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At least 595 records · Page 33Linked to original sources
PubMed2005

Diltiazem inhibits human intestinal cytochrome P450 3A (CYP3A) activity in vivo without altering the expression of intestinal mRNA or protein.

AIMS: To determine the effect of diltiazem on intestinal CYP3A activity and protein and mRNA expression in vivo in healthy subjects. METHODS: Intestinal biopsies were obtained from ten healthy controls and from ten healthy subjects after receiving diltiazem 120 mg bid for 7 days. Intestinal CYP3A activity, CYP3A4 protein and mRNA concentrations were quantified in both groups. Intestinal CYP3A activity was determined by incubation of small bowel homogenate with midazolam (25 microM) and NADPH for 5 min and the rate of formation of 1'-hydroxymidazolam was quantified. RESULTS: All subjects in the treatment group had detectable diltiazem concentration in the serum. While there was no significant difference in CYP3A4 protein and mRNA expression between the control and treatment groups, the formation of 1'-hydroxymidazolam (446 pmol min(-1) mg(-1) 6 (control) vs. 170 (CI 112, 228) pmol min(-1) mg(-1) 95% confidence interval (CI 269, 623) (diltiazem group)) was significantly reduced (P < 0.05). CONCLUSION: Diltiazem decreased small bowel CYP3A activity by 62% as a result of irreversible inhibition with no corresponding change in intestinal CYP3A4 mRNA or protein concentrations.

Adult↗
PubMed2006

Immunohistochemical distinction of intestinal-type sinonasal adenocarcinoma from metastatic adenocarcinoma of intestinal origin.

OBJECTIVES: Distinction of intestinal-type sinonasal adenocarcinoma (ITAC) from adenocarcinoma of intestinal origin metastatic to the sinonasal cavity may be extremely difficult on histologic grounds alone. We studied the role of cytokeratin (CK) and mucin (MUC) expression in differentiating ITAC, metastatic adenocarcinoma of intestinal origin, and non-intestinal-type sinonasal adenocarcinoma (non-ITAC). METHODS: We stained specimens from 5 cases of ITAC and 4 cases of non-ITAC, along with 4 colonic and 3 duodenal adenocarcinoma controls, with CK7 and CK20, MUC2 and MUC5, neuron-specific enolase (NSE), chromogranin (CHR), and carcinoembryonic antigen (CEA) in order to examine the possible combinations of markers that best aid in the diagnosis of these lesions. We also performed a retrospective review of our clinical experience with these rare lesions. RESULTS: CK7 staining was positive in all ITAC and non-ITAC cases, whereas all cases displaying gastrointestinal-type differentiation (ITAC and metastatic intestinal cases) stained positive for both CK20 and MUC2. Staining for MUC5, NSE, CHR, and CEA was variable. CONCLUSIONS: Tumors with the CK7+, CK20+, MUC2+ immunophenotype are likely primary sinonasal lesions, whereas tumors with the CK7-, CK20+, MUC2+ profile warrant further clinical evaluation to exclude metastatic disease from the gastrointestinal tract. Complete surgical resection of ITAC remains the mainstay of therapy.

Adenocarcinoma↗
PubMed2005

Practical guide to intestinal rehabilitation for postresection intestinal failure: a case study.

After massive small-intestinal resection or combined small-intestinal and colonic resection, diarrhea with resulting dehydration, electrolyte abnormalities, and malnutrition occur. Many patients become dependent on IV fluids and nutrition. An adaptation process manifested clinically by decreased diarrhea and improved nutrient absorption according to decreased parenteral nutrition and fluid requirements has been noted to occur over time. In some patients, adaptation is inadequate and may require special techniques to enhance and augment this process. This is a case of a 52-year-old woman who experienced increased stoma output 1 week after major intestinal resection, resulting in dehydration. She required IV fluids in order to maintain hydration. After the initiation of an intestinal rehabilitation program, which included modified diet, soluble fiber, oral rehydration solution (ORS), and medications, IV fluids were successfully weaned off in 3 months. She continues not to receive IV fluids and continues to follow the intestinal rehabilitation plan.

Crohn Disease↗
PubMed2001

Secretory transport of p-aminohippuric acid across intestinal epithelial cells in Caco-2 cells and isolated intestinal tissue.

The intestinal transport of an organic anion, p-aminohippuric acid (PAH), was studied in Caco-2 cell monolayers and rat intestinal tissue mounted in Ussing chambers. In both experimental methods, PAH exhibited vectorial transport with significantly greater permeability in the secretory direction than the absorptive direction, indicating net secretion. This secretory transport required metabolic energy, but protons or hydroxyl ions were not involved as the driving force. In Caco-2 monolayers, secretory transport of [3H]PAH was decreased, and the intracellular accumulation of PAH was increased with increasing concentration of unlabelled PAH at the basolateral side. Addition of probenecid and genistein at the basolateral side decreased the secretory transport of [3H]PAH; the accumulation was not changed by probenecid, but was increased by genistein. In addition, the initial uptake rate of [3H]PAH from the basolateral side was decreased by both PAH and probenecid, but not by genistein. Therefore, it is suggested that the transport of PAH in Caco-2 cells is regulated by several transporters: a genistein-sensitive transporter on the apical membrane and probenecid-sensitive transporters on both the basolateral and apical membranes. In rat intestinal tissues, the transport rate of PAH showed regional variation (ileum > jejunum > duodenum), suggesting that secretory transporters with high activity exist predominantly in the lower region of the small intestine. The results suggest that PAH transport in both Caco-2 cells and rat intestinal tissues is regulated by multiple transporters on the apical and basolateral membranes, and these transporters have different characteristics.

Animals↗
PubMed1999

[Guidelines on intestinal dysmicrobism (SIBO Small Intestine Bacterial Overgrowth)].

Bacterial flora consisting of Gram-positive and Gram-negative germs, aerobes and anaerobes, is distributed along the digestive tract in varying quantities from zero to a maximum of 10(12)/ml of endoluminal aspirate. This bacterial ecosystem counterbalances with the ecological niche of the host organism and harmonizes with the various digestive, secretory, motor, absorption and sensitivity functions of the entire intestine. This dynamic equilibrium between environment, bacterial flora and host may be interrupted due to a variety of complex reasons, leading to quantitative and qualitative modifications of the normal intestinal microbial flora that can cause Small Intestinal Bacterial Overgrowth (SIBO). SIBO is thus due to an invasion of the small intestine, from the upper part, by pathogenic strains of oro-alimentary origin, and from the lower part by colo-fecal germs through an incontinent Bauhin's valve. These germs alter the normal intestinal functions and give rise to a form of diarrhoea in which the characteristics of malabsorption prevail, with all the inherent diagnostic problems. The diagnostic gold standard is the culture of the duodenal-jejunal aspirate which, being difficult to perform and providing unreliable results, is not easily included in the daily clinical routine. Indirect tests include the breath test, which is widely accepted by patients but burdened by diagnostic doubts on the part of medical personnel. Diagnostic confirmation is therefore greatly conditioned by clinical subjectivity and objectivity, as well as by the response to medical therapy. In cases of declared malabsorption, medical therapy is necessary by means of appropriate diet, prebiotics, probiotics and antibiotics. The difficulty in identifying the specific bacterial population and the part of the digestive tract that is affected indicate the appropriateness of a broad-spectrum antibiotic therapy, capable of eradicating aerobes and anaerobes, preferably with a topical rather than a general action, frequently cause of undesired effects.

English Abstract↗
PubMed1980

Dependence of gastro-intestinal tumors on gastro-intestinal hormones: pentagastrin stimulates growth of transplanted colon adenocarcinoma in mice.

Gastrin was administered several times to mice with transplantable hepatoma, sarcomas, colon adenocarcinoma and adenocarcinoma of small intestine. Injections of gastrin stimulated the growth of colon adenocarcinoma in mice but not of the other tumors tested. Dependence upon gastro-intestinal hormones of "spontaneous" carcinogenesis in gastro-intestinal tract and the growth of many gastro-intestinal pancreatic and liver tumors is suggested. This hormone dependence could be used for the treatment and prophylaxis of some tumors of the gastro-intestinal tract.

Adenocarcinoma↗
PubMed1997

Bacterial lipopolysaccharide reduced intestinal barrier function and altered localization of 7H6 antigen in IEC-6 rat intestinal crypt cells.

The intestinal epithelial barrier restricts the passage of potentially toxic substances into the systemic circulation and is considered to be mostly mediated by tight junctions, though the mechanisms involved in the regulation of intestinal tight junctions are not yet fully understood. In the present study, we examined whether bacterial lipopolysaccharide (LPS) altered the barrier function of tight junction and localization of tight junctional proteins, ZO-1 and 7H6 antigen, in IEC-6 intestinal cells. Administration of LPS to the basolateral surface of IEC-6 cells disrupted the barrier function and caused the disappearance of 7H6 antigen from the cell border, whereas LPS administered to the apical surface altered neither the barrier function nor the localization of 7H6 antigen in IEC-6 cells. On the other hand, the localization of ZO-1 was not influenced by these treatments of LPS. These results suggest that the interaction of LPS with the basolateral surface of intestinal epithelial cells disrupts the barrier function and 7H6 antigen take part in the maintenance of the barrier function in IEC-6 cells.

Animals↗
PubMed1995

Mature cystic teratomas of the ovary with intestinal wall structures harboring intestinal- type epithelial neoplasms.

Mature cystic teratomas of the ovary frequently contain intestinal-type tissues, but these rarely organize into complete intestinal walls, including all layers, and even more rarely develop secondary neoplasms. The present report documents two mature teratomas with formation of complete segments of intestinal wall, one also containing a benign mucinous cystadenoma of the appendiceal type and the other an intestinal-type adenocarcinoma infiltrating into the neoplastic bowel wall but not the surrounding ovarian parenchyma. The latter patient is alive and well 5 years after surgery. These cases expand the repertoire of secondary neoplasms, benign and malignant, developing in mature cystic teratomas.

Adenocarcinoma↗
PubMed1995

Quadruple colocalization of calretinin, calcitonin gene-related peptide, vasoactive intestinal peptide, and substance P in fibers within the villi of the rat intestine.

Double-labeling immunofluorescent histochemistry demonstrates that calretinin, a calcium-binding protein, coexists with calcitonin gene-related peptide, vasoactive intestinal peptide, and substance P in the fibers innervating the lamina propria of the rat intestinal villi. An acetylcholinesterase histochemical stain revealed that the majority of calretinin-containing cells in the myenteric ganglia were cholinergic and that about one half of the submucosal calretinin-containing cells colocalized with acetylcholinesterase. In situ hybridization studies confirmed the presence of calretinin mRNA in the dorsal root ganglia, and a ribonuclease protection assay verified the presence of calretinin message in the intestine. The coexistence of calretinin in calcitonin-gene-related-peptide-containing cells that also contained substance P and vasoactive intestinal polypeptide in the dorsal root ganglia suggest that these ganglia are the source of the quadruple colocalization within the sensory fibers of the villi. Although the function of calretinin in these nerves is unknown, it is hypothesized that the coexistence of three potent vasodilatory peptides influences the uptake of metabolized food products within the vasculature of the villi.

Animals↗
PubMed1992

Intestinal fatty acid-binding protein as a sensitive marker of intestinal ischemia.

Determination of the serum level of intestinal fatty acid-binding protein has been used to detect rat intestinal ischemia following ligation or 30-min occlusion of the superior mesenteric artery. The normal values were under the minimal detectable level of less than 2 ng/ml in all the 10 rats. The serum fatty acid-binding protein level increased rapidly, to 340.7 +/- 54.6, 438.5 +/- 40.1, 388.1 +/- 37.4, and 292.2 +/- 95.7 ng/ml (P less than 0.01) at 1, 2, 4, and 8 hr after ligation, respectively. It also increased, to 347.2 +/- 127.7 ng/ml (P less than 0.01) at 1 hr, after a 30-min transient occlusion and then returned to a normal level. Histological studies showed destruction of the villi, disappearance of the mucosa, and transmural necrosis with the progress of time after ligation, while no remarkable morphological change was observed following 30-min transient occlusion. These observations strongly suggest that the intestinal fatty acid-binding protein is a useful biochemical marker for intestinal ischemia, particularly in the early reversible phase.

Alkaline Phosphatase↗
PubMed1978

[Closed intestinal decompression in postoperative paralysis: intestinal intubation (author's transl)].

Paralytic distension is a causative or important factor in the pathogenesis of early postoperative intestinal obstruction. The elimination of intestinal distension initiates a decisive change in the course of this disease. The long intestinal tube--comparable to an "intraluminary stoma"--renders the necessary intestinal decompression. The controlled placement of the tube using a gastroscope rules out technical problems. The procedure is highly effective, contributes to the reduction of relaparotomies, and avoids enterotomies with all their inherent risks in the state of ileus.

Gastroscopy↗
PubMed1999

Small-intestinal enteroliths--unusual cause of small-intestinal obstruction: report of three cases.

PURPOSE: The aim of this study was to report on a rare cause of small-intestinal obstruction caused by small-intestinal enteroliths. METHODS: We present three different cases of enterolith formation in the small intestine. One occurred after nontropical sprue, one patient had multiple jejunal diverticula, and another patient had enterolith formation in a blind loop after a small-bowel side-to-side anastomosis. RESULTS: After initial conservative therapeutic approach all patients underwent surgery. In two patients the enteroliths were removed by ileotomy or jejunostomy. In the third patient the bowel anastomosis had to be revised after removal of the enterolith. CONCLUSION: Small-intestinal enteroliths may cause small-bowel obstruction. The first therapeutic approach is nonsurgical; however, if obstruction proceeds, surgical removal with or without revision of underlying pathology is necessary. We discuss the causes and therapeutic management of enteroliths and give a review of related literature.

Adult↗
PubMed1977

Acute distal intestinal obstruction in gnotobiotic rats. Intestinal morphology and cell renewal.

1. Complete mechanical obstruction of the distal small intestine was produced in gnotobiotic rats. 72 h after the operation small intestinal morphology and epithelial cell renewal were investigated proximal and distal to the site of obstruction. 2. Proximal to the site of obstruction there were minor changes in villus height, base length and in villus cell number, a large increase in depth and diameter of the crypts and an approximately threefold increase in cell renewal. 3. Distal to the site of obstruction there were no differences between the intestines of rats with obstruction and controls. 4. The apparent lack of secretion by the goblet cells and the reduced number of intraepithelial leucocytes suggest that the barrier function of the small intestine is impaired in obstruction.

Animals↗
PubMed1998

Phenotypic and functional characteristics of intestinal intraepithelial lymphocytes during acute rejection of small intestinal allografts.

Infiltration of a transplanted organ by host lymphoid cells is the hallmark of acute rejection. However, after intestinal transplantation, physiological lymphocyte migration may lead to host cell infiltration of the graft even in the absence of rejection. It is unclear whether this lymphocyte migration also involves the intraepithelial compartment of the graft or whether infiltration there is indicative of acute rejection. We demonstrate here that host cell infiltration of the intestinal mucosa occurs both during acute rejection of a small bowel allograft and, to a lesser extent, when rejection is prevented by immunosuppression with FK506. The infiltrating host cells consisted of CD3+ T cells with a predominant CD4-CD8+ phenotype resembling intraepithelial lymphocytes (IELs). Functional studies showed that the nonspecific cytolytic activity of IELs was not affected by acute rejection or by immunosuppression with FK506. These findings indicate that host cell infiltration of the intestinal mucosa does not connote an ongoing acute rejection. Furthermore, the decreased mucosal barrier function during acute rejection of intestinal allgrafts is probably not due to impaired cytolytic activity of IELs.

Animals↗
PubMed1997

Anally projecting neurons exhibiting immunoreactivity to galanin, nitric oxide synthase and vasoactive intestinal peptide, detected by confocal laser scanning microscopy, in the intestine of the Atlantic cod, Gadus morhua.

The projections of enteric neurons showing immunoreactivity for vasoactive intestinal peptide (VIP), nitric oxide synthase (NOS) and galanin were investigated in the myenteric plexus of the intestine of the Atlantic cod, Gadus morhua. Quantification of immunoreactive material on the proximal and distal side of a myotomy was performed by means of confocal laser scanning microscopy. NOS immunoreactivity was reduced anal to the myotomy, whereas there was an accumulation of immunoreactivity for VIP and for galanin oral to the cut. These results suggest the presence of VIP, NOS and galanin in neurons with oral-to-anal projections along the intestine of the cod. Since descending neurons in the myenteric plexus of many other vertebrates also contain these substances, we conclude that the oral-to-anal projections of neurons containing VIP, NOS and galanin are highly conserved features and important for the descending phase of intestinal peristalsis on an evolutionary basis.

Anal Canal↗
PubMed1999

Intestinal permeability, leaky gut, and intestinal disorders.

A major task of the intestine is to form a defensive barrier to prevent absorption of damaging substances from the external environment. This protective function of the intestinal mucosa is called permeability. Clinicians can use inert, nonmetabolized sugars such as mannitol, rhamnose, or lactulose to measure the permeability barrier or the degree of leakiness of the intestinal mucosa. Ample evidence indicates that permeability is increased in most patients with Crohn's disease and in 10% to 20% of their clinically healthy relatives. The abnormal leakiness of the mucosa in Crohn's patients and their relatives can be greatly amplified by aspirin preadministration. Permeability measurements in Crohn's patients reflect the activity, extent, and distribution of the disease and may allow us to predict the likelihood of recurrence after surgery or medically induced remission. Permeability is also increased in celiac disease and by trauma, burns, and nonsteroidal anti-inflammatory drugs. The major determinant of the rate of intestinal permeability is the opening or closure of the tight junctions between enterocytes in the paracellular space. As we broaden our understanding of the mechanisms and agents that control the degree of leakiness of the tight junctions, we will be increasingly able to use permeability measurements to study the etiology and pathogenesis of various disorders and to design or monitor therapies for their management.

Celiac Disease↗
PubMed1985

Intestinal pseudoobstruction caused by diffuse lymphoid infiltration of the small intestine.

Four young women presented with diarrhea, malabsorption, and intestinal pseudoobstruction. Intestinal biopsy specimens (both peroral and full-thickness) showed flat small intestinal mucosa, sparsity of crypts, and a widespread lymphoid infiltrate in the lamina propria, muscularis propria, and myenteric plexus. There was no neuron or nerve fiber loss or damage in the plexus; muscle cell absence in the vicinity of lymphoid cell infiltration in the muscularis propria probably accounted for the pathogenesis of pseudoobstruction. Immunochemical stains showed that the infiltrate was polyclonal, and none of the patients has developed lymphoma on clinical follow-up of 4-16 yr. Transient improvement in symptoms occurred after antibiotic therapy in 3 patients, and 1 patient had improvement after treatment with cyclophosphamide and prednisone; however, symptoms of pseudoobstruction persist in all. These cases illustrate yet another cause of intestinal pseudoobstruction which is histologically distinct from visceral myopathies and neuropathies. The pathogenesis of this illness may be related to that of diffuse immunoproliferative diseases seen in Third World countries.

Adolescent↗
PubMed1989

Effects of prepro-vasoactive intestinal polypeptide-derived peptides on net fluid flux in small intestine of anesthetized rats.

Intravenous infusion of low doses of vasoactive intestinal polypeptide, peptide histidine valine-42, and peptide histidine methionine (and the rat equivalent, peptide histidine isoleucine) into anesthetized rats caused a reduction in net absorption of fluid from the small intestine. Larger doses caused a net fluid secretion. At the same nominal infusion rates, peptide histidine valine-42 appeared to be the most potent. In terms of plasma concentrations achieved, however, vasoactive intestinal polypeptide was approximately six times more active than the other two human peptides. If confirmed in humans, these results would suggest that peptide histidine methionine and peptide histidine valine may be as important as vasoactive intestinal polypeptide in causing the watery diarrhea seen in the Verner-Morrison syndrome in which plasma levels of all three peptides are raised.

Absorption↗