The effect of COVID-19 on development of hair and nail disorders: a Turkish multicenter, controlled study.

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.

Left ventricular outflow tract gradient is associated with reduced capillary density in hypertrophic cardiomyopathy irrespective of genotype.

BACKGROUND: Coronary microvascular dysfunction (CMD) is an important feature of hypertrophic cardiomyopathy (HCM), which contributes negatively to symptoms and long-term outcome. Previous in vivo imaging studies in HCM suggest that left ventricular outflow tract (LVOT) gradient and genetic status are important contributors to CMD. CMD may be caused by reduced capillary density. Here, we investigated whether a reduction in capillary density is related to genetic status or LVOT gradient severity in an in vitro study of HCM cardiac samples. METHODS: Using immunofluorescence microscopy, we analysed capillaries (Cap) and cardiomyocytes (CM) in myectomy specimens from 18 HCM patients with maximum left ventricular (LV) wall thickness ≥15 mm. All subjects exhibited significant LVOT obstruction, necessitating septal myectomy. In addition, control myocardium from the LV septal wall was collected at autopsy of 6 individuals that suffered a noncardiac death. RESULTS: CM area was higher in patients with HCM compared to controls. Capillary density was significantly lower in patients with HCM compared with controls (1425 ± 262 vs. 2543 ± 509 Cap/mm(2) , P < 0·001), as was the number of Cap per CM corrected for CM area (2·2 ± 0·5 vs. 4·2 ± 0·9 Cap/CM area, P < 0·001). Capillary density did not differ between genotype-negative and genotype-positive HCM patients at similar resting LVOT gradients. A significant correlation was present between resting LVOT gradient and CM area (r = 0·73, P < 0·001), capillary density (r = -0·74, P < 0·001) and the number of Cap per CM corrected for CM area (r = -0·82, P < 0·001). CONCLUSIONS: Our data indicate that LVOT gradient, rather than genetic status, is associated with reduced capillary density in HCM.