Background: Nail changes, including onychomadesis (nail shedding) and Beau’s line, following hand-foot-mouth disease (HFMD) are a common emergence at the stage of late complications of HFMD. However, the exact mechanism is still unknown. Therefore, we conducted this study to elucidate the mechanism of nail changes following HFMD. Methods: We collected 11 patients suffering from onychomadesis following HFMD. Nail samples from all of them were collected. Real time reverse transcription polymerase chain reaction (RT-PCR) and sequencing for human enteroviruses (HEV) were performed. Throat swabs for RT-PCR and sequencing for HEV were performed for three cases. Results: RT-PCR demonstrated the presence of Coxackievirus A6 (CVA6) in nail samples from three patients and one with Echovirus. Conclusion: In conclusion, we believe that the major cause of onychomadesis following HFMD is that certain novel viruses, mostly CVA6, are virulent and may damage nail matrix. Direct injury caused by cutaneous lesions of HFMD around nail matrix is a minor cause. There are still other virulent HEV which may result in onychomadesis. In addition, the novel strain of CVA6 also causes atypical clinical presentations, such as adult involvement and delayed-onset palmar and plantar desquamation. Physicians should be familiar with atypical presentations caused by novel viruses to avoid misdiagnosis and even inform patients of the possibility of onychomadesis that may take place weeks later to reassure patients.

Studies on the impact of syphilis on the cardiovascular system in large populations are limited. This study investigated the effects of syphilis on cardiovascular outcomes. Medical records from 2010 to 2015 were retrieved from the Taiwan National Health Insurance Research Database, linked to the Notifiable Infectious Diseases database from the Taiwan Centers for Disease Control. Patients with syphilis were identified, excluding those with missing information, under 20 years of age, or with a history of human immunodeficiency virus infection, acute myocardial infarction, heart failure, aortic regurgitation, replacement of the aortic valve, aneurysm and/or dissection of the aorta, atrial fibrillation, ischaemic stroke, haemorrhagic stroke, and venous thromboembolism. Primary outcomes included new-onset acute myocardial infarction, heart failure, aortic regurgitation, aneurysm and dissection of the aorta, atrial fibrillation, ischaemic stroke, haemorrhagic stroke, venous thromboembolism, cardiovascular death, and all-cause mortality. A total of 28 796 patients with syphilis were identified from 2010 to 2015. After exclusions and frequency matching, 20 601 syphilis patients and 20 601 non-syphilis patients were analysed. The relative rate (RR) was utilized in the analysis, as the competing risk of death was not considered. Compared with patients without syphilis, patients with syphilis had increased risks of acute myocardial infarction (RR 38%, 95% confidence interval [CI] 1.19–1.60, P < .001), heart failure (RR 88%, 95% CI 1.64–2.14, P < .001), aortic regurgitation (RR 81%, 95% CI 1.18–2.75, P = .006), atrial fibrillation (RR 45%, 95% CI 1.20–1.76, P < .001), ischaemic stroke (RR 68%, 95% CI 1.52–1.87, P < .001), haemorrhagic stroke (RR 114%, 95% CI 1.74–2.64, P < .001), venous thromboembolism (RR 67%, 95% CI 1.23–2.26, P = .001), cardiovascular death (RR 155%, 95% CI 2.11–3.08, P < .001), and all-cause death (RR 196%, 95% CI 2.74–3.19, P < .001) but not for aneurysm and dissection of the aorta. This study demonstrates that patients with syphilis have a higher risk of cardiovascular events and all-cause mortality compared with those without syphilis. This visual summary delineates the cardiovascular risks and mortality associated with syphilis infection, presenting hazard ratios for key outcomes. These include new-onset acute myocardial infarction, heart failure, aortic regurgitation, aneurysm and/or dissection of the aorta, atrial fibrillation, ischaemic stroke, haemorrhagic stroke, venous thromboembolism (deep vein thrombosis or pulmonary embolism), cardiovascular death, and all-cause mortality.

Background: Historically, acute kidney injury (AKI) has been a common severe complication of acute myocardial infarction (MI). As percutaneous coronary interventions have become more widely used, AMI outcomes have significantly improved. However, post-AMI AKI epidemiology and its associated factors are not well-understood in the age of interventional cardiology. Materials and methods: This is a retrospective study examining changes in creatinine levels in all patients admitted for AMI in a single medical center between August 2009 and February 2019. KDIGO criteria were used to define the different stages of post-AMI AKI. Results: The study included 1299 eligible cases, among which 213 (16.4%) developed AKI during AMI index admission; and 128 (60.1%), 46 (21.6%), and 39 (18.3%) were classified as KDIGO stages 1, 2, and 3, respectively. Compared with non-AKI subjects, the AKI group had a higher prevalence of non-STEMI (48.4% vs. 29.1%, p < 0.001), higher Killip class (3 or 4), and higher in-hospital mortality (15% vs. 2.5%, p < 0.001). During the index MI hospitalization, 13.6% (29/213) of the post-MI AKI patients received hemodialysis. Baseline abnormal creatinine (≥1.5 mg/dL), dyslipidemia, and more advanced KDIGO stages (2 or 3) were associated with an increased risk of requiring in-hospital hemodialysis. Moreover, a more advanced KDIGO stage (≥2) was correlated with higher all-cause in-hospital mortality. Conclusion: AMI patients remain at risk of AKI, which negatively affects their survival in the modern age.