Systematic review of sarcopenia in inflammatory bowel disease.

INTRODUCTION: There is growing evidence of increased muscle atrophy in IBD patients, likely resulting in a higher sarcopenia prevalence in IBD. The aims of this systematic review are A1; to estimate sarcopenia prevalence in IBD patients, A2; to investigate its impact on IBD patients, and A3; the effectiveness of nutritional interventions on muscle mass and/or strength in IBD patients. METHODS: On 28 July 2021, three electronic databases were used to identify eligible studies, including peer-reviewed studies (randomised controlled trials [RCTs], non-RCTs, observation studies) in adult (⩾ 18 years) IBD patients. For A1 and A2 only, studies defined low muscle mass and/or strength cut-off points. For A2, studies assessed association between sarcopenia and IBD complication. For A3, studies assessed the nutrition effect among IBD patients. RESULTS: 35 studies were included, 34 for A1, 20 for A2, and three for A3. 42% of adult IBD patients have myopenia, 34% have pre-sarcopenia, and 17% sarcopenia. Myopenic IBD was significantly associated with therapy failure including IBD-related surgery risk in six studies, risk of medical therapy failure in four studies, risk of hospitalisation in one study. A significant association existed with postoperative complications risk in IBD patients in four studies, reduction in BMD in two studies, and increased incidence of non-alcoholic fatty liver disease (NAFLD) in one study. Sarcopenia in IBD was significantly associated with a reduction in BMD in one study. Two studies found a personalised nutrition plan (high protein) in IBD patients significantly improved muscle mass. One study found a significant positive association between muscle mass and dietary intake including high protein intake. CONCLUSION: Over one third of adult IBD patients have myopenia and pre-sarcopenia, and nearly a fifth have sarcopenia. Myopeninc IBD is significantly associated with increased risk of IBD therapy failure, postoperative complications, and low BMD, with possible association with increased NAFLD risk. Nutritional therapy may play a role in reversing low muscle mass though yet unclear if this is through disease activity reversal. Further studies on adult IBD patients focusing on sarcopenia/myopenia are needed with recommended study designs of 1) standardised population-based definitions with recommended standard methods used to measure skeletal muscle mass, 2) prospective studies with IBD patients stratified by Montreal classification, disease activity, disease duration and concomitant medication to observe muscle changes, 3) mechanistic studies on sarcopenia aetiology, specifically focusing on protein handling atrophy and absorption, 4) properly designed RCT to assess nutrition intervention in sarcopenic IBD patients.

A case of idiopathic chylous ascites.

Chylous ascites is a rare condition found in 1 in 20 000 patients admitted to hospital with abdominal distention. It is caused by a limited number of pathologies but can, in rare situations, be idiopathic. Its management is difficult and usually involves correcting the primary pathology, making idiopathic chylous ascites particularly difficult to manage. We present a case of idiopathic chylous ascites extensively investigated over a period of several years. An incidental finding of B cell lymphoma was initially suspected to have been the primary cause of the ascites; however, after successful treatment of this condition, the patient's ascites did not resolve. Diagnostic difficulties and management are discussed and an overview of the diagnostic process is outlined through this case.

ACE Inhibitor Therapy Does Not Influence the Survival Outcomes of Patients with Colorectal Liver Metastases Following Liver Resection.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors have been shown to possibly influence the survival outcomes in certain cancers. The aim of this study was to evaluate the impact of ACE inhibitors on the outcomes of patients undergoing liver resection for colorectal liver metastases (CRLM). The secondary aim was to determine whether ACE inhibitors influenced histopathological changes in CRLM. METHODS: Patients treated with liver resection for CRLM over a 13-year period were identified from a prospectively maintained database. Data including demographics, primary tumour treatment, surgical data, histopathology analysis and clinical outcome were collated and analysed. RESULTS: A total of 586 patients underwent primary hepatic resections for CRLM during this period including 100 patients on ACE inhibitors. The median follow-up period was 23 (range: 12-96) months, in which 267 patients developed recurrent disease and 131 patients died. Independent predictors of disease-free survival on multivariate analysis included synchronous presentation, neoadjuvant chemotherapy, major liver resection, tumour size and number, extent of hepatic steatosis, R0 resection and presence of perineural invasion. Poorer overall survival was associated with neoadjuvant treatment, major liver resection, presence of multiple metastases, perineural invasion and positive resection margins on multivariate analysis. ACE inhibitors did not influence the survival outcome or histological presentation in CRLM. CONCLUSION: The use of ACE inhibitors did not affect the survival outcome or tumour biology in patients with CRLM following liver resection.

Retrospective cohort study of statin therapy effect on resected colorectal liver metastases.

BACKGROUND: Above and beyond their role in cardiovascular risk reduction, statins appear to have a chemopreventive role in some gastro-intestinal cancers. In the quest for new chemopreventive agents, some existing established drugs such as statins have shown potential for re-purposing as chemoprevention. Probing existing drugs, whose pharmacodynamics are familiar, for novel beneficial effects offers a more cost-effective and less time-consuming strategy than establishing brand new drugs whose pharmacodynamic profile is unfamiliar. Observational studies show statins decrease the risk of developing colorectal cancer but there are no published studies exploring the potential impact of statins on carcinogenesis in colorectal liver metastases (CRLM). AIM: To evaluate impact of statins on outcomes of CRLM resection, and secondarily to assess if statins influence CRLM histo-pathology. METHODS: We conducted a retrospective cohort study of patients operated for CRLM over a 13-year period from 2005 to 2017. Patients were identified from a prospective database maintained in our Tertiary care hospital. All 586 patients included the study had undergone resection of CRLM following discussion at multidisclipinary team meeting, some patients requiring neoadjuvant chemotherapy to downstage CRLM prior to surgery. We analysed patient demographics, operative details, CRLM histopathology, Index of Deprivation, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio and chemotherapy use in relation to clinical outcome. Statistics were performed using SPSS version 16.0; significance taken at 5%. RESULTS: Liver resection for CRLM was undertaken in 586 patients at a median age of 68 (range 19 to 88) years. Statin therapy was used by 181 patients. Median follow-up time was 23 (range 12-96) mo and further colorectal cancer metastases developed in 267 patients. A total of 131 patients died. Multi-variate analysis identified 6 independent predictors of poorer disease-free survival: Synchronous presentation, multiple tumours, tumour size ≥ 5 cm, moderate-severe steatosis, peri-neural invasion, and R1-resection margin. Poorer overall survival was significantly associated with neo-adjuvant chemotherapy, major hepatectomy, peri-neural invasion and R1-resection margin. Neither histo-pathological nor radiological traits of CRLM were affected by statins, and, there was no demonstrable effect of statin therapy on patient outcomes. CONCLUSION: Statin therapy does not affect patient survival following liver resection for CRLM. We postulate the reason for this key finding is that statins do not modulate tumour biology of CRLM.