19) has increased the incidence of several dermatological disorders, including hair loss (HL). This article aims to review the literature regarding the incidence of HL and telogen effluvium (TE) in COVID-19 patients and critically appraise the available evidence regarding the role of regenerative strategies like Platelet-Rich Plasma (PRP) and Human Follicle Stem Cells (HFSCs). A literature review regarding the correlation of HL and TE in COVID-19 patients analyzing the biomolecular pathway involved and the role of regenerative strategies was performed using PubMed, MEDLINE, Embase, PreMEDLINE, Scopus, and the Cochrane databases. Observational studies revealed an escalated incidence of pattern HL and TE in COVID-19 patients. Psychological stress, systemic inflammation, and oxidative stress are potential culprits. Proinflammatory cytokines and stress hormones negatively affect the normal metabolism of proteoglycans. Reduced anagenic expression of proteoglycans is a potential mediating mechanism that connects HL to COVID-19. Currently, only one study has been published on PRP against HL in COVID-19 patients. Further controlled trials are required to confirm PRP and HFSCs efficacy in COVID-19 patients.

The role of autologous micrografts injection from the scalp tissue in the treatment of COVID-19 associated telogen effluvium: Clinical and trichoscopic evaluation.

The clinical presentation of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2 COVID-19) varies from asymptomatic infection to a life-threatening, multiorgan disease. One of these manifestations is telogen effluvium (TE) which is characterized by diffuse hair loss occurring in patients previously infected with SARS-CoV-2 and lasts ~3 months, after which excessive hair loss follows. Hair follicles are known to contain a well-characterized niche for adult stem cells which is the bulge containing epithelial and melanocytic stem cells. Stem cells in the hair bulge, a demarcated structure within the lower permanent portion of hair follicles, can generate the interfollicular epidermis, hair follicle structures, and sebaceous glands. This study aims to evaluate autologous micrografts from scalp tissues as a therapeutic modality in the management of TE caused by COVID-19. Twenty patients of previous COVID-19 infection suffered from TE were included in this study for human follicle stem cells micrograft scalp treatment and they were evaluated after 3 months of treatment and after 6 months. There was significant improvement of the hair thickness and density compared with the start of the treatment and 6 months of follow-up. Autologous micrograft of the scalp showed marked improvement in the treatment of COVID-19 TE.

Understanding the significance of cytokines and chemokines in the pathogenesis of alopecia areata.

Alopecia areata has basically been understood as a type 1 inflammatory disease. Activated NKG2D+ CD8+ cells produce the Th1 cytokine interferon-γ, which leads to the disruption of immune tolerance of hair follicles and the exposure of self-antigens. This results in dense inflammatory cell infiltration and apoptosis around hair follicles, inducing hair loss. A well-known complication of alopecia areata is atopic dermatitis, a typical type 2 inflammatory disease. Hair scientists have shied away from confronting and understanding how alopecia areata, a type 1 inflammatory disease, and atopic dermatitis, a type 2 inflammatory disease, can occur together. This review summarizes the research on the cytokine balance in alopecia areata and then focuses on the classification of the cytokine balance in alopecia areata, including the classification of atopic dermatitis into extrinsic and intrinsic types. Dupilumab reportedly showed dual efficacy in a patient with concomitant atopic dermatitis and alopecia areata, supporting our own experience. Elevated Th2 cytokine levels have also been reported in patients with alopecia areata, with increased serum IL-4, IL-5, IL-6 levels, high IgE levels and elevated eosinophil levels. Because local immunotherapy is a treatment that induces Th2-type inflammation, it may worsen the condition of alopecia areata patients with extrinsic atopic dermatitis. It is desirable to select appropriate treatments with consideration of the cytokine balance.

Onset of alopecia areata after Epstein-Barr virus infectious mononucleosis.

BACKGROUND: The pathogenesis of alopecia areata (AA) is incompletely known. A positive family history in some points to a genetic predisposition, and discordance of the disease in identical twins suggests environmental triggers exist. OBJECTIVE: We sought to determine whether the Epstein-Barr virus (EBV) is a possible environmental trigger for AA. METHODS: We queried the National AA Registry for all patients who self-reported sudden onset of AA with concurrent EBV mononucleosis. RESULTS: Among the 6256 individuals registered between December 2001 and August 2007, 1586 patients reported an environmental trigger-including 12 individuals who had an EBV infection within 6 months before the onset of AA. LIMITATIONS: This study relies on self-reported data, and not all medical records confirming EBV infections were available for review. CONCLUSION: The association between EBV and AA is worthy of further investigation.

Role of cytomegalovirus replication in alopecia areata pathogenesis.

BACKGROUND: Cytomegalovirus (CMV) infection has been correlated with various autoimmune disorders. Using molecular biology techniques, DNA sequences of CMV have been reported in paraffin sections of alopecia areata (AA) lesions. Reactivation of the CMV infection has been postulated as one of the pathogenic mechanisms in AA. Other studies, using different techniques however have demonstrated no correlation between CMV and AA. OBJECTIVES: This study was to clarify the role of CMV infection and to demonstrate the absence of replication of other autoimmune diseases-related herpes virus (EBV) in the pathogenesis of AA. METHODS: After extraction of mRNA from tissue samples of a patient with active patchy AA, reverse transcriptase-polymerase chain reaction was carried out using primers specific for some viral members of the beta-herpes viridae family (CMV, EBV, HSV). RESULTS: No replication of the CMV or other beta-herpes viridae has been detected in any of the samples collected. CONCLUSIONS: The results strongly support the hypothesis that CMV is not the triggering factor in AA, neither as a re-activator of the immune response nor as a trigger of the autoimmunity. No other herpes virus is implicated in the pathogenesis of this disease.