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PubMedDate not supplied

Transjugular intrahepatic portosystemic stent shunt.

The transjugular intrahepatic portosystemic stent shunt (TIPSS) is essentially a side-to-side portocaval shunt performed by interventional radiological methods which connects the hepatic vein to the portal vein via the liver parenchyma. It can be performed successfully in 85% to 95% patients. The procedure mortality is low (1% to 2%) and is mainly from intraperitoneal bleeding. Major indications for TIPSS are in patients in whom sclerotherapy for bleeding varices has failed, those who have recurrent variceal haemorrhage after sclerotherapy or band ligation and in patients with refractory ascites, hypersplenism and portal gastropathy. It has also been used in some patients with the Budd-Chiari syndrome, portal vein thrombosis and cirrhotic hydrothorax. TIPSS is followed by variceal rebleeding and encephalopathy in about 10% to 20% of cases, deterioration in liver function in about 25% to 35% and shunt dysfunction in 15% to 60%. Further research should be directed at developing newer types of stents to prevent shunt dysfunction.

Algorithms↗

PubMed1996

[Crenotherapy in sports medicine: the state of the art].

The existing relationship linking thermal and sport medicine has developed with time. This is shown by the established beneficial effects of thermal treatments (mineral waters, mud baths, balneotherapy, aerosol applications) in a wide range of sport and non-sport related injuries. The muscle fatigue syndrome is a condition particularly worrisome for sports practising individuals. This condition impairs the cardiovascular system, as well as hematologic, renal and gastrointestinal functions, acting via biochemical and metabolic modifications of the organism, which have effects also on the psyche of the subject. The treatment of this syndrome includes the use of specific mineral waters, which underscores that the correct hydration of the organisms is a precondition to achieve high performance levels. Traumas involving muscles and skeletal segments, and precocious arthrosis occur with higher frequency in sportsmen after continuous and intense stresses. Within the scope of rheumatology, mud-baths and balneotherapy have curative and rehabilitative potentials leading to a reduction, and often a disappearance, of pain with a faster recovery of the locomotory system. The gastrointestinal system is a target of psychic as well as physical stresses displaying symptoms or diseases which may be favourably addressed with the aid of mineral waters. This treatment has proved effective in secretory and motility dysfunctions of the biliary tree allowing a rapid functional recovery. Mineral water treatments are successfully employed in the treatment of urologic disturbance and ORL and dermatological pathologies, where local applications such as mud baths, balneotherapy, showers and aerosols, play a critical role.

Balneology↗

PubMedDate not supplied

[The current pathogenetic aspects of MODS in the sepsis patient].

MODS, a phenomenon observed in many critically ill patients, is the progressive failure of two or more organ system which results from nonspecific systemic responses to abnormal intravascular inflammation. It is triggered by a number of cellular humoral and biochemical mediators (more than 100). This article takes up the role of individual organ system dysfunction in the development of MODS. Cardiopulmonary, renal and hepatic responses to injury and infection and the relation of these responses to the subsequent development of MODS have been the subject of intense investigations; recently the gastrointestinal tract was identified as another target organ in such patients.

Disease Progression↗

PubMed1991

Gastrointestinal complications of chronic spinal cord injury.

Gastrointestinal problems are important in the chronic stage of spinal cord injury. We review the literature on problems of specific segments of the alimentary tract in this setting and add observations based on clinical experience. Emphasis is placed on the colon and rectum, where most clinically apparent problems occur. While bowel management programs are often successful in the near-term, long-term dysfunctions are common and difficult to treat. Studies to determine colonic transit time and rectal physiologic responses are useful to provide scientific basis of management of such patients. More information is needed on the relative roles of extrinsic and intrinsic nervous system in GI function.

Digestive System↗

PubMed2002

Abnormal esophageal motility in children with congenital central hypoventilation syndrome.

BACKGROUND & AIMS: Congenital central hypoventilation syndrome, an unexplained disorder of the central control of breathing that may reflect widespread dysfunction of brainstem structures, is regarded as a form of neuro cristopathy. Because swallowing-induced peristalsis is centrally controlled and depends on neural crest-derived esophageal innervation, we looked for esophageal dysmotility in patients with congenital central hypoventilation syndrome. METHODS: Seven patients without dysphagia or any other upper gastrointestinal tract symptoms were studied prospectively (5 girls and 2 boys; median age, 14 years; range, 11-18 years). They were compared with 7 age- and sex-matched controls. Esophageal manometry was performed using a low-compliance infusion system and the station pull-through technique. At least 10 wet swallows were analyzed in each subject. RESULTS: Pressure wave propagation was abnormal in all 7 patients (median percentage of swallows propagated, 18%, and range, 0-66; controls, 90% and 80-100; P < 0.001). Lower esophageal sphincter relaxation was abnormal in 5 patients (patients, 73% and 53-100; controls, 95% and 90-100; P = 0.01). In 2 patients, lower esophageal sphincter pressure was above the 95th percentile of control values. CONCLUSIONS: These abnormalities are strong evidence of lower esophageal dysfunction in congenital central hypoventilation syndrome. We speculate that the underlying mechanism may be dysfunction of the central structures that control swallowing.

Adolescent↗

PubMed2003

Regulation of gastrointestinal mucosal growth during aging.

The increase in the aging population has led to a growing interest in achieving a better understanding of the aging process and of diseases that are predominantly expressed during advancing age. Since the structural and, in turn, the functional integrity of the mucosa of the gastrointestinal tract (GI) are maintained by constant renewal of cells, a detailed knowledge of the events that initiate and regulate mucosal proliferative processes is essential for a better understanding of the normal aging process as well as age-associated dysfunctions, including malignancy that represent disorders of tissue growth. In Fischer-344 rats, aging is associated with increased mucosal proliferative activity in much of the GI tract. On the other hand, the functional properties are either decreased or remain unchanged during advancing age. Basal gastric acid and pepsin output decline during aging, as is gastrin secretion. In contrast, antral gastrin levels increase during this period, as is mucosal histidine decarboxylase activity. The age-related decline in gastrin secretion could partly be attributed to a higher ratio of somatostatin (D) to gastrin (G) cells in the antral mucosa. The age-related rise in GI mucosal proliferative activity could not be attributed to the trophic action of either gastrin or bombesin, since they caused no significant change in mucosal proliferation in aged rats. On the other hand, EGF and TGF-alpha appear to be involved in regulating mucosal proliferation during aging. Aging is associated with increased activation of EGF-receptor (EGFR), the common receptor for EGF and TGF-alpha. This could be due to (a) increased levels of membrane-bound precursor form(s) of TGF-alpha resulting in increased activation EGFR signaling processes through an autocrine/paracrine mechanism, (b) heightened sensitivity of mucosal EGFR to EGF and TGF-alpha such that comparatively lower levels of these peptides are required to activate EGFR in aged than in young animals and/or (c) loss of EGFR regulatory factor(s) such as ERRP (EGFR Related Protein), a "negative regulator" of EGFR.

Aging↗

PubMed2001

Nitric oxide prevents intestinal mitochondrial dysfunction induced by surgical stress.

BACKGROUND: The intestine is highly susceptible to free radical-induced damage and earlier work has shown that surgical stress induces generation of oxygen free radicals in enterocytes, resulting in intestinal damage along with changes in mitochondrial structure and function. Nitric oxide is an important mediator of gastrointestinal function and this study looked at the effect of nitric oxide on surgical stress-induced intestinal mitochondrial alterations. METHODS: Controls and rats pretreated with the nitric oxide donor L-arginine were subjected to surgical stress by opening the abdominal wall and handling the intestine. Enterocytes were isolated, mitochondria prepared and the protection offered by L-arginine against damage due to surgical stress was determined. Protection to structural as well as functional aspects of mitochondria was examined. RESULTS: Mild handling of the intestine affected the enterocyte mitochondrial structure as assessed by lipid composition and electron microscopy. Mitochondria were also functionally impaired with altered calcium flux and decreased respiratory control ratio. Pretreatment with the nitric oxide synthase substrate L-arginine prevented these damaging effects of surgical stress. Protection with arginine was abolished by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester, indicating the role of nitric oxide. CONCLUSION: Surgical stress in the small intestine can affect enterocyte mitochondrial structure and function. These damaging effects can be prevented by nitric oxide, an important modulator of cellular function.

Animals↗

PubMed2001

Loss of interstitial cells of Cajal and development of electrical dysfunction in murine small bowel obstruction.

1. Partial obstruction of the murine ileum led to changes in the gross morphology and ultrastructure of the tunica muscularis. Populations of interstitial cells of Cajal (ICC) decreased oral, but not aboral, to the site of obstruction. Since ICC generate and propagate electrical slow waves in gastrointestinal muscles, we investigated whether the loss of ICC leads to loss of function in partial bowel obstruction. 2. Changes in ICC networks and electrical activity were monitored in the obstructed murine intestine using immunohistochemistry, electron microscopy and intracellular electrophysiological techniques. 3. Two weeks following the onset of a partial obstruction, the bowel increased in diameter and hypertrophy of the tunica muscularis was observed oral to the obstruction site. ICC networks were disrupted oral to the obstruction, and this disruption was accompanied by the loss of electrical slow waves and responses to enteric nerve stimulation. These defects were not observed aboral to the obstruction. 4. Ultrastructural analysis revealed no evidence of cell death in regions where the lesion in ICC networks was developing. Cells with a morphology intermediate between smooth muscle cells and fibroblasts were found in locations that are typically populated by ICC. These cells may have been the redifferentiated remnants of ICC networks. 5. Removal of the obstruction led to the redevelopment of ICC networks and recovery of slow wave activity within 30 days. Neural responses were partially restored in 30 days. 6. These data describe the plasticity of ICC networks in response to partial obstruction. After obstruction the ICC phenotype was lost, but these cells regenerated when the obstruction was removed. This model may be an important tool for evaluating the cellular/molecular factors responsible for the regulation and maintenance of the ICC phenotype.

Animals↗

PubMedDate not supplied

Effect of renal dysfunction in fulminant hepatic failure.

BACKGROUND: Effect of renal dysfunction in fulminant hepatic failure is not studied extensively. METHODS: Fifty consecutive patients of fulminant hepatic failure were studied prospectively to determine the prevalence of renal failure and its effect on survival. RESULTS: The mean age of these patients was 36 +/- 7.2 years and there were 21 males and 29 females. Twenty two patients (44%) were hepatitis B surface antigen (HBsAg) positive. Renal dysfunction was observed in 19 patients (38%). Acute tubular necrosis was seen in 7 patients (38%) while prerenal azotemia and functional renal failure occurred in six patients each (37%). Renal failure occurred more commonly in patients with jaundice. In these patients it occurred in less than four days and prior to onset of encephalopathy, ascites, and gastrointestinal hemorrhage. Histopathological examination of kidney (done in 8 patients) revealed acute tubular necrosis in 4 patients while patients with functional renal failure and prerenal azotemia had normal histology. A good correlation was observed between biochemical parameters and histology of kidney in all the patients. The survival amongst the patients with FHF was 28% (14 of 50 patients). Poor prognostic indicators were a leukocyte count of more than 16.5 x 10(9)/liter, prothrombin index of less than 34%, a peak serum bilirubin of more than 376 mumol/liter and presence of renal failure. Only 3 of 19 patients with renal failure survived. CONCLUSIONS: Renal dysfunction is a major indicator of poor prognosis in patients with FHF.

Acute Kidney Injury↗

PubMed1999

Folate deficiency beyond megaloblastic anemia: hyperhomocysteinemia and other manifestations of dysfunctional folate status.

Folate plays a key role in nucleic acid synthesis. As a consequence, the most conspicuous complication of folate deficiency or of derangements of folate metabolism is megaloblastic macrocytic anemia caused by interdiction of normal proliferation of rapidly dividing bone marrow cells. Other rapidly dividing cells, including those in the gastrointestinal tract, may also be affected by the megaloblastic process. This may result in malabsorption. However, there is mounting evidence to indicate that there are other earlier manifestations of folate deficiency or of longstanding suboptimal folate nutrition. Chief among these manifestations of folate deficiency are an increased predisposition to occlusive vascular disease and thrombosis, which have been linked to increased levels of homocysteine found in folate deficiency and abnormal states of folate metabolism. In addition, folate deficiency, previously considered free of neurological consequences, is now known to be associated with disturbances of mood, and even spinal cord syndromes similar to those seen in vitamin B12 deficiency. Finally, there is both experimental and clinical evidence to suggest that folate deficiency may interfere with immunologic status and may be associated with an increased predisposition to neoplasia. Nutritional as well as genetic factors may contribute to these various nonhematological manifestations of folate insufficiency.

Anemia, Megaloblastic↗

PubMed1994

Enhancement by KW-5092, a novel gastroprokinetic agent, of the gastrointestinal motor activity in dogs.

KW-5092 ([1-[2-[[[5-(piperidinomethyl)-2- furanyl]methyl]amino]ethyl]-2-imidazolidinylidene) propanedinitrile fumarate) is a novel gastroprokinetic agent with acetylcholinesterase (AChE) inhibitory activity and acetylcholine (ACh) release facilitatory activity. The present study examined the effects of KW-5092 on gastrointestinal (GI) motor activity in dogs. In anesthetized dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. dose-dependently enhanced the gastric antral and the colonic motor activity. Neostigmine, an AChE inhibitor, enhanced the motor activity at 0.03 and 0.1 mg/kg, i.v. Ranitidine, a histamine H2-receptor antagonist with AChE inhibitory activity and ACh release facilitatory activity, enhanced the motor activity but decreased blood pressure at 1 to 10 mg/kg, i.v. In conscious dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. or 1 to 10 mg/kg, p.o. dose-dependently enhanced the gastric antral, duodenal, ileal and the colonic motor activities. Neostigmine at 0.1 mg/kg, i.v. or 3 mg/kg, p.o. enhanced the duodenal, ileal and colonic motor activities, but induced excitement, slavering, vomiting and diarrhea. Ranitidine at 3 mg/kg, i.v. enhanced the gastric antral and colonic motor activities, but induced collapse or akinesia. The present results suggest that KW-5092 enhances the GI motor activity in a wide range from the gastric antrum to the colon and does not induce behavioral and cardiovascular side effects. KW-5092 may be a useful drug for the treatment of GI motility dysfunctions.

Acetylcholine↗

PubMed1996

Dose-intensive melphalan with blood stem cell support for the treatment of AL amyloidosis: one-year follow-up in five patients.

The morbidity and lethality of AL amyloidosis is caused by the deposition of lg light chains as fibrillar amyloid protein in vital organs, disrupting their function, and not by the generally low burden of clonal plasma cells that produce the paraproteins. Survival of patients with AL amyloidosis is no more than 1 to 2 years from the time of diagnosis with current management approaches. Clearly, more effective therapies are needed for this rapidly lethal disease. Five patients were treated with dose-intensive melphalan and blood stem cell support and followed for a period of 1 year. Patients were diagnosed with AL amyloidosis by tissue biopsy and categorized by performance status and organ involvement. Their plasma cell dyscrasias were evaluated with immunofixation electrophoresis of serum and urine specimens, quantitative serum lgs, and immunohistochemical staining of bone marrow biopsy specimens. After treatment with dose-intensive intravenous melphalan followed by infusion of autologous growth-factor-mobilized blood stem cells, clinical evaluations and plasma cell studies were repeated at 3 and 12 months. Three men and 2 women aged 38 to 53 years were treated. Median performance status (SWOG) was 2 (1 to 3), and clinical presentations included nephrotic syndrome (n = 1), symptomatic cardiomyopathy (n = 1), gastrointestinal involvement with polyneuropathy (n = 2), and hepatomegaly (n = 1). With a median follow-up of 13 months (12 to 17 months), all five patients are well and have shown stable or improved performance status and clinical remission of organ-related dysfunction, including a 50% reduction in daily proteinuria with no change in creatinine, reversal of symptoms of cardiomyopathy and reductions of posterior wall and septal thickening, reversal of polyneuropathy and gastric atony, and resolution of hepatomegaly by computed tomographic scan. In 3 of the 5 patients (60%) at 12 months after treatment, plasma cell dyscrasias could not be detected. Dose-intensive chemotherapy with intravenous melphalan and growth-factor-mobilized blood stem cell support is feasible therapy for patients with AL amyloidosis, even when there is clinical evidence of cardiac involvement. At least some patients with AL amyloidosis achieve complete remission of their plasma cell dyscrasia, improvement in performance status, and clinical remission of organ-specific disease after this form of treatment.

Adult↗

PubMed1996

Is motility impaired in the entire upper gastrointestinal tract in patients with gastro-oesophageal reflux disease?

BACKGROUND: Although the pathogenesis of gastro-oesophageal reflux disease is multifactorial, abnormal function of the lower oesophageal sphincter has been established, and in some cases motility defects in the oesophageal body has been described. In some patients with gastro-oesophageal reflux disease delayed gastric emptying has also been observed. METHODS: Oesophageal and gastric motor function, as evaluated by use of scintigraphy and manometry, were studied concomitantly in 105 patients with chronic, gastro-oesophageal reflux disease before and after antireflux surgery. In a subgroup of these patients (n = 29) similar data were retrieved also at 2.7 years after antireflux surgery. RESULTS: Impaired oesophageal motor function expressed as delayed transit of a labelled bolus was closely associated with motor dysfunction also recorded in the stomach as determined by delayed emptying of labelled solid food items. A similar relationship was found when oesophageal motor dysfunction was characterized as the frequency of failed primary peristalses after water swallows during manometry. When the 105 patients were studied half a year after an antireflux operation, noncorrelation between oesophageal and gastric motor function could be recorded. CONCLUSIONS: These data further substantiate the view that gastro-oesophageal reflux disease is associated with a disturbed motor function within the entire upper gastrointestinal tract.

Adult↗

PubMed2000

Portal vein thrombosis and liver disease.

Portal vein thrombosis can occur secondary to infection, surgical intervention, or as a result of liver dysfunction. Its development can precipitate the need for emergency interventions including endoscopy, transjugular intrahepatic portosystemic stents (TIPS), portacaval shunts, or even liver transplantation. Portal vein thrombosis occurs slowly and silently. Portal vein thrombosis is not discovered until gastrointestinal hemorrhage develops in the patient unless the thrombosis is diagnosed on routine surveillance diagnostic testing. Portal vein thrombosis can be diagnosed by Doppler ultrasonography, computed tomography scan, or magnetic resonance imaging. Late identification of portal vein thrombosis can lead to increased morbidity and mortality of the patient population. Patients with portal vein thrombosis can be successfully managed with early identification and collaboration between the patient and the health care team for ongoing monitoring and treatment. Patient education involves assisting the patient in the understanding of esophageal varices, the various treatment modalities, their physical limitations, and the need for monitoring and management of the portal hypertension.

Adult↗

PubMed2006

Intestinal disease in Hermansky-Pudlak syndrome: occurrence of colitis and relation to genotype.

BACKGROUND & AIMS: Hermansky-Pudlak syndrome (HPS), a rare autosomal recessive disorder characterized by oculocutaneous albinism and platelet dysfunction, results from mutations in 1 of at least 7 different genes. Some patients develop a fatal pulmonary fibrosis and others a disabling colitis. This study aimed to document the occurrence of colitis among HPS patients, characterize gastrointestinal tract involvement in HPS, and analyze the distribution of colitis among HPS genotypes. METHODS: Of the 122 HPS patients followed at the National Institutes of Health Clinical Center between 1993 and 2005, 24 were evaluated by endoscopy for gastrointestinal complaints. The histology of gastrointestinal biopsies was retrospectively examined to assess for inflammatory changes, granulomata, and pigmented macrophages. These data were compared with symptoms and HPS genetic subtypes. RESULTS: At colonoscopy, 7 of 23 patients (30%) had endoscopic mucosal abnormalities, including nodularity, erythema, petechiae, or erosions. Six of these 7 patients (86%) had findings of colitis on biopsy. Of the 16 patients with normal-appearing colonic mucosa, 2 patients (12%) had colitis on biopsy. Pigmented macrophages were also observed in the colonic lamina propria in 16 of the 23 patients (70%). Of the 8 patients with confirmed colitis, 7 had the HPS-1 subtype, and 1 had the HPS-4 subtype. CONCLUSIONS: There is an increased frequency of colitis in our population of 122 HPS patients (8/122, 7%) and in HPS patients referred specifically for symptom evaluation (8/24, 33%). Colitis was found in patients with HPS-1 and HPS-4 genotypes.

Adolescent↗

PubMed2001

Intestinal adaptation: structure, function, and regulation.

After massive small bowel resection (SBR), the remnant intestine undergoes an adaptive process characterized by increases in wet weight, protein and DNA content, villus height and crypt depth, and absorptive surface area. These changes are the result of a proliferative stimulus that increases crypt cell mitosis and augments cellular progression along the villus axis. Functionally, there is upregulation of the Na(+)/glucose cotransporter, Na(+)/H(+) exchanger, and other enzymes involved in intestinal digestion and absorption. These physiologic events are a compensatory response to the sudden loss of digestive and absorptive capacity by the remnant intestine. A major consequence of inadequate intestinal adaptation is lifelong dependence on parenteral nutrition, which results ultimately in cholestatic liver dysfunction. Furthermore, adaptation may be associated with changes in intestinal permeability and an increased risk of bacterial translocation and sepsis. Several mediators thought to be integral to the postresection adaptive response have been proposed, including luminal nutrients, gastrointestinal secretions, and humoral factors. A thorough understanding of intestinal adaptation will be essential in the rational development of new and innovative therapies that amplify this complex but important process.

Animals↗

PubMed2005

[Abdominal ultrasound after endoscopic or percutaneous stenting and drainage].

Stents and prostheses in the hepatobiliary system are visible by ultrasound examination and can be checked for their function. The reappearance of mechanical cholestasis, stent dislocation or formation of sludge on the stent tip is signs of stent dysfunction. Graduation of the biliary obstruction can help to find the best time for changing the stent. After intervention hematoma, abscess, intraabdominal fluid or gas may occur and can be diagnosed by ultrasound. Tumor stenosis in the gastrointestinal tract can be treated by self expandable metallic stents. Ultrasound helps to localize the stent in the correct position and to observe the reduction of occlusive ileus. Percutaneous and gastrointestinal drainage of pancreatic cysts, necrosis and abscesses are often controlled by ultrasound to evaluate size, echogenicity and localized pain. Many procedures and interventions in gastroenterology can be monitored by an experienced ultrasound examiner in an effective and inexpensive manner.

Abdomen↗

PubMed1991

Does serum CAR-3 play a role in pancreatic cancer diagnosis?

A new tumour marker, CAR-3, was isolated using the monoclonal antibody technique and measured in the sera of 27 patients with pancreatic cancer, 25 chronic pancreatitis, 30 extra-pancreatic diseases and in that of 18 healthy controls in order (1) to evaluate the diagnostic role of CAR-3 in patients with pancreatic cancer and (2) to ascertain whether liver dysfunction influences CAR-3 serum levels. The increased levels were found in 12/27 patients with pancreatic cancer (sensitivity 44.4%). No increase was found in patients with chronic pancreatitis, whereas abnormal levels were found in patients with other gastrointestinal diseases, especially those of the liver and biliary tract. Correlations were found between serum CAR-3 and (1) total bilirubin and (2) alkaline phosphatase. In conclusion, CAR-3, an antigen structurally related to CA 19-9, does not appear to be accurate enough to be considered a tumour marker. Cholestasis seems to increase CAR-3 levels as well as those of other glycoproteic tumour markers, probably by interfering with the hepatic clearance of these substances.

Adult↗