HLA-DQ2/DQ8 and HLA-DQB1*02 homozygosity typing by real-time polymerase chain reaction for the assessment of celiac disease genetic risk: evaluation of a Spanish celiac population.

Celiac disease (CD) is a complex autoimmune disorder caused by ingestion of gluten in genetically susceptible individuals. Different genetic risk factors have been identified, but virtually all patients are human leukocyte antigen (HLA)-DQ2 and/or HLA-DQ8 positive. We describe a new, fast, accurate and simple real-time polymerase chain reaction (PCR)-based assay for the genotyping and homozygosity analysis of the CD-related HLA alleles. The assay overcomes the major limitations of protocols currently in use, allowing HLA-DQ2/DQ8 genotyping by using only three real-time PCR reactions. For the appraisal of DQ2 homozygosity, only one more reaction is needed. These reactions are easily automated and suitable for large screening studies in diagnostic procedures, as it is demonstrated by their successful application in our HLA diagnostic laboratory. Finally, we assessed the clinical relevance of this real-time PCR-based assay by studying a cohort of fully characterized patients. As expected, all CD patients had at least one of the CD-associated alleles, and the highest CD risk was indicated by the presence of the HLA-DQ2.5 heterodimer (HLA-DQA1*05-DQB1*02) with HLA-DQB1*02 in homozygosity.

ANP32E, a Protein Involved in Steroid-Refractoriness in Ulcerative Colitis, Identified by a Systems Biology Approach.

BACKGROUND AND AIMS: Steroid-refractoriness is a common and unpredictable phenomenon in ulcerative colitis [UC], but there are no conclusive studies on the molecular functions involved. We aimed to assess the mechanism of action related to steroid failure by integrating transcriptomic data from UC patients, and updated molecular data on UC and glucocorticoids. METHODS: MicroRNA [miRNA] and mRNA expression were evaluated by sequencing and microarrays, respectively, from rectal biopsies of patients with moderately-to-severe active UC, obtained before and on the third day of steroid treatment. The differential results were integrated into the mathematical models generated by a systems biology approach. RESULTS: This computational approach identified 18 proteins that stand out either by being associated with the mechanism of action or by providing a means to classify the patients according to steroid response. Their biological functions have been linked to inflammation, glucocorticoid-induced transcription and angiogenesis. All the selected proteins except ANP32E [a chaperone which has been linked to the exchange of H2A.z histone and promotes glucocorticoid receptor-induced transcription] had previously been related to UC and/or glucocorticoid-induced biological actions. Western blot and immunofluorescence assays confirmed the implication of this chaperone in steroid failure in patients with active UC. CONCLUSIONS: A systems biology approach allowed us to identify a comprehensive mechanism of action of steroid-refractoriness, highlighting the key role of steroid-induced transcription and the potential implication of ANP32E in this phenomenon.

Reduced liver injury in the interleukin-6 knockout mice by chronic carbon tetrachloride administration.

BACKGROUND: Interleukin-6 has been involved in restoration of liver function after partial hepatectomy and toxic liver injury. However, normal liver regeneration in interleukin-6 knockout mice has also been reported. The aim of this work was to investigate the effect of interleukin-6 deficiency on liver injury and its regeneration in a model of long term carbon tetrachloride (CCl4) administration. DESIGN: Serum and whole livers from wild type and interleukin-6 knockout mice treated with carbon tetrachloride (0.25 mL kg(-1)) twice a week were obtained after 4, 6 and 8 weeks (n = 4-6). Sections were assessed for liver regeneration, liver injury and hepatocyte apoptosis whereas sera were assayed for aminotransferase levels. Nuclear extracts and total liver lysates were assayed for transcription factor activation and apoptosis related proteins, respectively. RESULTS: When compared to wild type, interleukin-6 knockout mice showed reduced liver damage scores, lower aminotransferase levels and diminished apoptosis, as well as reduced nuclear factor kappa B activation. Although the level of active protein was lower, activation of signal transducer and activator of transcription 3 still takes place in knockout mice. Furthermore, liver regeneration measured by bromodeoxyuridine incorporation showed no differences between wild type and knockout animals after 6 and 8 weeks of treatment. CONCLUSIONS: Compared to the wild type mice liver regeneration after chronic treatment with carbon tetrachloride proceeds at a slower rate in interleukin-6 deficient mice. However, this low recovery rate is accompanied by a reduction not only in hepatocyte apoptosis, but also in activation of nuclear factor kappa B and liver injury.

Phenotype and natural history of elderly onset inflammatory bowel disease: a multicentre, case-control study.

BACKGROUND: Onset during old age has been reported in upto 10% of total cases of inflammatory bowel disease (IBD). AIM: To evaluate phenotypic characteristics and the use of therapeutic resources in patients with elderly onset IBD. METHODS: Case-control study including all those patients diagnosed with IBD over the age of 60 years since 2000 who were followed-up for >12 months, identified from the IBD databases. Elderly onset cases were compared with IBD patients aged 18 to 40 years at diagnosis, matched by year of diagnosis, gender and type of IBD (adult-onset). RESULTS: One thousand three hundred and seventy-four elderly onset and 1374 adult-onset cases were included (62% ulcerative colitis (UC), 38% Crohn's disease (CD)). Among UC patients, elderly onset cases had a lower proportion of extensive disease (33% vs 39%; P < 0.0001). In CD, elderly onset cases showed an increased rate of stenosing pattern (24% vs 13%; P < 0.0001) and exclusive colonic location (28% vs 16%; P < 0.0001), whereas penetrating pattern (12% vs 19%; P < 0.0001) was significantly less frequent. Regarding the use of therapeutic resources, there was a significantly lower use of corticosteroids (P < 0.0001), immunosuppressants (P < 0.0001) and anti-TNFs agents (P < 0.0001) in elderly onset cases. Regarding surgery, we found a significantly higher surgery rate among elderly onset UC cases (8.3% vs 5.1%; P < 0.009). Finally, elderly onset cases were characterised by a higher rate of hospitalisations (66% vs 49%; P < 0.0001) and neoplasms (14% vs 0.5%; P < 0.0001). CONCLUSIONS: Elderly onset IBD shows specific characteristics and they are managed differently, with a lower use of immunosuppressants and a higher rate of surgery in UC.

ESPEN Guidelines on Enteral Nutrition: Liver disease.

Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility to increase or to insure nutrient intake in case of insufficient oral food intake. The present guideline is intended to give evidence-based recommendations for the use of ONS and TF in patients with liver disease (LD). It was developed by an interdisciplinary expert group in accordance with officially accepted standards and is based on all relevant publications since 1985. The guideline was discussed and accepted in a consensus conference. EN by means of ONS is recommended for patients with chronic LD in whom undernutrition is very common. ONS improve nutritional status and survival in severely malnourished patients with alcoholic hepatitis. In patients with cirrhosis, TF improves nutritional status and liver function, reduces the rate of complications and prolongs survival. TF commenced early after liver transplantation can reduce complication rate and cost and is preferable to parenteral nutrition. In acute liver failure TF is feasible and used in the majority of patients.

Clinical evolution of luminal and perianal Crohn's disease after inducing remission with infliximab: how long should patients be treated?

BACKGROUND: Few data are available regarding the evolution of Crohn's disease after discontinuing a successful course of infliximab. AIM: To evaluate clinical outcome of Crohn's disease after induction of remission with three infliximab infusions (luminal disease) and after maintenance of remission with 1-year course of infliximab every 8 weeks (luminal and perianal). METHODS: Twenty-three patients with active luminal Crohn's disease who responded to three infusions of infliximab (0, 2, and 6 weeks), and 23 patients with sustained response to infliximab every 8 weeks during 1 year, were included. Patients were followed-up until relapse or for at least 6 months after infliximab discontinuation. Clinical outcomes and factors associated to relapse were evaluated. RESULTS: In luminal Crohn's disease, a three-infusion infliximab regimen achieved a sustained response in most patients, especially if a complete response occurred at the time of the third infusion. In patients treated for 1-year, infliximab discontinuation was also successful, with a cumulative probability of being free of relapse of 69% at 12 months. In perianal disease, early relapse was the rule after stopping infliximab treatment, with only 34% of patient maintaining remission at 1 year. CONCLUSIONS: Short regimens of infliximab might be evaluated in patients with luminal Crohn's disease. However, infliximab discontinuation is not recommended in perianal Crohn's disease, because of a high rate of early relapse.

[Gasometric alterations in hospitalized cirrhotic patients]. / Alteraciones gasométricas en pacientes cirróticos hospitalizados.

BACKGROUND AND OBJECTIVES: Gas exchange alterations have been described in cirrhotic patients; but by the moment, a few prospective studies have focused in them. The aim of this study was to describe the frequency and severity of gasometric alterations in hospitalized cirrhotic patients, a their correlation with hepatocellular disfunction. PATIENTS AND METHODS: 50 consecutive cirrhotic patients (41 males) admitted for liver decompensation (ascites, liver encephalopathy, alcoholic hepatitis and upper gastrointestinal bleeding) without acute or chronic cardiopulmonary disfunction were included in the study. Patients were classified according with Child-Pugh score (A, n = 13; B, n = 21; C, n = 16). Severe alcoholic hepatitis (SAH) was confirmed in 7 patients. Arterial gasometry was performed in all patients before discharge. Contrast echocardiography was performed in any case of suspicion of hepatopulmonary syndrome (HPS). RESULTS: Light hypoxemia was observed (80.9 mmHg), without differences with Child-Pugh. Hypocapnia was significantly more evident in Child C than in A and B (31.2 +/- 3.1 vs. 38.1 +/- 4.3 y 36.3 +/- 5 mmHg; p < 0,05), respectively. Cirrhotic patients with SAH showed a significantly higher hypocapnia by comparison with others (31.2 +/- 3.1 vs. a 36.3+/-5 mmHg; p < 0.05). In multivariate analysis, independent prognostic variables for hypocapnica were plasmatic levels of protrombin time, albumin and sodium. HPS was confirmed in 8 patients (16%). CONCLUSIONS: The most prevalent gas exchange abnormality in cirrhosis was the alteration of alveolar-arterial oxygen tension gradient, directly correlated with hepatocellur disfunction. Hypocapnia could be a compensatory mechanism or the result of the activation of central respiratory centres by non-depurated substances by the liver.

Factors related to the plasma fatty acid profile in healthy subjects, with special reference to antioxidant micronutrient status: a multivariate analysis.

The plasma lipid fatty acid (FA) profile was measured in 83 healthy subjects (35 men, 48 women; ages 18-82 y). The association of 19 variables (including serum antioxidant micronutrients) with saturated (SFA), monounsaturated (MUFA), essential (EFA), and polyunsaturated fatty acid (PUFA) status was assessed by stepwise multiple-linear regression. Serum selenium was directly associated with percent EFA and n-6 PUFA (r = 0.38, P = 0.0004 for both) and inversely related to percent SFA in phospholipids (r = -0.38, P = 0.0004). Serum selenium was the only predictor of the unsaturation index of this fraction (r = 0.45, P = 0.0000). Although associations of plasma FA pattern with age, serum cholesterol, bilirubin, vitamin E, and zinc were also disclosed, only for selenium did the antioxidant effect seem to explain this relationship. These results suggest that antioxidant micronutrients should be measured when PUFA metabolism is studied. The relationship between plasma FA and antioxidant micronutrients in disease states needs further research.

Determinants of plasma Fatty Acid abnormalities in patients with active inflammatory bowel disease: a multivariate analysis.

: Patients with active inflammatory bowel disease (IBD) have increased levels of n3 and decreased levels of n6 plasma long-chain polyunsaturated fatty acids (LC-PUFA). Using multivariate statistical techniques, this study assessed the influence of the potentially important factors of diagnosis (ulcerative colitis versus Crohn's disease), disease activity, malnutrition, location of disease, therapy, age, and sex on these plasma fatty acid abnormalities. Plasma fatty acids were analyzed by semicapillary column gas-liquid chromatography in 73 patients with IBD and 107 healthy controls. The effect of each confounder upon either "low" (below the first quartile of the control group) or "high" (above the third quartile of the control group) levels of each fatty acid (FA) was assessed by means of stepwise logistic regression analyses. After controlling for these factors, disease activity remained the primary factor associated with changes in the plasma FA profile. Moderate/severe activity was significantly associated with low n6 LC-PUFA and was inversely related to high n3 LC-PUFA. Corticosteroid therapy was independently associated with high C16:0 and C18:2n6 plasma values and low C20:3n6 values and unsaturation index. Sulfasalazine therapy was inversely associated with low percentages of both C18:0 and C20:3n6. Hypoalbuminemia was significantly related only to low values of C18:0. No relationship between any confounder and high levels of n3 LC-PUFA was found. The observed relationships may be of importance in the pathogenesis and treatment of IBD.

Azathioprine without oral ciclosporin in the long-term maintenance of remission induced by intravenous ciclosporin in severe, steroid-refractory ulcerative colitis.

BACKGROUND: Intravenous ciclosporin is considered to be the only alternative to avoid surgery in severe, steroid-refractory ulcerative colitis. In responders, some authors recommend a switch to oral ciclosporin to act as a 'bridge' until the therapeutic action of azathioprine is achieved for maintenance treatment. AIM: To report the short- and long-term outcome of intravenous ciclosporin-responsive ulcerative colitis patients treated with oral azathioprine without oral ciclosporin. METHODS: The records of all patients treated with intravenous ciclosporin for severe, steroid-refractory ulcerative colitis were reviewed. Responders following treatment with azathioprine but without oral ciclosporin as maintenance therapy were included. Patients with colonic cytomegalovirus infection and/or follow-up of less than 1 year were excluded. RESULTS: Twenty-seven patients were included. Steroids were discontinued in 24 (89%). The median follow-up was 36 months. Eighteen (75%) patients presented mild or moderate relapses, which were easily managed with salicylates or steroids. Cumulative probabilities of relapse were 42%, 72% and 77% at 1, 3 and 5 years, respectively. Eleven (40.7%) patients underwent elective colectomy. Cumulative probabilities of colectomy were 29%, 35% and 42% at 1, 3 and 5 years, respectively. No opportunistic infections were observed. CONCLUSIONS: Oral azathioprine seems to be enough to maintain long-term remission induced by intravenous ciclosporin in patients with steroid-refractory ulcerative colitis. The 'bridging step' with oral ciclosporin may not be necessary in this subset of patients, although a randomized controlled trial is warranted to confirm this hypothesis.

Malnutrition-related polyunsaturated fatty acid changes in plasma lipid fractions of cirrhotic patients.

Cirrhotic patients have both impaired liver function and nutritional derangement. In fact, the prevalence of protein-energy malnutrition (PEM) is very high in these patients. The aim of the present study was to elucidate whether the nutritional status in cirrhosis could be an additional factor that would affect levels of plasma lipids. Plasma lipid phosphorus, cholesterol, and triglycerides (TG), and fatty acid profiles in plasma and plasma fractions were determined in 50 healthy subjects and 92 patients with liver cirrhosis. The cirrhotic patients were prospectively included in three groups according to the result of nutritional assessment: group 1 (n = 38), acceptable nutritional status (including well-nourished and mildly malnourished patients); group 2 (n = 29), moderate PEM; and group 3 (n = 25), severe PEM. The main findings of this study were that the decrease in plasma cholesterol and linoleic, dihomo-gamma-linolenic, and arachidonic acid levels of cirrhotic patients was related to the degree of PEM. Cholesteryl esters (CE) appeared to be the most sensitive indicator of lipid changes in cirrhosis. We consider that the role of malnutrition in the changes observed for polyunsaturated fatty acid (PUFA) profiles in plasma lipids of cirrhotic patients may be of major importance, since severe malnourished subjects exhibited the lowest levels of those compounds. Dietary supplementation of both essential fatty acids (EFA) and long-chain PUFA in adequate amounts to the cirrhotic patient might be of importance in the management of the disease.

Changes in mucosal fatty acid profile in inflammatorybowel disease and in experimental colitis: a common response to bowel inflammation.

BACKGROUND AND AIMS: Plasma polyunsaturated fatty acid profile in patients with inflammatory bowel disease is abnormal. We aimed to assess the mucosal fatty acid pattern in patients with ulcerative colitis and Crohn's disease, and in rats with trinitrobenzene-sulfonic acid (TNB) induced colitis. METHODS: Fatty acids were measured in colonic mucosa of patients with ulcerative colitis (n = 30), Crohn's disease (n = 21), and healthy controls (n = 13). Likewise, they were assessed in the colonic mucosa of rats with TNB- and sham-colitis. RESULTS: There was an increase of the end-products (C22:5n3, C22:6n3, C20:4n6, C22:5n6) and a decrease of the precursors (C18:3n3, C18:2n6) of both n3 and n6 polyunsaturated fatty acids in the mucosa of active ulcerative colitis and TNB-colitis. Also, high values of saturated (C16:0, C18:0) and low values of monounsaturated fatty acids (C18:1n9) were observed. Furthermore, the mucosa of active Crohn's disease showed substantial changes in saturated, monounsaturated and essential fatty acids, but not in polyunsaturated fatty acids. Mucosa of patients with inactive disease showed intermediate fatty acid values between the mucosa of active patients and healthy controls. CONCLUSIONS: Colonic inflammation causes a characteristic modification of the mucosal fatty acid profile which appears to be common to different aetiologies and seems to be related to the degree of inflammation.

Nutritional support in liver disease.

Protein-energy malnutrition is highly prevalent in patients with chronic liver disease, especially in those with advanced cirrhosis, and seems to influence their survival. Enteral and parenteral approaches to the treatment of alcoholic hepatitis have yielded controversial results. The use of polyunsaturated lecithin might be a promising alternative for the future. Enteral nutrition is the preferred way of providing artificial nutrition to patients with advanced cirrhosis. In some trials, it appears to improve the short-term survival of these patients. The long-term use of oral nutritional supplements may widen the scope of enteral nutrition in cirrhotic patients.

Low serum selenium concentration in a healthy population resident in Catalunya: a preliminary report.

Serum selenium levels were determined in 92 healthy subjects [40 men, 52 women; mean age 33.5 +/- 1.6 (s.e.m.) years, range 16-71 years] living in the province of Barcelona, Catalunya, Spain. Only well-nourished individuals with unremarkable clinical history, normal blood chemistry and haematological tests were selected. The subjects were divided into 6 age groups for each sex. Serum samples were analysed using a modification of the standard electrothermal graphite furnace atomic absorption spectrophotometry method to shorten the procedure while maintaining its accuracy. A significant correlation (y = -1.31 + 1.51 x; r = 0.9967, P less than 0.001) was observed between our method and the standard assay method. The mean serum selenium concentration was 60.39 micrograms/l, 95 per cent CI 53.35-67.45 micrograms/l. There were age- but no sex-group differences (P less than 0.001). This result is similar to that found in countries whose low selenium levels have been related to an increased risk of some disease states. Clinical and health implications of this suboptimal selenium status are discussed.

Polyunsaturated fatty acid deficiency in liver diseases: pathophysiological and clinical significance.

Polyunsaturated fatty acid (PUFA) deficiency occurs in advanced cirrhosis and other liver diseases (acute hepatitis, cholestasis). Long-chain PUFA deficit in cirrhosis is due to both essential fatty-acid (EFA) deficiency and impaired PUFA biosynthesis. Although hepatic insufficiency itself mostly accounts for this phenomenon, other factors such as associated malnutrition also play a role. PUFA deficiency in cirrhosis probably has a wide array of both cellular and clinical consequences, but, at present, they have been difficult to prove. In addition, the route, dosage, and safety of PUFA supplementation in these patients needs extensive investigation in the future.

How effective is enteral nutrition in inducing clinical remission in active Crohn's disease? A meta-analysis of the randomized clinical trials.

BACKGROUND: The purpose of the study was to evaluate, using meta-analysis techniques, whether enteral nutrition is effective in inducing clinical remission in active Crohn's disease. METHODS: Randomized trials either comparing enteral nutrition with steroids or comparing elemental (amino acid-based) with nonelemental diets were selected using MEDLINE (1984 to 1994), reference lists from published articles, reviews, and abstracts from major gastrointestinal meetings. Sixteen studies fulfilled the inclusion criteria (four published as abstracts). Crude rates for induction of remission were collected on an intention-to-treat basis by three independent observers. Each study was given a quality score, based on predetermined criteria. RESULTS: The pooled odds ratio (OR) for all type of enteral diets compared with steroid therapy was 0.35 (95% CI, 0.23 to 0.53). This result was similar for the best studies (by quality score) combined, for trials using tube feeding combined, and when noncompliant patients were withdrawn. Further subgroup analyses were conducted on the basis of the type of diet administered. Peptide-based diets were significantly inferior to steroids (pooled OR, 0.32; CI, 0.20 to 0.52). There was a trend to lower remission rate after elemental diets than after steroids (pooled OR, 0.44; CI 0.17 to 1.12). On the other hand, pooled OR for whole protein-based diets compared with elemental diets was 1.28 (CI, 0.40 to 4.02). CONCLUSIONS: Data available to date show that steroids are better than enteral nutrition to induce remission in active Crohn's disease. These results are more evident when peptide-based diets are administered, but they are not conclusive when either elemental or whole protein-based diets are used.

Impact of portacaval anastomosis on plasma fatty acid profile in cirrhosis: a randomized 24-month follow-up study.

BACKGROUND: Portacaval anastomosis has an hypolipemic effect in familial hypercholesterolemia and in healthy animals. In cirrhosis, it raises serum cholesterol, but there is no information on its effect upon plasma fatty acids. However, indirect data suggest that portacaval shunting might contribute to the polyunsaturated fatty acid deficit of these patients. We assessed the effect of portacaval anastomosis on plasma fatty acid profile in cirrhosis. METHODS: Forty-four Child-Pugh class A/B bleeding cirrhotics were randomized to be treated with portacaval anastomosis (n = 20) or nonsurgical therapy (n = 24). Fatty acid profile in plasma total lipids, alcohol intake, anthropometry, Child-Pugh score, serum cholesterol, triglycerides, and antioxidant micronutrients were assessed before and 3, 6, 12, 18, and 24 months after surgery or the start of nonsurgical therapy. Time course of plasma fatty acids was assessed using unbalanced repeated measures models with the above mentioned variables acting as covariates. RESULTS: No changes in the time course of percent plasma saturated, monounsaturated, and essential fatty acids were found between groups. Percent long-chain omega-6 and omega-3 polyunsaturated fatty acids decreased during follow-up in shunted patients compared with controls (p = .007 and p < .0005). However, this was not due to a true decrease in polyunsaturated fatty acid levels but to greater increases in saturated and monounsaturated fatty acid concentrations in shunted patients compared with control patients (p = .047 and p = .006). CONCLUSIONS: Portacaval anastomosis does not worsen plasma polyunsaturated fatty acid deficiency in cirrhosis. However, by increasing saturated and monounsaturated fatty acids, it further decreases plasma lipid unsaturation.

Liver function tests abnormalities in patients with inflammatory bowel disease receiving artificial nutrition: a prospective randomized study of total enteral nutrition vs total parenteral nutrition.

Liver and biliary abnormalities are well-known complications of inflammatory bowel disease (IBD). It has been suggested that using total parenteral nutrition (TPN) may further impair liver function in these patients; this seems not to be so with total enteral nutrition (TEN). However, prospective trials comparing the incidence of liver function test (LFT) abnormalities with either TPN or TEN have not been carried out. Twenty-nine IBD inpatients with normal LFT, randomized to receive either TEN with a polymeric diet or isocaloric, isonitrogenous "all-in-one" TPN because of protein-energy malnutrition and/or severe disease, were included in the study. Sixteen patients (five with ulcerative colitis and 11 with Crohn's disease) received TEN, and 13 patients (eight ulcerative colitis and five Crohn's disease) were on TPN. All patients were on systemic steroids, and nine of them were on oral metronidazole. Both groups were homogeneous regarding age, sex, diagnosis, disease activity, nutritional status, daily nutrient supply, and days on artificial nutrition. Serum albumin levels significantly increased with TEN (32 +/- 1 to 38.2 +/- 1.6 g/liter, p less than 0.01), but not with TPN (32.1 +/- 2.2 to 33.9 +/- 1.4 g/liter, NS). Clinical improvement occurred in both groups of patients as shown by the change in the disease activity indexes. In all cases, measurements of serum alkaline phosphatase, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase were performed weekly. There were no significant differences in the initial LFT between both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in liver function tests in patients with inflammatory bowel disease on enteral nutrition.

Morphologic and functional hepatic changes occur in inflammatory bowel disease (IBD). Patients with this disease often require the administration of artificial nutritional support. Liver function tests (LFT) derangement is a widely recognized side-effect of total parenteral nutrition (TPN). Therefore, the use of this modality of nutritional support may be an additional factor to cause hepatic damage in IBD patients. However whether or not the same occurs in patients receiving total enteral nutrition (TEN) is not well-established. The aim of the present study was to evaluate the effect of TEN upon LFT in patients with moderate to severe acute attacks of IBD, by means of a prospective, controlled, and nonrandomized design. Forty-nine patients were included; 29 (11 patients with ulcerative colitis and 18 with Crohn's disease) received TEN, and 20 (11 with ulcerative colitis and 9 with Crohn's disease) did not. Both groups were homogeneous regarding age, sex, disease activity index, nutritional status, and length of the study (24.8 +/- 1.3 vs 23.9 +/- 16.8 days). In all cases, weekly measurements of serum alkaline phosphatase, GOT, and GPT were performed. There were no significant differences in LFT at the beginning of the study between groups. The percentage of patients showing derangement of some LFT during the study did not differ between both groups: six of 29 (20.6%) in TEN group vs three of 20 (15%) in control group. Six out of the nine patients (in both groups) who developed LFT derangement had one or more causes, other than TEN for explaining hepatic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma polyunsaturated fatty acids in liver cirrhosis with or without chronic hepatic encephalopathy: a preliminary study.

Fatty acid levels (from C14:0 to C22:6n3) in plasma lipid fractions were prospectively studied in 11 cirrhotic patients with chronic hepatic encephalopathy and compared with those in 23 cirrhotic patients without chronic hepatic encephalopathy with similar age, sex distribution, and liver and nutritional status, and in 11 age- and sex-matched, healthy subjects. Plasma lipid fractions were separated by thin-layer chromatography and fatty acids were identified by capillary column gas-liquid chromatography. Total n6 polyunsaturated fatty acid plasma levels were lower in cirrhotic patients--with and without chronic hepatic encephalopathy--than in control subjects. In addition, arachidonic acid levels, both in total lipids and fractions, were lower in patients with than in those without chronic encephalopathy. On the other hand, a selective decrease of plasma docosahexaenoic acid (a major component of neuronal membranes) was observed in those patients with chronic encephalopathy as compared with both control and cirrhotic subjects without chronic encephalopathy. These findings may be due to various mechanisms. Differences in long-chain polyunsaturated fatty acid content in fish- and meat-restricted diets partly may account for these findings. However, it could be speculated that polyunsaturated fatty acid biosynthesis may be reduced further in patients with chronic hepatic encephalopathy because of either a decrease in portal essential fatty acid extraction in the postabsorptive phase due to portal-systemic shunting or to the effect of protein-restricted diets. Furthermore, the finding of low plasma docosahexaenoic acid in these patients raises the possibility that this deficiency might be an additional pathogenic factor in chronic hepatic encephalopathy.