Modified dietary fat intake for treatment of gallstone disease

Madden AM, Trivedi D, Smeeton NC, Culkin A., 'Modified dietary fat intake for treatment of gallstone disease', Cochrane Database of Systematic Reviews 2017, Issue 3. Art. No.: CD012608, DOI: 10.1002/14651858.CD012608. Copyright © 2017 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.Protocol: To assess the benefits and harms of modifying dietary fat intake in the treatment of gallstone disease.Peer reviewedFinal Published versio

Modified dietary fat intake for treatment of gallstone disease (Protocol)

© 2017 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.This is a protocol for a Cochrane Review (Intervention). To assess the benefits and harms of modifying dietary fat intake in the treatment of gallstone disease.Peer reviewe

Modified dietary fat intake for treatment of gallstone disease in people of any age

© 2024 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.Background The prevalenceof gallstones varies between less than 1% and 64% in different populations andis thought to be increasing in response to changes in nutritional intake andincreasing obesity. Some people with gallstones have no symptoms butapproximately 2% to 4% develop them each year, predominantly including severeabdominal pain. People who experience symptoms have a greater risk ofdeveloping complications. The main treatment for symptomatic gallstones ischolecystectomy. Traditionally, a low-fat diet has also been advised to managegallstone symptoms, but there is uncertainty over the evidence to support this. Objectives To evaluatethe benefits and harms of modified dietary fat intake in the treatment ofgallstone disease in people of any age. Search methods We searchedthe Cochrane Hepato-Biliary Group Controlled Trials Register, the CochraneCentral Register of Controlled Trials in the Cochrane Library, MEDLINE ALLOvid, Embase Ovid, and three other databases to 17 February 2023 to identifyrandomised clinical trials in people with gallstones. We also searched onlinetrial registries and pharmaceutical company sources, for ongoing or unpublishedtrials to March 2023. Selectioncriteria We includedrandomised clinical trials (irrespective of language, blinding, or status) inpeople with gallstones diagnosed using ultrasonography or conclusive imagingmethods. We excluded participants diagnosed with another condition that maycompromise dietary fat tolerance. We excluded trials where data fromparticipants with gallstones were not reported separately from data from participantswho did not have gallstones. We included trials that investigated otherinterventions (e.g. trials of drugs or other dietary (non-fat) components)providing that the trial groups had received the same proportion of drug orother dietary (non-fat) components in the intervention. Data collectionand analysis We intended toundertake meta-analysis and present the findings according to Cochranerecommendations. However, as we identified only five trials, with dataunsuitable and insufficient for analyses, we described the data narratively. Main results We includedfive trials but only one randomised clinical trial (69 adults), published in1986, reported outcomes of interest to the review. The trial had four dietaryintervention groups, three of which were relevant to this review. We assessedthe trial at high risk of bias. The dietary fat modifications included amodified cholesterol intake and medium-chain triglyceride supplementation. Thecontrol treatment was a standard diet. The trial did not report on any of theprimary outcomes in this review (i.e. all-cause mortality, serious adverseevents, and health-related quality of life). The trial reported on gallstonedissolution, one of our secondary outcomes. We were unable to apply the GRADEapproach to determine certainty of evidence because the included trial did notprovide data that could be used to generate an estimate of the effect on thisor any other outcome. The trial expressed its finding as "no significant effectof a low-cholesterol diet in the presence of ursodeoxycholic acid on gallstonedissolution." There were no serious adverse events reported. The includedtrial reported that they received no funding that could bias the trial resultsthrough conflicts of interest. We found no ongoing trials. Authors'conclusions The evidenceabout the effects of modifying dietary fat on gallstone disease versus standard diet is scant. We lack results from high-quality randomised clinical trialswhich investigate the effects of modification of dietary fat and other nutrientintakes with adequate follow-up. There is a need for well-designed trials thatshould include important clinical outcomes such as mortality, quality of life,impact on dissolution of gallstones, hospital admissions, surgicalintervention, and adverse events.Peer reviewe

The nutritional management and immune status in patients with chronic intestinal failure

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

A dangerous combination of binge and purge

We present a 36-year-old female diagnosed with Crohn's disease at the age of 11 years. In 2001, she underwent a total colectomy and further small bowel resection as a result of active Crohn's. Her residual anatomy consisted of 150 cm of small bowel to an end jejunostomy. Subsequently, she developed short bowel syndrome with recurrent episodes of hypomagnesaemia, hypocalcaemia, and hypokalaemia. Dietetic assessment revealed her to be severely underweight at 37 kg with a bodymass index (BMI) of 14.4 kg/m2. During her admission, our patient underwent psychiatric assessment and was established on home parenteral nutrition (HPN). At the time of discharge, 1 month later, her weight had increased to 44 kg (BMI = 17.7 kg/m2). Over the following 12-month period, she lost weight (BMI, 15.4 mg/m2; weight, 39.5 kg) and she described a high stoma output (up to 17 L) and dehydration. Assessment of her oral intake found she was consuming an estimated 14,000 kcal and 600 g protein per day. At this time, the possibility of a new form of eating disorder was discussed with the patient and she agreed that her behavior i.e., using her stoma as a purging device, fulfilled the criteria for a diagnosis of bulimia nervosa and she was referred to a specialist eating disorder unit

Revisiting the refeeding syndrome: Results of a systematic review.

OBJECTIVE Although described >70 y ago, the refeeding syndrome (RFS) remains understudied with lack of standardized definition and treatment recommendations. The aim of this systematic review was to gather evidence regarding standardized definition, incidence rate and time course of occurrence, association with adverse clinical outcomes, risk factors, and therapeutic strategies to prevent or treat this condition. METHODS We searched MEDLINE and EMBASE for interventional and observational clinical trials focusing on RFS, excluding case reports and reviews. We extracted data based on a predefined case report form and assessed bias. RESULTS Of 2207 potential abstracts, 45 records with a total of 6608 patients were included (3 interventional trials, 16 studies focusing on anorexic patients). Definitions for RFS were highly heterogenous with most studies relying on blood electrolyte disturbances only and others also including clinical symptoms. Incidence rates varied between 0% and 80%, depending on the definition and patient population studied. Occurrence was mostly within the first 72 h of start of nutritional therapy. Most of the risk factors were in accordance with National Institute for Health and Care Excellence guidelines, with older age and enteral feeding being additional factors. There was no strong evidence regarding association of RFS and adverse outcomes, as well as regarding preventive measures and treatment algorithms. CONCLUSION This systematic review focusing on RFS found consensus regarding risk factors and timing of occurrence, but wide variations regarding definition, reported incidence rates, preventive measures and treatment recommendations. Further research to fill this gap is urgently needed

Management and prevention of refeeding syndrome in medical inpatients: An evidence-based and consensus-supported algorithm

Objectives:Refeeding syndrome (RFS) can be a life-threatening metabolic condition after nutritional re-plenishment if not recognized early and treated adequately. There is a lack of evidence-based treatmentand monitoring algorithm for daily clinical practice. The aim of the study was to propose an expert con-sensus guideline for RFS for the medical inpatient (not including anorexic patients) regarding risk factors,diagnostic criteria, and preventive and therapeutic measures based on a previous systematic literaturesearch.Methods:Based on a recent qualitative systematic review on the topic, we developed clinically relevantrecommendations as well as a treatment and monitoring algorithm for the clinical management of in-patients regarding RFS. With international experts, these recommendations were discussed and agreementwith the recommendation was rated.Results:Upon hospital admission, we recommend the use of specific screening criteria (i.e., low bodymass index, large unintentional weight loss, little or no nutritional intake, history of alcohol or drug abuse)for risk assessment regarding the occurrence of RFS. According to the patient’s individual risk for RFS, acareful start of nutritional therapy with a stepwise increase in energy and fluids goals and supplemen-tation of electrolyte and vitamins, as well as close clinical monitoring, is recommended. We also proposecriteria for the diagnosis of imminent and manifest RFS with practical treatment recommendations withadoption of the nutritional therapy.Conclusion:Based on the available evidence, we developed a practical algorithm for risk assessment, treat-ment, and monitoring of RFS in medical inpatients. In daily routine clinical care, this may help to optimizeand standardize the management of this vulnerable patient population. We encourage future quality studiesto further refine these recommendations

Sexual differentiation of neural mechanisms of stress sensitivity during puberty.

Anxiety disorders are a major public health concern and current treatments are inadequate for many individuals. Anxiety is more common in women than men and this difference arises during puberty. Sex differences in physiological stress responses may contribute to this variability. During puberty, gonadal hormones shape brain structure and function, but the extent to which these changes affect stress sensitivity is unknown. We examined how pubertal androgens shape behavioral and neural responses to social stress in California mice (Peromyscus californicus), a model species for studying sex differences in stress responses. In adults, social defeat reduces social approach and increases social vigilance in females but not males. We show this sex difference is absent in juveniles, and that prepubertal castration sensitizes adult males to social defeat. Adult gonadectomy does not alter behavioral responses to defeat, indicating that gonadal hormones act during puberty to program behavioral responses to stress in adulthood. Calcium imaging in the medioventral bed nucleus of the stria terminalis (BNST) showed that social threats increased neural activity and that prepubertal castration generalized these responses to less threatening social contexts. These results support recent hypotheses that the BNST responds to immediate threats. Prepubertal treatment with the nonaromatizable androgen dihydrotestosterone acts in males and females to reduce the effects of defeat on social approach and vigilance in adults. These data indicate that activation of androgen receptors during puberty is critical for programming behavioral responses to stress in adulthood