Background A broad spectrum of skin diseases, including hair and nails, can be directly or indirectly triggered by COVID‐19. It is aimed to examine the type and frequency of hair and nail disorders after COVID‐19 infection. Methods This is a multicenter study conducted on consecutive 2171 post‐COVID‐19 patients. Patients who developed hair and nail disorders and did not develop hair and nail disorders were recruited as subject and control groups. The type and frequency of hair and nail disorders were examined. Results The rate of the previous admission in hospital due to COVID‐19 was statistically significantly more common in patients who developed hair loss after getting infected with COVID‐19 ( P < 0.001). Telogen effluvium (85%) was the most common hair loss type followed by worsening of androgenetic alopecia (7%) after COVID‐19 infection. The mean stress scores during and after getting infected with COVID‐19 were 6.88 ± 2.77 and 3.64 ± 3.04, respectively, in the hair loss group and were 5.77 ± 3.18 and 2.81 ± 2.84, respectively, in the control group ( P < 0.001, P < 0.001). The frequency of recurrent COVID‐19 was statistically significantly higher in men with severe androgenetic alopecia (Grades 4–7 HNS) ( P = 0.012; Odds ratio: 2.931 [1.222–7.027]). The most common nail disorders were leukonychia, onycholysis, Beau's lines, onychomadesis, and onychoschisis, respectively. The symptoms of COVID‐19 were statistically significantly more common in patients having nail disorders after getting infected with COVID‐19 when compared to the control group ( P < 0.05). Conclusion The development of both nail and hair disorders after COVID‐19 seems to be related to a history of severe COVID‐19.
Background The COVID‐19 pandemic has substantially affected the healthcare systems around the world. It has also induced some changes in working habits at dermatology clinics. The majority of dermatology clinics limited the number of patients at outpatient clinics and postponed the elective procedures. Aims and Objectives To evaluate the working conditions and habits of dermatologists in Turkey during the COVID‐19 pandemic. Methods This is a survey study with seventeen questions in which two hundred fifteen dermatologists working in Turkey participated. Results Our results revealed that 53.5% of the participants worked in the areas related to COVID‐19 during the pandemic. The average number of dermatology outpatient days in a week was five among the 48.8% of dermatologists, 21.4% of those had three working days, and 18.1% of those had four days. During the pandemic, the most common reasons for referral to outpatient clinics were acne and acneiform eruptions (88.8%), dermatitis (73.5%), and hair loss (71.2%). Participants hesitated to use the following treatments: long‐term systemic steroid (77.7%), cyclosporine (69.8%), and methotrexate (60%). Conclusion It is observed that the COVID‐19 pandemic had affected the working habits and conditions of the dermatologists, which might be considered for the designing of new working approaches.
Background: This study aims to investigate the anti-inflammatory effects of cinnamaldehyde in atopic dermatitis (AD) in the mouse model. Materials and Methods: Twenty-four mice were divided into four groups: Group A (control), group B [AD with no treatment (AD + NoTre)], group C [AD with corticosteroids (AD + Cort)] and group D [AD with cinnamaldehyde (AD + Cin)]. 2,4-dinitrofluorobenzene was used to form the AD model. Topical corticosteroid was applied to group C, and oral cinnamaldehyde was administered to group D. Dorsal skin biopsies were evaluated immunohistochemically with interleukin (IL)-25, IL-33, thymic stromal lymphopoietin and caspase-3. Results: Epithelial thicknesses were significantly higher in group B–D mice compared to group A ( P = 0.002, 0.009, 0.004, respectively). Significantly, higher staining with IL-25 was observed in group B (AD + NoTre) and group D (AD + Cin) than in group A (control) ( P = 0.003, 0.002, respectively). However, no significant difference was observed between group D (AD + Cin) and group B (AD + NoTre). All three groups (B–D) had significantly higher staining in terms of diffuseness of IL-33 compared to group A (control) ( P = 0.002, 0.002, 0.002, respectively). Caspase-3 staining was significantly lower in group D (AD + Cin) than in group B (AD + NoTre) ( P = 0.003, 0.002, respectively). Moreover, caspase-3 staining intensity was significantly lower in group D (AD + Cin) than in group C (AD + Cort) ( P = 0.002). Conclusions: Our study demonstrated that IL-33, IL-25 and caspase-3 have a role in the pathogenesis of AD. Furthermore, cinnamaldehyde reduced caspase-3 activity more than topical corticosteroids and anti-inflammatory effects might be investigated in AD therapy with future studies.
Background: The etiopathogenesis and cold stimulation mechanism are not fully understood in cold urticaria (CU). Substance P (SP) is released from skin neurons as a result of cold stimulation. It causes mast cell degranulation and therefore causes mast cell chymase (MCC) release. Angiotensin-converting enzyme (ACE) plays a role in removing SP from the environment. ACE also catalyses the conversion of angiotensin I (AT1) to angiotensin II (AT2), like MCC. This study aims to investigate the role of SP, ACE and MCC in the pathogenesis of CU. Methods: Patients with acquired CU were included in the study. Two punch biopsies were taken from the urticaria plaque resulting from the stimulation and the intact skin without lesions. The samples were evaluated histopathologically. All samples were stained immunohistochemically with SP, ACE and MCC antibodies. Results: The number of patients included in the study was 21. In the plaque lesion, the presence of dermal neutrophil and eosinophil, neutrophil in the vascular lumen were found to be statistically significantly higher than intact tissue (p = 0.046, P = 0.014, P = 0.014). Strong positive staining was detected in the full thickness of the epidermis, vascular endothelial cells, eccrine and sebaceous glands with ACE. MCC was statistically significantly higher in lesional skin than lesion-free skin samples (p < 0.001). Conclusions: Mast cell maintains its central role in CU pathogenesis. SP, which causes neurogenic inflammation, may not be detected due to its rapid destruction in the tissue. Strong staining of ACE, which takes part in the local renin-angiotensin-aldosterone (RAS) system in the skin, should be documented quantitatively.
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