New-onset diabetes is considered one of the most serious complications of transplantation, impacting heavily on graft function and survival and patient morbidity and mortality, as well as on quality of life and healthcare costs. Furthermore, development of diabetes after transplantation is a major determinant of the increased cardiovascular morbidity and mortality observed in transplant recipients, imposing a greater relative risk than hyperlipidemia and hypertension in this patient population (1). The additional risk for serious macrovascular and microvascular complications comparable to type 1 and type 2 diabetes mellitus compound the already complex management of the transplant recipient, adding to the posttransplantation care requirements and imposing further significant economic burden on healthcare systems (2).Despite consistent improvements in transplant graft survival with the advent of new immunosuppressive drugs, the incidence of new-onset diabetes after transplantation remains high yet underreported, with recorded incidences varying between 2% and 53% in the first year after transplantation (3). These variable data reflect the need for a standard definition for new-onset diabetes after transplantation and highlight the lack of awareness of this serious complication among the transplant community. Because the immunosuppressive regimen plays a major role in the development of diabetes after transplantation, the approach to management before and after transplantation is equally important. Indeed, a higher rate of new-onset diabetes after transplantation has been observed with the calcineurin inhibitor tacrolimus compared with cyclosporine (4), despite a trend to use less steroids. Consequently, guidelines have been warranted for many years to provide recommendations (i) for a standard definition and diagnostic criteria for newonset diabetes after transplantation; (ii) to minimize the risk of developing diabetes; (iii) for monitoring patients after transplantation; and (iv) for the management of patients who develop new-onset diabetes after transplantation.With this in mind, I commend the recent international consensus guidelines for new-onset diabetes after transplan-tation recently reported by Davidson et al. (5), which build on and compliment recommendations developed by the Canadian working group (6). These guidelines examine the impact of new-onset diabetes after transplantation and provide practical recommendations for the diagnosis and management of this condition as a priority in transplant recipients. The guidelines highlight the need for risk assessment and counseling for each patient before transplantation and appropriate tailoring and adjustment of immunosuppressive therapy. Strategies to minimize the risk for development of diabetes after transplantation include avoidance or minimization of steroids and tacrolimus and conversion to less diabetogenic regimens (eg, cyclosporine). Although further research into new-onset diabetes after transplantation is warranted, these guidelines will help to r...

No abstract

Enteroviruses (EVs) can induce nonspecific respiratory tract infections in children, but their epidemiological, virological, and clinical features remain to be assessed. In the present study, we analyzed 252 EV-related infection cases (median age of subjects, 5.1 years) diagnosed among 11,509 consecutive children visiting emergency departments within a 7-year period in the north of France. EV strains were isolated from nasopharyngeal samples by viral cell culture, identified by seroneutralization assay, and genetically compared by partial amplification and sequencing of the VP1 gene. ؊3 ) occurring more often in infants aged 1 to 12 months (P ‫؍‬ 0.0002), with spring-fall seasonality. Viruses ECHO 11, 6, and 13 were the more frequently identified respiratory strains (24, 13, and 11%, respectively). The VP1 gene phylogenetic analysis showed the concomitant or successive circulation of genetically distinct EV respiratory strains (species A or B) during the same month or annual epidemic period. Our findings indicated that respiratory tract infections accounted for the 30% of EV-induced pediatric pathologies, contributing to LRTIs in 54% of these cases. Moreover, the concomitant or successive circulation of genetically distinct EV strains indicated the possibility of pediatric repeated respiratory infections within the same epidemic season.Enteroviruses (EVs) (Picornaviridae) are among the most common viruses infecting human beings worldwide (13,23,25). Current taxonomy divides nonpolio human EV into four species (human EVs A to D), including a total of 89 serotypes (24, 38). Individual serotypes have different temporal patterns of circulation and can be associated with different clinical manifestations (24, 39). Although the majority of human EV infections remain asymptomatic, these viruses are associated with diverse clinical syndromes, ranging from minor febrile illness to severe and potentially fatal pathologies, including aseptic meningitis, encephalitis, myopericarditis, acute flaccid paralysis, and severe neonatal sepsis-like disease (24). Moreover, EV can induce nonspecific respiratory illnesses in infants or adults, including upper respiratory tract infections but also lower respiratory tract infections (LRTIs), resulting in bronchitis, bronchiolitis (37), and pneumonia (13). Different human EV strains-including EV 68 and 71, coxsackie A9, A21, B2 and B4 viruses, and echovirus 9, 11 and 22-have been isolated from nasopharyngeal samples, tracheal aspirates, bronchoalveolar lavages, or lung tissues by classical cell culture assays and identified as the cause of severe or fatal viral bronchopneumonia (4,6,10,11,29,32,35). At present, our understanding of the epidemiology and clinical profile of EV pediatric respiratory infections is restricted to the prevalence and the epidemiological significance of EV respiratory infections as the cause of bronchiolitis or acute wheezing in cohorts of hospitalized infants (1,22,31,33). In these reports, no serotyping identification or molecular comparative analysis of EV res...

Our data suggest that HBoV at a high viral load could be an etiologic agent of respiratory tract disease, whereas the exact role of HBoV at a low viral load, as etiological cause or as pathophysiological co-factor of respiratory diseases, remains to be determined.