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BackgroundThe YOMEGA study (Y-study) was a randomized trial comparing one anastomosis gastric bypass (OAGB) and Roux-en-Y gastric bypass (RYGB). Here, we aim to compare the Y-study and our pioneer trial from Taiwan (T-study).MethodsData from the Y-study and the T-study were collected and compared.ResultsThe Y-study recruited 234 patients with a mean body mass index (BMI) of 43.9 and age of 43.5 years. The T-study recruited 80 patients with a similar mean BMI of 44.3 and mean age of 31.4 years. The studies had similar findings including (1) OAGB is easier and possibly safer procedure than RYGB. Both studies showed that OAGB had a shorter operation time than RYGB, but a lower surgical complication rate was only demonstrated in T-study. (2) Both procedures have similar weight loss but OAGB features better glycemic control than RYGB. Weight loss at 2 years after surgery was similar between two procedures, but OAGB reduced HbA1c to a greater degree than RYGB at 2 years in Y-study (− 2.3% vs. − 1.3%; p = 0.025). The resolution of the metabolic syndrome was 100% for both groups in the T-study. (3) OAGB carried a higher risk of malnutrition. OAGB had more malabsorptive problems with a lower hemoglobin level than RYGB at 2 years after surgery. Adverse malnutrition events occurred in nine (7.8%) OAGB patients in the Y-study. Four (3.4%) patients of OAGB received revision surgery in Y-study but none in T-study. (4) Bile reflux was noted in OAGB patients but did not influence quality of life or revision rate. Y-study found that bile in the gastric pouch was present in 16% of patients in the OAGB group versus none in the RYGB, but no inter-group difference in quality of life was detected. There was a trend for RYGB patients to experience more abdominal pain than OAGB.ConclusionsBoth studies showed that OAGB is a technically easier procedure and features better glycemic control than RYGB, but has a mal-absorptive effect. However, the bile reflux and abdominal pain controversies persisted.

Background Dietary fat malabsorption contributes to poor nutritional status in patients with cystic fibrosis (CF) and exocrine pancreatic insufficiency (EPI). Prescribing gastric acid-reducing agents such as proton-pump inhibitors (PPI) as an adjunct to pancreatic enzyme replacement therapy (PERT) to improve dietary fat absorption has been accepted in clinical practice despite limited evidence. Aims This was a pilot randomized, double-blind, placebo-controlled crossover trial of subjects aged 12 and older with CF and EPI assessed on placebo and omeprazole to determine if PPI improved the efficacy of PERT as indicated by measures of dietary fat absorption. Methods Fat malabsorption via stool coefficient of fat absorption (CFA) and malabsorption blood test (MBT), gastrointestinal pH (wireless motility capsule [WMC]), and quality of life (QOL) were assessed after 14 days on both placebo or PPI (omeprazole). Results Total 19 subjects enrolled, 13 were randomized, and 9 provided paired results on placebo and PPI. The 3 subject results for CFA were as follows: 1 increased, 1 decreased, and 1 was within the reference range in both tests for fat absorption. For 9 MBT subjects, 7 decreased and 2 increased fat absorption. For the 4 WMC studies, no change in transit times, nor in pH profiles were noted. No differences were seen in the domains of the two QOL questionnaires comparing placebo and PPI. Conclusions These limited descriptive pilot study results in participants with CF and EPI on PERT evaluated by stool, blood, and QOL tests did not suggest improvement in fat absorption attributable to PPI.

Lactose is the main source of calories in milk, an essential nutriedigestion, patients with visceral hypersensitivity nt in infancy and a key part of the diet in populations that maintain the ability to digest this disaccharide in adulthood. Lactase deficiency (LD) is the failure to express the enzyme that hydrolyses lactose into galactose and glucose in the small intestine. The genetic mechanism of lactase persistence in adult Caucasians is mediated by a single C→T nucleotide polymorphism at the LCTbo −13’910 locus on chromosome-2. Lactose malabsorption (LM) refers to any cause of failure to digest and/or absorb lactose in the small intestine. This includes primary genetic and also secondary LD due to infection or other conditions that affect the mucosal integrity of the small bowel. Lactose intolerance (LI) is defined as the onset of abdominal symptoms such as abdominal pain, bloating and diarrhoea after lactose ingestion by an individual with LM. The likelihood of LI depends on the lactose dose, lactase expression and the intestinal microbiome. Independent of lactose digestion, patients with visceral hypersensitivity associated with anxiety or the Irritable Bowel Syndrome (IBS) are at increased risk of the condition. Diagnostic investigations available to diagnose LM and LI include genetic, endoscopic and physiological tests. The association between self-reported LI, objective findings and clinical outcome of dietary intervention is variable. Treatment of LI can include low-lactose diet, lactase supplementation and, potentially, colonic adaptation by prebiotics. The clinical outcome of these treatments is modest, because lactose is just one of a number of poorly absorbed carbohydrates which can cause symptoms by similar mechanisms.

PurposeAn amino acid-containing elemental diet (ED) does not require digestion for nutritional absorption, making it a good option for patients with gastrointestinal malabsorption. We conducted a randomized trial to confirm that perioperative ED enhanced the recovery of patients undergoing laparoscopic colectomy.MethodsPatients in the intervention arm received commercially available ED from the day prior to surgery until postoperative day (POD) 3, whereas patients in the control group received a conventional perioperative diet program. To verify the endpoints, “estimated minimum length of stay in hospital after surgery” (emLOS) was defined as the number of days necessary to reach all the five criteria; namely, “sufficient oral intake”, “sufficient pain control”, “withdrawal of intravenous alimentation”, “no abnormal findings in routine examinations”, and “no rise in fever”.ResultsA total of 102 patients were randomized, 94 of whom were analyzed (ED 45, control 49). There was no morbidity or mortality. Shorter emLOS (POD 4 vs. POD 7; p = 0.018), earlier resumption of sufficient oral intake (POD 3 vs. POD 4; p = 0.034) and faster recovery to defecation (2.2 vs. 3.1 days; p = 0.005) were observed in the ED group vs. the control group.ConclusionsThe perioperative ingestion of ED by patients undergoing laparoscopic colectomy is safe and can reduce the postoperative hospital stay by supporting the acceleration of oral intake.

The present randomised trial investigated the effects of feeding Zambian infants from 6 to 18 months old either a richly or basal micronutrient-fortified complementary/replacement food on gut integrity and systemic inflammation. Blood samples were obtained from all infants ( n 743) at 6 and 18 months for the assessment of serum C-reactive protein (CRP) and α1-acid glycoprotein (AGP). A subsample of 502 infants, selected from the main cohort to include a larger proportion of infants with HIV-positive mothers, was assigned to lactulose/mannitol gut permeability tests. Lactulose:mannitol (L:M) ratio analyses were adjusted for baseline urinary L:M ratio, socio-economic status, mother's education, season of birth and baseline stunting, and stratified by maternal antenatal HIV status, child's sex, concurrent breast-feeding status and anaemia at baseline. There was no significant difference in geometric mean L:M ratio between the richly fortified and basal-fortified porridge arms at 12 months (0·47 (95 % CI 0·41, 0·55) v. 0·41 (95 % CI 0·34, 0·49); P  = 0·16 adjusted). At 18 months, the richly fortified porridge group had a significantly higher geometric mean L:M ratio than the basal-fortified group (0·23 (95 % CI 0·19, 0·28) v. 0·15 (95 % CI 0·12, 0·19); P  = 0·02 adjusted). This effect was evident for all stratifications, significantly among boys ( P  = 0·04), among the infants of HIV-negative mothers ( P  = 0·01), among the infants of HIV-negative mothers not concurrently breast-fed ( P  = 0·01) and among those who were not anaemic at baseline ( P  = 0·03). CRP, but not AGP, was positively associated with L:M ratio, but there were no significant effects of the diet on either CRP or AGP. In conclusion, a richly fortified complementary/replacement food did not benefit and may have worsened intestinal permeability.

This review intends to act as an overview of fructose malabsorption (FM) and its role in the aetiology of diseases including, but not limited to, irritable bowel syndrome (IBS) and infantile colic and the relationship between fructose absorption and the propagation of some cancers. IBS results in a variety of symptoms including stomach pains, cramps and bloating. Patients can be categorised into two groups, depending on whether the patients’ experiences either constipation (IBS-C) or diarrhoea (IBS-D). FM has been proposed as a potential cause of IBS-D and other diseases, such as infantile colic. However, our knowledge of FM is limited by our understanding of the biochemistry related to the absorption of fructose in the small intestine and FM’s relationship with small intestinal bacterial overgrowth. It is important to consider the dietary effects on FM and most importantly, the quantity of excess free fructose consumed. The diagnosis of FM is difficult and often requires indirect means that may result in false positives. Current treatments of FM include dietary intervention, such as low fermentable oligo-, di-, monosaccharides and polyols diets and enzymatic treatments, such as the use of xylose isomerase. More research is needed to accurately diagnose and effectively treat FM. This review is designed with the goal of providing a detailed outline of the issues regarding the causes, diagnosis and treatment of FM.

In cystic fibrosis (CF), pancreatic insufficiency and a diminished bile acid pool cause malabsorption of important nutrients and dietary components leading to deficiency, poor nutritional status, and oxidative stress. Of particular significance is the malabsorption of fat-soluble nutrients and antioxidants, which are important for normal immune and neurologic function. Patients with CF often are deficient in these compounds despite supplementation with the current standard of care therapy. The objective was to compare the pharmacokinetic profile of this water-soluble vitamin E formulation (Aqua-E) with an oil-based softgel formulation in a malabsorbing patient population. Patients with CF who had documented malabsorption were recruited for participation in this pharmacokinetic study. Patients who met inclusion and exclusion criteria discontinued vitamin E supplementation, except for that in a multivitamin, for 7 to 21 days before the day of dosing. Patients were randomized to a single dose of 20 ml of Aqua-E or three oil-based softgels, which contained equivalent amounts of tocopherols. Blood was drawn from patients at time 0, 2, 4, 8, 24, 48, and 168 hr and analyzed for tocopherols. Eight patients were enrolled in the study and randomized to Aqua-E or softgels. The primary outcome, the absorption of gamma-tocopherol in Aqua-E (AUC=115 micro g/ml(*)hr), was significantly greater than that of oil-based softgels (AUC=25.3 micro g/ml(*)hr; P=0.013). Total-tocopherols (alpha+gamma+delta) in Aqua-E (AUC=294 micro g/ml(*)hr) showed a strong trend toward increased absorption compared with that of oil-based softgels (AUC=117 micro g/ml(*)hr; P=0.09). In conclusion, this novel, water-soluble formulation showed a marked and statistically significant increase in absorption of gamma-tocopherol in malabsorbing patients with CF compared with an oil-based formulation.

BackgroundThe indications for intestinal transplantation (ITx) are still debated. Knowing survival rates and causes of death on home parenteral nutrition (HPN) will improve decisions.MethodsA prospective 5-year study compared 389 non-candidates (no indication, no contraindication) and 156 candidates (indication, no contraindication) for ITx. Indications were: HPN failure (liver failure; multiple episodes of catheter-related venous thrombosis or sepsis; severe dehydration), high-risk underlying disease (intra-abdominal desmoids; congenital mucosal disorders; ultra-short bowel), high morbidity intestinal failure. Causes of death were defined as: HPN-related, underlying disease, or other cause.ResultsThe survival rate was 87% in non-candidates, 73% in candidates with HPN failure, 84% in those with high-risk underlying disease, 100% in those with high morbidity intestinal failure and 54%, in ITx recipients (one non-candidate and 21 candidates) (p<0.001). The primary cause of death on HPN was underlying disease-related in patients with HPN duration ≤2 years, and HPN-related in those on HPN duration >2 years (p=0.006). In candidates, the death HRs were increased in those with desmoids (7.1; 95% CI 2.5 to 20.5; p=0.003) or liver failure (3.4; 95% CI 1.6 to 7.3; p=0.002) compared to non-candidates. In deceased candidates, the indications for ITx were the causes of death in 92% of those with desmoids or liver failure, and in 38% of those with other indications (p=0.041). In candidates with catheter-related complications or ultra-short bowel, the survival rate was 83% in those who remained on HPN and 78% after ITx (p=0.767).ConclusionsHPN is confirmed as the primary treatment for intestinal failure. Desmoids and HPN-related liver failure constitute indications for life-saving ITx. Catheter-related complications and ultra-short bowel might be indications for pre-emptive/rehabilitative ITx. In the early years after commencing HPN a life-saving ITx could be required for some patients at higher risk of death from their underlying disease.

Malabsorption in children presents significant diagnostic and therapeutic challenges due to its diverse etiologies and broad spectrum of symptoms. This review aims to support pediatric clinicians by providing a structured guide for recognizing, diagnosing, and managing malabsorption syndromes in children, promoting early intervention to prevent long-term complications. Malabsorption, defined as the inefficient absorption of nutrients, manifests with symptoms such as diarrhea, failure to thrive, and systemic nutritional deficiencies. The etiologies are categorized into intestinal, pancreatic, hepatobiliary, and extraintestinal causes, necessitating a multidisciplinary approach tailored to the patient’s age and clinical presentation. Diagnostic strategies emphasize stool analysis, serological testing, and imaging to identify conditions such as Celiac disease, Crohn’s disease, or exocrine pancreatic insufficiency. The review explores the gastrointestinal system's complexity, detailing critical phases of digestion—luminal, mucosal, and transport—and processes specific to neonates and infants. Common issues like lactose intolerance, small intestinal bacterial overgrowth (SIBO), and bile acid malabsorption are addressed, alongside rare genetic and metabolic disorders that require targeted diagnostic approaches. Management focuses on dietary modifications, enzyme replacement therapy, and condition-specific interventions to ensure optimal growth and development. Special attention is given to the unique challenges of neonatal and infant cases, where developmental immaturity and congenital disorders often complicate evaluation and treatment. By synthesizing current evidence and clinical guidelines, this review provides pediatricians with a practical framework for addressing the multifaceted challenges of malabsorption. It emphasizes the importance of early recognition and multidisciplinary care to improve patient outcomes and quality of life. •Comprehensive guide to diagnosing pediatric malabsorption across all age groups.•Emphasizes stool analysis and targeted tests for early recognition of rare syndromes.•Structured approach aids in identifying fat, carbohydrate, and bile absorption issues.•Diagnostic algorithms are provided for neonates, infants, and children with malabsorption.•Highlights the role of diet, enzymes, and multidisciplinary care in pediatric treatment plans.

Carbohydrate intolerance is a poorly understood and potentially overlooked cause of unexplained gastrointestinal symptoms, particularly among patients with disorders of gut-brain interaction. Symptoms related to carbohydrate intolerance arise from bacterial fermentation of unabsorbed carbohydrates leading to increased gases and osmotic load within the gastrointestinal tract. This mechanism is shared across various carbohydrates, including lactose, sucrose, maltose, fructose, and fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. Primary forms of carbohydrate maldigestion typically affect one specific type of carbohydrate and result from inherited defects in specific brush-border enzymes or transport mechanisms, whereas secondary, or acquired, forms of carbohydrate maldigestion can arise from conditions that affect the structural integrity or function of the pancreas and small intestine. Although confirmation of a disaccharidase deficiency does not imply clinical relevance, obtaining a careful patient history with appropriate use of breath testing, duodenal disaccharidase assay, and response to dietary modification can help identify patients whose symptoms are associated with carbohydrate maldigestion and who may benefit from treatment. Dietary modification remains the cornerstone of therapy for patients with carbohydrate intolerance and should focus on determining the most liberal diet for patients that allows symptom control. Given the complexity and time-consuming nature of this process, clinicians are encouraged to engage the help of dietitians with expertise in the treatment of disorders of gut-brain interaction where available. Enzyme replacement therapy can also be an important adjunct to dietary management, with sacrosidase improving symptoms in sucrase-isomaltase deficiency and helping patients to liberalize their diet.