Impact of the malnutrition on mortality in Rheumatoid arthritis patients: A cohort study from NHANES 1999-2014.

Background: Patients with Rheumatoid arthritis (RA) are prone to malnutrition. However, it is rare studies assessing the relationship between malnutrition and all-cause mortality in patients with RA. Objective: To investigate the relationship between malnutrition and all-cause mortality in patients with RA in a large national sample cohort. Methods: We analyzed data on 1,976 adults ≥ 18 years of age during National Health and Nutrition Examination Survey (NHANES) 1999-2014. We chose the Controlled Nutritional Status Score (CONUT) and the Nutritional Risk Index (NRI) to assess the nutritional status of patients with RA. The Kaplan-Meier (KM) survival curves Cox proportional hazards regression models were used to analyze the associations between malnutrition and all-cause mortality. Results: Of the 1,976 patients with RA (57.38 ± 0.40 years, female 59.9%, non-Hispanic white 69.9%), the prevalence of malnutrition was 18.8% by used the CONUT and 26.6% by used the NRI. The KM survival curves showed that malnutrition was associated with a higher incidence of all-cause mortality during the 10-year follow-up period (log-rank test, P < 0.001). In the fully corrected model, the adjusting hazard ratio (aHR) for all-cause mortality in patients with moderate to severe malnutrition with CONUT and NRI were 5.63 (95% CI, 2.55-12.45; P < 0.001) and 2.56 (95% CI, 1.81-3.62; P < 0.001), respectively, compared with patients without malnutrition. Conclusion: Malnutrition is very prevalent in patients with RA, approximately 18.8% (CONUT) to 26.6% (NRI). Malnutrition is strongly associated with an increased risk of all-cause mortality. These findings underscore the importance of attention and intervention in the nutritional status of patients with RA. Further clinical trials are needed to prospectively assess the effect of nutritional interventions on the prognosis of patients with RA.

Evaluation of the neonatal sequential organ failure assessment and mortality risk in neonates with respiratory distress syndrome: A retrospective cohort study.

Background: Respiratory distress syndrome (RDS) is one of the leading causes of neonatal death in the neonatal intensive care unit (NICU). Previous studies have suggested that the development of neonatal RDS may be associated with inflammation and lead to organ dysfunction. The neonatal sequential organ failure assessment (nSOFA) scoring system is an operational definition of organ dysfunction, but whether it can be used to predict mortality in neonates RDS is unknown. The aim of this study was to clarify the performance of the nSOFA score in predicting mortality in patients with neonatal RDS, with the aim of broadening the clinical application of the nSOFA score. Methods: Neonates with RDS were identified from the Medical Information Mart for Intensive Care (MIMIC)-III database. Cox proportional hazards model were used to assess the association between nSOFA score and mortality. Propensity score matched analysis were used to assess the robustness of the analytical results. Results: In this study of 1,281 patients with RDS of which 57.2% were male, death occurred in 40 cases (3.1%). Patients with high nSOFA scores had a higher mortality rate of 10.7% compared with low nSOFA scores at 0.3%. After adjusting for confounding, multivariate Cox proportional risk analysis showed that an increase in nSOFA score was significantly associated with increased mortality in patients with RDS [adjusted Hazards Ratio (aHR): 1.48, 95% Confidence Interval (CI): 1.32-1.67; p < 0.001]. Similarly, the High nSOFA group was significantly associated with higher mortality in RDS patients (aHR: 19.35, 95% CI: 4.41-84.95; p < 0.001) compared with the low nSOFA group. Conclusion: The nSOFA score was positively associated with the risk of mortality in cases of neonatal RDS in the NICU, where its use may help clinicians to quickly and accurately identify high risk neonates and implement more aggressive intervention.

Impact of the Malnutrition on Mortality in Patients With Osteoporosis: A Cohort Study From NHANES 2005-2010.

Background: Osteoporosis is the most common metabolic bone disease. Recent studies have shown that malnutrition can promote the development of osteoporosis. However, the incidence of malnutrition in patients with osteoporosis and the relationship between malnutrition and all-cause mortality has not been adequately studied. Therefore, our study investigated the relationship between malnutrition and all-cause mortality in patients with osteoporosis. Methods: We analyzed data on 7,700 adults ≥20 years of age during National Health and Nutrition Examination Survey (NHANES) 2005-2010. Each patient was assigned to one of three groups: normal nutritional status, mild malnutrition, and moderate to severe malnutrition. Survival curves and univariate and multivariable cox regressions based on the NHANES recommended weights were used to assess the association between malnutrition status and mortality. Moreover, cox proportional hazards regression analyses were performed on the matched pairs. Results: Overall, 7,700 eligible individuals with osteoporosis were included in the final analysis, and the mean age was 52.0 ± 0.4 years. From the Kaplan-Meier curves for long-term all-cause mortality of malnutrition, worsening malnutrition status was associated with higher incidence of all-cause mortality. In the fully adjusted models, the adjusted hazard ratio (aHR) was 1.54 [95% confidence interval (CI), 1.02-2.31, p = 0.039] at mild malnutrition status and 2.70 (95%CI, 1.95-3.74, p < 0.001) at moderate to severe malnutrition status. The cox model after matching indicated that malnutrition was still a high mortality risk than no malnutrition (aHR = 2.23, 95% CI, 1.66-3.01, p < 0.001). Conclusions: Poor malnutrition status, common in osteoporotic patients, is strongly associated with a risk for all-cause mortality comparable to that seen with normal nutritional status. These findings highlight the importance of risk stratification for nutritional status in osteoporotic patients and the implementation of strategies that is now available to help prevent malnutrition in these patients.

Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin.

It has previously been demonstrated that bradykinin receptor B1 (B1R) agonists evoke an itch-related scratching response in inflamed skin via the B1 receptor; however, the mechanisms responsible for this abnormal itch sensation remain unclear. Therefore, the present study utilized a complete Freund's adjuvant (CFA)-induced mouse model of inflammation to elucidate the mechanisms responsible. Over a period of 30 min, scratching behavior was quantified by the number of hind limb scratches of the area surrounding the drug injection site on the neck. Furthermore, western blot analysis was used to investigate the potential role of extracellular signal-regulated kinase (ERK) 1/2 signaling as a mediator of itch in CFA-treated mice. The results demonstrated that CFA-induced inflammation at the back of the neck is associated with sustained enhancement of ERK1/2 activation in the spinal cord. Moreover, B1R agonist treatment resulted in increased expression of phosphorylated ERK1/2 in the spinal cord, which peaked at 45 min. Consistent with these findings, inhibition of either mitogen-activated protein/ERK kinase or ERK1/2, as well as inhibition of ERK1/2 activation following inflammation, attenuated B1 receptor-mediated scratching responses to a greater extent, as compared with control mice. Collectively, the results of the present study indicated that enhanced and persistent ERK1/2 activation in the spinal cord may be required to induce a scratching response to B1R agonists following CFA-induced inflammation.

The kinin B1 receptor mediates alloknesis in a murine model of inflammation.

Noxious stimuli and non-noxious mechanical stimuli elicit itch (alloknesis) instead of pain on skin lesions of patients with atopic dermatitis. We previously found that bradykinin evokes an itch-related scratching response through activation of kinin B1 receptor in skin inflamed using complete Freund's adjuvant. In this study we investigated whether alloknesis is evoked in CFA-inflamed skin and the involvement of kinin receptors. In our results, alloknesis was elicited four days after CFA-inflammation. Furthermore, pretreatment with a B1 receptor antagonist or µ-opioid receptor antagonist significantly reduced alloknesis. In contrast, treatment with a B2 receptor antagonist significantly increased alloknesis. These results suggest that the alloknesis response is mediated by the activation of kinin B1 receptor but antagonized by the B2 receptor in CFA-inflamed mice.