Spectrum of gluten-sensitive enteropathy in first-degree relatives of patients with coeliac disease: clinical relevance of lymphocytic enteritis.

BACKGROUND: Limited data on a short series of patients suggest that lymphocytic enteritis (classically considered as latent coeliac disease) may produce symptoms of malabsorption, although the true prevalence of this situation is unknown. Serological markers of coeliac disease are of little diagnostic value in identifying these patients. AIMS: To evaluate the usefulness of human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy for the detection of gluten-sensitive enteropathy in first-degree relatives of patients with coeliac disease and to assess the clinical relevance of lymphocytic enteritis diagnosed with this screening strategy. PATIENTS AND METHODS: 221 first-degree relatives of 82 DQ2+ patients with coeliac disease were consecutively included. Duodenal biopsy (for histological examination and tissue transglutaminase antibody assay in culture supernatant) was carried out on all DQ2+ relatives. Clinical features, biochemical parameters and bone mineral density were recorded. RESULTS: 130 relatives (58.8%) were DQ2+, showing the following histological stages: 64 (49.2%) Marsh 0; 32 (24.6%) Marsh I; 1 (0.8%) Marsh II; 13 (10.0%) Marsh III; 15.4% refused the biopsy. 49 relatives showed gluten sensitive enteropathy, 46 with histological abnormalities and 3 with Marsh 0 but positive tissue transglutaminase antibody in culture supernatant. Only 17 of 221 relatives had positive serological markers. Differences in the diagnostic yield between the proposed strategy and serology were significant (22.2% v 7.2%, p<0.001). Relatives with Marsh I and Marsh II-III were more often symptomatic (56.3% and 53.8%, respectively) than relatives with normal mucosa (21.1%; p = 0.002). Marsh I relatives had more severe abdominal pain (p = 0.006), severe distension (p = 0.047) and anaemia (p = 0.038) than those with Marsh 0. The prevalence of abnormal bone mineral density was similar in relatives with Marsh I (37%) and Marsh III (44.4%). CONCLUSIONS: The high number of symptomatic patients with lymphocytic enteritis (Marsh I) supports the need for a strategy based on human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy in relatives of patients with coeliac disease and modifies the current concept that villous atrophy is required to prescribe a gluten-free diet.

Serum selenium and risk of large size colorectal adenomas in a geographical area with a low selenium status.

OBJECTIVE: Selenium is a fundamental nutrient to human health that might have anticarcinogenic effects. Previous studies have assessed the possible relationship of selenium status to colorectal adenomas with controversial results. We primarily aimed to assess the relationship of serum selenium status with the presence of large size colorectal adenomas in subjects living in a poor selenium region. The serum selenium status in colorectal cancer was also evaluated. METHODS: Serum selenium levels were measured in 28 patients with large size sporadic adenomatous polyps, 24 patients with colorectal adenocarcinomas, and 35 age-matched healthy individuals. A logistic regression analysis was performed to assess the relationship of serum selenium to colorectal adenomatous polyps after adjusting for confounding variables (age, sex, smoking habit, and alcohol drinking). RESULTS: Among subjects aged < or = 60 yr, mean serum selenium levels were significantly lower in both patient groups (adenoma, 57.9 +/- 4.3 microg/L; cancer, 43.7 +/- 6.6 microg/L) than in healthy controls (88.9 +/- 8 microg/L) (p = 0.0001). There were no difference among subjects > 60 yr old. A significant inverse association between selenium status and the diagnosis of large size adenomatous polyps after adjusting for confounding variables was found (adjusted p = 0.029). Subjects with higher selenium status (> or = 75th percentile value of 82.11 microg/L) had a lower probability (OR = 0.17, 95% CI = 0.03-0.84) to be in the adenoma group than subjects with lower selenium status (< 82.11 microg/L). This association was more marked in subjects aged < or = 60 yr (adjusted p value = 0.04, OR = 0.08, 95% CI = 0.007-0.91), and was not significant in older subjects. CONCLUSIONS: Results suggest that high selenium status may decrease the risk of large size adenomas in a low selenium region, and that this preventive effect seems to be exclusive to subjects < or = 60 yr. These results will need to be confirmed in additional epidemiological studies before recommending selenium supplementation in patients with colon adenomas.

Factors related to the presence of IgA class antineutrophil cytoplasmic antibodies in ulcerative colitis.

OBJECTIVES: Few studies have assessed the IgA antineutrophil cytoplasmic antibody (ANCA) positivity in ulcerative colitis patients and there is no information about factors related to its synthesis and its status after colectomy. The aims of the study were to assess the serum IgA ANCA prevalence in ulcerative colitis patients, both nonoperated and operated, and to determine the clinical factors related to this positivity. METHODS: Fifty-four ulcerative colitis patients, 63 ulcerative colitis colectomized patients (32 with Brooke's ileostomy and 31 with ileal pouch anal anastomosis), and 24 controls were studied. Antineutrophil cytoplasmic antibodies were detected by specific indirect immunofluorescent assays. RESULTS: The percentage of IgA ANCA was significantly higher in patients with ileal pouch anal anastomosis (45%) than in patients with Brooke's ileostomy (22%). There were no differences related to the presence of pouchitis in ileal pouch anal anastomosis patients. Patients with nonoperated extensive colitis (47%) had a significantly higher percentage of IgA ANCA than patients with proctitis (19%). Total percentage of ANCA (IgA and/or IgG) tended to be higher in ulcerative colitis and in patients with ileal pouch anal anastomosis than in patients with Brooke's ileostomy. However, in ileal pouch anal anastomosis patients, ANCA positivity was mainly due to exclusive IgA production. CONCLUSIONS: A substantial percentage of ulcerative colitis patients, and especially colectomized patients with ileal pouch anal anastomosis, had IgA ANCA, suggesting that ANCA production in ulcerative colitis might be stimulated by an immune reaction in the intestinal mucosa.

Plasma and mucosal fatty acid pattern in colectomized ulcerative colitis patients.

Patients with inflammatory bowel disease (IBD) have increased plasma n3 polyunsaturated fatty acids (PUFAs), which in ulcerative colitis (UC) patients persists six months after colectomy, suggesting a primary abnormality in fatty acid (FA) metabolism in IBD. This finding needed to be confirmed in a larger series of UC long-term colectomized patients. We aimed to assess the plasma FA pattern in UC colectomized patients with either Brooke's ileostomy (UC-BI) or ileal pouch anal anastomosis (UC-IPAA) and the mucosal FA pattern in the ileal reservoir of the UC-IPAA patients. Plasma FAs were assessed in 63 UC colectomized patients (31 with BI and 32 with IPAA) and 30 controls. In 26 UC-IPAA (8 with pouchitis and 18 without pouchitis) and in 13 healthy controls gut mucosal FAs were also investigated. FAs were detected by capillary column gas-liquid chromatography. Increased levels of saturated fatty acids (SFAs) and decreased percentages of monounsaturated fatty acids (MUFAs) were observed in both groups of patients. There were no changes in plasma n3 and n6 PUFAs. The mucosal FA pattern of the ileal reservoir consisted of increased long-chain PUFAs, specially n6 PUFA, and a decrease of their essential precursors. High percentages of SFAs and low percentages of MUFAs were also seen. The plasma FA profile previously described in IBD is not observed long-term after colectomy in UC, suggesting that it is related with the presence of inflamed intestine. High concentrations of SFAs and decreased percentages of MUFAs might represent early events in disturbed FA metabolism in IBD. The changes in FAs of the ileal reservoir, which closely resemble those found in human and experimental IBD, probably represent a common pattern of intestinal inflammation.

Antineutrophil cytoplasmic antibodies in sera from colectomised ulcerative colitis patients and its relation to the presence of pouchitis.

BACKGROUND: Few studies have evaluated the influence of colectomy on antineutrophil cytoplasmic antibody (ANCA) positivity in ulcerative colitis (UC). In small series of patients it has been suggested that ANCA positivity in UC might be predictive for development of pouchitis after colectomy. AIMS: To assess the prevalence of ANCA in UC patients treated by colectomy and a Brooke's ileostomy (UC-BI) or ileal pouch anal anastomosis (UC-IPAA), and the relation between the presence of ANCA, the type of surgery, and the presence of pouchitis. SUBJECTS: 63 UC patients treated by colectomy (32 with UC-BI and 31 with UC-IPAA), 54 UC, and 24 controls. METHODS: Samples were obtained at least two years after colectomy. ANCA were detected by indirect immunofluorescent assay. RESULTS: There were no differences between patients with (36.3%) or without pouchitis (35.0%) and between patients with UC (55%), UC-BI (40.6%), and UC-IPAA (35.4%). However, ANCA prevalence significantly decreases in the whole group of operated patients (38.0%) compared with non-operated UC (p = 0.044). CONCLUSIONS: The prevalence of ANCA in operated patients was significantly lower than in non-operated UC, suggesting that it might be related either to the presence of inflamed or diseased tissue. ANCA persistence is not related to the surgical procedure and it should not be used as a marker for predicting the development of pouchitis.

Changes of the mucosal n3 and n6 fatty acid status occur early in the colorectal adenoma-carcinoma sequence.

Despite data favouring a role of dietary fat in colonic carcinogenesis, no study has focused on tissue n3 and n6 fatty acid (FA) status in human colon adenoma-carcinoma sequence. Thus, FA profile was measured in plasma phospholipids of patients with colorectal cancer (n = 22), sporadic adenoma (n = 27), and normal colon (n = 12) (control group). Additionally, mucosal FAs were assessed in both diseased and normal mucosa of cancer (n = 15) and adenoma (n = 21) patients, and from normal mucosa of controls (n = 8). There were no differences in FA profile of both plasma phospholipids and normal mucosa, between adenoma and control patients. There were considerable differences, however, in FAs between diseased and paired normal mucosa of adenoma patients, with increases of linoleic (p = 0.02), dihomogammalinolenic (p = 0.014), and eicosapentaenoic (p = 0.012) acids, and decreases of alpha linolenic (p = 0.001) and arachidonic (p = 0.02) acids in diseased mucosa. A stepwise reduction of eicosapentaenoic acid concentrations in diseased mucosa from benign adenoma to the most advanced colon cancer was seen (p = 0.009). Cancer patients showed lower alpha linolenate (p = 0.002) and higher dihomogammalinolenate (p = 0.003) in diseased than in paired normal mucosa. In conclusion changes in tissue n3 and n6 FA status might participate in the early phases of the human colorectal carcinogenesis.

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.

Factors associated with low values of biochemical vitamin parameters in healthy subjects.

Levels of vitamins A, E, C, B1, B2, B6, B12, folate and beta-carotene were assessed in plasma or whole blood in a group of 114 healthy adults. Biochemical vitamin status was classified into acceptable or suboptimal (moderate or severe). The independent association of various factors with the finding of a suboptimal vitamin status was studied by means of logistic regression analyses. Seventy seven per cent of subjects had suboptimal vitamin status for vitamin B2, 20% for vitamin A, and 84% for beta-carotene. Although few subjects had suboptimal biochemical levels for vitamin E, plasma levels of this vitamin were significantly lower in smokers than in non-smokers (p < 0.01). Likewise, plasma folate levels were significantly related to body mass index and the season of blood sampling (p < 0.05). Old age was protective (OR 0.15; 95% CI 0.03-0.67), whereas current smoking was harmful (OR 3.63; 95% CI 1.09-12.1) for riboflavin status. Age group of 25-59 years was independently associated to a low risk of suboptimal vitamin A status (OR 0.29; 95% CI 0.09-0.88). On the other hand, female sex had a negative effect on plasma vitamin A levels (OR 2.39; 95% CI 0.82-6.92) and smoking had a harmful effect on biochemical beta-carotene status (OR 2.72; 95% CI 0.82-8.99). This cross sectional study provides information about the determinants of vitamin inadequacy, and may be the basis for further pathophysiological studies.

Abnormal plasma polyunsaturated fatty acid pattern in non-active inflammatory bowel disease.

An abnormal plasma polyunsaturated fatty acid pattern (PUFA) (increased n3 and decreased n6 PUFA) has been reported in active inflammatory bowel disease (IBD). The possibility of a primary defect in the PUFA metabolism in IBD was hypothesised. The aim of this study was to assess plasma PUFA pattern in inactive inflammatory bowel disease and to ascertain whether patients who had had a colectomy and who were suffering from ulcerative colitis have a similar PUFA pattern than those patients with non-active ulcerative colitis and who had not had a colectomy. Plasma fatty acids were analysed by semi-capillary column gas-liquid chromatography in three groups of patients with inactive IBD (24 patients with inactive ulcerative colitis who had not had a colectomy, 15 patients with ulcerative colitis who had had a colectomy, and 27 patients with Crohn's disease). Plasma concentration and percentage of C22:6n3 and unsaturation index were significantly higher in patients with inactive ulcerative colitis without a colectomy and the Crohn's disease group (p < 0.0001) than in controls. Plasma concentration and percentage of C22:6n3 and the unsaturation index remained significantly higher, in both the operated and non-operated ulcerative colitis patients when compared with controls (p < 0.0001). These results suggest that in inactive IBD, an increased PUFA biosynthesis might be the cause of the high values of n3 compounds. These findings although seen in active disease, are more noticeable in remission because of the lack of artefactual factors (malnutrition, steroids, inflammation). In addition, persistence of high values in both groups of ulcerative colitis patients--that is, those who had had a colectomy and those who had not suggests the existence of a primary abnormality in the PUFA metabolism in IBD.

Polymeric enteral diets as primary treatment of active Crohn's disease: a prospective steroid controlled trial.

Thirty two patients with active Crohn's disease were included in a controlled randomised trial to determine the efficacy and safety of polymeric enteral nutrition compared with steroids, to achieve and maintain clinical remission. The polymeric diet was administered through a fine bore nasogastric tube by continuous, pump assisted infusion (2800 (SEM 120) kcal/day). The steroid group received 1 mg/kg/day of prednisone. Both treatments were effective in inducing clinical remission: 15 of the 17 patients given steroids and 12 of the 15 patients assigned to the polymeric diet went into clinical remission (defined by a Van Hees index < 120) within four weeks of treatment. The percentage reduction of the Van Hees index was 34.8 (4.9)% for steroids and 32.3 (5)% for enteral nutrition (mean difference 2.5%; 95% CI--11.8% to +16.8%). Mean time elapsed to achieve remission was similar in both groups (2.0 (1) v 2.4 (1.2) weeks). Tolerance of the enteral diet was excellent. Four patients in the steroid group had mild complications attributable to this treatment. Ten patients (66.6%) in the steroid group and five (41.6%) in the enteral nutrition group relapsed within a year of discharge, but no differences were found in the cumulative probability of relapse during the follow up period. These results suggest that polymeric enteral nutrition is as safe and effective as steroids in inducing short term remission in active Crohn's disease.

The relationship of plasma polyunsaturated fatty acid deficiency with survival in advanced liver cirrhosis: multivariate analysis.

Total plasma fatty acids were measured in 101 cirrhotic inpatients (64 men, 37 women, aged 64.3 +/- 1.2 (SEM) yr; range, 34-80) who were subsequently followed for survival for a mean of 14.8 +/- 1.0 months. Data on plasma fatty acids have been published elsewhere. Individual values of these variables were categorized in a binary fashion using the 5th or the 95th percentiles of a group of 44 well-nourished healthy controls (24 men, 20 women, aged 51.3 +/- 2.1 yr; range, 32-76) as the cutoff limit. Forty-nine patients died during follow-up (2-yr cumulative probability of survival, 52%). Deficiency of palmitate, dihomo-tau-linolenate, and arachidonate (values below the 5th percentile) were univariately associated with death (long-rank test). However, after a multivariate analysis (Cox's proportional hazards regression), only the existence of plasma arachidonate deficiency was included in the final model (beta, 0.62; relative risk, 1.86; 95% CI, 1.06-3.25; p < 0.05). We conclude that arachidonic acid deficiency significantly increases the mortality risk in patients with advanced liver cirrhosis.

Routine tests of renal function, alcoholism, and nutrition improve the prognostic accuracy of Child-Pugh score in nonbleeding advanced cirrhotics.

In an attempt to improve the prognostic capacity of Child-Pugh score in nonbleeding cirrhotics, 110 consecutive in-patients without gastrointestinal hemorrhage at admission were studied and followed up for 24 months or until death. Fifty-five of the 110 patients (50%) died during this period. Mean survival time was 18.8 +/- 1.4 months (mean +/- SEM). In addition to Child-Pugh score, eight variables, including anthropometric nutritional parameters, routine renal function tests, and alcoholism markers, were recorded at admission. The ability of these variables to improve the prognostic capacity of the Child-Pugh score was assessed with the proportional hazard Cox's regression procedure, using a stepwise method for covariate selection, after including the Child-Pugh score at the first step. Thus, in addition to Child-Pugh score (beta = 0.302), three variables were included in the final model: serum urea (beta = 0.113), MCV (beta = 0.027), and mid-arm muscle circumference (beta = -0.025). According to the contribution of each of these factors to the model, a prognostic index was obtained to estimate survival in the individual patient. An assessment of the predictive power of the model was made by means of a split-sample technique. The prognostic index described in this study may contribute to improve the selection of nonbleeding patients with advanced cirrhosis to receive specific therapies such as transplantation. However, its true clinical relevance will be established only by prospectively comparing its prognostic value with that of the Child-Pugh score in a new sample of patients.

Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis.

To ascertain the role of total enteral nutrition, compared with total parenteral nutrition, as adjunct therapy to steroids in patients with severe acute ulcerative colitis, a prospective randomized trial was conducted in 42 of such patients. Inclusion criteria were the persistence of a moderate or severe attack of the disease (Truelove's index) after 48 h on full steroid treatment (prednisone 1 mg/kg/day). Patients were randomized to receive polymeric total enteral nutrition or isocaloric, isonitrogenous total parenteral nutrition as the sole nutritional support. Remission rate and need for colectomy were similar in both groups. No significant changes in anthropometric parameters were observed in either nutritional group at the end of the study. Median increase in serum albumin was 16.7% (-0.5% to +30.4%) in the enteral feeding group, and only 4.6% (-12.0% to +13.7%) in the parenteral nutrition patients (p = 0.019). Adverse effects related to artificial nutritional support were less frequent (9% vs. 35%, p = 0.046) and milder in enterally fed patients. Postoperative infections occurred more often with parenteral nutrition (p = 0.028). These results suggest that total enteral nutrition is safe and nutritionally effective in severe attacks of ulcerative colitis. It is also cheaper and associated with fewer complications than parenteral nutrition. Total enteral nutrition should be regarded as the most suitable type of nutritional support in these patients.

Prognostic factors of hepatic encephalopathy after portacaval anastomosis: a multivariate analysis in 50 patients.

Portacaval anastomosis has proved to be effective in avoiding active and recurrent hemorrhage from gastroesophageal varices in liver cirrhosis. However, hepatic encephalopathy is the most common and serious complication of this procedure. The aim of this study was to investigate by multivariate analysis the predictive factors of development of hepatic encephalopathy in 50 Child's A and B cirrhotic patients whose variceal bleeding was treated with emergency (n = 17) or elective (n = 33) portacaval anastomosis. The etiology of the cirrhosis was alcoholic in 74% of cases. The mean follow-up was 22.7 +/- 16.6 months (range 1-60 months). The 2-yr probability of suffering from at least one episode of hepatic encephalopathy in the overall group was 43%. The multivariate analyses (Cox's regression method) of 37 variables based upon clinical history, physical examination, and laboratory data disclosed that only five of these variables had independent predictive value: need for diuretic treatment in the days prior to surgery, absence of hepatomegaly, and serum levels of total bilirubin, gamma-globulin, and hemoglobin. According to the contribution of each one of these factors to the final model, a prognostic index was obtained which allowed the division of patients in two different groups of risk for developing hepatic encephalopathy (20% and 74%, respectively, after 2 yr of surgery; p = 0.0002). This index may help to better choose those candidates for portacaval anastomosis.

Plasma polyunsaturated fatty acid pattern in active inflammatory bowel disease.

Plasma fatty acid patterns were assessed by gas liquid chromatography in 73 patients with active inflammatory bowel disease and 107 healthy controls. The influence of the disease activity on fatty acid profile was also investigated. Plasma fatty acid patterns in patients with ulcerative colitis and Crohn's disease were similar. Plasma C18:3n3 and C22:6n3 were significantly higher in active ulcerative colitis (p = 0.0143 and p < 0.00001 respectively) and in Crohn's disease (p < 0.00001 for both) than in controls, whereas C20:3n6 was significantly lower in patients than in controls, both in ulcerative colitis (p = 0.0001) and in Crohn's disease (p = 0.0041). In more severe disease, plasma polyunsaturated fatty acid concentrations fell with a significant stepwise decrease in the desaturation index (p = 0.0031 in ulcerative colitis and p = 0.0355 in Crohn's disease). Even in patients with severe disease, however, plasma n3 fatty acids (C18:3n3 and C22:6n3) never fell below those of healthy controls. These findings suggest that in active inflammatory bowel disease, an increased biosynthesis might coexist with an increased consumption of polyunsaturated fatty acids. These observations may be of relevance in the pathogenesis of the disease as polyunsaturated fatty acids are involved in tissue eicosanoid synthesis and cellular membrane function, including that of immunocompetent cells. These results also question the rationale of using n3 polyunsaturated fatty acids in the treatment of inflammatory bowel disease.

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.

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.

Acute effects of abdominopelvic irradiation on the orocecal transit time: its relation to clinical symptoms, and bile salt and lactose malabsorption.

Twenty-five patients with abdominopelvic malignant tumors receiving irradiation were studied. The following items were assessed before, during, and at the end of the radiation period: 1) clinical symptoms, scored on the basis of their severity; 2) orocecal transit time (lactulose-H2 breath test); and 3) absorption of lactose and bile salts. Ninety-two percent of the patients showed clinical symptoms suggestive of acute radiation enteropathy, mainly diarrhea. A significant acceleration of the orocecal transit was observed during the study: 70 +/- 6.9 min vs 63.3 +/- 6.3 min vs 44.3 +/- 5.1 min (F = 5.49, p = 0.008), being faster in patients with severe diarrhea (F = 3.25, p = 0.05). Forty-four percent and 57% of the patients developed lactose and bile salt malabsorption, respectively. A decrease in the transit time was observed, independent of the absorption or malabsorption of such substances. However, the orocecal transit was faster in those lactose malabsorbers with severe diarrhea, than in those with mild diarrhea (F = 4.2, p = 0.03). The results suggest that acceleration of orocecal transit may be a major factor in the pathophysiology of radiation-induced diarrhea, whereas lactose malabsorption may contribute to the severity of the diarrhea.