The Impact of Malnutrition on the Hospital and Infectious Outcomes of Patients Admitted With Alcoholic Hepatitis: 2011 to 2017 Analysis of US Hospitals.

GOALS: We specifically evaluate the effect of malnutrition on the infection risks of patients admitted with alcoholic hepatitis using a national registry of hospitalized patients in the United States. BACKGROUND: Malnutrition is a common manifestation of alcoholic hepatitis that affects patient outcomes. STUDY: 2011 to 2017 National Inpatient Sample was used to isolated patients with alcoholic hepatitis, stratified using malnutrition (protein-calorie malnutrition, sarcopenia, and weight loss/cachexia) and matched using age, gender, and race with 1:1 nearest neighbor matching method. Endpoints included mortality and infectious endpoints. RESULTS: After matching, there were 10,520 with malnutrition and 10,520 malnutrition-absent controls. Mortality was higher in the malnutrition cohort [5.02 vs. 2.29%, P<0.001, odds ratio (OR): 2.25, 95% confidence interval (CI): 1.93-2.63], as were sepsis (14.2 vs. 5.46, P<0.001, OR: 2.87, 95% CI: 2.60-3.18), pneumonia (10.9 vs. 4.63%, P<0.001, OR: 2.51, 95% CI: 2.25-2.81), urinary tract infection (14.8 vs. 9.01%, P<0.001, OR: 1.76, 95% CI: 1.61-1.91), cellulitis (3.17 vs. 2.18%, P<0.001, OR: 1.47, 95% CI: 1.24-1.74), cholangitis (0.52 vs. 0.20%, P<0.001, OR: 2.63, 95% CI: 1.59-4.35), and Clostridium difficile infection (1.67 vs. 0.91%, P<0.001, OR: 1.85, 95% CI: 1.44-2.37). In multivariate models, malnutrition was associated with mortality [P<0.001, adjusted odds ratio (aOR): 1.61, 95% CI: 1.37-1.90] and infectious endpoints: sepsis (P<0.001, aOR: 2.42, 95% CI: 2.18-2.69), pneumonia (P<0.001, aOR: 2.19, 95% CI: 1.96-2.46), urinary tract infection (P<0.001, aOR: 1.68, 95% CI: 1.53-1.84), cellulitis (P<0.001, aOR: 1.46, 95% CI: 1.22-1.74), cholangitis (P=0.002, aOR: 2.27, 95% CI: 1.36-3.80), and C. difficile infection (P<0.001, aOR: 1.89, 95% CI: 1.46-2.44). CONCLUSION: This study shows the presence of malnutrition is an independent risk factor of mortality and local/systemic infections in patients admitted with alcoholic hepatitis.

The Clinical Impact of Cirrhosis on the Hospital Outcomes of Patients Admitted With Influenza Infection: Propensity Score Matched Analysis of 2011-2017 US Hospital Data.

BACKGROUND/OBJECTIVES: Patients with cirrhosis have liver-related immune dysfunction that potentially predisposes the patients to increased influenza infection risk. Our study evaluates this cross-sectional relationship using a national registry of hospital patients. METHODS: This study included the 2011-2017 National Inpatient Sample database. From this, respiratory influenza cases were isolated and stratified using the presence of cirrhosis into a cirrhosis-present study cohort and cirrhosis-absent controls; propensity score matching method was used to match the controls to the study cohort (cirrhosis-present) using a 1:1 matching ratio. The endpoints included mortality, length of stay, hospitalization costs, and influenza-related complications. RESULTS: Following the match, there were 2,040 with cirrhosis and matched 2,040 without cirrhosis admitted with respiratory influenza infection. Compared to the controls, cirrhosis patients had higher in-hospital mortality (7.79 vs 3.43% p < 0.001, OR 2.38 95% CI 1.78-3.17), longer length of stay (7.25 vs 6.52 d p < 0.001), higher hospitalization costs ($70,009 vs $65,035 p < 0.001), and were more likely be discharged to a skilled nursing facility and home healthcare (vs routine home discharges). In terms of influenza-related complications, the cirrhosis cohort had higher rates of sepsis (29.8 vs 22% p < 0.001, OR 1.51 95% CI 1.31-1.74). In the multivariate regression analysis, cirrhosis was associated with higher mortality (p < 0.001, aOR 2.31 95% CI 1.59-3.35) and length of stay (p = 0.018, aOR 1.03 95% CI 1.01-1.06). In subgroup analysis of patients with decompensated (n = 597) versus compensated cirrhosis (n = 1443), those with decompensated cirrhosis had higher rates of in-hospital mortality (12.7 vs 5.75% p < 0.001, OR 2.39 95% CI 1.72-3.32), length of stay (8.85 vs 6.59 d p < 0.001), and hospitalization costs ($92,858 vs $60,556 p < 0.001). In the multivariate analysis, decompensated cirrhosis was associated with increased mortality (p < 0.001, aOR 2.86 95% CI 1.90-4.32). CONCLUSION: This study shows the presence of cirrhosis to result in higher hospital mortality and postinfluenza complications in patients with influenza infection.

The clinical impact of cirrhosis on the postoperative outcomes of patients undergoing bariatric surgery: propensity score-matched analysis of 2011-2017 US hospitals.

Objectives: Since there is increasing number of patients with cirrhosis who require the bariatric procedure due to obesity and obesity-related nonalcoholic steatohepatitis fibrosis, we evaluate the effect of cirrhosis on post-bariatric surgery outcomes.Methods: 2011-2017 National Inpatient Sample was used to isolate bariatric cases, which were stratified by cirrhosis; controls were propensity-score matched to cases and compared to endpoints: mortality, length of stay (LOS), costs, and postoperative complications.Results: From 190,753 patients undergoing bariatric surgery, there were 957 with cirrhosis and 957 matched controls. There was no difference in mortality (0.94 vs 0.52% p = 0.42, OR 1.81 95%CI 0.60-5.41); however, cirrhosis patients had higher LOS (3.36 vs 2.89d p = 0.002), costs ($68,671 vs $61,301 p < 0.001), and bleeding (2.09 vs 0.72% p < 0.001, OR 2.95 95%CI 1.89-4.61). In multivariate, there was no difference in mortality (p = 0.330, aOR 1.73 95%CI 0.58-5.19). In subgroup comparison of cirrhosis patients, those with decompensated cirrhosis had higher mortality (7.69 vs 0.94% p < 0.001, OR 8.78 95%CI 3.41-22.59).Conclusion: The results of this study show compensated cirrhosis does not pose an increased risk toward post-bariatric surgery mortality; however, hepatic decompensation increases the postsurgical risks.

The effect of malnutrition on the infectious outcomes of hospitalized patients with cirrhosis: analysis of the 2011-2017 hospital data.

BACKGROUND: In patients with cirrhosis, there is a clinical concern that the development of protein-calorie malnutrition will affect the immune system and predispose these patients to increased infectious outcomes. AIMS: In this study, we evaluate the effects of malnutrition on the infectious outcomes of patients admitted with cirrhosis. MATERIALS AND METHODS: This study used the 2011-2017 National Inpatient Sample to identify patients with cirrhosis. These patients were stratified using malnutrition (protein-calorie malnutrition, cachexia, and sarcopenia) and matched using age, gender, and race with 1:1 nearest neighbor matching method. The endpoints included mortality and infectious outcomes. RESULTS: After matching, there were 96 842 malnutrition-present cohort and equal number of controls. In univariate analysis, the malnutrition cohort had higher hospital mortality [10.40 vs. 5.04% P < 0.01, odds ratio (OR) 2.18, 95% confidence interval (CI) 2.11-2.26]. In multivariate models, malnutrition was associated with increased mortality [P < 0.01, adjusted odds ratio (aOR) 1.32, 95% CI 1.27-1.37] and infectious outcomes, including sepsis (P < 0.01, aOR 1.94, 95% CI 1.89-2.00), pneumonia (P < 0.01, aOR 1.68, 95% CI 1.63-1.73), UTI (P < 0.01, aOR 1.39, 95% CI 1.35-1.43), cellulitis (P < 0.01, aOR 1.09, 95% CI 1.05-1.13), cholangitis (P < 0.01, aOR 1.39, 95% CI 1.26-1.55), and clostridium difficile (P < 0.01, aOR 2.11, 95% CI 1.92-2.31). CONCLUSION: The results of this study indicate that malnutrition is an independent risk factor of hospital mortality and local/systemic infections in patients admitted with cirrhosis.

Improving the public health utility of global cardiovascular mortality data: the rise of ischemic heart disease.

BACKGROUND: High-quality, cause-specific mortality data are critical for effective health policy. Yet vague cause of death codes, such as heart failure, are highly prevalent in global mortality data. We propose an empirical method correcting mortality data for the use of heart failure as an underlying cause of death. METHODS: We performed a regression analysis stratified by sex, age, and country development status on all available ICD-10 mortality data, consisting of 142 million deaths across 838 country-years. The analysis yielded predicted fractions with which to redistribute heart failure-attributed deaths to the appropriate underlying causes of death. Age-adjusted death rates and rank causes of death before and after correction were calculated. RESULTS: Heart failure accounts for 3.1% of all deaths in the dataset. Ischemic heart disease has the highest redistribution proportion for ages 15-49 and 50+ in both sexes and country development levels, causing gains in age-adjusted death rates in both developed and developing countries. COPD and hypertensive heart disease also make significant rank gains. Reproductive-aged women in developing country-years yield the most diverse range of heart failure causes. CONCLUSIONS: Ischemic heart disease becomes the No. 1 cause of death in several developed countries, including France and Japan, underscoring the cardiovascular epidemic in high-income countries. Age-adjusted death rate increases for ischemic heart disease in low- and middle-income countries, such as Argentina and South Africa, highlight the rise of the cardiovascular epidemic in regions where public health efforts have historically focused on infectious diseases. This method maximizes the use of available data, providing better evidence on major causes of death to inform policymakers in allocating finite resources.

The history of liposuction.

This article aims to familiarize the reader with the history of liposuction. The author documents the landmark events and characters in the development of this revolutionary and widely known procedure. Included is a historical discussion of the obstacles and the triumphs the practitioners and the procedure itself has seen, as well as a review of relevant scientific data placed in its appropriate historical context up through modern day.

The Peng flap: reviewed and refined.

BACKGROUND: The Peng flap was first described in 1987 and there has been only one subsequent article published about its use. The Peng flap is very versatile and has a greater range of application than previously described. It can be used for central and eccentric defects of the nasal tip and it is also an excellent choice for defects that bridge the proximal nasal tip with the distal dorsum. OBJECTIVE: In this series, we present several new modifications to the Peng flap. METHODS: We describe conceptual changes in the movement dynamics of the flap based on these design refinements. Additional detail regarding flap execution is provided. RESULTS: Presented here is retrospective data on the last 30 patients from our tumor registry who received Peng flap repairs between 2001 and 2006. The average defect size was 1.8 x 1.5 cm. CONCLUSIONS: Described herein is a refined flap design that: (1) hides incisions in cosmetic junctions, (2) achieves a wider pedicle, and (3) utilizes a larger component of cheek advancement than previously described.

Upregulation of CTLA-4 by HIV-specific CD4+ T cells correlates with disease progression and defines a reversible immune dysfunction.

In progressive viral infection, antiviral T cell function is impaired by poorly understood mechanisms. Here we report that the inhibitory immunoregulatory receptor CTLA-4 was selectively upregulated in human immunodeficiency virus (HIV)-specific CD4(+) T cells but not CD8(+) T cells in all categories of HIV-infected subjects evaluated, with the exception of rare people able to control viremia in the absence of antiretroviral therapy. CTLA-4 expression correlated positively with disease progression and negatively with the capacity of CD4(+) T cells to produce interleukin 2 in response to viral antigen. Most HIV-specific CD4(+) T cells coexpressed CTLA-4 and another inhibitory immunoregulatory receptor, PD-1. In vitro blockade of CTLA-4 augmented HIV-specific CD4(+) T cell function. These data, indicating a reversible immunoregulatory pathway selectively associated with CD4(+) T cell dysfunction, provide a potential target for immunotherapy in HIV-infected patients.

Evolution of innate and adaptive effector cell functions during acute HIV-1 infection.

Early events during acute human immunodeficiency virus type 1 (HIV-1) infection are critical in determining the course of disease progression. Cells of the innate and adaptive immune responses are involved in this acute response to infection; however, little is known about the coevolution of innate and adaptive effector cell populations during the initial phase of HIV-1 infection. Here, we have characterized the development of innate natural killer (NK) cell and adaptive HIV-1-specific CD8(+) T cell function during acute HIV-1 infection. Although NK cell populations were significantly expanded during acute infection before HIV-1 seroconversion, HIV-1-specific CD8(+) T cell responses were absent or weak and were inversely correlated with the level of NK cell activity. NK cell activity was directly correlated with the level of viral replication during acute HIV-1 infection and declined rapidly in subjects who initiated highly active antiretroviral therapy, whereas NK cell activity remained elevated in subjects who did not initiate therapy. Yet, reexposure to HIV-1 antigen during treatment discontinuation in chronic infection resulted in a synchronous increase in NK and CD8(+) T cell activity. Overall, these data demonstrate that expansion of the NK cell population precedes the development of adaptive HIV-1-specific CD8(+) T cells during acute infection but that both effector cell subsets respond with similar kinetics during chronic HIV-1 infection.