Sarcopenia is associated with an increased risk of advanced colorectal neoplasia

Background/aims

Although sarcopenia is associated with an increased risk for mortality after the curative resection of colorectal cancer, its influence on the development of advanced colonic neoplasia remains unclear.

Methods

This study included 1270 subjects aged 40 years or older evaluated with first-time screening colonoscopy at Seoul National University Boramae Health Care Center from January 2010 to February 2015. Skeletal muscle mass was measured with a body composition analyzer (direct segmental multifrequency bioelectrical impedance analysis method). Multiple logistic regression analysis was performed to determine whether sarcopenia is associated with advanced colorectal neoplasia.

Results

Of 1270 subjects, 139 (10.9%) were categorized into the sarcopenia group and 1131 (89.1%) into the non-sarcopenia group. In the non-sarcopenia group, 55 subjects (4.9%) had advanced colorectal neoplasia. However, in the sarcopenia group, 19 subjects (13.7%) had advanced colorectal neoplasia, including 1 subject with invasive colorectal cancer (0.7%). In addition, subjects with sarcopenia had a higher prevalence of advanced adenoma (P < 0.001) than those without sarcopenia. According to the multiple logistic regression analysis adjusted for variable confounders, age (odds ratio 1.062, 95% confidence interval 1.032–1.093; P < 0.001), male sex (odds ratio 1.749, 95% confidence interval 1.008–3.036; P = 0.047), and sarcopenia (odds ratio 2.347, 95% confidence interval 1.311–4.202; P = 0.004) were associated with an advanced colorectal neoplasia.

Conclusion

Sarcopenia is associated with an increased risk of advanced colorectal neoplasia.

     

Can sarcopenia be a predictor of prognosis for patients with non-metastatic colorectal cancer? A systematic review and meta-analysis

Purpose

We aimed to explore whether sarcopenia diagnosed with the third lumbar vertebra skeletal muscle index (L3 SMI) can be a predictor of prognosis for colorectal cancer (CRC) patients.

Methods

A systematic review and meta-analysis was conducted using PubMed, Embase, and the Web of Science databases. All original comparative studies published in English that were related to sarcopenia versus non-sarcopenia in non-metastatic CRC patients based on postoperative and survival outcomes were included. Data synthesis and statistical analysis were carried out using Stata software.

Results

A total of 12 studies including 5337 patients were included in our meta-analysis. In our overall analyses of postoperative outcomes, we indicated that CRC patients with sarcopenia would have longer hospital stays, higher incidence of total postoperative morbidity (OR?=?1.70, 95% CI?=?1.07–2.70, P?<?0.01), mortality (OR?=?3.45, 95% CI?=?1.69–7.02, P?<?0.01), and infection (OR?=?2.21, 95% CI?=?1.50–3.25, P?<?0.01) but not anastomosis leakage or intestinal obstruction when compared to non-sarcopenia patients. Regarding survival outcomes, our results showed that sarcopenia predicted a decreased overall survival (HR?=?1.63, 95% CI?=?1.24–2.14, P?<?0.01), disease-free survival, and cancer-specific survival for non-metastatic CRC patients. Moreover, our subgroup analyses showed similar tendency with our overall analyzed results.

Conclusions

Sarcopenia diagnosed with L3 SMI can be a negative predictor of postoperative and survival outcomes for non-metastatic CRC patients. Prospective studies with a uniform definition of sarcopenia are needed to update our findings.

     

Should Sarcopenia Increase Priority for Transplant or Is It a Contraindication?

Purpose of Review

The purpose of this review is to discuss the current evidence regarding the impact of sarcopenia on patients with cirrhosis awaiting liver transplantation and to determine if its presence should be considered a criterion for expedited transplantation or a contraindication for transplantation.

Recent Findings

Sarcopenia is a negative predictor of survival in patients on a waiting list and after liver transplant. The gut-liver axis and the liver-muscle axis have been explored to understand the complex pathophysiology of sarcopenia.

Summary

Sarcopenia is a frequent finding in patients with cirrhosis. The diagnosis is ideally based on cross-sectional image analysis (CT or MRI) and treatment consists of optimization of caloric and protein intake. To date, prioritizing tools for liver transplantation have not included nutrition or sarcopenia parameters. Patients with a low Model for End-Stage Liver Disease (MELD) or MELD-Na score and sarcopenia would benefit from prioritization for transplant in order to reduce time on waiting list and therefore mortality.

     

IL-17A Promotes Initiation and Development of Intestinal Fibrosis Through EMT

Background

Intestinal fibrosis is a common complication of Crohn’s disease (CD). Its exact mechanism is still unclear, and effective treatments to control or reverse the fibrosis process are unavailable. Epithelial–mesenchymal transition (EMT) may promote intestinal fibrosis by increasing deposition of extracellular matrix protein. IL-17A is a pro-inflammatory cytokine, and it has been shown as a profibrotic factor as its association with fibrosis of multiple organs was reported.

Aims

To assess the roles of IL-17A and EMT in the initiation and development of intestinal fibrosis and to verify the potential inductive effect of IL-17A on EMT.

Methods

In this study, we evaluated the expression of IL-17A and EMT-related genes in colonic mucosal biopsy tissues of CD patients and control individuals. Then, we examined the changes of EMT-related genes and fibrosis-related genes of IEC-6 cells which cultured for 72 h under increasing concentrations of IL-17A or with TGF-β1, to verify the potential inductive effect of IL-17A on EMT in vitro. We blocked the IL-17A of the mouse model of TNBS-induced experimental intestinal colitis and fibrosis to further verify the potential inductive effect of IL-17A on EMT in vivo.

Results

We found the occurrence of EMT and high-level expression of IL-17A in intestinal mucosa of CD patients. Using IEC-6 cells, we showed that IL-17A may induce EMT in intestinal epithelial cells that come with reduced E-cadherin expression and increased expression of vimentin, snail, and α-SMA. We further found that anti-IL-17A treatment alleviated intestinal fibrosis through reducing EMT in mouse intestine.

Conclusions

Our study confirmed the involvement of IL-17A in the development of intestinal fibrosis through inducing EMT.

     

Paricalcitol reduces oxidative stress and inflammation in hemodialysis patients

Background

Treatment with selective vitamin D receptor activators such as paricalcitol have been shown to exert an anti-inflammatory effect in patients on hemodialysis, in addition to their action on mineral metabolism and independently of parathyroid hormone (PTH) levels. The objective of this study was to evaluate the additional antioxidant capacity of paricalcitol in a clinical setting.

Methods

The study included 19 patients with renal disease on hemodialysis, of whom peripheral blood was obtained for analysis at baseline and three months after starting intravenous paricalcitol treatment. The following oxidizing and inflammatory markers were quantified: malondialdehyde (MDA), nitrites and carbonyl groups, indoleamine 2,3-dioxygenase (IDO), tumor necrosis factor alfa (TNF-α), interleukin-6 (IL-6), interleukin-18 (IL-18) and C-reactive protein (CRP). Of the antioxidants and anti-inflammatory markers, superoxide dismutase (SOD), catalase, reduced glutathione (GSH), thioredoxin, and interleukin-10 (IL-10) levels were obtained.

Results

Baseline levels of oxidation markers MDA, nitric oxide and protein carbonyl groups significantly decreased after three months on paricalcitol treatment, while levels of GSH, thioredoxin, catalase and SOD activity significantly increased. After paricalcitol treatment, levels of the inflammatory markers CRP, TNF-α, IL-6 and IL-18 were significantly reduced in serum and the level of anti-inflammatory cytokine IL-10 was increased.

Conclusions

In renal patients undergoing hemodialysis, paricalcitol treatment significantly reduces oxidative stress and inflammation, two well known factors leading to cardiovascular damage.

     

A study of association between regulatory polymorphism in the IL-10 gene promoter region and acute viral hepatitis,and acute liver failure

Background

The level of inflammatory cytokine Interleukin (IL)-10 is increased in patients infected with hepatitis-related acute liver failure (ALF), and this was thought to be because of the regulatory polymorphism in the IL-10 gene promoter region. The present study was designed to analyze the possible association between IL-10 gene promoter polymorphism and acute viral hepatitis (AVH), and ALF. An attempt was made to quantify IL-10 levels at admission, during the hospital stay, and at the final outcome to study its relationship with liver injury among patients with AVH, ALF, and controls.

Methods

The study included 40 patients each with ALF and AVH. IL-10 gene promoter polymorphism was detected by the PCR-RFLP method. Quantification of IL-10 was done using commercially available ELISA kits.

Results

The individuals with ?592 AC, ?819 TC, ?1082 AA genotypes were found to have a significantly higher risk of ALF whereas those with ?592 AA and ??819 CC polymorphism were found to be less susceptible. Individuals with ??819 CC were found to be more susceptible to AVH while those with ?592 AA and ?819 TT were less susceptible as compared to controls. Mean serum IL-10 at admission was significantly elevated in patients with ALF (38.4±11.3 pg/mL) as compared to patients with AVH (16.7±5.4 pg/mL) and control population (8.3±3.6 pg/mL, p?<?0.05).

Conclusion

Regulatory polymorphism in the IL-10 gene promoter has a possible and significant association with severity and outcome in patients with AVH and ALF. Raised levels of IL-10 could be predictive of prognosis in patients with ALF.

     

Reduced IL-37 Production Increases Spontaneous Chemokine Expressions in Colon Epithelial Cells

Background and Aim

Microscopic colitis, comprising collagenous colitis and lymphocytic colitis, is a common cause of chronic diarrhea. Previously, we showed enhanced chemokine productions in microscopic colitis patients, indicating dysregulated immune cell chemotaxis in the immunopathogenesis. We also showed decreased mRNA of IL-37, mainly regarded as an anti-inflammatory cytokine, in the colonic mucosa of these patients, potentially an important factor for the chronicity of the colitis. Our aim in this study was to understand the possible role of IL-37 in chemokine production using a cell line model.

Methods

A colon epithelial cell line, T84, was stimulated with the TLR5 ligand flagellin. IL-37 protein production was reduced 20% using the CRISPR/Cas9 system, and the changes in chemokine mRNA and protein expressions were compared to cells transfected with empty plasmid.

Results

The 20% reduction in IL-37 protein levels spontaneously increased CCL5, CXCL8, CXCL10, and CXCL11 mRNA and protein expressions. CCL2 mRNA and protein levels were enhanced upon TLR5 stimulation. CCL3, CCL20, and CX₃CL1 mRNA expressions were increased either spontaneously or following TLR5 stimulation, whereas CCL4 and CCL22 mRNA expressions were significantly decreased.

Conclusions

Even a minor decrease in the ability of colon epithelial cells to produce IL-37 results in altered chemokine expression, mainly an increase in the production of several chemokines. Our results indicate that a decreased IL-37 expression by colon epithelial cells may be an important factor for increasing the recruitment of immune cells and subsequently developing microscopic colitis.

     

Morphologic change of the psoas muscle as a surrogate marker of sarcopenia and predictor of complications after colorectal cancer surgery

Purpose

Sarcopenia is reported to be associated with complications after surgery. However, there is no established optimal parameter to determine sarcopenia affecting surgical outcome. This study investigated whether morphologic change of the psoas muscle (MPM) reflects sarcopenia and could be a predictor of complications after colorectal cancer surgery.

Methods

Colorectal cancer patients who underwent primary tumor resection with anastomosis between 2015 and 2016 were analyzed. MPM score was evaluated as the ratio of the short-to-long axis of the psoas muscle in CT images at the L3 vertebrae and classified into five MPM grades. Then, the impact of MPM grade on development of postoperative complications was investigated.

Results

A total of 133 patients were studied. MPM score was significantly correlated to the sectional areas of the psoas muscle at the L3 vertebrae which was evaluated by manual tracing. 21.1% of the subjects were classified into severe MPM (defined as MPM grade 3–4). Overall and infectious complications were noted in 37 (27.8%) and 16 (12.0%) patients. Severe MPM (odds ratio [OR] 2.71, 95% confidence interval [CI] 1.09–6.73), longer operative time (OR 1.01, 95%CI 1.001–1.01), and open surgery (OR 2.73, 95%CI 1.17–6.35) were identified as independent risk factors of overall complications. Severe MPM (OR 4.26,95%CI 1.38–13.10) and open surgery (OR 3.42, 95%CI 1.11–10.48) were identified as independent factors associated with infectious complications.

Conclusions

MPM grade may be used as a simple and convenient marker of sarcopenia and to identify patients at increased risk of complications after colorectal cancer surgery.

     

Increased Sputum IL-17A Level in Non-asthmatic Eosinophilic Bronchitis

Background

Non-asthmatic eosinophilic bronchitis (NAEB) is one common cause of chronic cough which is characterized as airway eosinophilic inflammation like asthma but lack of airway hyper-responsiveness. Previous studies showed that Th2-pathway plays a role in NAEB, but the role of non-Th2 pathway in mechanism of NAEB remains unknown. Recently, IL-17A, a Th17-pathway cytokine, has been demonstrated to be involved in asthma development. However, the relationship between Th17-pathway and NAEB is unknown.

Methods

We aim to assess the airway level of IL-17A in the subjects with NAEB. Relationships between the IL-17A level and airway function in NAEB or asthma are also observed. We measured IL-17A concentrations in the sputum supernatant from 12 subjects with EB, 16 subjects with asthma [9 eosinophilic asthmatic (EA) and 7 non-eosinophilic asthmatic (NEA) according to the sputum eosinophil ≥?3%], and 9 healthy control subjects.

Results

Increasing IL-17A level was found in NAEB group (29.65?±?8.13 pg/ml), EA group (32.45?±?3.22 pg/ml), and NEA group (29.62?±?6.91 pg/ml) compared with the healthy control group (17.05?±?10.30 pg/ml) (P?<?0.05, P?<?0.01, P?<?0.05, respectively). The sputum IL-17A level was correlated with FENO (r?=?0.44, P?<?0.01), FEV1/FVC% (r?=???0.38, P?<?0.05), MMEF%pred (r?=???0.34, P?<?0.05), and sputum neutrophil% (r?=?0.33, P?<?0.05) in total.

Conclusion

Th17-pathway may play a role not only in asthmatics, but also in subjects with NAEB, as reflected by increasing IL-17A concentrations in sputum supernatant.

     

Aryl Hydrocarbon Receptor Activation Down-Regulates IL-7 and Reduces Inflammation in a Mouse Model of DSS-Induced Colitis

Background and Aims

The pathogenesis of inflammatory bowel disease (IBD) is associated with dysregulation of intestinal immune system. Aryl hydrocarbon receptor (AHR) is believed to control the chronic inflammation in the gut. Besides, interleukin-7 (IL-7) is proved to be an important cytokine that activates mucosal inflammation in IBD. Moreover, intraepithelial lymphocytes (IELs) are one of the key immunological compartments involved in regulating intestinal inflammation. In this study, we investigated the function of 6-formylindolo (3,2-b) carbazole (Ficz), a ligand of AHR, on IL-7, colitis, and IEL phenotypes.

Methods

Colitis was induced by administration of dextran sulfate sodium (DSS) to wild-type C57BL/6J mice for 7 days. Mice were weighted, colon tissues were collected and measured, and histology analyses were performed. IELs were isolated from colon, and the phenotype and activation of IELs were examined using flow cytometry detection. The expression of AHR and IL-7 was measured by immunofluorescence, Western blot, and RT-PCR.

Results

Ficz down-regulated epithelial-derived IL-7 expression in mice with DSS-induced colitis and ameliorated DSS-induced colitis. Ficz also decreased CD8αβ⁺ and CD8⁺ IEL subpopulations, enhanced TCRγδ⁺ IEL subpopulation, and reduced the percentage of activated CD4⁺ and CD8⁺ subpopulations.

Conclusions

Ficz could down-regulate epithelial-derived IL-7 expression in mice with DSS-induced colitis and inhibit inflammation in the gastrointestinal tract of mice. AHR-related compounds might be the new and promising therapeutic medicaments for the treatment of patients with IBD.

     

Tumor Necrosis Factor-α in Heart Failure: an Updated Review

Purpose of the Review

Proinflammatory cytokines are consistently elevated in congestive heart failure. In the current review, we provide an overview on the current understanding of how tumor necrosis factor-α (TNFα), a key proinflammatory cytokine, potentiates heart failure by overwhelming the anti-inflammatory responses disrupting the homeostasis.

Recent Findings

Studies have shown co-relationship between severity of heart failure and levels of the proinflammatory cytokine TNFα and one of its secondary mediators interleukin-6 (IL-6), suggesting their potential as biomarkers. Recent efforts have focused on understanding the mechanisms of how proinflammatory cytokines contribute towards cardiac dysfunction and failure. In addition, how unchecked proinflammatory cytokines and their cross-talk with sympathetic system overrides the anti-inflammatory response underlying failure.

Summary

The review offers insights on how TNFα and IL-6 contribute to cardiac dysfunction and failure. Furthermore, this provides a forum to begin the discussion on the cross-talk between sympathetic drive and proinflammatory cytokines and its determinant role in deleterious outcomes.

     

The Role of Interleukin-10 in the Pathophysiology of Preeclampsia

Purpose of Review

The pathophysiology of preeclampsia is complex and not entirely understood. A key feature in preeclampsia development is an immunological imbalance that shifts the maternal immune response from one of tolerance towards one promoting chronic inflammation and endothelial dysfunction. As a key regulator of immunity, IL-10 not only has immunomodulatory activity, but also directly benefits vasculature and promotes successful cellular interactions at the maternal-fetal interface. Here we focus on the mechanisms by which the dysregulation of IL-10 may contribute to the pathophysiology of preeclampsia.

Recent Findings

Dysregulation of IL-10 has been demonstrated in various animal models of preeclampsia. Decreased IL-10 production in both placenta and peripheral blood mononuclear cells has been reported in human studies, but with inconsistent results.

Summary

The significance of IL-10 in preeclampsia has shifted from a key biomarker to one with therapeutic potential. As such, a better understanding of the role of this cytokine in the pathophysiology of preeclampsia is of paramount importance.

     

Possible Role of IL-25 in Eosinophilic Lung Inflammation in Patients with Chronic Eosinophilic Pneumonia

Purpose

Interleukin (IL)-25 and IL-33 induce IL-5 production by various types of cells, such as type 2 helper T (Th2) cells and type 2 innate lymphoid cells. The number of Th2 cells and concentration of IL-5 in the bronchoalveolar lavage fluid (BALF) are increased in patients with eosinophilic pneumonia (EP). To examine the contribution of IL-25 and IL-33 to eosinophilic inflammation of the lung in humans, we evaluated IL-5, IL-25 and IL-33 levels in the BALF of patients with EP.

Methods

IL-5, IL-25, and IL-33 concentrations in the BALF were measured by enzyme-linked immunosorbent assay in patients with acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), idiopathic pulmonary fibrosis (IPF), and sarcoidosis.

Results

The absolute number of eosinophils, and IL-5 levels, but not IL-33 levels, in the BALF were significantly higher in patients with EP than in patients with IPF and sarcoidosis. IL-25 levels in the BALF were significantly higher in patients with CEP, but not in patients with AEP, than in patients with IPF and sarcoidosis. The absolute number of eosinophils was significantly correlated with the IL-5 concentration in the BALF of patients with EP. IL-5 concentrations were significantly correlated with IL-25 concentrations in the BALF of patients with CEP, but not in patients with AEP. IL-5 levels were not correlated with IL-33 levels in the BALF of patients with EP.

Conclusions

Our findings suggest that IL-25 plays an important role via IL-5 in eosinophilic lung inflammation in patients with CEP.

     

Transgenic Expression of Vitamin D Receptor in Gut Epithelial Cells Ameliorates Spontaneous Colitis Caused by Interleukin-10 Deficiency

Background

Vitamin D deficiency is common in patients with inflammatory bowel diseases. The vitamin D receptor (VDR) is a nuclear hormone receptor mediating the activity of vitamin D hormone. Our previous studies showed that intestinal epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this activity is independent of non-epithelial immune VDR actions. Interleukin (IL)-10-deficient mouse is a chronic colitis model that develops colitis due to aberrant immune responses. Here we used IL-10 null (IL-10KO) model to assess the anti-colitic activity of epithelial VDR in the setting of an aberrant immune system.

Methods

We crossed IL-10KO mice with villin promoter-driven human (h) VDR transgenic (Tg) mice to generate IL-10KO mice that carry the hVDR transgene in intestinal epithelial cells (IL-10KO/Tg). IL-10KO and IL-10KO/Tg littermates were studied in parallel and followed for up to 25 weeks.

Results

By 25 weeks of age, accumulatively 79 % IL-10KO mice developed prolapse, whereas only 40 % IL-10KO/Tg mice did so (P < 0.001). Compared with IL-10KO mice, IL-10KO/Tg littermates showed markedly reduced mucosal inflammation in both small and large intestines, manifested by attenuation in immune cell infiltration and histological damage and a marked decrease in pro-inflammatory cytokine production. IL-10KO/Tg mice also showed reduced intestinal epithelial cell apoptosis as a result of diminished PUMA induction and caspase 3 activation.

Conclusion

These observations demonstrate that targeting hVDR expression to intestinal epithelial cells is sufficient to attenuate spontaneous colitis caused by an ill-regulated immune system, confirming a critical role of the epithelial VDR signaling in blocking colitis development.

     

Depletion of Foxp3+ Regulatory T Cells Promotes Profibrogenic Milieu of Cholestasis-Induced Liver Injury

Background

Accumulating evidence suggests that Foxp3+ regulatory T (Treg) cells act as inhibitory mediators of inflammation; however, the in vivo mechanism underlying this protection remains elusive in liver diseases.

Aims

To clarify the in vivo role of Foxp3+ Treg cells in liver fibrosis, we used the DEREG mouse, which expresses the diphtheria toxin receptor under control of the Foxp3 promoter, allowing for specific deletion of Foxp3+ Treg cells.

Methods

Bile duct ligation-induced liver injury and fibrosis were assessed by histopathology, fibrogenic gene expression, and measurement of cytokine and chemokine levels.

Results

Depletion of Foxp3+ Treg cells enhanced Th17 cell response as demonstrated by the increase of IL-17+ cells and related gene expressions including Il17f, Il17ra, and Rorgt in the fibrotic livers of DEREG mice. Of note, infiltration of CD8+ T cells and Cd8 gene expression was significantly increased in the livers of DEREG mice. Consistent with increased IL-17+ and CD8+ T cell responses, DEREG mice generated higher levels of inflammatory cytokines (TNF-α, IL-6, and IL-12p70) and chemokines (MCP-1, MIP-1α, and RANTES). These results were concordant with severity of liver fibrosis and hepatic enzyme levels (ALT and ALP).

Conclusions

The present findings demonstrate that Foxp3+ Treg cells inhibit the profibrogenic inflammatory milieu through suppression of pro-fibrogenic CD8+ and IL-17+ T cells.

     

Differential modulation of IL-12 family cytokines in autoimmune islet graft failure in mice

Aims/hypothesis

The relative contribution of T helper (Th)1 and Th17 cells in graft rejection is inconclusive, on the basis of evidence provided by different T cell-related cytokine-deficient animal models and graft types.

Methods

We used novel antigen-presenting-cell-specific Il-12p35 (also known as Il12a)-knockout (KO), IL-23p19-knockdown (KD) and IL-27p28-KD strategies to investigate T cell differentiation in islet graft rejection.

Results

In vitro dendritic cell–T cell coculture experiments revealed that dendritic cells from Il-12p35-KO and IL-23p19-KD mice showed reduced ability to stimulate IFN-γ and IL-17 production in T cells, respectively. To further explore the T cell responses in islet graft rejection, we transplanted islets into streptozotocin-induced diabetic NOD/severe combined immunodeficiency (SCID) recipient mice with IL-12-, IL-23-, or IL-27-deficient backgrounds and then challenged them with NOD.BDC2.5 T cells. The survival of islet grafts was significantly prolonged in Il-12p35-KO and IL-23p19-KD recipients compared with the control recipients. T cell infiltrations and Th1 cell populations were also decreased in the grafts, correlating with prolonged graft survival.

Conclusions/interpretation

Our results suggest that IL-12 and IL-23 promote and/or maintain Th1 cell-mediated islet graft rejection. Thus, blockade of IL-12 and IL-23 might act as therapeutic strategies for reducing rejection responses.

     

Die Rolle der Selbsthilfegruppen in der Onkologie

Background

Little is known about self-help associations and their possibilities. Obstacles often prevent early contacts between affected people.

Objectives

The psychosocial support given by self-help associations in different phases is evaluated.

Materials and methods

Based on the experience of the Deutsche ILCO and from cooperation with other organizations and institutions, various dimensions of self-help groups are investigated.

Results

On the professional side, there is a lack of knowledge and of attitude. Suitable structures are rare.

Conclusions

The removal of barriers and development of effective structures are overdue.

     

Nutritional Assessment and Management for Hospitalized Patients with Cirrhosis

Purpose of Review

The purpose of this review is to summarize recent knowledge on malnutrition and sarcopenia in liver cirrhosis with special focus on hospitalized cirrhotic patients. Assessment tools and treatment options are briefly discussed.

Recent Findings

During hospitalization, cirrhotic patients frequently deteriorate their nutritional status due to multiple factors. Evaluation of nutritional risk followed by nutritional assessment has been suggested in cirrhotic patients and may alert the need of special nutritional care in those hospitalized. Few recent studies, although in small series, proposed to ameliorate sarcopenia in cirrhotic patients by protein/calorie supplementation and also encouraging physical activity.

Summary

Malnutrition and sarcopenia are negative predictors of morbidity and mortality in hospitalized cirrhotic patients. When malnutrition is diagnosed, care should be taken to provide adequate nutritional support. Physical movement, whenever possible, has been suggested for prevention of muscle loss.

     

Use of Interleukin-1 Blockers in Pericardial and Cardiovascular Diseases

Purpose of Review

This review aims to summarize the role of the interleukin-1 (IL-1) blocking agents in cardiovascular diseases, briefly describing the pathogenetic rationale and the most relevant clinical studies.

Recent Findings

IL-1 is a pivotal cytokine of the innate immune system. Anti-IL-1 agents are currently used for the treatment of several autoimmune and autoinflammatory conditions. Recently, the role of IL-1 has also emerged in cardiovascular diseases. Indeed, two recent randomized controlled trials have shown that the IL-1 receptor antagonist anakinra is effective for the treatment of idiopathic recurrent pericarditis and the IL-1β blocking agent canakinumab is effective in reducing myocardial infarction in people at risk. Interestingly, interfering with IL-1 has proved to be also effective in other cardiovascular manifestations, such as myocarditis, arrhythmias, and heart failure.

Summary

Blocking the IL-1 pathway is a possible new therapeutic strategy, potentially leading to innovative therapies in many acute and chronic cardiovascular diseases.