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At least 1,009 records · Page 56Linked to original sources
PubMed2004

Cytokines as therapeutic targets for the gastrointestinal manifestations of scleroderma.

Systemic sclerosis (SSc), or scleroderma, is a connective tissue disorder characterized by progressive fibrosis of the skin and internal organs. It has significance for gastroenterologists because the gastrointestinal tract is involved in 90% of SSc patients, who often present with esophageal dysfunction. Though the exact pathogenesis of SSc is unknown, there is increasing evidence supporting an immune mechanism. Cytokines are the soluble mediators of immune activation, altered fibroblast proliferation and extracellular matrix accumulation in SSc and thereby provide important therapeutic targets. In the present review, the involvement of cytokines in SSc is discussed with particular emphasis on cytokines and growth factors that have been implicated in the disease process and likely play an important role in the gastrointestinal manifestations of scleroderma. The role of cytokines as therapeutic targets in scleroderma forms the basis of this timely review.

Chemokine CCL2↗
PubMed2005

Dystrophin glycoprotein complex dysfunction: a regulatory link between muscular dystrophy and cancer cachexia.

Cachexia contributes to nearly a third of all cancer deaths, yet the mechanisms underlying skeletal muscle wasting in this syndrome remain poorly defined. We report that tumor-induced alterations in the muscular dystrophy-associated dystrophin glycoprotein complex (DGC) represent a key early event in cachexia. Muscles from tumor-bearing mice exhibited membrane abnormalities accompanied by reduced levels of dystrophin and increased glycosylation on DGC proteins. Wasting was accentuated in tumor mdx mice lacking a DGC but spared in dystrophin transgenic mice that blocked induction of muscle E3 ubiquitin ligases. Furthermore, DGC deregulation correlated positively with cachexia in patients with gastrointestinal cancers. Based on these results, we propose that, similar to muscular dystrophy, DGC dysfunction plays a critical role in cancer-induced wasting.

Adult↗
PubMed1986

Pyloric dysfunction in diabetics with recurrent nausea and vomiting.

Diabetes mellitus has been associated with a variety of gastrointestinal motor disturbances. Pyloric activity, however, has not been specifically investigated. We have quantified the pyloric manometric profile in 24 diabetics with recurrent nausea or vomiting, or both, without evidence of mechanical obstruction. Twelve healthy volunteers served as controls. A multilumen pneumohydraulic perfusion assembly with five side openings, each 1 cm apart, was positioned fluoroscopically across the antroduodenal junction and used to monitor pressure activity for 5 h (3 h fasting and 2 h fed). Three patterns of pyloric activity were defined and quantified: (a) baseline elevation of greater than or equal to 3 mmHg for greater than or equal to 1 min (tonic pattern); (b) antral-type phasic pressure activity mixed with duodenal phasic activity (phasic pattern); and (c) phasic pattern superimposed on tonic activity (combined tonic-phasic pattern). The duration of the total pyloric activity before and after the meal was greater in diabetics than in controls (p less than 0.005). Furthermore, episodes of unusually prolonged (greater than or equal to 3 min) and intense (greater than or equal to 10 mmHg) tonic contraction, "pylorospasm," were observed in 14 of 24 diabetics but in only 1 control (p = 0.025). In diabetics, episodes of pylorospasm had a peak amplitude of tonic activity of 13 +/- 1 mmHg and a duration of 7 +/- 0.7 min (mean +/- SE). We conclude that pyloric dysmotility forms part of the widespread disruption of gut motility that affects some patients with diabetes.

Adult↗
PubMed2005

Disordered enterocyte signaling and intestinal barrier dysfunction in the pathogenesis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in neonates, and is characterized by the development of diffuse intestinal necrosis in the stressed, pre-term infant. Systemic stress causes a breakdown in the intestinal mucosal barrier, which leads to translocation of bacteria and endotoxin and the initiation of a signaling response within the enterocyte. This review summarizes recent evidence defining a clear role that defective enterocyte signaling plays in the pathogenesis of NEC through the following mechanisms: 1) The localized production of nitric oxide by villus enterocytes results in an increase in enterocyte apoptosis and impaired proliferation; 2) The translocation of endotoxin results in a PI3K-dependent activation of RhoA-GTPase within the enterocyte leading to decreased enterocyte migration and impaired restitution; 3) Dysregulated sodium-proton exchange within the enterocyte by endotoxin renders the enterocyte monolayer more susceptible to damage in the face of the acidic microenvironment characteristic of systemic sepsis; and 4) Endotoxin causes a p38-dependent release of the pro-inflammatory molecule COX-2 by the enterocyte, which potentiates the systemic inflammatory response. An understanding of the mechanisms by which disordered enterocyte signaling contributes to the pathogenesis of barrier failure and NEC--through these and other mechanisms--may lead to the identification of novel therapeutic approaches for this devastating disease.

Bacterial Translocation↗
PubMed2006

[Pancreatic elastase-1 in the stool for the determination of exocrine pancreas function of postoperative patients with early enteral nutrition -- a pilot study].

BACKGROUND AND OBJECTIVE: There are only incomplete data about exocrine pancreatic function after major gastrointestinal surgery. Early enteral nutrition with high-molecular diets is increasingly administered to these patients. A knowledge of exocrine secretion of the pancreas is crucial, because pancreatic enzymes are needed for the adsorption of the high-molecular diets. To determine the exocrine pancreatic secretion the fecal elastase-1 is a sensitive method for measuring exocrine pancreatic secretion. PATIENTS AND METHODS: In a prospective study fecal elastase-1 was measured in patients on enteral nutrition (n=12) early after major gastrointestinal operations. They were given a high molecular diet via an intraoperatively placed small-needle catheter jejunostomy, starting 12 hours after operation with a continuous infusion of 20 ml/h (1 kcal/ml),increased to 80 ml/h during the next few days. Samples from the first and second stools after beginning the enteral nutrition were taken for measuring the fecal elastase-1. RESULTS: All patients fed enterally had no relevant feeding-associated complications and no diarrhea. The elastase-1 concentrations were normal in both the first and the second stool samples in all patients (normal stool elastase is > 200 g/g). The average elastase concentration in the first stool sample was 361,4 mg/g (median: 317 mg/g) and 454 mg/g in the second (median: 466,6 mg/g). Thus no exocrine pancreatic insufficiency was detected in any of the patients. CONCLUSION: The results of elastase-1 in stool demonstrate that severe exocrine pancreas dysfunction is not generally present in patients on early enteral nutrition after major gastrointestinal surgery.

Aged↗
PubMed1987

Ketoconazole prevents Candida sepsis in critically ill surgical patients.

We conducted a prospective, randomized, double-blind, placebo-controlled study to determine whether or not ketoconazole could prevent yeast colonization or invasion in critically ill adult surgical patients. Fifty-seven patients in a surgical intensive care unit (SICU) with three or more clinical risk factors for Candida infection were randomized to receive ketoconazole, 200 mg via the gastrointestinal tract daily (27 patients), or placebo (30 patients). Patients with hepatic dysfunction were excluded. The study was continued for 21 days or until one week after discharge from the SICU, whichever was longer. Stool cultures were obtained every three days and other cultures as indicated clinically. Patients were observed for yeast colonization (sputum, urine, stool, or wound) and invasion (fungemia or deep tissue focus). The incidence of Candida colonization was significantly lower in the ketoconazole group than the placebo group. Invasive yeast sepsis developed in five (17%) of the placebo-treated patients and in no patient in the ketoconazole group, a significant difference. Length of stay in the SICU was significantly lower in the ketoconazole group, as were the basic SICU patient charges. Sixty percent of the patients with invasive fungal sepsis died.

Adult↗
PubMedDate not supplied

Unusual and early hyperglycemia following amiodarone infusion in two infants.

Amiodarone is an effective antiarrhythmic agent that is widely used for tachyarrhythmias, especially ventricular tachycardia and supraventricular tachycardia. It has some mild short-term (e.g., skin rashes, gastrointestinal symptoms, and corneal microdeposits) and long-term side effects (thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, and hepatitis). We present two infants who had hyperglycemia following amiodarone infusion during the early postoperative period.

Amiodarone↗
PubMed1986

Proctectomy for inflammatory bowel disease.

Between July 1973 and October 1984, we performed proctectomy either as part of a primary proctocolectomy or as a secondary staged procedure in 388 patients with ulcerative colitis and in 39 patients with Crohn's disease. The proctectomies were performed using a two-team synchronous approach. An intersphincteric or perimuscular technique was employed. All perineal wounds were closed and drained by suction drainage and the pelvic peritoneum was closed in all cases. Two patients died in the early postoperative period, one from a pulmonary embolus and one from sepsis. Three patients had to be reexplored for postoperative hemorrhage, in all cases from a branch of the superior hemorrhoidal artery. Postoperative perineal hematoma developed in two patients and perineal abscess developed in four patients which necessitated opening of the perineal skin wound. Nonhealing of the perineal wound occurred in 3 of 388 patients with ulcerative colitis and in 5 of 39 patients with Crohn's disease. No perineal dehiscence or hernias were seen. Postoperatively, one man was permanently impotent and two had prolonged but temporary impotence. Three patients had retrograde ejaculation at last follow-up.

Abscess↗
PubMed2004

Clinical consult: iron overload--hereditary hemochromatosis.

One of the most common genetic causes of iron overload is hereditary hemochromatosis (HHC), a condition characterized by overabsorption of dietary iron from the gastrointestinal tract. This condition can lead to excessive iron accumulation with resulting dysfunction in multiple organs, including the liver, skin, heart,joints, pancreas, and testes. The clinical consequences of HHC if undetected and untreated can be severe and include liver cirrhosis,hepatocellular carcinoma, diabetes mellitus, cardiac arrhythmias and failure, arthritis, and hypogonadism. HHC is one of the most common heritable conditions in white populations of Northern European origin. This article presents a case study of HHC, describing inheritance and genetics, disease characteristics and natural history, diagnosis, differential diagnosis, and management.

Hemochromatosis↗
PubMed1987

Chloramphenicol and tetracyclines.

Tetracyclines have a broad range of clinical usefulness because of their broad antimicrobial spectrum of activity. For most routine gram positive and gram negative infections, alternative agents are available, but for Chlamydiae, Rickettsiae, Brucella, and Borrelia they still remain agents of choice. To some extent, gastrointestinal intolerance and inability to use these agents in patients with renal dysfunction have been overcome by the availability of doxycycline. Phototoxicity is a problem with this agent, however. Tetracycline is still useful as a sclerogenic agent for malignant effusions, and demeclocycline often is an agent of choice in therapy of inappropriate antidiuretic hormone secretion.

Bacterial Infections↗
PubMed1998

Diagnosis and treatment of sphincter of Oddi dysfunction.

UNLABELLED: BACKGROUND Sphincter of Oddi dysfunction is a challenge from both the diagnostic and therapeutic point of view. There is much ongoing debate about the accuracy and usefulness of various diagnostic tests, as there is about the effectiveness of proposed therapeutic alternatives. METHODS: A comprehensive review of the past 15 years' literature was undertaken, using the Medline database and cross-referencing of major articles on the subject. RESULTS AND CONCLUSION: Endoscopic and surgical treatments result in similar outcomes, with considerable failure rates. The latter reflect the difficulties in accurate diagnosis and a lack of sound objective criteria for selecting patients for intervention. In addition, in some patients sphincter of Oddi dysfunction may be only part of a generalized motility disorder of the gastrointestinal tract.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed2005

Molecular, cellular and developmental biology of urothelium as a basis of bladder regeneration.

Urinary bladder malfunction and disorders are caused by congenital diseases, trauma, inflammation, radiation, and nerve injuries. Loss of normal bladder function results in urinary tract infection, incontinence, renal failure, and end-stage renal dysfunction. In severe cases, bladder augmentation is required using segments of the gastrointestinal tract. However, use of gastrointestinal mucosa can result in complications such as electrolyte imbalance, stone formation, urinary tract infection, mucous production, and malignancy. Recent tissue engineering techniques use acellular grafts, cultured cells combined with biodegradable scaffolds, and cell sheets. These techniques are not all currently applicable for human bladder reconstruction. However, new avenues for bladder reconstruction maybe facilitated by a better understanding of urogenital development, the cellular and molecular biology of urothelium, and cell-cell interactions, which modulate tissue repair, homeostasis, and disease progression.

Animals↗
PubMed2004

Pneumonectomy: four case studies and a comparative review.

Pneumonectomy is the resection of all lung lobes in either the left or right lung field. The surgical technique and postoperative results of pneumonectomy for clinical disease have not been reported in companion animals. Pneumonectomy was performed in three dogs and one cat to treat pulmonary or pleural disease, and the postoperative outcome compared with the complications and results reported in the human literature. One dog died immediately postoperatively due to suspected respiratory insufficiency and the remaining three animals survived the perioperative period. Postoperative complications were reported in two animals. Cardiac complications occurred in the cat, with perioperative arrhythmias and progressive congestive heart failure. Gastrointestinal complications were diagnosed in one dog, with mediastinal shift and oesophageal dysfunction. Left- and right-sided pneumonectomy is feasible in companion animals, and the postoperative outcome and complications encountered in this series were similar to those reported in humans.

Animals↗
PubMed1987

A case of postganglionic cholinergic dysautonomia.

A 24 year old female presented with signs and symptoms of postganglionic cholinergic autonomic dysfunction manifested by impaired lachrymation and salivation, mydriasis of the pupil, decreased gastrointestinal motility, atony of the bladder, and sweating and taste disturbance. Clinical and pharmacological studies confirmed that the abnormalities were restricted mainly to the postganglionic cholinergic autonomic systems. The titre of serum complement was low, antinuclear antibodies revealed a diffuse pattern, and anti SS-A antibody was positive, suggesting that this disorder was caused by an immune mechanism.

Adult↗
PubMedDate not supplied

[Multiple organ dysfunction syndrome].

Multiple organ dysfunction syndrome (MODS) is a clinical situation that has been described as a result of the rapid progress and advances that have been made in recent decades in the physiology, diagnosis, and therapeutic support of critically ill patients. In 1991, in view of the confusing terminology used to characterize processes coursing with systemic inflammatory response syndrome (SIRS), a consensus conference was held. A series of basic definitions were established and the term "multiple organ failure" was replace by MODS. In response to outside aggression, the organism tries to defend itself with two mechanisms: a non-specific humoral and cellular response called inflammation, and a specific antigenic response that modifies the genetic codes of cells of the defense system and constitutes an immunological response. At present it is thought that the inflammatory response is activated (SIRS) in response to an uncontrolled aggression, but an antiinflammatory response syndrome (ARS) exists as well. An exaggerated SIRS can lead to MODS. MODS usually debuts with pulmonary dysfunction. If the aggression persists, cardiovascular, renal, hepatic, coagulation, central nervous system, gastrointestinal metabolism, neuroendocrine and musculoskeletal failure follow. A series of causes often trigger this syndrome and certain factors favor it. Prevention of these causes and factors in fundamental for controlling the occurrence of MODS. At present, there is no clear treatment for MODS, although numerous studies designed to block the release of certain proinflammatory mediators or to neutralize antiinflammatory responses are being carried out.

Consensus Statements as Topic↗
PubMed2006

Placental umbilical cord whole blood transfusion to combat anemia in the background of advanced rheumatoid arthritis and emaciation and its potential role as immunoadjuvant therapy.

Rheumatoid arthritis is the commonest form of inflammatory arthritis and affects about 1-3% of the population in the West and even more in the developing world due to the compounded factors of late detection and inadequate treatment in the overall background of poverty, deprivation, and improper macro and micronutrients in the diet in a sizeable segment of the population. Nearly 90% of patients with aggressive disease will become clinically disabled within 20 years. Furthermore, in patients with severe disease or extra-articular symptoms, mortality is equal to that for patients with triple artery coronary artery disease or Stage IV Hodgkin's lymphoma. Anemia is a very common comorbidity of rheumatoid arthritis. Anemia in rheumatoid arthritis is caused by various factors, for instance, cytokine impact of the advanced arthritic process on the host, or lack of proper nutrition and essential micronutrients in the diet, or coexistent helminthiasis, and/or impact of antiarthritic drugs on the host system, i.e., high steroid induced gastritis or ulcerations in gastric mucosa or subclinical or clinical hepatitis due to methotrexate or salazopyrin effects on bone marrow, only to name a few. Other pre-existing or compounding gastrointestinal problems, which alter the available iron stores or cause bone marrow dysfunction, may also help in adding to an anemic condition. If the anemia is 8 g/dl or less, blood transfusion or erythropoietin injection with adequate hematinic reserve is effective in normal situations, but is not that effective in anemia with a chronic disease background like rheumatoid arthritis. Cord blood, because of its rich mix of fetal and adult hemoglobin, high platelet and white blood cell (WBC) counts, and a plasma filled with cytokine and growth factors, as well as its hypo antigenic nature and altered metabolic profile, has all the potential of a real and safe alternative to adult blood transfusion. Seventy-eight units (42 ml -136 ml mean 80.6 ml +/- 3.6 ml SD, median 82.4 ml, mean packed cell volume 48.2 +/- 2.1 SD, mean percent hemoglobin concentration 16.4 g/dl +/- 1.5 g/dl SD) of placental umbilical cord whole blood was transfused (from 1 April 1999 to April 2005) after lower uterine cesarean section (LUCS) from consenting mothers to 28 informed consenting patients with advanced rheumatoid arthritis who had plasma hemoglobin of 8 g/dl or less. After collection, the blood was immediately transfused following the standard adult blood transfusion protocol. Each case was passed through the institutional ethical committee. The patients received two to six units of freshly collected placental umbilical cord blood without encountering any clinical, immunological or non-immunological reactions. Three days after completion of the transfusion of placental umbilical cord blood, the peripheral blood hematopoietic stem cell (CD34) estimation revealed a rise from the pretransfusion base level (.09%), varying from 2.03 to 23%, which returned to base level in most of the cases at the three-month CD34 re-estimation, without provoking any clinical graft vs host reaction in any of the patients.

Adolescent↗