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PubMedDate not supplied

It is not what you eat, but how you eat it digestion, life-style, nutrition.

Each year, over 30 million Americans suffer from acute or chronic digestive dysfunction. Much of this dysfunction is associated with occupational and behavioral stresses, which, although not life threatening, cause absenteeism and claim considerable health services. Central nervous system gastrointestinal (GI) peptide hormones partly control the quantity and quality of food eaten and its digestion. Because digestion is modified by occupational stress and behavior patterns, including smoking and consumption of alcohol and coffee, the physiological status of the individual plays a major role in the absorption of luminal nutrients. Whereas a Western, versus vegetarian, diet has been associated with an increase in coronary heart disease and diet-related cancers, inadequate attention has been given to the effects of life-style and occupation. This review is concerned with the adverse environmental effects on digestion that act via changes in GI function. To reduce the incidence of digestive dysfunction and diet-related diseases, more attention must be given to environmental factors other than diet, which affects the absorption of nutrients.

Diet↗
PubMed2005

Intentional self-poisoning with the chlorophenoxy herbicide 4-chloro-2-methylphenoxyacetic acid (MCPA).

STUDY OBJECTIVE: Data on poisoning with MCPA (4-chloro-2-methyl-phenoxyacetic acid) are limited to 6 case reports. Our objective is to describe outcomes from intentional self-poisoning with MCPA in a prospective case series of 181 patients presenting to hospitals in Sri Lanka. METHODS: Patient information was collected by on-site study physicians as part of an ongoing prospective cohort study of poisoned patients. Medical history, clinical details, and blood samples were obtained prospectively. RESULTS: Overall clinical toxicity was minimal in 85% of patients, including mild gastrointestinal symptoms in 44% of patients. More severe clinical signs of chlorophenoxy poisoning reported previously, such as rhabdomyolysis, renal dysfunction, and coma, also occurred but were uncommon. Eight patients died (4.4%). Most deaths occurred suddenly from cardiorespiratory arrest within 48 hours of poisoning; the pathophysiological mechanism of death was not apparent. The correlation between admission plasma MCPA concentration and clinical markers of severity of toxicity (physical signs, symptoms, and increased creatine kinase level) was poor. CONCLUSION: Intentional self-poisoning with MCPA generally causes mild toxicity, but cardiorespiratory arrest and death may occur. All patients should receive routine resuscitation and supportive care. It seems reasonable to correct acidosis and maintain an adequate urine output, but there is insufficient evidence to support other specific interventions. Our data do not support a clinical role for measurement of plasma MCPA in the acute management of poisoning, and insufficient data were available to fully examine the utility of measured electrolytes and creatine kinase levels.

2-Methyl-4-chlorophenoxyacetic Acid↗
PubMed2005

Efficacy of argon plasma coagulation for gastric antral vascular ectasia associated with chronic liver disease.

Gastric antral vascular ectasia (GAVE) is a rare cause of chronic gastrointestinal bleeding. The aim of this study was to evaluate the relationship between GAVE with cirrhotic patients and liver dysfunction, portal hypertension and the safety and efficacy of argon plasma coagulation (APC) in treating GAVE with cirrhotic patients. Eight cirrhotic patients with the characteristic endoscopic findings of GAVE were registered. In this study, APC was performed for GAVE in all eight patients. The patients-liver function was classified by Child-Pugh classification and classifications were: two class A, five class B and one class C (mean score: 7.8). Five patients had previously received prophylactic endoscopic injection sclerotherapy for esophageal varices and one had esophageal varices. Balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices had been performed in other one patient. Portal hypertensive gastropathy (PHG) was recognized in only one case. APC was performed in all eight patients and one to three treatment sessions were needed (mean: 1.8 sessions). No complications were observed in the initial treatment. During follow-up, endoscopies revealed the recurrence of GAVE in two patients requiring further treatment by APC (recurrence rate: 25%). After APC treatment, the recurrence of GAVE was not observed with endoscopy in the other six patients. The results suggest that GAVE is related to severe liver damage and portal hypertension in cirrhotic patients. APC is a safe and effective treatment against GAVE.

Journal Article↗
PubMed1988

VP-16 and carboplatin in previously untreated patients with extensive small cell lung cancer: a study of the National Cancer Institute of Canada Clinical Trials Group.

Thirty-four previously untreated patients with extensive small cell lung cancer were treated with a combination of carboplatin 300 mg m-2 i.v. on day 1 and etoposide 100 mg m-2 i.v. on days 1, 2 and 3 every 28 days. Thirty-two patients were assessable for response. Eighteen patients (56%) achieved an objective response (95% confidence limits 38%-73%). Five (16%) had a complete response and 13 (41.0%) had a partial response. The median time to response was 7.8 weeks and the median duration of response was 23.1 weeks (range 6.2 to 54 weeks). The median survival of all 34 extensive disease patients was 34.7 weeks (range 1.3-59.3 weeks). Myelosuppression (leukopenia) was the main toxicity. There was one early death that may have been treatment-related. Biochemical renal dysfunction was noted in two patients. Paresthesiae and tinnitus/hearing loss were described by three and two patients respectively. Serious gastrointestinal toxicity was infrequent. This and other studies have shown this combination to be active and well tolerated in small cell lung cancer; however, it is not yet clear if it is as efficacious as the more commonly used VP-16-cisplatin regimen.

Adult↗
PubMed1985

Zinc metabolism in malabsorption syndromes.

Zinc deficiency may complicate many gastrointestinal malabsorptive states. Zinc deficiency may manifest itself in a myriad of ways, ranging from skin lesions to immune dysfunction. This paper reports many of the ways in which zinc deficiency may appear in malabsorption syndromes and possible mechanisms for the development of this zinc deficiency.

Acrodermatitis↗
PubMed2000

Clinical aspects of bleeding complications in cirrhotic patients.

Liver disease is a frequent cause of haemostatic abnormalities, which may lead to overt or occult bleeding. Clinical manifestations of hepatic coagulopathy include upper and lower gastrointestinal haemorrhage, easy bruising and bleeding from gums, nose or the female genital tract. The most significant bleeding problem among patients with chronic liver disease is blood loss due to portal hypertension. About 30% of subjects with oesophageal or gastric varices resulting from cirrhosis have an episode of gastrointestinal bleeding in their lifetime. Risk factors for the first episode of variceal bleeding include the severity of liver dysfunction, large varices, and the presence of endoscopic red colour signs. Bacterial infection in patients with variceal haemorrhage may be critical in triggering bleeding. Nongastrointestinal bleeding events, either spontaneous or induced by minor trauma, are also a common complication of advanced cirrhosis. In women, for instance, dysfunctional uterine bleeding may become so severe that hysterectomy is required. In addition, invasive diagnostic tests (mostly solid tissue biopsies) and surgical procedures have a high risk of haemorrhage and are sometimes withheld in cirrhotic patients for fear of complications. In patients with portal hypertension, surgical procedures aggravate the injury of the hepatic parenchyma and may worsen the condition.

Bacterial Infections↗
PubMed2001

Exocrine dysfunction of the pancreas in patients with chronic polyarthritis.

We studied the extent to which exocrine dysfunction of the pancreas is seen among patients with severe chronic polyarthritis and whether it might account for some gastrointestinal symptoms. Our series consisted of 50 such chronic polyarthritis cases; most had rheumatoid arthritis but had neither diagnosed or suspected pancreatitis nor primary Sjögren's syndrome. They were asked about gastrointestinal (GI) and sicca symptoms. The exocrine function of each pancreas was evaluated by the fecal elastase-1-enzyme test. Thirty-two patients had GI symptoms at least weekly. Forty had sicca eye syndrome and 26 had dry mouth. There were two cases (4%; 95% confidence interval, 1-14%) with abnormally low fecal elastase-1-enzyme test level. Chronic GI and sicca symptoms are frequent among patients with severe chronic polyarthritis. Secondary Sjögren's syndrome may cause exocrine insufficiency in the pancreas. That circumstance was not common here, but it is worth remembering because it can be diagnosed by a noninvasive method, and enzyme preparation treatment is available for the symptoms, especially for postprandial pain and distention of the stomach.

Journal Article↗
PubMed1984

General aspects of cadmium: transport, uptake and metabolism by the kidney.

Cadmium taken up from lung and gastrointestinal tract is transported via blood to liver and kidney. On long-term exposure to cadmium, renal tubular dysfunction develops in humans and experimental animals. Data from animal experiments demonstrate that initially after exposure cadmium in blood is bound to albumin and proteins with higher molecular weight. Such cadmium is mainly taken up in liver. For a few days after exposure cadmium exists as metallothionein in plasma and blood cells. After both single and long-term administration of cadmium bound to metallothionein, cadmium is taken up by the kidney. The concentration of metallothionein-bound cadmium in plasma is quite low due to continuous renal clearance. Cadmium from metallothionein is taken up in renal tubules by pinocytosis and subsequently degraded in lysosomes, thereby releasing cadmium which stimulates de novo synthesis of metallothionein but also binds to reabsorbed metallothionein. Catabolizing and rebinding are continuous and prevent excretion of cadmium. Because of differences in transport, renal metabolic handling forms of cadmium are also different for different forms of cadmium administered and rate of administration. A single dose of metallothionein-bound cadmium given intravenously is almost immediately and completely taken up in the renal tubule. Under such conditions, resynthesis and rebinding processes are insufficient to sequester cadmium from sensitive tissue receptors, and renal damage occurs at total tissue concentrations much lower than when renal cadmium concentrations rise slowly. This explains the wide range (10-200 micrograms Cd/g wet weight) of cadmium in the renal cortex that associated with renal tubular dysfunction in experimental animals.

Animals↗
PubMed2002

Cyclo-oxygenase-2 inhibitors and the kidney: a case for caution.

Cyclo-oxygenase (COX) is one of the key enzymes in the biosynthesis of prostaglandins. Two isoforms of this enzyme COX-1 and COX-2 are known to exist. Among other functions, prostaglandins play an important role in the protection of the gastric mucosa and maintenance of renal function in pathophysiological conditions which would otherwise threaten it. Conventional nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin synthesis, resulting in gastric mucosal injury and renal dysfunction in susceptible individuals. The recent introduction of selective COX-2 inhibitors, celecoxib and rofecoxib, appear to induce less gastrointestinal morbidity. Although conclusive data are still lacking, there is evidence to suggest that COX-2 antagonists may be capable of causing some of the same renal syndromes seen in association with the older, less selective NSAIDs.

Animals↗
PubMed1994

Clinical management of intractable constipation.

PURPOSE: To review current management of intractable constipation. DATA SOURCES: Original articles and reviews published in the English-language literature between 1965 and 1993 identified by MEDLINE search. Verbal feedback from attendees after presentation of the document as a clinical symposium at the 14th International Symposium on Gastrointestinal Motility in September 1993. STUDY SELECTION: Key words included constipation, epidemiology, colonic inertia, pseudo-obstruction, pelvic floor dysfunction, and results of therapeutic interventions, particularly the effects of biofeedback training and subtotal colectomy. RESULTS: In most patients, constipation is usually due to lack of dietary fiber and responds to simple measures to correct these factors, often without consulting a physician. In some, probably fewer than 10% of patients who consult their physicians, structural diseases of the colon and rectum, systemic disease, or medications that slow gut transit should be excluded, and regular exercise, dietary fiber, and an osmotic laxative prescribed. In a series of 277 highly selected patients from a tertiary referral center who had intractable constipation, only 29% had a definable abnormality; identification of abnormal transit facilitates selection of patients for further investigations identifying colonic inertia or pelvic floor dysfunction. CONCLUSION: An algorithmic approach can carefully select patients with intractable constipation for behavioral modification and biofeedback; the long-term outcome is excellent, with at least 75% success in several series. In a minority of patients with slow transit constipation unresponsive to medical treatment, subtotal colectomy with ileorectostomy is indicated and effective.

Algorithms↗
PubMed2002

[Digestive manifestations in systemic sclerosis].

Gastrointestinal involvement occurs in most patients with systemic sclerosis. Pathology is characterized by vasculopathy, resulting in tissue ischemia, progressive dysfunction and fibrosis. In its diffuse and visceral pattern, digestive manifestations may involve most of the intestinal tract and are the most frequent before renal, cardiac and pulmonary involvement. Whatever the visceral extension, about 80% of patients have digestive manifestations including gastroesophageal reflux, abnormalities of intestinal motility leading to chronic intestinal pseudo-obstruction and small bowel bacterial overgrowth and malnutrition. Long-term treatment of reflux with high-dose proton pump inhibitors appears safe and effective for symptom relief and may prevent recurrence of esophagitis and stricture. Prokinetic agents effective in pseudoobstruction include metoclopramide, domperidone, octreotide, and erythromycin.

Digestive System↗
PubMed2006

[Pulmonary infection of Pneumocystis carinii and Cytomegalo virus in the treatment of cholesterol crystal embolism].

Cholesterol crystal embolism (CCE) is a multivisceral disease caused by occlusion of small arteries with cholesterol crystal emboli deriving from eroded atherosclerotic plaques of the aorta and/or large feeder arteries. The factors precipitating CCE are manipulation of the aorta or other large arteries during arteriography or surgery, and anticoagulant or thrombolytic therapy. CCE has been reported to be a life threatening condition involving multiple vital organ dysfunction, including renal failure, cardiac failure, skin ischemic lesions such as livedo reticularis, patchy skin necrosis, and purple toes, gastrointestinal ischemia, and/or visual disturbance. We report a 63-year-old male patient of CCE after percutaneous transluminal coronary angioplasty, who contracted severe pneumonia of Pneumocystis carinii and Cytomegalo virus during steroid therapy (prednisolone 20 mg for 3 months). He was treated successfully with mechanical ventilation, hemodialysis, and appropriate antibiotic therapy. Although corticosteroid therapy has been reported to be effective in some CCE patients, the indications of steroid therapy, dosage of corticosteroids, duration of the treatment, or efficacy of prophylactic administration of antibiotics are not yet established. Further interventional studies are required in order to evaluate the benefit of corticosteroid therapy for CCE.

Angioplasty, Balloon, Coronary↗
PubMed1983

Intermittent high-dose aclarubicin in patients with advanced cancer: a phase I study with special reference to cardiac toxicity.

Aclarubicin was given iv every 3 weeks to 21 patients with a variety of solid tumors. Four dose levels were tested: 80, 100, 120, and 140 mg/m2. The median cumulative dose was 270 mg/m2 (range, 80-900). No objective responses were observed. Hematologic toxicity was dose-limiting. All patients experienced moderate to severe gastrointestinal toxicity. Five of 13 patients evaluable for cardiac function showed clinical signs and ECG changes suggestive of cardiac dysfunction. The suggested maximum dose for phase II trials is 120-140 mg/m2 iv given in an intermittent 3-week schedule.

Aclarubicin↗
PubMed1996

Gastric emptying in diabetes: an overview.

Gastric emptying is delayed in 30%-50% of patients with longstanding diabetes mellitus. The prevalence of disordered gastric emptying in patients with "early" Type 2 diabetes is controversial, but it has been suggested that gastric emptying is often accelerated. The pathogenesis of delayed gastric emptying in diabetes is poorly understood. It is, however, clear that acute changes in the blood glucose concentration have a major effect on gastric motor function and gastric emptying. There is an inverse relationship between the rate of gastric emptying and the blood glucose concentration, so that emptying is slower during hyperglycaemia and faster during hypoglycaemia. The motor dysfunctions responsible for delayed gastric emptying in patients with diabetes are heterogeneous. There is a high prevalence of upper gastrointestinal symptoms in diabetes. However, the correlation between symptoms and delay in gastric emptying is poor. Recent studies indicate that the blood glucose concentration modulates the perception of some sensations arising from the gastrointestinal tract. In both normal subjects and patients with diabetes the blood glucose response to oral carbohydrate and gastric emptying are related and there is evidence that modulation of the rate of gastric emptying, by dietary or pharmacological means, could be used to optimise glycaemic control. The use of prokinetic drugs, particularly cisapride, is currently the most effective approach to the treatment of symptomatic patients with gastroparesis. An improved understanding of the pathophysiology of both symptoms and delayed gastric emptying is fundamental to the development of more effective treatments.

Appetite↗
PubMed1997

Zinc toxicosis in a Celebes ape (Macaca nigra) following ingestion of pennies.

An adult Celebes ape (Macaca nigra) was presented for a routine yearly evaluation. Abdominal radiographs revealed four radiodense metallic foreign objects resembling coins within the gastrointestinal tract. Hematologic abnormalities included a mild nonregenerative anemia and a mild leukocytosis, and the biochemical profile reflected renal dysfunction. Serum zinc levels were elevated. The animal was denied food for 24 hr in preparation for the endoscopic removal of the foreign objects. During this period, two partially eroded pennies were passed in the feces. Endoscopy was temporarily postponed, and the animal was offered food. Two days later a third penny was passed. When the fourth coin did not pass within the next 2 days, the animal was once again denied food, and the fourth coin was passed within 24 hr. Because of the temporal association between the fasting cycles and the passage of the coins, a causal relationship is suggested. Following the passage of all coins, serum zinc levels decreased, and hematologic and serum biochemical abnormalities improved. Six months later, all abnormalities had resolved.

Animals↗
PubMed1997

Delayed colonic transit times in amyotrophic lateral sclerosis assessed with radio-opaque markers.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder, characterized by progressive loss of motor neurons. However, ALS has been recognized to involve several non-motor systems, subclinically. Cardiac and sudomotor autonomic involvement in ALS has been described. Recently, delayed gastric emptying was reported. The aim of this study was to assess colonic transit time in patients with ALS. Therefore, measurement of total and segmental colonic transit times using radio-opaque markers was performed in 14 patients with ALS and 14 healthy age-matched volunteers. Multiple-ingestion, single-radiograph technique was used. Segmental and colonic transit times were calculated from the number of retained markers. Nine of 14 patients with ALS showed markedly delayed colonic transit times if compared to healthy controls. Colonic transit in ALS patients was significantly delayed in the right and left colon; the rectosigmoid transit did not show major delay. The colonic transit times did not correlate with bulbar involvement, Norris score, walking disability or duration of the disease. In summary, colonic dysfunction in ALS may be a result of inactivity or inadequate fiber intake. However, it also may represent a gastrointestinal autonomic involvement due to nerval degeneration. Considering ALS as a multisystem disorder including the autonomic nervous system may have implications for research into pathogenesis and therapy of neurodegenerative disease.

Abdominal Pain↗
PubMed2001

Basic pathophysiologic mechanisms in irritable bowel syndrome.

Converging evidence supports the concept that the irritable bowel syndrome (IBS) symptom complex results from altered regulation of gastrointestinal motility and epithelial function, as well as an altered perception of visceral events. Despite similar symptoms, there is likely heterogeneity of underlying dysfunction and pathogenesis in different subgroups of IBS patients: the syndrome may be produced by primary alterations in the central nervous system (CNS; top down model), or by primary alterations in the periphery (bottom up model), or by a combination of both. One plausible mechanism by which alterations in the CNS result in symptoms, is the enhanced responsiveness of central stress/emotion circuits. The physiological effects of psychological and physical stressors on gut function and brain-gut interactions are mediated by outputs of the emotional motor system in terms of autonomic, neuroendocrine, attentional and pain modulatory responses. IBS patients show an enhanced responsiveness of this system manifesting in altered modulation of gastrointestinal motility, secretion, immune function and in alterations in the perceptual and emotional response to visceral events.

Animals↗