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Biomedical subjects

E Stüber

Publications and source records attributed to E Stüber.

At least 19 recordsLinked to original sources
PubMed2005

Glutamine-enriched total parenteral nutrition in patients with inflammatory bowel disease.

BACKGROUND: Studies in animal models of inflammatory bowel disease (IBD) suggest that supplementation of total parenteral nutrition with glutamine (gln), a conditionally essential amino acid in catabolic conditions, increases gln plasma concentrations, reduces intestinal damage, improves nitrogen balance and may improve the course of the disease. However, human data supporting this assumption are missing. METHODS: A total of 24 consecutive patients with an acute exacerbation of IBD (19 Crohn's disease; five ulcerative colitis) and scheduled for total parenteral nutrition (TPN) (>7 days) were randomised. Parallel to a standardised anti-inflammatory therapy, the patients received either a TPN with 1.5 g/kg body weight of a standard amino acid or an isonitrogenic, isocaloric TPN with 1.2 g/kg body weight of a standard amino acid and 0.3 g/kg L-alanine-L-glutamine. Primary end points were gln plasma concentrations and intestinal permeability assessed by urinary lactulose and D-xylose ratio. RESULTS: Gln plasma levels did not differ significantly in either group throughout the study. Intestinal permeability did not change within 7 days either with or without gln supplementation (Delta-lactulose/xylose ratio: 0.01+/-0.05 (gln+) vs 0.02+/-0.1 (gln-)). The observed changes in inflammatory and nutritional parameters, and also disease activity, length of TPN and hospital stay, were independent of glutamine substitution. Five (41%) patients in the gln+ group and three (25%) patients in the gln- group needed surgical intervention. CONCLUSION: Although limited by the sample size, these results do not support the hypothesis that glutamine substitution has an obvious biochemical or clinical benefit in patients with active IBD scheduled for total parenteral nutrition.

Acute Disease↗
PubMed2002

Unusual course of colonic tattooing with India ink.

We here report the successful but unusual course of colonic tattooing in a patient with a carcinoma in situ in a polyp. A 70-year-old woman was admitted for persistent diarrhea, occult fecal blood, and anemia. During colonoscopy, a pedunculated large polyp in the sigmoid colon occluding the lumen was removed successfully. Histopathological examination revealed a carcinoma in situ with a resection of the peduncle in sano. At the second sigmoidoscopy, the polypectomy site was marked with India ink to facilitate the recovery of the polypectomy site in follow-up endoscopies. Three months later, the India ink had spread in the submucosal layer and a segment measuring 15 cm was colored dark blue. At the original polypectomy site, an uncolored flat mucosal proliferation was found above the dark colonic wall. After mucosectomy, the tissue was classified as hyperplastic. Six weeks later, a second control sigmoidoscopy did not show any suspicious mucosal alterations.

Adenoma, Villous↗
PubMed2002

[Recurrent sanguineous and mucous diarrhea and spasms in a 46-year-old woman--manifestation of endometriosis in the colon sigmoideum].

Intestinal endometriosis is the most frequent extragenital manifestation of this disease. Sometimes patients even present with acute bowel obstruction. We report on a 46-year-old woman complaining about recurrent sanguineous and mucous diarrhea and spasms for several years. Colonoscopy showed a stenosis in the sigmoid colon without macroscopically visible alterations of the mucosa. Computertomography, ultrasound and barium contrast enema did not provide us with further information about the origin of the stenosis. Biopsies out of the mucosa at the stenosis showed typical endometriosis tissue. After starting a conservative therapy with GnRH-agonist gosereline the patient became completely free of symptoms. The coincidence of endometriosis and M. Crohn has to be taken into consideration. Therapy planning should include a close co-operation with gynaecologists and surgeons to transfer the patient to surgical intervention when needed.

Colon, Sigmoid↗
PubMed2001

Identification of CCK-B/gastrin receptor splice variants in human peripheral blood mononuclear cells.

There is increasing evidence for a direct interaction of the enteric nervous and immune system. Receptors for neuropeptides such as VIP, somatostatin, and substance P have been characterised in human immuno-haematopoietic cells but little is known about the functional significance and expression of receptors for cholecystokinin (CCK) on cells of the immune system. There are only few studies that describe the expression of CCK receptors on human leukaemia-derived cell lines but the receptor structure and function in normal leukocytes have not been clearly established. We therefore sought to determine CCK receptor expression, structure, and function in nontransformed human peripheral blood mononuclear cells.Full-length cDNA clones encoding the human CCK-A and CCK-B/gastrin receptor are expressed in peripheral blood mononuclear cells from healthy volunteers without haematopoietic malignancy. In addition to wild-type CCK-B/gastrin receptor cDNAs, we isolated a splice variant with an in frame insertion of 69 amino acids within its putative third intracellular receptor loop. Dideoxy sequence analysis revealed that the cDNA of this splice variant comprises exons 1-4 but retains intron 4 (207 bp) in the absence of mutations within the splice donor sites. Transient expression of this splice variant in COS-7 cells reveals wild-type affinity for CCK-8, Gastrin-17, and antagonist L-365,260. Affinity for glycine-extended gastrin-17 was not increased when compared to the wild-type CCK-B/gastrin receptor. In vitro, gastrin decreased 3H-thymidine labelling in phytohaemagglutinin-pretreated mononuclear cells at a half-maximally effective concentration of 1.5 nM. We also isolated a cDNA encoding another splice variant of the CCK-B/gastrin receptor with a 158 bp deletion of the entire exon 4 sequence. We conclude that wild-type transcripts of both CCK receptor subtypes and splice variants of the CCK-B/gastrin receptor are expressed in nontransformed human mononuclear cells and that gastrin exhibits antiproliferative effects.

Alternative Splicing↗
PubMed2001

Interferon-gamma is not involved in the intestinal manifestations of the acute murine semiallogenic graft-versus-host disease.

BACKGROUND: The acute murine semiallogenic graft-versus-host disease (GvHD) is known to be associated with Th1 cytokines secreting lymphocytes in the spleen and lymph nodes. However, whether this cytokine secretion pattern is also involved in the intestinal manifestations of acute GvHD (crypt hyperplasia and villous atrophy) is not known, so far. METHODS: We first investigated the secretion of interleukin (IL) 4 (indicative of Th2-type differentiation) and interferon (IFN) 7 (Th1-type differentiation) by splenic and by small bowel lamina propria lymphocytes. In addition, animals were treated with neutralizing antibodies to IL-4 or IL-12. The effect of this treatment on the intestinal morphology was examined. Second, we also investigated the effect of donor-derived IFN-gamma by using donor lymphocytes from IFN-gamma knock-out animals. Third, animals were treated with the fusion protein OX40-Ig which interferes with the OX40-OX40L interaction and thereby inhibits the intestinal manifestations of acute GvHD. RESULTS: We found that, whereas splenic lymphocytes secrete an excess of IFN-gamma, lymphocytes of the intestinal lamina propria secrete less IFN-gamma and IL-4 than control animals. When OX40-Ig is administered to animals with acute GvHD, the intestinal histology normalizes as well as the secretion of IFN-y and IL-4, indicating that the intestinal morphology is not affected by the secretion of IFN-gamma by lamina propria lymphocytes. The treatment of animals suffering from acute GvHD with anti-IL-4 and anti-IL-12, which blocks the differentiation of IFN-gamma secreting T-lymphocytes, did not significantly affect the development of crypt hyperplasia or villous atrophy. Furthermore, donor lymphocytes of IFN-gamma knock-out animals also induced the intestinal manifestations of acute GvHD. CONCLUSIONS: These findings indicate that IFN-gamma is not crucial for the development of crypt hyperplasia and villous atrophy in the murine semiallogenic GvHD.

Animals↗
PubMed2000

The expression of OX40 in immunologically mediated diseases of the gastrointestinal tract (celiac disease, Crohn's disease, ulcerative colitis).

BACKGROUND: The membrane bound receptor OX40 (CD134) - a member of the TNF-R/NGF-R superfamily - is expressed on activated CD4+-T cells in humans and rodents. The interaction of OX40 with its ligand (OX40L) has been shown to be important in T-cell dependent B cell-stimulation and T-cell costimulation in vitro and in vivo. Several studies in experimental animal models for immunologically mediated GI-diseases have stressed the important role of the OX40-OX40L interaction for their manifestations. To assess if the OX40-OX40L interaction is also crucial in the pathogenesis of immunologically mediated diseases of the human gastrointestinal tract (e.g. celiac disease, Crohn's disease, ulcerative colitis) we investigated, in a first line of experiments, the expression of OX40 in biopsy specimens of patients suffering from these diseases. METHODS: The biopsies were formalin fixed and paraffin-embedded and cut into 5 microm slides. To demask the antigen, the slides were consecutively cooked in citrate buffer for 20 min. Binding of anti-OX40 antibody was detected using the alkaline phosphatase-anti-alkaline phosphatase (APAAP) method. RESULTS: Nine of 11 biopsy specimens of patients with celiac disease were OX40-positive; none of the 20 control duodenal biopsies demonstrated OX40-positivity; and all biopsies of patients with ulcerative colitis (n = 11) or Crohn's disease (n = 11), respectively, stained positively for OX40. One of the 20 control biopsies showed OX40 staining. DISCUSSION: OX40 is highly expressed in the gastrointestinal tissue of patients with immunologically mediated bowel diseases. Together with previous studies in animal models for these diseases, the present results point to a potential role of OX40 in their pathogenesis.

Adolescent↗
PubMed2000

Gallstones, the choledochoduodenal junction and initiation of acute pancreatitis: are two stones the culprits rather than one stone?

Reflux of biliary secretions into the pancreatic duct following gallstone obstruction of the common biliary pancreatic ampulla has been implicated as a cause of acute pancreatitis. However, the pancreatic duct pressure is higher than the biliary pressure and, therefore, the simple obstruction of the choledochoduodenal junction by one gallstone does not result in biliary pancreatic reflux. We propose a mechanism whereby simultaneous migration and sequential impaction above and below the common biliary pancreatic ampulla of two gallstones allows for the creation of a toxic bile-pancreatic juice mixture in the common bile duct, subsequent reversal of the pressure gradient and reflux of the toxic secretions into the pancreatic duct.

Acute Disease↗
PubMed1999

The effect of anti-gp39 treatment on the intestinal manifestations of acute murine graft-versus-host disease.

The changes in the intestinal morphology of murine T-cell-mediated acute semi-allogenic graft-versus-host disease (GvH) are characterized by lymphocytic infiltrates, crypt hyperplasia, and villous atrophy. In the present study, the role of CD40L (gp39)-an important member of the TNF/NGF superfamily of receptors and their ligands-for T-cell costimulation in vivo during the development of mucosal atrophy was investigated. We found that the inhibition of the CD40L-CD40 interaction in GvH animals by the administration of an anti-CD40L antibody (MR-1) completely prevents the development of crypt hyperplasia and villous atrophy in GvH animals. This includes a normalization of the rate of crypt cell apoptosis, which is augmented in untreated GvH animals. In conclusion, the CD40L-CD40 interaction is crucial in the pathogenesis of T-cell-mediated mucosal atrophy.

Acute Disease↗
PubMed1999

Linear IgA disease associated with lymphocytic colitis.

A 66-year-old woman presented with a bullous skin eruption and chronic diarrhoea. Lesional skin showed subepidermal blistering, and direct immunofluorescence of perilesional skin revealed linear deposits of IgA at the dermoepidermal junction, establishing a diagnosis of linear IgA disease (LAD). Chronic watery diarrhoea complicated by substantial loss of body weight preceded the skin eruption for several months. On endoscopy, the colon appeared macroscopically normal. On histology, the colon mucosa showed increased numbers of intraepithelial lymphocytes and infiltrates of mononuclear cells in the lamina propria, indicative of lymphocytic colitis. Treatment with methylprednisolone and dapsone led to complete clearing of the bullous skin eruption and marked improvement of the patient's diarrhoea. Gastrointestinal disorders such as lymphocytic colitis have rarely been reported in patients with LAD. Whether the simultaneous occurrence of these two diseases is coincidental or due to related pathogenetic mechanisms remains to be seen.

Aged↗
PubMed1999

Biliary pancreatic reflux-induced acute pancreatitis--myth or possibility?

OBJECTIVE: The mechanism whereby gallstone passage through the choledochoduodenal junction initiates acute pancreatitis is not known. We mimicked different patterns of stone impaction at the choledochoduodenal junction in a rabbit model and studied whether these result in biliary pancreatic reflux and the initiation of pancreatic inflammation. METHODS: In rabbits, catheters were introduced into the common bile duct (CBD) and the pancreatic duct. In five experiments, obstruction of these catheters at various time intervals mimicked different patterns of stone obstruction of both ducts prior to a stone impaction at the papilla of Vater: experiment I--no obstruction of the pancreatic duct and the CBD; experiment II--separate obstruction of the CBD and the pancreatic duct; experiment III--selective obstruction of the CBD; experiment IV--separate obstruction of the CBD and the pancreatic duct and subsequent decompression of the pancreatic duct; experiment V--obstruction pattern as in experiment IV associated with a bacterial infection of bile (10(8) E. coli/ml). Ductal pressures were recorded for 24 h. In order to study the effects of a subsequent impaction of the stone at the papilla of Vater, the catheters in the CBD and in the pancreatic duct were connected and mimicked a common channel behind a papillary stone. The flow direction of bile and pancreatic juice was directly observed. Pancreatic histology was analysed 24 h later. RESULTS: In experiments I-III, neither biliary pancreatic reflux nor acute pancreatitis was observed. In experiments IV and V, obstruction of the CBD caused an increase in the biliary pressure to 17 +/- 3 cm H2O, whereas the pancreatic duct pressure dropped to subnormal levels following obstruction and selective decompression (2 +/- 0.5 cm H2O). After the creation of a 'common channel', biliary pancreatic reflux was observed for 118 +/- 21 min. Flow of sterile bile into the pancreas was not harmful to the gland. Infected biliary pancreatic reflux initiated acute pancreatitis. CONCLUSIONS: 1. Bile flow into the pancreas may occur. 2. Biliary pancreatic reflux may initiate acute pancreatitis. 3. Bile reflux-induced acute pancreatitis requires previous biliary hypertension, temporary pancreatic duct obstruction, and the bacterial infection of choledochal secretions.

Acute Disease↗
PubMed1999

Intestinal crypt cell apoptosis in murine acute graft versus host disease is mediated by tumour necrosis factor alpha and not by the FasL-Fas interaction: effect of pentoxifylline on the development of mucosal atrophy.

BACKGROUND: Murine T cell mediated acute semiallogeneic graft versus host disease (GVHD) is characterised by lymphocytic infiltrates, crypt hyperplasia, and villous atrophy. It has been shown that programmed cell death (apoptosis) of the crypt epithelium takes place during the intestinal manifestation of acute GVHD. AIMS: To investigate which of the two most investigated inductors of apoptosis (Fas ligand (FasL) and tumour necrosis factor alpha (TNF-alpha)) is responsible for the induction of apoptosis in this animal model. METHODS: Animals undergoing acute semiallogeneic GvH reaction were treated with neutralising anti-TNF-alpha, two different anti-FasL antibodies, or pentoxifylline. RESULTS: Anti-TNF-alpha application inhibited the appearance of apoptotic cells in the intestinal mucosa, whereas anti-FasL antibodies had no influence on mucosal apoptosis. In addition, the transfer of FasL deficient (gld) donor lymphocytes still induced crypt cell apoptosis, villous atrophy, and crypt hyperplasia. Furthermore, when the animals were treated with pentoxifylline, a known inhibitor of TNF-alpha secretion in vitro and in vivo, there was significant normalisation of the intestinal morphology accompanied by inhibition of epithelial apoptosis. CONCLUSIONS: The FasL-Fas interaction is not involved in the induction of apoptosis during acute GVHD. However, neutralisation of TNF-alpha by an antibody or by pentoxifylline inhibits the occurrence of apoptosis and of mucosal atrophy in this animal model. These results have implications for the treatment of immunologically mediated human atrophic gut diseases-for example, diet refractory cases of coeliac disease.

Animals↗
PubMed1999

Association of lymphocytic colitis with linear IgA dermatosis.

The case of a 66-year-old female patient is presented, who suffered from chronic watery diarrhea. In addition, she developed linear IgA dermatosis after oral treatment of a presumed yeast infection with nystatin. To evaluate the reason for her diarrhea, colonoscopy was performed. The macroscopic aspect of the colon mucosa was described as normal with no specific alterations for chronic inflammatory bowel disease or for bacterial infections. In contrast, the histologic examination revealed the typical characteristics of lymphocytic colitis. This disease is thought to be caused by immunological reactions against as yet unknown luminal antigens. After treatment with steroids and dapsone the diarrhea as well as the skin disease disappeared. To our knowledge, the present report describes for the first time the association of linear IgA dermatosis with lymphocytic colitis after oral treatment with nystatin. A possible causative link between these two disease entities is discussed.

Administration, Oral↗