To identify risk factors for mortality in a cohort of carbapenem-resistant enterobacteriaceae (CRE) carriers, focusing on immunosuppression and other risk factors known at the time of CRE carriage detection.
Methods
We prospectively followed all new and known CRE carriers admitted between June 2016 and June 2017 to a single tertiary center in Israel. Patients were included in the study after confirmation of the carrier state. Demographic and clinical data were documented on admission or CRE acquisition and patients were followed prospectively post-discharge until January 2018 or death. Risk factors for mortality known at the time of the first encounter with a CRE carrier were sought. Adjusted hazard ratios (HR) for mortality at end of follow-up with 95% confidence intervals (CI) were assessed using Cox regression analysis.
Results
A total of 115 patients were included in the analysis. During the study period, 66 (57.4%) patients died. Immunosuppression was associated with mortality (HR 1.95, CI 95% 1.12–3.44), adjusted to the Charlson co-morbidity score, functional status, chronic renal disease and Klebsiella pneumonia CRE, the latter three also significantly associated with mortality. CRE bacteremia occurred among 24 (20.9%) carriers during follow up, more frequently among immunosuppressed patients and was significantly associated with mortality at end of follow-up (p?=?0.015).
Conclusion
Immunosuppression is independently associated with mortality among CRE carriers, possibly related to CRE bacteremia that is frequent among these patients. Further research is needed on interventions to prevent deaths among CRE carriers. 相似文献
Despite the significant progress made over the past decade with combination of molecular profiling data and the development of new clinical strategies, our understanding of metastasis remains elusive. Bone metastasis is a complex process and a major cause of mortality in breast and prostate cancer patients, for which there is no effective treatment to-date. The current review summarizes the routes taken by the metastatic cells and the interactions between them and the bone microenvironment. We emphasize the role of the specified niches and cues that promote cellular adhesion, colonization, prolonged dormancy, and reactivation. Understanding these mechanisms will provide better insights for future studies and treatment strategies for bone metastatic conditions.
People with kidney failure face a multitude of psychosocial stressors that affect disease trajectory and health outcomes.
Objectives
To investigate psychosocial factors affecting people with kidney failure before or at start of kidney replacement therapy (KRT) and kidney supportive and palliative care (KSPC) phases of illness and to explore role of social worker during the illness trajectory.
Methods
We conducted a secondary data audit of patients either before or at start of KRT (Phase 1) and at the KSPC (Phase 2) of illness and had psychosocial assessments between March 2012 and March 2020 in an Australian setting.
Results
Seventy-nine individuals, aged 70 ± 12 years, had at least two psychosocial assessments, one in each of the two phases of illness. The median time between social worker evaluations in Phase 1 and Phase 2 was 522 (116−943) days. Adjustment to illness and treatment (90%) was the most prevalent psychosocial issue identified in Phase 1, which declined to 39% in Phase 2. Need for aged care assistance (7.6%−63%; p < 0.001) and carer support (7.6%−42%; p < 0.001) increased significantly from Phase 1 to Phase 2. There was a significant increase in psychosocial interventions by the social worker in Phase 2, including supportive counselling (53%−73%; p < 0.05), provision of education and information (43%−65%; p < 0.01), and referrals (28%−62%; p < 0.01).
Conclusion
Adults nearing or at the start of KRT experience immense psychosocial burden and adaptive demands that recognisably change during the course of illness. The positive role played by the nephrology social worker warrants further investigation. 相似文献
Childhood growth hormone deficiency (GHD) decreases left-ventricular (LV) mass, but impairment of cardiac function has never
been documented. The objective of this study was to assess the cardiac effects of GHD and recombinant human growth hormone
(rhGH) treatment using conventional echocardiography and tissue Doppler imaging. Complete two-dimensional, M-mode, pulse-wave
Doppler echocardiography and pulse-wave tissue Doppler imaging were performed in 12 children (6 male and 6 female patients)
with GHD at baseline and at 5.86 ± 1.61 months after rhGH therapy. Recombinant human growth hormone treatment was associated
with a significant increase in LV mass index (63.8 ± 27.1 to 79.3 ± 30.3 g/m2; P < 0.01) and LV internal dimensions (21.4 ± 2.63 to 24.0 ± 4.13 mm in systole [P = 0.03] and 36.5 ± 3.90 to 39.5 ± 4.94 mm in diastole [P < 0.01]). There were statistical differences of parameters, such as deceleration time of early peak velocity of mitral, isovolumic
relaxation time, and myocardial performance index (103 ± 15.4 to 139 ± 21.2 ms [P < 0.01], 55.5 ± 9.24 to 69.2 ± 3.74 ms [P < 0.01], and 37.8 ± 4.46 to 44.9 ± 5.44% [P < 0.01], respectively). Before and during rhGH therapy, there were no significant differences in fractional shortening of
the left ventricle, peak mitral, and tricuspid wave velocities with ratios determined using conventional echocardiography
and tissue Doppler imaging. In children, GHD affects heart morphology by inducing a decrease in cardiac size, but it does
not modify cardiac function. Recombinant human growth hormone treatment increases cardiac mass, deceleration time of early
peak velocity of the mitral valve, isovolumic relaxation time, and myocardial performance index, but it does not make a difference
in other parameters of conventional echocardiography and tissue Doppler imaging. 相似文献
While individuals with Huntington disease (HD) show memory impairment that indicates hippocampal dysfunction, the available literature does not consistently identify structural evidence for involvement of the whole hippocampus but rather suggests that hippocampal atrophy may be confined to certain hippocampal subregions.
Methods
We processed T1-weighted MRI from IMAGE-HD study using FreeSurfer 7.0 and compared the volumes of the hippocampal subfields among 36 early motor symptomatic (symp-HD), 40 pre-symptomatic (pre-HD), and 36 healthy control individuals across three timepoints over 36 months.
Results
Mixed-model analyses revealed significantly lower subfield volumes in symp-HD, compared with pre-HD and control groups, in the subicular regions of the perforant-pathway: presubiculum, subiculum, dentate gyrus, tail, and right molecular layer. These adjoining subfields aggregated into a single principal component, which demonstrated an accelerated rate of atrophy in the symp-HD. Volumes between pre-HD and controls did not show any significant difference. In the combined HD groups, CAG repeat length and disease burden score were associated with presubiculum, molecular layer, tail, and perforant-pathway subfield volumes. Hippocampal left tail and perforant-pathway subfields were associated with motor onset in the pre-HD group.
Conclusions
Hippocampal subfields atrophy in early symptomatic HD affects key regions of the perforant-pathway, which may implicate the distinctive memory impairment at this stage of illness. Their volumetric associations with genetic and clinical markers suggest the selective susceptibility of these subfields to mutant Huntingtin and disease progression. 相似文献