Administration Of Lactulose Research Articles

THE CORRELATION BETWEEN SMALL INTESTINAL BACTERIA OVERGROWTH AND DENDRITIC CELLS PHENOTYPE AND FUNCTION IN CIRRHOTIC PATIENTS WITH HEPATITIS B

Objective: To investigate the relationship between dendritic cells (DCs) and small intestinal bacteria overgrowth (SIBO) in cirrhotic patients with hepatitis B. Methods: Flow cytometry was used to analyze the phenotype of peripheral blood DCs in 47 cirrhotic patients with hepatitis B and 15 healthy controls. Small intestinal bacterial overgrowth was determined by lactulose hydrogen breath test (LHBT). A basal breath hydrogen >20 ppm or arise by >12 ppm above baseline following lactulose administration was taken as positive test. LHBT aggregate value, as another indicator to evaluate the growth of the small intestinal bacteria, is the sum of the LHBT within 90 min. Plasma total bilirubin and plasma albumin were measured in all subjects. Data analysis was using SPSS 17.0. Results: Of the 47 cirrhotics, 22 (46.8%) had SIBO, compared to healthy controls (6.7%; P= 0.005).The prevalence of SIBO increased with Child Pugh classification of cirrhosis (A18.2%, B 43.8% and C65.0%). The prevalence of SIBO in cirrhotic patients of Child Pugh class B and C was significantly higher than that of healthy controls (P=0.037; P=0.001). While the prevalence of SIBO in cirrhotic patients of Child Pugh class A was no statistically significant than that of healthy controls (P=0.556). The prevalence of SIBO in cirrhotic patients of de compensatory phase was significantly higher than that of compensatory phase (χ2 = 4.727, P=0.030). The plasma total bilirubin was positively correlated with LHBT aggregate value (r=0.907, P=0.000), While plasma albumin was negatively correlated (Ir= 0.810 P=0.000). The expressions of CD1a, CD80, CD83 on the surface of DCs in cirrhotic patients were all significant lower than that in healthy controls (P<0.05), while the expression of HLA DR was no statistically significant than that in healthy control. The expressions rate of CD80, CD83, CD1a and HLA DR on the DCs surface in SIBO positive cirrhotic patients were lower than those in SIBO negative [(17.22 ± 2.08) % vs (22.13 ± 2.34) %, (24.65 ± 1.47) % vs ( 34.52 ± 2.84) %, (14.05 ± 1.33) % vs (17.40 ± 3.22) %, (81.47 ± 7.56)% vs (70.15 ± 6.32) %; (P < 0.05)]. Conclusions: The prevalence of SIBO is correlated with severity of cirrhosis. The phenotype and function of peripheral blood DCs in cirrhotic patients with hepatitis B is associated with the presence of SIBO.

Lactulose increases bacterial diversity and modulates the swine faecal microbiome as revealed by 454-pyrosequencing

Lactulose is a synthetic by-product of the isomerization of lactose to disaccharide galactosyl β-(1→4) fructose, and is widely applied as an oral therapeutic and laxative. As a prebiotic, lactulose is thought to control gastrointestinal diseases associated with weaning both in humans and animals. This study focuses on the effect of lactulose as a prebiotic supplement in modulating the microbial community composition and diversity in 30 piglets. The swine faecal microbiome was investigated using 16S rRNA gene barcoded-pyrosequencing before and after lactulose administration for 2 weeks. Major shifts in bacterial composition were detected from the phylum to species level. An increased abundance of Firmicutes phylum and lower abundance of the Bacteroidetes phylum were observed in pigs fed with lactulose compared with the control group. Interestingly, there was a negative relationship between lactulose administration and abundance of the genus Escherichia. In addition, a marked increase in the abundance of Lactobacillus reuteri (1.15–6.28%) was observed in the lactulose group. The canonical loading plot showed that three genera, Prevotella, Subdoligranulum, and Clostridium, were highly discriminating genera that explain the separation of swine faecal microbiota by lactulose administration. Overall, our results showed that lactulose administration could effectively increase diversity and create a distinct microbial community in weaned piglets, which is believed to be important and beneficial to health and performance.

Supplementation of Lactulose Modulates Intestinal Environment

Lactulose, a non‐digestible carbohydrate composed of a galactose and a fructose, is widely used as a food and pharmaceutical ingredient for common health issues such as chronic constipation, hyperammonemia and hepatic encephalopathy. Production of lactulose has been divided into chemical reaction and enzymatic reaction. Most of chemical reaction has some safety issues such as residual catalyst and colored by‐products. In this study, we prepared lactulose by using enzymatic reaction process and investigated the effect of lactulose on in vitro growth of selected strains of probiotic bacteria. We also confirmed whether oral administration of lactulose affected the growth of fecal bifidobacteria by determining the cecal short chain fatty acid (SCFA) levels, intestinal glucagon‐like peptide‐1 (GLP‐1) and peptide YY (PYY) mRNA expression. As a result, we proposed that prebiotic properties of lactulose could be a potential functional ingredient for food application.This research was supported by a grant from the Fundamental R&amp;D Program for Technology of World Premier Materials funded by the Ministry of Trade, Industry and Energy, Republic of Korea

Lactulose accelerates liver regeneration in rats by inducing hydrogen

BackgroundOxidative stress and inflammation are implicated in the process of liver regeneration. Lactulose orally administered can be bacterially fermented and induces dramatic amounts of endogenous hydrogen. Hydrogen has been confirmed to have antioxidant and anti-inflammatory properties. This study investigated the potential influence of lactulose administration on liver regeneration. Materials and methodsAntibiotics were used to suppress bacterial fermentation of lactulose, and hydrogen-rich saline was used as a supplementary measure of exogenous hydrogen. The liver regeneration model was produced in Sprague–Dawley rats through 70% partial hepatectomy. ResultsCompared with non–lactulose-treated group, lactulose administration remarkably increased the weights of remnant liver and inhibited increases in serum levels of transaminases more notably. In the lactulose-treated group, increases of markers for regeneration, such as proliferating cell nuclear antigen and cyclin D1, were highly elevated. Biochemically, lactulose administration increased liver superoxide dismutase activity and decreased malondialdehyde content. In the lactulose-treated group, excessive increases in inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, were inhibited significantly. Increased heme oxygenase-1 and superoxide dismutase 2 expression were also observed after lactulose treatment. The antibiotics suppressed the regeneration-promoting effect of lactulose by reducing hydrogen production, whereas supplementing hydrogen by hydrogen-rich saline would get a similar regeneration-promoting effect as lactulose administration. ConclusionsLactulose administration accelerates posthepatectomized liver regeneration in rats by inducing hydrogen, which may result from attenuation of the oxidative stress response and excessive inflammatory response.

Lactulose ameliorates cerebral ischemia–reperfusion injury in ratsby inducing hydrogen by activating Nrf2 expression

Molecular hydrogen has been proven effective in ameliorating cerebral ischemia/reperfusion (I/R) injury by selectively neutralizing reactive oxygen species. Lactulose can produce a considerable amount of hydrogen through fermentation by the bacteria in the gastrointestinal tract. To determine the neuroprotective effects of lactulose against cerebral I/R injury in rats and explore the probable mechanisms, we carried out this study. The stroke model was produced in Sprague–Dawley rats through middle cerebral artery occlusion. Intragastric administration of lactulose substantially increased breath hydrogen concentration. Behavioral and histopathological verifications matched biochemical findings. Behaviorally, rats in the lactulose administration group won higher neurological scores and showed shorter escape latency time in the Morris test. Morphologically, 2,3,5-triphenyltetrazolium chloride showed smaller infarction volume; Nissl staining manifested relatively clear and intact neurons and TUNEL staining showed fewer apoptotic neurons. Biochemically, lactulose decreased brain malondialdehyde content, caspase-3 activity, and 3-nitrotyrosine and 8-hydroxy-2-deoxyguanosine concentration and increased superoxide dismutase activity. The effects of lactulose were superior to those of edaravone. Lactulose orally administered activated the expression of NF-E2-related factor 2 (Nrf2) in the brain as verified by RT-PCR and Western blot. The antibiotics suppressed the neuroprotective effects of lactulose by reducing hydrogen production. Our study for the first time demonstrates a novel therapeutic effect of lactulose on cerebral ischemia/reperfusion injury and the probable underlying mechanisms. Lactulose intragastrically administered possessed neuroprotective effects on cerebral I/R injury in rats, which could be attributed to hydrogen production by the fermentation of lactulose through intestinal bacteria and Nrf2 activation.

Lactulose mediates suppression of dextran sulfate sodium-induced colon inflammation

ObjectiveAssessment of digestion colonic flora lactulose can be induced to produce hydrogen and prove lactulose with a potential anti-inflammatory effects. MethodsWe established a mouse model of human ulcerative colitis (UC) by supplying mice with water containing dextran sulfate sodium (DSS). At 7-day, DSS-induced pathogenic outcomes, including loss of body weight, increase of colitis score, pathogenic shortening of colon length, elevated level of TNF-α, IL-1β, malondialdehyde (MDA) and myeloperoxidase (MPO) deficiency in colon lesions, were significantly suppressed by lactulose administration and intraperitoneally injected hydrogen water. ResultsAfter eliminating colon microflora by antibiotics, the anti-inflammatory effects of lactulose were significantly compromised. Histological analysis also revealed that the DSS mediated colonic tissue destruction accompanied by neutrophils infiltration was remarkably suppressed by lactulose and hydrogen water. ConclusionThe present study indicated that lactulose can prevent the development of DSS-induced colitis and alleviate oxidative stress state in colitis.

Effects of Cyclophosphamide and Lactulose on the Release of Ammonia and Medium-Molecular-Weight Substances from the Intestine into Blood in Rats

The effects of lactulose on the release of ammonia and medium-molecular-weight substances from the intestine into the blood and on the severity of cyclophosphamide intoxication were studied in rats. The pH and urease-dependent component of ammonia-producing activity of the cecal chyme decreased over 6 h after lactulose administration, while ammonia content in the chyme increased. Cyclophosphamide caused an increase in ammonia and, less so, glutamine level in the portal blood and in the blood collected after decapitation; this drug stimulated release of methylene blue and endogenous substances of medium-molecular-weight to the portal blood. Lactulose was virtually inessential for these changes and for the neurological status, mortality, and medium life span of rats. Hence, lactulose did not prevent cyclophosphamide-induced leakage of ammonia and medium-molecular-weight substances from the gastrointestinal tract into blood and did not reduce the severity of intoxication.

Lactulose Mediates Suppression of Dextran Sodium Sulfate-Induced Colon Inflammation by Increasing Hydrogen Production

Molecular hydrogen (H2) is a potent antioxidant and able to protect organs from oxidative stress injuries. Orally administered lactulose, a potent H2 inducer, is digested by colon microflora and significantly increases H2 production, indicating its potential anti-inflammatory action. To evaluate the anti-inflammatory effects of lactulose on dextran sodium sulfate (DSS)-induced colitis in mice. Mice were randomly assigned into seven groups, receiving regular distilled water, H2-rich saline (peritoneal injection), DSS, oral lactulose (0.1, 0.15, 0.2ml/10g, respectively), and lactulose (0.2ml/10g) + oral antibiotics. The mouse model of human ulcerative colitis was established by supplying mice with water containing DSS. The H2 breath test was used to determine the exhaled H2 concentration. Body weight, colitis score, colon length, pathological features and tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), maleic dialdehyde (MDA) and marrow peroxidase (MPO) levels in colon lesions were evaluated. After 7days, DSS-induced loss of body weight, increase of colitis score, shortening of colon length, pathological changes and elevated levels of TNF-α, IL-1β, MDA, and MPO in colon lesions, were significantly suppressed by oral lactulose administration and intraperitoneally injected H2-rich saline. Ingestion of antibiotics significantly compromised the anti-inflammatory effects of lactulose. The H2 breath test showed that lactulose administration significantly induced hydrogen production and that antibiotics administration could inhibit H2 production. Lactulose can prevent the development of DSS-induced colitis and alleviate oxidative stress in the colon, as measured by MDA and MPO, probably by increasing endogenous H2 production.

Functional Decline After an Emergency Shelter Stay: Misleading Evidence

Differentiation of delirium from dementia requires the utmost care, especially when the symptoms lack some core features.1 Detection becomes even more difficult with the absence of suggestive medical history or laboratory findings, which occurs in nonalcoholic steatohepatitis (NASH).2 We report the case of an elderly woman who developed delirium after an emergency shelter stay. She was originally misdiagnosed with dementia with disuse syndrome. In June 2011, an 87-year-old woman's son admitted her, claiming that she had become “senile” after a month-long emergency shelter stay due to damage caused by the March 2011 earthquake and tsunami. Because of the destruction, water was unavailable for flushing toilets. Therefore, most of the evacuees limited food and liquid intake to minimize stool and urine production. After returning home, the woman manifested functional decline; she often mistook the time and forgot to take her medication, her gait became somewhat unstable, and slight edema developed in both legs. She had consulted doctors at several hospitals, where access to detailed tests were limited because of the destruction. Because her brain computed tomography (CT) scan and blood screening tests were normal, she was repeatedly diagnosed with dementia, reinforced by the effect of the disaster and lack of exercise.3 One day, her hands were noted to be shaking briefly. Although this symptom appeared only once, her son decided to admit her to the hospital. The woman's only significant medical history was hypertension, controlled with daily candesartan and nilvadipine (8 mg each); she had no significant family history of disease. No abnormalities, except obesity (body mass index (BMI) 29.4 kg/m2), had been noted over several years of regular examinations. Her edema, which expanded to her upper and lower extremities, was classified as pitting and fast, indicating hypoalbuminemia as the major cause.4 Pyramidal and extra-pyramidal signs and ataxia were not manifested; her muscle strength was well preserved. Mini-Mental State Examination revealed immediate recall failure. The forward and backward digit span test showed lower score, suggesting that her forgetfulness was inattention rather than memory impairment.5 She spoke slowly and showed careless behavior, such as leaving the toilet without flushing after excretion. Because most of her symptoms seemed to be related to inattention, it was speculated that she had delirium rather than dementia, although fluctuation of symptoms or hyperactivity was unapparent. The concomitance of “subsyndromal delirium”1 and edema caused by hypoalbuminemia with mild throm;?>bocytopenia (Figure 1A) suggested hepatic encephalopathy (HE),6 which a blood ammonia level of 194 pg/mL and electroencephalographic findings confirmed. Abdominal ultrasonography showed cirrhosis without fluid retention (Child Class B). CT showed that her liver and spleen were of almost the same density (Figure 1B). Autoantibodies were negative. Her history and CT findings strongly indicated that cirrhosis occurred due to NASH, which often occurs in people with obesity or diabetes mellitus.5 Insulin resistance was detected later; it had been missed in her annual examinations.7 Her transaminase levels were normal in her regular examinations, suggesting that she had developed compensated cirrhosis several years earlier. Her nutrition had already improved by the time she developed HE, but sanitary water remained unavailable. These facts suggested that constipation, rather than malnutrition, was the likely cause of her encephalopathy. After 20 days of lactulose (19.5 g/d) and branched-chain amino acid (12 g/d) administration, her behavior and her performance on neuropsychological tests improved markedly (Figure 1A). Comprehensive evaluation of edema, cognition, and behavior played a major role in diagnosis. Even without full access to detailed examinations, detection of subsyndromal delirium and speculation regarding its etiology were achieved through comprehensive assessment. The major cause of misdiagnosis was NASH, which tends to be missed in the absence of suggestive history (e.g., excessive alcohol intake or hepatitis infection) and normal transaminase levels. Furthermore, if NASH has developed into cirrhosis, diabetes mellitus and insulin resistance (both causes of NASH) might be obscured. Its diagnosis should not depend heavily on laboratory findings or medical history alone. Another cause of misdiagnosis was the subacute progression and lack of fluctuation of symptoms, which resulted from a variation in clinical progression of HE and difficulties in detecting fluctuation within low-stage HE.6 Acute onset and fluctuation of symptoms are considered essential features of delirium,8 but the possibility of delirium should not be excluded if any one of the core features exists. The present case also indicates that maintaining appropriate lavatory conditions at emergency shelters is important not only for preventing infections,9 but also for maintaining good excretory habits. Conflict of Interest: None. Author Contributions: Naoki Tomita: patient diagnosis and care and manuscript preparation. Kaori Une and Takashi Ohrui: patient diagnosis and advice on the manuscript. Takae Ebihara, Youichi Kosaka, Shoji Okinaga, Katsutoshi Furukawa, Hiroyuki Arai: patient diagnosis. All of the authors read the final version of the manuscript. Sponsor's Role: None.

Lactulose in the treatment of hepatic encephalopathy: New evidence for an old modality

See article in J. Gastroenterol. Hepatol. 2012; 27: 1329–1335.

Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors

Altered intestinal permeability has been shown to be associated with metabolic alterations in animal models of obesity, but not in humans. The aim of this study was to assess intestinal permeability in obese women and verify if there is any association with anthropometric measurements, body composition or biochemical variables. Twenty lean and twenty obese females participated in the study. Anthropometric measurements, body composition and blood pressure were assessed and biochemical analyses were performed. Administration of lactulose and mannitol followed by their quantification in urine was used to assess the intestinal permeability of volunteers. The obese group showed lower HDL (p < 0.05), higher fasting glucose, insulin, HOMA index and lactulose excretion than the lean group (p < 0.05), suggesting increased paracellular permeability. Lactulose excretion showed positive correlation (p < 0.05) with waist and abdominal circumference. Blood insulin and the HOMA index also increased with the increase in mannitol and lactulose excretion and in the L/M ratio (p < 0.05). L/M ratio presented a negative correlation with HDL concentration (p < 0.05). We demonstrated that intestinal permeability parameters in obese women are positively correlated with anthropometric measurements and metabolic variables. Therapeutic interventions focused on intestine health and the modulation of intestinal permeability should be explored in the context of obesity.

Physical exercise and intermittent administration of lactulose may improve autism symptoms through hydrogen production

Autism is neuro-developmental disorder. Oxidative stress is enhanced in some children with autism. Hydrogen is a gas with anti-oxidative effects suggested for treating or prevention of some medical problems. It is hypothesized that lactulose or hydrogen water may provide hydrogen to reduce oxidative stress in autism.

Analysis of the urinary glucose-[15N, 15N]-ureide content in the study of the lactose-[15N, 15N]-ureide metabolism in healthy humans

Lactose-[(15)N, (15)N]-ureide is used to study the fate of the colonic urea-nitrogen metabolism. During the passage through the gastrointestinal tract, lactose ureide is hydrolysed to glucose ureide, which is absorbed to a limited extent from the small intestine and is excreted urinarily. In the present study, a procedure has been developed to quantify the urinary excretion of glucose-[(15)N, (15)N]-ureide. In addition, urine and faecal samples obtained during a dietary intervention study with the prebiotic lactulose were retrospectively analysed. The glucose ureide and lactose ureide content was measured by GC-MS in 19 healthy volunteers. After consumption of a standard test meal containing 75 mg lactose-[(15)N, (15)N]-ureide, six healthy volunteers performed a fractionated 24 h urine collection to investigate the urinary excretion of glucose-[(15)N, (15)N]-ureide. In 13 volunteers, the effect of lactulose administration on the urinary excretion of glucose-[(15)N, (15)N]-ureide was analysed. The urinary excretion of glucose-[(15)N, (15)N]-ureide reached its maximum level in the 3-6 h urine collection and decreased in the 6-9 h urine. The label was still detectable in the 9-24 h urine collection. The cumulative excretion of (15)N-labelled glucose ureide after 24 h amounted 12.91%. No significant differences in glucose-[(15)N, (15)N]-ureide excretion were found in either of the urine fractions after administration of lactulose, compared with baseline. In none of the urine samples lactose-[(15)N, (15)N]-ureide was detected. In conclusion, the results obtained in the present study indicated that the percentage dose glucose-[(15)N, (15)N]-ureide recovered in urine is rather constant and not influenced by the presence of lactulose.

Metronidazole-induced encephalopathy in a patient with liver cirrhosis

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.

A case of adult-onset type II citrullinemia induced by hospital diet.

A 47-year-old Japanese man was first admitted to our hospital for 8days because of an asthma attack. After discharge he changed his diet. On the 12th day after his discharge, he was re-admitted to our hospital because he exhibited transient loss of consciousness with flapping tremor. His plasma ammonia level was extremely high (245μg/dL; normal, <90μg/dL), suggesting hepatic encephalopathy. He underwent intravenous administration of branched-chain amino acids (Aminoleban(®)) and oral administration of lactulose and kanamycin sulfate; however, the hyperammonemia did not improve. Analysis of the amino acids and citrin gene led to the diagnosis of adult-onset type II citrullinemia (CTLN2). Following this diagnosis, the carbohydrate content of his diet was mildly restricted. As a result, his plasma ammonia level markedly improved (ammonia, 40-60μg/dL) and he became symptom-free without any medication. CTLN2 is a metabolic disorder characterized by increased plasma concentrations of citrulline and ammonia, which occurs by the failure of compensatory mechanisms associated with diet. Here, we report a case of a patient for whom a change in eating habits during his hospitalization disturbed his compensatory mechanism resulting in clinical CTLN2, which was reversed with an appropriate diet.

Hepatic encephalopathy and mild lack of awareness

Sirs, In his review Bajaj stated, ‘The administration of lactulose while the patient is admitted with HE is associated with improvement’.1 To support his statement, he cited Blanc et al. whose real conclusion of their article was, ‘Lactulose-neomycin combination should not be used in the treatment of acute hepatic encephalopathy’.2 A few lines before, Bajaj indicated that ‘the Cochrane review did not find any significant difference in outcomes in patients treated with and without lactulose’. After more than 30 years of use, lactulose should no longer be part of standard care for a patient with hepatic encephalopathy. Declaration of personal and funding interests: None.

Benefits of breath hydrogen testing after lactulose administration in analysing carbohydrate malabsorption

Breath hydrogen testing after lactulose administration may yield findings of clinical value, but whether it should be a routine part of breath testing has not been evaluated. We examined the contribution of breath testing after lactulose administration to the conduct and interpretation of breath hydrogen responses after fructose and lactose administration. Two hundred consecutive patients were given lactulose, fructose or lactose on separate days (at least 2 days apart); breath hydrogen was monitored every 15 min after the administration of each sugar. Peak breath hydrogen levels after lactulose administration correlated with those after fructose (r = 0.26; P = 0.03) and lactose (r = 0.44; P = 0.004). Of the patients with a reduced response to lactulose, 51% had definite or borderline evidence of fructose malabsorption (FM); similarly, 23% of patients had definite or borderline lactose malabsorption. After lactulose administration, an increase in breath hydrogen levels occurred after the same amount of time or longer than after the administration of fructose or lactose (>120 min). The earlier the first rise in breath hydrogen levels after lactulose administration, the more frequently FM occurred, indicating an association between FM and rapid transit and/or small intestinal bacterial overgrowth. Routine breath hydrogen testing with lactulose administration before other sugars cannot be used to define non-hydrogen producers, but might, by indicating the vigour of hydrogen production in the individual, allow more rational interpretation of results after testing with other sugars. It permits the duration of testing to be judged and provides information on possible mechanisms of FM.

Influence of colectomy on hydrogen excretion in breath

Hydrogen breath test is the most commonly used method to analyze carbohydrate absorption and diagnose carbohydrate malabsorption. The result of the H(2) breath test is influenced by different factors, which are mostly related to quantitative or qualitative aspects of colonic flora. A scarcely studied variable is the effect of colonic anatomical integrity on H(2) excretion in breath. The present study aims to determine whether loss of colonic integrity reduces H(2) excretion capacity after an oral load of an unabsorbable carbohydrate. An observational study was conducted in three patient groups: controls with preserved colon, patients with partial colectomy, and patients with complete colectomy and ileostomy. H(2) concentration in breath was measured by gas chromatography every 10 min for 3 h after oral lactulose administration. Twenty-two patients with partial colectomy, 18 controls with preserved colon, and seven patients with ileostomy were included. H(2) excretion after lactulose did not differ between patients with partial colectomy and controls (basal excretion = 8.5 vs 4 ppm; delta increase = 50.0 vs 47.5 ppm; area under the curve = 4,480.0 vs 4,710.5 ppm/min). In contrast, H(2) excretion was significantly lower in the ileostomy group. Partial colectomy does not influence the capacity for H(2) excretion after oral unabsorbable carbohydrate administration.

Intestinal Permeability in Preterm Infants by Feeding Type: Mother's Milk Versus Formula

Intestinal permeability in preterm infants represents a critical balance between absorption of nutritional agents and protection from dangerous pathogens. This study identified the relationship between feeding type (human milk and formula) and intestinal permeability as measured by lactulose to mannitol ratio in preterm infants in the first postnatal month. Sixty-two preterm (<or=32 weeks of gestation) infants had assessment of feeding type and evaluation with enteral lactulose and mannitol administration and urinary measurement at three time points in the first postnatal month. Infants who received the majority of feeding as human milk (>75%) demonstrated significantly lower intestinal permeability when compared to infants receiving minimal or no human milk (<25% or none) at postnatal days 7, 14, and 30 (p = 0.02, 0.02, and 0.047, respectively). When infants receiving any human milk were compared to infants receiving formula only, a significant difference existed at day 7 and day 14 but not for day 30 (p = 0.04, 0.02, and 0.15, respectively). With evaluation over the complete study period, exclusively formula-fed infants demonstrated a 2.8-fold higher composite median lactulose/mannitol ratio when compared with those who received any human milk. Infants who received >75% of enteral feeding as mother's milk demonstrated a 3.8-fold lower composite median ratio when compared to infants receiving <25% or no mother's milk. Preterm infant intestinal permeability was significantly decreased for those receiving human milk versus formula in a dose-related manner in the first postnatal month.

Valproic acid-induced encephalopathy in very long course treated patients

Primary objective: In patients receiving valproate (VPA) treatment, valproate induced-encephalopathy (VIE) is among the most serious adverse side-effects and hyperammonaemia is a frequent and well-recognized event. This report evaluates adult patients receiving VPA for several years.Research design: This study was conducted in adult patients receiving VPA for several years. Many studies have evaluated blood ammonia levels and VPA-related encephalopathy in patients whose treatment was initiated for a few months. Most studies were conducted in children.Methods and procedures: This study looked at retrospectively occurrences of VIE in 63 patients who were receiving VPA for a minimum duration of at least 2 years. At the beginning of the study basal ammonaemia was measured for all patients.Main outcomes and results: This study reports a rather frequent onset of VIE. Long duration of VPA treatment was not correlated with encephalopathy onset. In seven cases temporary administration of lactulose alone was effective and VPA was continued.Conclusions: This study confirms that, under VPA treatment, hyperammonaemia is a current event; 25.4% patients presented isolated elevated ammonaemia when receiving VPA for very long durations. VPA therapy should be monitored closely and clinicians must be warned of VPA encephalopathy signs.