AIM: To investigate the prevalence of undernutrition, risk of malnutrition and obesity in the Italian gastroenterological population. METHODS: The Italian Hospital Gastroenterology Association ...conducted an observational, cross-sectional multicenter study. Weight, weight loss, and body mass index were evaluated. Undernutrition was defined as unintentional weight loss > 10% in the last threesix months. Values of Malnutrition Universal Screening Tool(MUST) > 2, NRS-2002 > 3, and Mini Nutritional Assessment(MNA) from 17 to 25 identified risk of malnutrition in outpatients, inpatients and elderly patients, respectively. A body mass index ≥ 30 indicated obesity. Gastrointestinal pathologies were categorized into acute, chronic and neoplastic diseases. RESULTS: A total of 513 patients participated in the study. The prevalence of undernutrition was 4.6% in outpatients and 19.6% in inpatients. Moreover, undernutrition was present in 4.3% of the gastrointestinal patients with chronic disease, 11.0% of those with acute disease, and 17.6% of those with cancer. The risk of malnutrition increased progressively and significantly in chronic, acute and neoplastic gastrointestinal diseases in inpatients and the elderly population. Logistical regression analysis confirmed that cancer was a risk factor for undernutrition(OR = 2.7; 95%CI: 1.2-6.44, P = 0.02). Obesity and overweight were more frequent in outpatients. CONCLUSION: More than 63% of outpatients and 80% of inpatients in gastroenterological centers suffered from significant changes in body composition and required specific nutritional competence and treatment.
No data are available on the variability in the clinical management of ulcerative colitis (UC) patients by Italian gastroenterologists. Therefore, improving the standards of UC care as provided by ...the National Welfare Clinical Path (PDTA), in accordance with the European Crohn’s and Colitis Organization (ECCO) guidelines for UC, is not easy.
To assess the management of UC by Italian gastroenterologists in a real-life setting taking into account its variability.
This prospective, cross-sectional, observational study included IBD-specialized gastroenterologists (GSIBDs) and general gastroenterologists (GGs) working in Italian public hospital units. Consecutive patients with an UC flare were enrolled and the medical treatment evaluated. For each center, the physician in charge of the study (16 GSIBDs and 10 GGs) was administered two electronic questionnaires.
Among 26 units, 573 UC patients were enrolled. Good adherence to the European guidelines was reported; GSIBDs reported greater adherence than GGs with a higher prescription of rectal and combination therapy in mild to moderate distal disease and a higher rate of hospitalization in severe UC.
The management of UC by Italian gastroenterologists in clinical practice is good according to the ECCO consensus recommendations, though some discrepancies are present between GSIBDs and GGs.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
3.
Leonardo da Vinci Meets Celiac Disease Zanchi, Chiara; Ventura, Giovanna; Di Leo, Grazia ...
Journal of pediatric gastroenterology and nutrition,
2013-February, Volume:
56, Issue:
2
Journal Article
Peer reviewed
Open access
ABSTRACT
Background and Aim:
Leonardo da Vinci's face symmetry derives from 3 equal craniofacial segments: trichion‐nasion (tn), which represents the superior third of the face, nasion‐subnasal (ns) ...that is the medium third of the face, and subnasal‐gnathion (sg) that is the length of the lower third of the face. It has been reported that adult subjects with celiac disease (CD) can be identified on the basis of a greater extension of the forehead in comparison to the medium third of the face, with a high tn/ns ratio. The aim of the present study was to investigate the correlation between facial asymmetry and CD in childhood and adulthood.
Methods:
We studied 126 biopsy‐proven patients with CD (76 children and 50 adults) and 102 healthy controls (43 children and 59 adults). Their faces were photographed; the pictures were edited using a software program to calculate the facial segments.
Results:
The tn length was significantly different between adult celiac and adult controls (7.43 ± 1.46 cm vs 6.38 ± 1.73 cm, P = 0.001). The cutoff of 6.5 cm tn, derived from receiver operating characteristic curve analysis, identified 43 of 50 patients (sensitivity 86%), but 34 of 59 controls were positive (specificity 54.2%). The positive predictive value was 56%; however, the tn/ns ratio was not significantly different between celiacs and controls. Neither the tn length nor the tn/ns ratio in celiacs correlated to the time of gluten exposure.
Conclusions:
Adults, but not children, with celiac disease show a forehead extension significantly greater than controls, but this test's specificity appears too low to be used in the screening of CD.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Abstract Objectives To evaluate the role of faecal calprotectin in consecutive outpatients referred for colonoscopy. Methods Outpatients undergoing colonoscopy at five participating institutions were ...eligible. Demographic and clinical data were collected. Faecal samples were tested at a single laboratory by means of a commercially available kit. Results We consecutively enrolled 870 patients. Mean levels of calprotectin were significantly higher in patients with neoplastic and inflammatory disorders when compared with subjects with a normal colonoscopy or trivial endoscopic findings. Elevated calprotectin levels (>50 mg/dl) were detected in 85% of patients with colorectal cancer, and 81% of those with inflammatory conditions but also in 37% of patients with normal or trivial endoscopic findings. In patients referred for chronic diarrhoea, sensitivity and negative predictive value were 100% in detecting either any organic colonic disease. In patients referred for symptoms of “suspected functional origin” sensitivity and negative predictive value for colorectal cancer were also 100%. Conclusions In unselected outpatients referred for colonoscopy, a single measurement of faecal calprotectin is not sufficiently accurate to identify those with significant colorectal disease. However, a normal result can help rule out organic disease among patients with diarrhoea and those with abdominal pain and/or constipation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
The pathogenesis of celiac disease (CD) is associated with polymorphisms in human leukocyte antigen (HLA) genes; however, compelling evidence suggests that additional non-HLA genes are associated ...with CD and related complications. The present study investigated whether killer cell immunoglobulin-like receptor (KIR)/HLA gene combinations are associated with CD and its clinical complications in the population of northeast Italy. The study included 61 adults affected by CD: 48 patients were at first diagnosis and 13 patients had CD-related complications (8 with refractory CD and 5 with cancer). Controls were 69 blood donors genotyped for KIR and HLA. Several statistically significant differences emerged between CD patients and blood donors. The results herein presented show that susceptibility to CD with refractory disease or cancer is associated with various genotypes including the 2DS2/2DL2+C1, 2DS3, 3DL1, and 2DL5B genes. In addition, the absence of the Bw4 ligand may be a predisposing factor for cancer. These results suggest that a KIR haplotype and HLA ligands may be involved in the susceptibility to important clinical CD complications such as tumors or refractoriness as a result of a gluten-free diet.
Celiac disease is induced by gliadin in genetically susceptible individuals expressing HLA-DQ2 or HLA-DQ8. The mechanisms underlying the expansion of interferon g-producing intraepithelial cytotoxic ...T lymphocytes (CTLs) and the destruction of the epithelial cells (EC) lining the small intestine of celiac patients have remained elusive. Intraepithelial lymphocytes (IELs) can undergo malignant transformation during the course of rare but severe complications of celiac disease: enteropathy associated T-cell lymphomas and refractory sprue. These complications support the idea that celiac disease IELs are permanently submitted to stimuli that promote their expansion and ultimately may favour their transformation. Altogether, these observations underline the importance of understanding the mechanism(s) that drives the expansion of IELs and their role in the pathogenesis of the epithelial lesions. A model enhanced presentation of gliadin peptides by DQ2 or DQ8 molecules to CD4 + cells in the lamina propria which results in secretion of interferon gamma and other cytokines that may be deleterious to gut epithelial cells, however gluten-specific IE-CTL could not be identified. To characterize T cells and protein expression in CD patients in relationship to severe complications, we used for the first time 2D-Dige approaches with well-characterized CD-associated gut biopsies. Fourteen adult patients diagnosed as CD were studied. All patients were characterized for the presence of anti-transglutaminase antibodies, VDJ-TcR and VDJ-BcR genescan pattern, HLA DQ and KIRs/ligand genotypes, villous atrophy, and to clinical response to gluten-free diet (13 out of 14 cases). One of these patients presented a restricted T cell population both in the peripheral blood as well as in the gut biopsy. Another patient presented a concomitant DLCL lymphoma. 2 further patients, with biopsies for intestinal disorders but with HLA-DQ2 and DQ8 negative, were used as controls. Patient with the T cell restriction pattern showed a prevalent Tg clone in peripheral blood and two identical over-expanded Tg clones in the peripheral blood a nd gut biopsy. Moreover in the gut biopsy it was also present a restricted Tb clone. Sequences from these 4 clones were reported in the EMBL database. HLA DQ2+D8 is found only in the case of CD-DLCL associated, 5 cases were DQ2 homozigote, 6 cases were DQ2 heterozygote (including the case with the restricted TCR pattern), 2 cases have neither DQ2 nor DQ8 heterodimer. A complete set of KIR with activating function (KIR2DS1, KIR2DS2, KIR2DS3, KIR2DS5 KIR3DS1) was present only in two samples, one of them with the T cell restricted pattern. Data from comparative protein expression obtained by 2D-Dige analysis, are in course. Although the number of control individuals and patients analysed were still low, the frequency of KIR with activating function was found to be higher in patients, particularly in sprue CD with T cell restriction, than in controls. This indicates that genotypic profiles of NK-T-CD patients may be characterized by an increased presence of activating KIRs.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Epomediol (EPO) is a synthetic terpenoid compound shown to be active in increasing bile flow and some enzymatic activities of liver plasma membranes in the rat. The possible effect of EPO treatment ...in the ethinyl-estradiol (EE) induced cholestasis in the rat was investigated by measuring the hepatic transport of sulfobromophthalein (BSP) (plasma clearance and biliary secretion) and bile flow. Liver plasma membrane fluidity was also determined by the steady state fluorescence polarization (P) of diphenylhexatriene (DPH). EE administration (5 mg/kg s.c. for 5 days) was followed by a significant, comparable reduction (P less than 0.001) in BSP plasma clearance and biliary excretion and in bile flow. Intraperitoneal administration of EPO (100 mg/kg) to EE-treated rats restored both parameters of BSP transport, as well as bile flow, to control values. Liver plasma membrane fluidity was markedly (P less than 0.01) decreased by EE administration with a concomitant reduction (P less than 0.01) in Na+/K+-ATPase activity. EPO administration significantly increased membrane fluidity to values higher either to cholestatic (P less than 0.05) or control (P less than 0.05) animals. On the contrary, EPO did not influence Na+/K+-ATPase activity in either EE-treated or control animals. These data indicate that EPO fully reverses the impairments of BSP transport and bile flow induced by EE, possibly by reversing the decrease in liver plasma membrane fluidity induced by the synthetic estrogen. On the contrary, the EE-mediated decrease in Na+/K+-ATPase activity was not reversed by EPO.
To investigate the role of sex steroids in the sex-related difference in the hepatic uptake of organic anions, sulphobromophthalein (bromsulphalein, BSP) transport was measured in hepatocytes ...isolated from rats either deprived of hormonal influence by castration at prepubertal age or after hormonal substitution. In control animals, the kinetics of BSP uptake showed the presence of two components: one saturable (0-3 microM), with high affinity and low capacity, and the other linear (9-30 microM), probably related to the non-specific component of BSP uptake. Sex difference was detected only in the saturable portion of the uptake process as the apparent Km was significantly lower in females than in males (3.8 +/- 0.7 vs. 6.1 +/- 1.8 microM, mean +/- S.D. of six animals, P less than 0.01). In contrast, no difference was observed in Vmax (2.3 +/- 0.3 vs. 2.2 +/- 0.7 nmol BSP.(mg protein)-1.min-1). Castration was associated with the disappearance of the saturable uptake site and abolished the sex difference. Progesterone treatment of castrated males failed to restore the saturable kinetics of BSP uptake. In contrast, administration of oestradiol to castrated males or testosterone to castrated females did restore the saturable kinetics of the high-affinity BSP uptake. Km and Vmax were comparable to those of adult females and males, respectively, with the exception of testosterone which induced a Vmax value higher than that observed in the other groups of animals. These data suggest that the influence of oestrogen and testosterone is necessary for the expression of the high-affinity, low-capacity carrier-mediated process of hepatic BSP uptake.
The diagnostic value of the nicotinic acid (NA)-induced hyperbilirubinaemia was compared with that resulting from caloric restriction in 40 patients with Gilbert's syndrome (GS) and 20 controls. Both ...tests resulted in a significant higher level of serum bilirubin in GS than in controls (P less than 0.001). When the serum bilirubin level 240 min after NA administration (5.9 mumol/kg i.v.) was higher than 18 mumoles/l, this test had a specificity and sensitivity of 100%, both in males and females with the syndrome. The discriminatory value of the test was lower when either the area under the time concentration curve or the maximal increment of serum unconjugated bilirubin were used. Reduction in caloric intake (400 calories/day) showed a lower specificity and sensitivity than the NA test, particularly in females. An increment of bilirubin at 24 h greater than 15 mumoles/l was more diagnostic than an increase by 100% or more over the pre-diet value. The efficacy was not improved by prolonging the test for additional 24 h. From these data we conclude that NA-induced hyperbilirubinaemia and, in particular the concentration of the pigment 240 min after drug administration, is more efficient than fasting-induced hyperbilirubinaemia in the diagnosis of the Gilbert's syndrome both in males and in females.
The increments in serum concentrations of unconjugated bilirubin and free fatty acids (FFA) were measured 24 and 48 h after reduction of the caloric intake (400 cal/day) in 17 patients with Gilbert's ...syndrome (GS) and in 12 healthy control subjects. In males, both normal and with GS, the rise in serum bilirubin was statistically higher (p less than 0.01) as compared to females. On the contrary, no sex difference was found in FFA concentrations. A linear correlation (p less than 0.01) between bilirubin and FFA serum levels was present in normal males and in patients with Gilbert's syndrome of both sexes. Because bilirubin and FFA partly share a common, bilitranslocase-mediated, hepatic uptake mechanism, data reported support the hypothesis that a bilitranslocase function may be one of the metabolic defects in Gilbert's syndrome.
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