Effects of fibre-supplemented enteral feeds on bowel function of non-critically ill tube-fed adults: a meta-analysis of randomised controlled trials.

Diarrhoea is common in enterally fed patients and can impact their nutritional and overall outcomes. This meta-analysis evaluates the potential benefits of fibre-supplemented (FS) feeds on incidence of diarrhoea and stool frequency in non-critically ill tube-fed adults. Databases including PubMed, Embase and CINAHL with full text were searched for randomised controlled trials (RCT) with adults on exclusive tube feeding, published until August 2022. The Cochrane Collaboration's tool was used for quality assessment. Studies with published results on incidence of diarrhoea and stool frequency were analysed using RevMan 5. Thirteen RCT with 847 non-critically ill patients between 20 and 90 years old without diarrhoea at the onset of enteral feeding were included. Study duration ranged from 3 to 35 d. Nine papers investigated the incidence of diarrhoea where intervention group was given FS and control was given non-fibre-supplemented (NFS) enteral feeds. Those receiving FS feeds were significantly less likely to experience diarrhoea as compared with those using NFS feeds (OR 0·44; 95 % CI 0·20, 0·95; P = 0·04; I2 = 71 %). Combined analysis showed no differences in stool frequency in those receiving NFS feeds (SMD 0·32; 95 % CI -0·53, 1·16; P = 0·47; I2 = 90 %). Results should be interpreted with caution due to considerable heterogeneity between study population, assessment tool for diarrhoea, potential conflict of interest and short duration of studies. This meta-analysis shows that FS feeds can reduce the incidence of diarrhoea in non-critically ill adults; however, the effects of stool frequency remain debatable.

Conflicting relationship between dietary intake and metabolic health in PTSD: A systematic review.

Posttraumatic stress disorder (PTSD) is a disabling psychological condition associated with significant physical comorbidities. There has been growing evidence to support the relationship between PTSD and cardiometabolic disease. Disordered eating behaviors often seen in people with PTSD symptoms may explain increased cardiometabolic risk. This systematic review aimed to assess the quality of evidence surrounding dietary intake of individuals with symptoms or a diagnosis of PTSD and their associated risk with cardiometabolic health outcomes. Online databases Scopus, ProQuest (Health), Embase, Medline, PsycINFO, and CINAHL with Full Text were searched for peer-reviewed English articles prior to December 2017 that examined dietary intake and cardiometabolic health outcomes in adults with PTSD symptoms or diagnosis. The quality of each study was graded based on the design and methodology using adapted quality assessment tools. Seven studies with five unique participant samples were included in the review. Study methods, design, populations, and outcomes were inconsistent across studies. Dietary intake was considerably varied and limited associations were demonstrated between dietary intake and cardiometabolic risk factors in the PTSD cohorts. Due to the variability of measures and study outcomes, there was insufficient evidence to determine the relationship between dietary intake and PTSD-related cardiometabolic health outcomes. Future studies are needed to examine these associations in individuals with PTSD: specifically higher quality descriptive studies are necessary to confirm a link between diet and cardiometabolic disease in PTSD.

Mutations in the N-terminal actin-binding domain of filamin C cause a distal myopathy.

Linkage analysis of the dominant distal myopathy we previously identified in a large Australian family demonstrated one significant linkage region located on chromosome 7 and encompassing 18.6 Mbp and 151 genes. The strongest candidate gene was FLNC because filamin C, the encoded protein, is muscle-specific and associated with myofibrillar myopathy. Sequencing of FLNC cDNA identified a c.752T>C (p.Met251Thr) mutation in the N-terminal actin-binding domain (ABD); this mutation segregated with the disease and was absent in 200 controls. We identified an Italian family with the same phenotype and found a c.577G>A (p.Ala193Thr) filamin C ABD mutation that segregated with the disease. Filamin C ABD mutations have not been described, although filamin A and filamin B ABD mutations cause multiple musculoskeletal disorders. The distal myopathy phenotype and muscle pathology in the two families differ from myofibrillar myopathies caused by filamin C rod and dimerization domain mutations because of the distinct involvement of hand muscles and lack of pathological protein aggregation. Thus, like the position of FLNA and B mutations, the position of the FLNC mutation determines disease phenotype. The two filamin C ABD mutations increase actin-binding affinity in a manner similar to filamin A and filamin B ABD mutations. Cell-culture expression of the c.752T>C (p.Met251)Thr mutant filamin C ABD demonstrated reduced nuclear localization as did mutant filamin A and filamin B ABDs. Expression of both filamin C ABD mutants as full-length proteins induced increased aggregation of filamin. We conclude filamin C ABD mutations cause a recognizable distal myopathy, most likely through increased actin affinity, similar to the pathological mechanism of filamin A and filamin B ABD mutations.

VATS thymectomy for nonthymomatous myasthenia gravis: standardized outcome assessment using the myasthenia gravis foundation of America clinical classification.

OBJECTIVE: : Video-assisted thoracoscopic (VATS) thymectomy has been practiced in Australia for nearly two decades. Our aim was to assess the complete stable remission and asymptomatic disease rates after VATS thymectomy in nonthymomatous myasthenia gravis. There remains doubt that minimally invasive techniques achieve equal remission rates to open maximal operations. Therefore, we report our outcomes using the Myasthenia Gravis Foundation of America (MGFA) Clinical Classification and Kaplan-Meier analysis and compare the results to the literature. METHODS: : A retrospective analysis of 78 consecutive patients undergoing right VATS thymectomy between April 1994 and March 2007 at two Thoracic Surgery Units in Melbourne, Australia, was undertaken. Patients with thymoma were excluded. Therefore, 57 patients were followed-up for a minimum of 12 months to apply the MGFA Clinical Classification. VATS thymectomy was performed by a three-port right side technique. RESULTS: : The complete stable remission rate was 15% at 3 years and 28% at 5 years. The asymptomatic disease rate was 59% at 5 years. Median follow-up was 32 months. No prognostic factors for remission were identified. The overall morbidity rate was 14% (8/57). CONCLUSIONS: : Right VATS thymectomy achieves comparable remission and asymptomatic disease rates to other minimally invasive and open techniques when compared with studies using either MGFA or older criteria.

Preliminary results of the Australasian Regional Anaesthesia Collaboration: a prospective audit of more than 7000 peripheral nerve and plexus blocks for neurologic and other complications.

BACKGROUND AND OBJECTIVES: Peripheral nerve blockade is associated with excellent patient outcomes after surgery; however, neurologic and other complications can be devastating for the patient. This article reports the development and preliminary results of a multicenter audit describing the quality and safety of peripheral nerve blockade. METHODS: From January 2006 to May 2008, patients who received peripheral nerve blockade had data relating to efficacy and complications entered into databases. All patients who received nerve blocks performed by all anesthetists during each hospital's contributing period were included. Patients were followed up by phone to detect potential neurologic complications. The timing of follow-up was either at 7 to 10 days or 6 weeks postoperatively, depending on practice location and time period. Late neurologic deficits were defined as a new onset of sensory and/or motor deficit consistent with a nerve/plexus distribution without other identifiable cause, and one of the following: electrophysiologic evidence of nerve damage, new neurologic signs, new onset of neuropathic pain in a nerve distribution area, paresthesia in relevant nerve/plexus distribution area. RESULTS: A total of 6950 patients received 8189 peripheral nerve or plexus blocks. Of the 6950 patients, 6069 patients were successfully followed up. In these 6069 patients, there were a total of 7156 blocks forming the denominator for late neurologic complications. Thirty patients (0.5%) had clinical features requiring referral for neurologic assessment. Three of the 30 patients had a block-related nerve injury, giving an incidence of 0.4 per 1000 blocks (95% confidence interval, 0.08-1.1:1000). The incidence of systemic local anesthetic toxicity was 0.98 per 1000 blocks (95% confidence interval, 0.42-1.9:1000). CONCLUSIONS: These results indicate that the incidence of serious complications after peripheral nerve blockade is uncommon and that the origin of neurologic symptoms/signs in the postoperative period is most likely to be unrelated to nerve blockade.

Limb-girdle muscular dystrophy: diagnostic evaluation, frequency and clues to pathogenesis.

We characterized the frequency of limb-girdle muscular dystrophy (LGMD) subtypes in a cohort of 76 Australian muscular dystrophy patients using protein and DNA sequence analysis. Calpainopathies (8%) and dysferlinopathies (5%) are the most common causes of LGMD in Australia. In contrast to European populations, cases of LGMD2I (due to mutations in FKRP) are rare in Australasia (3%). We have identified a cohort of patients in whom all common disease candidates have been excluded, providing a valuable resource for identification of new disease genes. Cytoplasmic localization of dysferlin correlates with fiber regeneration in a subset of muscular dystrophy patients. In addition, we have identified a group of patients with unidentified forms of LGMD and with markedly abnormal dysferlin localization that does not correlate with fiber regeneration. This pattern is mimicked in primary caveolinopathy, suggesting a subset of these patients may also possess mutations within proteins required for membrane targeting of dysferlin.