Do Specialized Bariatric Multivitamins Lower Deficiencies After Sleeve Gastrectomy?

BACKGROUND: Vitamin and mineral deficiencies are common after a sleeve gastrectomy (SG). The aim of this study is to examine the effectiveness of a specialized bariatric multivitamin (WLS Optimum) for SG patients on deficiencies compared with a regular multivitamin (MVS) for up to 5 years. METHODS: Data of all patients who underwent a SG procedure in the Catharina Hospital Eindhoven (CZE) between July 2011 and July 2016 were collected and retrospectively analyzed. All patients who completed a preoperative blood test and at least one blood withdrawal during the first operative year were included in this study. RESULTS: This study included 970 patients; 291 patients in the WLS-user group and 679 patients in the non-WLS-user group. In favor of the user group, significantly less de novo deficiencies were found of vitamin B1 (2 years) and vitamin B6 (two and three), folic acid (1 and 2 years), and vitamin B12 (at 1 year). Binomial logistic regression showed a significant influence of multivitamin supplementation mainly on ferritin; vitamins B1, B6, B12, and D; and folic acid, (all p < 0.05). The total number of de novo deficiencies was significantly reduced during the whole study for all WLS Optimum users. CONCLUSIONS: Vitamin deficiencies are common, and postoperative nutritional management after SG is underestimated. The use of a specialized multivitamin supplement resulted in higher mean serum concentrations and less deficiencies of vitamin B1, folic acid, and vitamin B12. This study shows that SG patients benefit from the specialized multivitamin supplements, but adjustments are required for iron and vitamin B6 content.

Environmental Enteric Dysfunction and Growth Failure/Stunting in Global Child Health.

Approximately 25% of the world's children aged <5 years have stunted growth, which is associated with increased mortality, cognitive dysfunction, and loss of productivity. Reducing by 40% the number of stunted children is a global target for 2030. The pathogenesis of stunting is poorly understood. Prenatal and postnatal nutritional deficits and enteric and systemic infections clearly contribute, but recent findings implicate a central role for environmental enteric dysfunction (EED), a generalized disturbance of small intestinal structure and function found at a high prevalence in children living under unsanitary conditions. Mechanisms contributing to growth failure in EED include intestinal leakiness and heightened permeability, gut inflammation, dysbiosis and bacterial translocation, systemic inflammation, and nutrient malabsorption. Because EED has multiple causal pathways, approaches to manage it need to be multifaceted. Potential interventions to tackle EED include: (1) reduction of exposure to feces and contact with animals through programs such as improved water, sanitation, and hygiene; (2) breastfeeding and enhanced dietary diversity; (3) probiotics and prebiotics; (4) nutrient supplements, including zinc, polyunsaturated fatty acids, and amino acids; (5) antiinflammatory agents such as 5-aminosalicyclic acid; and (6) antibiotics in the context of acute malnutrition and infection. Better understanding of the underlying causes of EED and development of noninvasive, practical, simple, and affordable point-of-care diagnostic tools remain key gaps. "Omics" technologies (genomics, epigenomics, transcriptomics, proteomics, and metabolomics) and stable isotope techniques (eg, 13C breath tests) targeted at children and their intestinal microbiota will enhance our ability to successfully identify, manage, and prevent this disorder.

Vitamin D deficiency in patients with intestinal malabsorption syndromes--think in and outside the gut.

There is a very high prevalence of vitamin D deficiency, which is defined by a serum level of 25-hydroxyvitamin D [25(OH)D] of lower than 20 ng/mL, in all populations of the world. Unfortunately, the prevalence of vitamin D deficiency in patients with intestinal malabsorption syndromes, including cystic fibrosis (CF), celiac disease (CD), short bowel syndrome and inflammatory bowel disease (IBD), is higher than that in the general population, indicating the presence of disease-specific causative factors. In this review, we aimed to present clinical findings to highlight the roles of insufficient exposure to sunlight and inflammation in the development of vitamin D deficiency in patients with intestinal malabsorption syndromes. Furthermore, we aimed to present experimental evidence that supported a role of vitamin D deficiency in the pathogenesis of IBD. Finally, we reviewed clinical intervention strategies aiming to normalize vitamin D status in and even to improve the conditions of patients and to discuss certain issues that needed to be addressed in future research.

Risk of Malnutrition, Trace Metal, and Vitamin Deficiency Post Roux-en-Y Gastric Bypass--a Prospective Study of 20 Patients with BMI < 35 kg/m².

BACKGROUND: Due to its reliable effects on type 2 diabetes mellitus (T2DM) remission, Roux-en-Y gastric bypass (RYGB) has recently been investigated as a treatment option for nonseverely obese patients with T2DM (body mass index (BMI) <35 kg/m(2)). The purpose of this study was to investigate whether RGYB induces malnutrition of macro- and micronutrients within 24 months in these patients. METHODS: A prospective cohort of 20 patients with longstanding, insulin-dependent T2DM and a BMI of 25-35 kg/m(2) were treated with RYGB. The patients were supplemented with over-the-counter, multivitamin, and micronutrient supplements. Serum concentrations of albumin, vitamins, and trace elements, hemoglobin, and bone density were measured preoperatively and over a 24-month period (DRKS00004605). RESULTS: RYGB did not result in underweight or protein malnutrition. No new onset of deficiencies of water- or fat-soluble vitamins developed over the study period. However, serum selenium, zinc, and ferritin decreased significantly (selenium, 1.17 ± 0.13 to 0.89 ± 0.11 µmol/l, p = 0.018; zinc, 13.9 ± 0.5 to 10.8 ± 0.5 µmol/l, p = 0.012; ferritin, 171.7 ± 26.9 to 31.8 ± 11.2 µg/l, p = 0.018). Hemoglobin remained stable. Vitamin D (13.7 ± 1.8 to 19.1 ± 1.1 ng/ml, p = 0.017) and osteocalcin (15.3 ± 1.7 to 25.4 ± 2.7 ng/ml, p = 0.025) rose significantly, whereas the parathyroid hormone remained stable. Despite increased bone formation, bone density decreased (T score hip, 0.15 ± 0.25 to -0.71 ± 0.34, p = 0.005) resulting in a significant increase in osteopenia rates (18 to 50 %, p = 0.046). CONCLUSIONS: This is the first prospective cohort to investigate malnutrition after RYGB in nonseverely obese patients. These patients are at risk of developing iron, selenium, and zinc deficiencies within 24 months, as well as osteopenia despite an increase in bone formation.

Environmental enteric dysfunction: an overview.

BACKGROUND: Environmental enteric dysfunction (EED) refers to an incompletely defined syndrome of inflammation, reduced absorptive capacity, and reduced barrier function in the small intestine. It is widespread among children and adults in low- and middle-income countries. Understanding of EED and its possible consequences for health is currently limited. OBJECTIVE: A narrative review of the current understanding of EED: epidemiology, pathogenesis, therapies, and relevance to child health. METHODS: Searches for key papers and ongoing trials were conducted using PUBMED 1966-June 2014; ClinicalTrials.gov; the WHO Clinical Trials Registry; the Cochrane Library; hand searches of the references of retrieved literature; discussions with experts; and personal experience from the field. RESULTS: EED is established during infancy and is associated with poor sanitation, certain gut infections, and micronutrient deficiencies. Helicobacter pylori infection, small intestinal bacterial overgrowth (SIBO), abnormal gut microbiota, undernutrition, and toxins may all play a role. EED is usually asymptomatic, but it is important due to its association with stunting. Diagnosis is frequently by the dual sugar absorption test, although other biomarkers are emerging. EED may partly explain the reduced efficacy of oral vaccines in low- and middle-income countries and the increased risk of serious infection seen in children with undernutrition. CONCLUSIONS: Despite its potentially significant impacts, it is currently unclear exactly what causes EED and how it can be treated or prevented. Ongoing trials involve nutritional supplements, water and sanitation interventions, and immunomodulators. Further research is needed to better understand this condition, which is of likely crucial importance for child health and development in low- and middle-income settings.

Nutritional status in children with Shwachman-diamond syndrome.

OBJECTIVE: In Shwachman-Diamond syndrome (SDS), pancreatic insufficiency can lead to malabsorption of fat-soluble vitamins and trace elements. The aim of this study was to assess the serum concentrations of vitamins A and E, zinc, copper, and selenium and their deficiencies. METHODS: This retrospective review was performed in 21 children (12 were male; median age, 7.8 years) with genetically confirmed SDS at a tertiary pediatric hospital. Pancreatic enzyme replacement therapy (PERT) and vitamin or trace elements supplements were documented. RESULTS: Twenty patients (95%) had pancreatic insufficiency receiving PERT, 10 (47%) had a combined vitamin and trace element deficiency, 6 (29%) had an isolated vitamin deficiency, and 4 (19%) had an isolated trace element deficiency. Vitamins A and E deficiency occurred in 16 (76%) and 4 (19%) of 21, respectively. Low serum selenium was found in 10 (47%), zinc deficiency in 7 (33%), and copper deficiency in 5 (24%). Eleven patients (52%) were on multivitamin supplementation, and 2 (10%) on zinc and selenium supplements. No statistical differences were found between repeated measurements for all micronutrients. CONCLUSIONS: More than 50% of the children had vitamin A and selenium deficiencies despite adequate supplementation of PERT and supplements. Micronutrients should be routinely measured in SDS patients to prevent significant complications.

Vitamin a deficiency in pregnancy: perspectives after bariatric surgery.

This study aims to describe the clinical consequences of vitamin A deficiency (VAD) in pregnant women after bariatric surgery. Included are studies on VAD during pregnancy and after bariatric surgery conducted in humans from 1993 to 2011. There are few investigations on the relationship between pregnancy and bariatric surgery and on the damage to the binomial mother-child resulting from VAD in this relationship. The high percentage of VAD in the postoperative period is a cause for concern, especially considering the function of this vitamin in certain biological moments and in moments of intense nutritional demand. This vitamin serum evaluation is recommended during the prenatal period.

Vitamin B12 malabsorption in patients with limited ileal resection.

OBJECTIVES: Patients with Crohn's disease who have terminal ileal resections are at risk for vitamin B12 malabsorption. Our aim was to determine whether the length of terminal ileum resected correlated with an abnormal Schilling test result. METHODS: Patients with a history of ileal resection had the length of small bowel removed determined by review of their pathology report. Patients who had a Schilling test within 3 mo of surgery or who had a documented normal terminal ileum at the time of the Schilling test were included in the study. RESULTS: Fifty-six patients were included in the study. Patients who had <20 cm of terminal ileum resected (n = 14) did not develop abnormal Schilling test results; 52% of the remainder (n = 42) had abnormal Schilling test results and there was no clear correlation between resection length and abnormal Schilling test result. CONCLUSIONS: Patients with Crohn's disease and terminal ileal resections <20 cm are not at risk of developing vitamin B12 deficiency. For patients with resections of 20-60 cm, options include doing a Schilling test and treating those with abnormal results, empirically treating patients on the presumption that they are at high risk of developing deficiency, or monitoring for biochemical evidence of deficiency. Further studies are needed to determine whether oral supplementation is effective in these patients.

Fat malabsorption induced by gastrointestinal lipase inhibitor leads to an increase in urinary oxalate excretion.

BACKGROUND: Unabsorbed fat and bile acids may react with calcium in the intestinal lumen, limiting the amount of free calcium binding with oxalate and thereby raising intestinal oxalate absorption leading to hyperoxaluria. The aim of the present study was to determine whether orlistat (Xenical), a gastrointestinal lipase inhibitor, might increase urinary oxalate in an experimental rat model. METHODS: Thirty-nine male adult Wistar rats were fed a standard diet alone (controls) or supplemented with either 2% sodium oxalate (NaOx) or 3.2 mL of soy oil, or with both (NaOx + soy oil) for 4 weeks (diet period). Orlistat (16 mg/day) was added to the diet from the 5th to the 8th week (diet + orlistat period). Urinary oxalate (uOx), calcium (uCa), magnesium (uMg), and citrate (uCit) were determined and the ion-activity product of calcium oxalate [AP (CaOx) index(rat)] was estimated. RESULTS: Compared to baseline uOx significantly increased after diet + orlistat in controls (0.64 +/- 0.1 mg/24 hours vs. 0.56 +/-0.1 mg/24 hours), soy oil (0.80 +/- 0.3 mg/24 hours vs. 0.49 +/-0.2 mg/24 hours), and NaOx (2.48 +/- 0.8 mg/24 hours vs. 0.57 +/- 0.2 mg/24 hours), but the most marked increase occurred in NaOx + soy oil (3.87 +/- 0.7 mg/24 hours vs. 0.47 +/- 0.1 mg/24 hours). All groups except controls presented a significant reduction in uCa and uMg. Orlistat induced a significant increase in AP (CaOx) index(rat) compared, respectively, to baseline and to the diet period in NaOx (4.52 +/- 2.34 mg/24 hours vs. 0.94 +/- 0.86 and 1.53 +/- 0.93 mg/24 hours) and NaOx + soy oil (6.49 +/- 4.03 mg/24 hours vs. 0.54 +/- 0.17 and 1.76 +/- 1.32 mg/24 hours). CONCLUSION: These data suggest that the use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation.