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PubMed1999

Renal allograft dysfunction associated with cytomegalovirus infection.

Renal transplant recipients are at an increased risk for cytomegalovirus (CMV) infection, which occurs as a primary infection or as a result of reactivation of a latent virus. The main risk factors for symptomatic CMV disease include a CMV-negative recipient of a kidney from a CMV-positive donor (primary infection) and treatment of rejection with monoclonal or polyclonal antibodies. In this study, we report a renal transplant recipient with multiple risk factors for the development of CMV infection. He developed three episodes of CMV disease; the first was associated with gastrointestinal tract involvement, and the second episode was diagnosed according to surveillance laboratory test results in the absence of symptoms. The third episode was associated with acute allograft dysfunction. The renal transplant biopsy specimen showed viral inclusions without acute rejection or glomerular abnormality. Despite the absence of morphological injury on biopsy, treatment of CMV with ganciclovir was accompanied by an improvement in renal function. Further studies are needed to establish the mechanism of allograft dysfunction in the absence of inflammatory changes.

Adult↗

PubMed2002

The results of total mesorectal excision for rectal carcinoma in a district general hospital before the era of surgical specialization.

OBJECTIVE: To evaluate the results of rectal cancer surgery performed by a gastrointestinal surgeon in a district general hospital prior to the introduction of specialization, and to compare these to the targets set by the Royal College of Surgeons for specialist units. METHODS: Data collection in 73 consecutive patients (prospective in 53) undergoing elective excisional surgery (sphincter conserving in 77%) for rectal cancer. While adjuvant radio/chemotherapy and pathological assessment evolved over the study period, a standardized surgical technique (total mesorectal excision) was used in all patients. RESULTS: Observed (and recommended) outcome measures were operative mortality 4.1% (<5), anastomotic leak 6.2% (<8), wound infection 2.7% (< 10), pelvic recurrence after curative resection 9.6% (< 10). Temporary defunctioning stomas were used in 32/48 (66.7%) of patients. Other complications, currently without recommended outcomes, were erectile dysfunction (13%), stoma related (7.1%) urinary retention (4.1%), urinary incontinence (2.7%) and benign anastomotic stricture (2.7%). CONCLUSION: All treatment outcome criteria were met. Trained gastrointestinal surgeons outside the setting of a specialist unit can achieve good results with acceptable complication rates.

Journal Article↗

PubMed2004

Selective decontamination of the digestive tract attenuated the myocardial inflammation and dysfunction that occur with burn injury.

This study examined the effects of oral antibiotics to selectively decontaminate the digestive tract (SDD) on postburn myocardial signaling, inflammation, and function. We hypothesized that antibiotic therapy to eliminate pathogens from the gastrointestinal (GI) tract would reduce myocardial inflammatory responses and improve postburn myocardial performance. Sprague-Dawley rats received polymyxin E (15 mg), tobramycin (6 mg), and 5-flucytosin (100 mg) by oral gavage twice daily for 3 days preburn and 24 h postburn. Experimental groups included 1) sham burn given vehicle (3 ml water), 2) sham plus SDD, 3) burn over 40% total body surface area (TBSA) plus SDD, and 4) burn over 40% TBSA given vehicle. All burns received lactated Ringer solution (4 mg.kg(-1).%burn(-1)); myocardial signaling (PKCepsilon/p38 MAPK/NF-kappaB) was studied 2, 4, and 24 h postburn; and cytokine secretion (systemic and myocyte secreted cytokines, ELISA) and cardiac function were examined 24 h postburn. Vehicle-treated burn injury increased myocardial PKCepsilon/p38 MAPK expression, promoted NF-kappaB nuclear translocation, promoted TNF-alpha, IL-1beta, IL-6, and IL-10 secretion, and impaired myocardial function. SDD attenuated burn-related proinflammatory myocardial signaling, cytokine secretion, and myocardial contractile defects. Our data suggest that burn-related loss of GI barrier function and translocation of microbial products serve as upstream mediators of postburn myocardial inflammatory signaling and dysfunction.

Animals↗

PubMed2002

Revision of the multiple organ failure score.

BACKGROUND AND AIM: The multiple organ failure (MOF) score published by Goris et al. in 1985 was one of the first attempts to quantify severity of organ dysfunction and failure based on expert opinion in surgical intensive care unit patients. Fifteen years later a reassessment of this score is mandatory. PATIENTS AND METHODS: Daily MOF scores were documented in patients admitted to the surgical ICUs in Nijmegen (NL) and Cologne (D). Patients with an ICU stay < or = 3 days were excluded. Organ dysfunction (1 point) and organ failure (2 points) were recorded for the following organ systems: lung, heart, kidney, liver, blood, gastrointestinal tract (GI), and central nervous system (CNS). Maximum scores were computed, and logistic regression analysis was used to optimize point weights for each organ system. Predictive power was analyzed using receiver operating characteristic (ROC) curves. RESULTS: In all, 147 patients, mean age 56 years, were included with a total of 2,354 observation days. Hospital mortality was 30.6%. GI failure was present on only 3.3% of days, without impact on mortality. Valid evaluation of CNS was impossible in most cases due to sedation and ventilation. Reweighting of the score items revealed only marginal improvements in prediction. Mortality consistently increased with increase in number of failed organs. This phenomenon was even more pronounced in older patients, e.g., 55% mortality (age > or = 60) versus 0% (age < 60) with two failing organs. CONCLUSION: Due to problems in definition and assessment (reliability) CNS and GI should not be considered in future assessments of the MOF score. The original point weights in the remaining five organ systems provide a valid and reliable risk stratification, at least in surgical ICU patients.

Adult↗

PubMed2004

Glucagon-like peptide 2 improves intestinal wound healing through induction of epithelial cell migration in vitro-evidence for a TGF--beta-mediated effect.

BACKGROUND/AIMS: In vitro studies suggest that glucagon-like peptide 2 (GLP-2), secreted from enteroendocrine cells in the gastrointestinal tract after food intake, is able to ameliorate mucosal injury in settings of human disease characterized by injury and dysfunction of the intestinal mucosal epithelium. We evaluated this potential of GLP-2 after epithelial trauma by using two in vitro models measuring intestinal epithelial cell proliferation and cell migration. MATERIALS AND METHODS: Injuries were induced in confluent monolayers of the small intestinal cells lines IEC-6 and IEC-18, as well as in the colonic cell lines Caco-2 and Colo 320. GLP-2 (50-500 nM) or other peptides were added to the media. Wound healing was investigated after 24 h by quantification of the number of cells migrating across the wound edge. Proliferation of cells was assessed by using photometric mitochondrial incorporation measurement of MTT (3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide). Monoclonal TGF-beta antibodies were added to wounded monolayers to examine whether the GLP-2-induced wound healing was TGF-beta-mediated. RESULTS: Migration assessments revealed a significant stimulation of GLP-2-induced migration in IEC-6 and IEC-18 monolayers compared to the placebo group. No effect was observed in the colon cancer cell lines Caco-2 and Colo 320. Results of the proliferation assays show a significant inhibition of proliferation by GLP-2 in small intestinal cell lines whereas a dose-dependent stimulation of proliferation in colonic epithelial cells was observed. Addition of neutralizing TGF-beta1 antibodies to wounded IEC-6 and IEC-18 monolayers incubated with GLP-2 significantly reduced the number of migrating cells to the level of the placebo group. CONCLUSIONS: In our in vitro model, it was shown that the GLP-2-induced improvement of intestinal wound healing is TGF-beta-mediated. These effects were predominant in the epithelium of the small intestine compared to colonic epithelium. Our findings provide further insight into mechanisms leading to GLP-2-induced mucosal wound healing. These results suggest that GLP-2 or analogues of this peptide may potentially be useful for the treatment of intestinal disorders characterized by injury and ineffective repair of the intestinal mucosa.

Animals↗

PubMed2002

Rescue of the acetylcholinesterase knockout mouse by feeding a liquid diet; phenotype of the adult acetylcholinesterase deficient mouse.

Acetylcholinesterase (AChE, EC3.1.1.7) functions in nerve impulse transmission, and possibly as a cell adhesion factor during neurite outgrowth. These functions predicted that a mouse with zero AChE activity would be unable to live. It was a surprise to find that AChE -/- mice were born alive and survived an average of 14 days. The emaciated appearance of AChE -/- mice suggested an inability to obtain sufficient nutrition and experiments were undertaken to increase caloric intake. Pregnant and lactating dams (+/-) were fed 11% high fat chow supplemented with liquid Ensure. AChE -/- pups were weaned early, on day 15, and fed liquid Ensure. Although nullizygous animals showed slow but steady weight gain with survival over 1 year (average 100 days), they remained small at all ages compared to littermates. They demonstrated delays in temperature regulation (day 22 vs. 15), eye opening (day 13 vs. 12), righting reflex (day 18 vs. 12), descent of testes (week 7-8 vs. 4), and estrous (week 15-16 vs. 6-7). Significant physical findings in adult AChE -/- mice included body tremors, abnormal gait and posture, absent grip strength, inability to eat solid food, pinpoint pupils, decreased pain response, vocalization, and early death caused by seizures or gastrointestinal tract ileus. Behavioral deficits included urination and defecation in the nest, lack of aggression, reduced pain perception, and sexual dysfunction. These findings support the classical role for AChE in nerve impulse conduction and further suggest that AChE is essential for timely physical development and higher brain function.

Acetylcholinesterase↗

PubMed2001

Interaction of human chagasic IgG with human colon muscarinic acetylcholine receptor: molecular and functional evidence.

BACKGROUND AND AIMS: Gastrointestinal disorders is one of the clinical manifestations of chronic Chagas' disease. The pathogenesis seems to be associated with autonomic dysfunction. Here, we consider the muscarinic cholinoceptor mediated alteration in distal colon function in chagasic megacolon. PATIENTS: Patients were divided into four groups: group I, chronic chagasic patients with megacolon; group II, chronic chagasic patients without megacolon; group III, non-chagasic patients with megacolon; and group IV, normal healthy volunteers (control). METHODS: Binding assay and immunoblot of cholinoceptors from human and rat colon and enzyme immunoassay (ELISA) using a synthetic 24mer peptide corresponding to the second extracellular loop of human M2 muscarinic acetylcholine receptors (mAChR) were used to detect the presence of serum antibodies. The effect of antibodies on basal tone and 3',5'-cyclic monophosphate (cAMP) production of human and rat distal colon strips were also tested. RESULTS: Group I but not the other groups had circulating antibodies capable of interacting with human colon activating M2 mAChR, as they competed with binding of specific radioligand to mAChR and interacted with the second extracellular loop of human M2 mAChR. Moreover, affinity purified anti-M2 peptide IgG from group I, in common with monoclonal antihuman M2 mAChR, recognised bands with a molecular weight corresponding to colon mAChR. This antibody also displayed an agonist-like activity, increasing basal tone and decreasing cAMP accumulation. Both effects were blunted by AF-DX 116 and neutralised by the synthetic peptide. CONCLUSIONS: In chagasic patients with megacolon there are antibodies that can recognise and activate M2 mAChR. The implications of these autoantibodies in the pathogenesis of chagasic megacolon is discussed.

Adult↗

PubMed2001

Transthyretin-associated neuropathic amyloidosis. Pathogenesis and treatment.

Hereditary amyloidoses form a clinically and genetically heterogeneous group of autosomal dominantly inherited diseases characterized by the deposit of insoluble protein fibrils in the extracellular matrix. They typically present with polyneuropathy, carpal tunnel syndrome, autonomic insufficiency, and cardiomyopathy and gastrointestinal features, occasionally accompanied by vitreous opacities and renal insufficiency. Other phenotypes are characterized by nephropathy, gastric ulcers, cranial nerve dysfunction, and corneal lattice dystrophy. Rarely, involvement of the leptomeningeal or cerebral structures dominates the clinical picture. The age at onset is as early as 17 and as late as 78 years. The basic constituents of amyloid fibers are physiologic proteins that have become amyloidogenic through genetically determined conformation changes. Mutated transthyretin (TTR), formerly termed prealbumin, is the most frequent offender in hereditary amyloidosis. Orthotopic liver transplantation (OLT) stops the progression of the disease, which is otherwise invariably fatal, by removing the main production site of amyloidogenic protein. The indications for OLT and its success depend on the grade of cardiovascular and autonomic dysfunction at the time of surgery, age, comorbidity, and type of mutation. Alternative treatment modalities with drugs stabilizing the native tetrameric conformation of TTR and inhibiting fibril formation are currently being studied.

Age of Onset↗

PubMed2000

Adverse effects of creatine supplementation: fact or fiction?

The consumption of oral creatine monohydrate has become increasingly common among professional and amateur athletes. Despite numerous publications on the ergogenic effects of this naturally occurring substance, there is little information on the possible adverse effects of this supplement. The objectives of this review are to identify the scientific facts and contrast them with reports in the news media, which have repeatedly emphasised the health risks of creatine supplementation and do not hesitate to draw broad conclusions from individual case reports. Exogenous creatine supplements are often consumed by athletes in amounts of up to 20 g/day for a few days, followed by 1 to 10 g/day for weeks, months and even years. Usually, consumers do not report any adverse effects, but body mass increases. There are few reports that creatine supplementation has protective effects in heart, muscle and neurological diseases. Gastrointestinal disturbances and muscle cramps have been reported occasionally in healthy individuals, but the effects are anecdotal. Liver and kidney dysfunction have also been suggested on the basis of small changes in markers of organ function and of occasional case reports, but well controlled studies on the adverse effects of exogenous creatine supplementation are almost nonexistent. We have investigated liver changes during medium term (4 weeks) creatine supplementation in young athletes. None showed any evidence of dysfunction on the basis of serum enzymes and urea production. Short term (5 days), medium term (9 weeks) and long term (up to 5 years) oral creatine supplementation has been studied in small cohorts of athletes whose kidney function was monitored by clearance methods and urine protein excretion rate. We did not find any adverse effects on renal function. The present review is not intended to reach conclusions on the effect of creatine supplementation on sport performance, but we believe that there is no evidence for deleterious effects in healthy individuals. Nevertheless, idiosyncratic effects may occur when large amounts of an exogenous substance containing an amino group are consumed, with the consequent increased load on the liver and kidneys. Regular monitoring is compulsory to avoid any abnormal reactions during oral creatine supplementation.

Administration, Oral↗

PubMed2001

[Anorexia nervosa or somatic disease].

We have studied 18 patients with anorexia nervosa with antroduodenal manometry for 24 hours and also 24 hours oesophageal pH studies. After the first 12 hours of measurements we started treatment with Cisapride (n = 8) or Erythromycin (n = 10) in a blind study. The results of measurements reveal a severe gastroesophageal reflux in 4 patients. Antroduodenal manometry showed dysfunctions in gastric motility, without relation with weight loss or duration of the disease. Cisapride and more so Erythromycin favor gastrointestinal motility.

Adolescent↗

PubMed1992

Hepatic encephalopathy in Saudi Arabia: retrospective analysis of 51 patients.

The clinical features, prognostic factors, and outcome of 51 patients with hepatic encephalopathy (HE), were retrospectively reviewed. The mean (+/- SD) age of patients was 47.2 (+/- 14.8) years. Seventy-five percent of patients were males and 73% were Saudi. All identified episodes of hepatic encephalopathy were associated with chronic underlying liver disease and no episode occurred as a result of acute fulminant hepatic failure. Most patients presented in advanced stage of hepatic dysfunction and had one or more precipitating factors. In-hospital mortality rate was 41% (21 out of 51 patients). Gastrointestinal tract bleeding, electrolytes imbalance and alkalosis were associated with significantly higher mortality rate. However, unadjusted analysis failed to identify certain base-line independent prognostic factors.

Adult↗

PubMed1979

High-dose methotrexate for advanced breast cancer.

High-dose infusions of methotrexate with citrovorum factor rescue were evaluated in 27 patients with advanced recurrent breast cancer who had previously been treated with various Adriamycin-containing regimens. Eight of 27 patients (29%) achieved objective tumor regression with a median duration of response of 26 weeks. Nineteen patients had previously received standard doses of methotrexate (less than 50 mg/m2/dose), while eight patients had had no prior exposure to methotrexate. The response rates observed in these two groups of patients were similar. Except for two drug-related deaths, toxic effects were acceptable. Myelosuppression was mild, transient, and noncumulative. Gastrointestinal toxic effects did not appear to be dose-related and were mild in most instances. Central nervous system dysfunction with lethargy, fatigability, confusion, and disorientation was the most significant toxic effect of this high-dose methotrexate therapy and was observed in six (22%) of the patients. In two patients treatment with this program was discontinued because of the development of renal dysfunction. High-dose methotrexate with citrovorum factor rescue appears to be an effective regimen in patients with advanced refractory breast cancer. However, in view of the enormous cost necessitated by this treatment approach, we do not feel further studies would be worthwhile.

Age Factors↗

PubMed1999

Sensory-motor and genito-sphincter dysfunctions in multiple sclerosis.

Multiple sclerosis is a chronic demyeliniting disease of the central nervous system which is characterized by an extreme multiplicity of clinical features. Multiple sclerosis can have a profound impact on the quality of life of patients. The induced handicap varies from one patient to an other, and depends on the location of the demyeliniting lesions. Among the symptoms, sensory-motor disorders and genito-sphincter dysfunctions are some of the more disabling. Thus, up to 70% of patients suffer from urinary troubles, and 15 years after the onset of the illness, 50% of patients have difficulties for deambulation. A good knowledge of these pathologies is necessary to improve the management of patients suffering from multiple sclerosis.

Female Urogenital Diseases↗

PubMed1998

[Aspects in monitoring and treatment of gastrointestinal underperfusion in sepsis. Diagnosis and therapy of gastrointestinal underperfusion in sepsis].

Tissue hypoxia, especially in the splanchnic area, is still considered to be an important cofactor in the pathogenesis of multiple organ failure. Thus, in the treatment of septic shock the specific effects of ino-tropic drugs on the splanchnic perfusion are of particular interest. To give strict recommendations for monitoring and for therapeutic strategies in the treatment of gastrointestinal failure in patients with sepsis is difficult not only due to the lack of data on clinical outcome and organ dysfunction, but also due to some limitations in the methods applied to assess splanchnic perfusion and oxygenation. A reasonable approach in the management of splanchnic underperfusion in septic patients includes: Measurement of gastric mucosal pH or CO2-gap because it is the only method for the assessment of splanchnic perfusion which can be useful in the clinical routine. Adequate volume loading likely is the most important step in the supportive treatment of patients with septic shock. Unfortunately, what kind of fluids, endpoints, and monitoring techniques should be used is still controversial. Nevertheless, techniques allowing us to achieve and tightly control volume loading and regional perfusion, e.g. the measurement of pHi or CO2-gap, may be helpful. Patients with high DO2 have had better outcome. However, measurement of parameters assessing global and regional oxygenation may be superior than to guide therapy by DO2. To maximize DO2 by the use of very high dosages of catecholamines can be harmful. The recommendation to use dobutamine as catecholamine of first choice seems to be justified. In critically ill patients, no negative effects of norepinephrine on regional perfusion have been demonstrated provided the patient is adequately volume resuscitated and the DO2 is normal or slightly elevated. Therefore, after volume resuscitation and treatment with dobutamine, norepinephrine should be used for achieving an adequate perfusion pressure. Epinephrine and dopamine should be avoided because they seem to restribute blood flow away from the splanchnic region. There are no convincing data yet to support the routine use of low dose dopamine or dopexamine in patients with sepsis. These recommendations are limited by the lack of outcome studies and optimal methods for the assessment of splanchnic perfusion/oxygenation.

Critical Care↗

PubMed2005

Changes in enteric neurone phenotype and intestinal functions in a transgenic mouse model of enteric glia disruption.

AIMS: The influence of enteric glia on the regulation of intestinal functions is unknown. Our aim was to determine the phenotype of enteric neurones in a model of glia alterations and the putative changes in intestinal motility and permeability. METHODS: Transgenic mice expressing haemagglutinin (HA) in glia were used. Glia disruption was induced by injection of activated HA specific CD8+ T cells. Control mice consisted of non-transgenic littermates injected with activated HA specific CD8+ T cells. Immunohistochemical staining for choline acetyltransferase (ChAT), substance P (SP), vasoactive intestinal peptide (VIP), and nitric oxide synthase (NOS) was performed on jejunal submucosal plexus (SMP) and myenteric plexus (MP). Neurally induced jejunal muscle activity was characterised in vitro. Gastrointestinal transit and paracellular permeability were measured using fluorescein isothiocyanate-dextran markers. RESULTS: CD3 positive T cells infiltrates were observed in the MP of transgenic mice. In the SMP, the proportions of VIP and SP positive neurones decreased in transgenic mice compared with control mice. ChAT remained unchanged. In the MP, the proportions of ChAT and NOS positive neurones increased and decreased, respectively, in transgenic mice. In contrast, VIP and SP remained unchanged. Neurally mediated jejunal relaxation was lower in transgenic mice than in controls. This relaxation was reduced by NG-nitro-L-arginine methyl ester in control mice but not in transgenic mice. Gastrointestinal transit was delayed and intestinal permeability increased in transgenic mice compared with control mice. CONCLUSION: Glia disruption induces changes in the neurochemical coding of enteric neurones, which may partly be responsible for dysfunctions in intestinal motility and permeability.

Adoptive Transfer↗

PubMed1994

Abdominal vagotomy alters the structure of the ingestive behavior of rats ingesting liquid diets.

A microstructural analysis of the licking behavior of the rat was used to investigate the effects of total abdominal vagotomy on ingestive behavior. Vagotomy decreased the meal size of milk and 3 concentrations of sucrose. The decrease was due to an increase in the decline in the rate of licking during the meal, suggesting that negative feedback from the gastrointestinal tract was enhanced by vagotomy, perhaps because of accelerated clearance of fluid from the stomach to the intestine. No evidence was found for motor dysfunction of licking or alterations in gustatory sensitivity to the test solution. The results suggest that vagotomy enhanced the strength of an extravagally mediated negative feedback signal from the intestine and that the vagus nerve normally prevents this from occurring by regulating gastric clearance.

Afferent Pathways↗

PubMed1988

Parenteral nutrition in the management of gastrointestinal Kaposi's sarcoma in a patient with AIDS.

A patient with acquired immunodeficiency syndrome (AIDS) who required aggressive nutritional intervention via home parenteral nutrition therapy is described, and nutritional status, etiology and therapeutic management of AIDS-associated malnutrition, role of nutrition support, and factors for consideration in using parenteral nutrition in AIDS patients are discussed. Parenteral nutrition therapy was initiated in a 30-year-old AIDS patient with Kaposi's sarcoma lesions of the gastrointestinal tract because of rapid weight loss, low serum protein levels, and malnutrition. He had previously undergone a small-bowel resection and a jejunojejunostomy, and radiation and antineoplastic-drug therapy was planned. During parenteral nutrition therapy, the patient demonstrated increased physical strength and was able to care for himself during most of the time spent at home or in a long-term-care facility. Aggressive measures, including parenteral nutrition therapy, were discontinued 11 days before the patient's death. Complications of therapy included one episode of sepsis and a tear in the external catheter tubing. Malabsorption and diarrhea mainly caused by gastrointestinal disease, reduced food intake because of oral and esophageal infections, adverse effects from medication, and depression are factors that can contribute to AIDS-associated malnutrition. Also, hypermetabolism resulting from infections and fevers may contribute to malnutrition in AIDS. The extent to which this malnutrition affects the underlying immune dysfunction occurring in the syndrome and the response to other more direct drug therapies in AIDS is not known. Available methods for nutritional intervention are based on clinical experience and anecdotal reports. Because of gastrointestinal disease, an oral diet, supplements, and enteral tube feedings may not meet nutritional goals for an AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed1990

Anxiety and the gastrointestinal system.

There is a growing recognition that a link exists between anxiety and the gastrointestinal tract. This is evident in studies examining the effects of stress on gastrointestinal function and also in studies assessing psychopathology in patients with functional gastrointestinal disorders which demonstrate a high prevalence of anxiety disorders and depression in these individuals. The recent conceptualization of anxiety as resulting from dysfunction in separable subsystems of the brain as well as experimental evidence linking the brain with the GI tract may allow for testing hypotheses that the high prevalence of anxiety in patients with functional GI disorders may be due to common or interacting pathophysiology. The similarity between the ENS and the CNS may also be a plausible explanation for this association. The high prevalence of anxiety disorders in functional GI patients suggests that medications useful in the treatment of anxiety disorders (anxiolytics and antidepressants) may be useful in the treatment of functional GI disorders especially refractory cases, but further treatment studies are needed.

Anxiety Disorders↗