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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with gastroparesis frequently present challenging clinical, diagnostic, and therapeutic problems. Data from 146 gastroparesis patients seen over six years were analyzed. Patients were evaluated at the time of initial diagnosis and at the most recent follow-up in terms of gastric emptying and gastrointestinal symptomatology. The psychological status and physical and sexual abuse history in female idiopathic gastroparesis patients were ascertained and an association between those factors and gastrointestinal symptomatology was sought. Eighty-two percent of patients were females (mean age: 45 years old). The mean age for onset of gastroparesis was 33.7 years. The etiologies in 146 patients are: 36% idiopathic, 29% diabetic, 13% postgastric surgery, 7.5% Parkinson's disease, 4.8% collagen vascular disorders, 4.1% intestinal pseudoobstruction, and 6% miscellaneous causes. Subgroups were identified within the idiopathic group: 12 patients (23%) had a presentation consistent with a viral etiology, 48% had very prominent abdominal pain. Other subgroups were gastroesophageal reflux disease and nonulcer dyspepsia (19%), depression (23%), and onset of symptoms immediately after cholecystectomy (8%). Sixty-two percent of women with idiopathic gastroparesis reported a history of physical or sexual abuse, and physical abuse was significantly associated with abdominal pain, somatization, depression, and lifetime surgeries. At the end of the follow-up period, 74% required continuous prokinetic therapy, 22% were able to stop prokinetics, 5% had undergone gastrectomy, 6.2% went onto gastric electrical stimulation (pacing), and 7% had died. At some point 21% had required nutrition support with a feeding jejunostomy tube or periods of parenteral nutrition. A good response to pharmacological agents can be expected in the viral and dyspeptic subgroups of idiopathics, Parkinson's disease, and the majority of diabetics, whereas a poorer outcome to prokinetics can be expected in postgastrectomy patients, those with connective tissue disease, a subgroup of diabetics, and the subset of idiopathic gastroparesis dominated by abdominal pain and history of physical and sexual abuse. Appreciation of the different etiologies and psychological status of the patients may help predict response to prokinetic therapy.
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PMID:Demography, clinical characteristics, psychological and abuse profiles, treatment, and long-term follow-up of patients with gastroparesis. 982 25

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Although aspiration is a relatively rare event during anaesthesia, it represent an important cause of anaesthesia related mortality and also of ventilator associated pneumonia in intensive care unit. The incidence of aspiration is markedly increased after trauma owing to the risk of recent ingestion of food, depression of consciousness and airways reflexes, and gastric stasis induced by raised sympathoadrenal tone. The factors which contribute to the likelihood of aspiration include the urgency of surgery, airways problems, inadequate depth of anaesthetic, use of the lithotomy position, gastrointestinal problems, depressed consciousness, increased severity of illness and obesity. Factors that predispose to aspiration pneumonia are: a gastric content with a pH less than 2.5 and a gastric volume of 0.4 ml kg-1; a reduction in lower oesophageal sphincter tone; a reduction of upper oesophageal sphincter tone and a not coordination between the pharyngeal muscle and the upper oesophageal sphincter tone during swallowing; and a depression of protective airway reflexes. Methods to minimize regurgitation and aspiration involve control of gastric contents (preoperative starvation is the method universal accepted), application of cricoid pressure and control of the airways.
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PMID:Gastric reflux and pulmonary aspiration in anaesthesia. 1276 74

A 5-year-old pet rabbit (Oryctolagus cuniculus) died after a 3-day history of anorexia and depression. At necropsy, the stomach was distended with dough-like ingesta and hair consistent with gastric stasis syndrome. The lungs had multifocal, raised red nodules with circumferential hemorrhage. Microscopic examination showed pulmonary hemorrhage with intravascular fibrin thrombi and bacterial colonies, which were present in lesser amounts in the kidney, heart, and liver. Bacterial culture of the lung produced a heavy pure growth of Actinobacillus capsulatus. Acute septicemia is a novel presentation for this pathogen. This is the first documented case of A. capsulatus disease in the contiguous United States and may represent an underdiagnosed to emerging disease of lagomorphs.
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PMID:Actinobacillus capsulatus septicemia in a domestic rabbit (Oryctolagus cuniculus). 1569 Sep 60

The key points of this article are anorexia and cachexia are: A major cause of cancer deaths. Several drugs are available to treat anorexia and cachexia. Dyspnea in cancer usually is caused by several factors. Treatment consists of reversing underlying causes, empiric bronchodilators, cortico-steroids--and in the terminally ill patients-opioids, benzodiazepines,and chlorpromazine. Delirium is associated with advanced cancer. Empiric treatment with neuroleptics while evaluating for reversible causes is a reasonable approach to management. Nausea and vomiting are caused by extra-abdominal factors (drugs,electrolyte abnormalities, central nervous system metastases) or intra-abdominal factors (gastroparesis, ileus, gastric outlet obstruction, bowel obstruction). The pattern of nausea and vomiting differs depending upon whether the cause is extra- or intra-abdominal. Reversible causes should be sought and empiric metoclopramide or haloperidol should be initiated. Fatigue may be caused by anemia, depression, endocrine abnormalities,or electrolyte disturbances that should be treated before using empiric methylphenidate. Constipation should be treated with laxatives and stool softeners. Both should start with the first opioid dose.
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PMID:Common symptoms in advanced cancer. 1583 69

Many patients with diabetes mellitus suffer from upper and lower GI symptoms. The reported prevalence of these symptoms varies among different ethnic groups/populations. The natural history of GI symptoms as well as their pathogenesis in patients with diabetes remains poorly understood, although it is known that gastric emptying is influenced by hyperglycemia, euglycemia, and hypoglycemia. Poor glycemic control over a long period of time can lead to neuropathy and damage the vagus nerve, resulting in diabetic gastroparesis whose signs and symptoms vary in the individual patient. Gastroparesis can further worsen glycemic control by adversely altering the pharmacokinetics of orally administered hypoglycemic agents as well as by altering the delivery of diet-derived calories to intestines from which absorption, subsequently, determines incipient blood glucose, and thus effectiveness of various injectable antidiabetics including various insulins and related insulin analogs. As GI symptoms may overlap with other disorders, including functional dyspepsia, irritable bowel syndrome, and depression, it is important to have such patients/patients with diabetes undergo standardized testing for measuring gastric emptying. Certain medications including metformin, amylin analogues (i.e. pramlintide), glucagon-like peptide 1 analogs (i.e. exenatide, liraglutide), anticholinergic agents, antidepressants, calcium-channel blockers, and others may contribute to GI symptoms observed in patients with diabetes. Given the global diabetes pandemic, it is of utmost importance to not only diagnose and treat present patients with diabetes mellitus and its comorbidities, but also to help prevent the development of further disease burden by educating children and adolescents about healthy lifestyle modifications (avoidance of overeating, portion control, healthy food choices, increased physical and reduced sedentary activity), as changing behavior in adulthood has proven to be notoriously difficult.
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PMID:Are gastrointestinal symptoms related to diabetes mellitus and glycemic control? 1879 3

Opioids are important as medication against postoperative pain in infants and children too. However, intraoperatively given opioids increase the analgesic demand in the postoperative period without an improvement of the postoperative pain. Nausea, vomiting, respiratory depression and gastroparesis develop. The apparent benefit of a stable anaesthetic has to be bought with relevant drawbacks. Modern concepts heavily rely on local anaesthetics and nonsteroidals for postoperative analgesia.
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PMID:[Generous use of opioids is advantageous for infants and children--Contra]. 2066 56

Patients with gastroparesis often present a challenge to the treating physician. Postprandial symptoms with nausea and vomiting may not only lead to nutritional and metabolic consequences, but also cause significant disruptions to social activities that often center around food. While the definition of gastroparesis focuses on impaired gastric emptying, treatment options that affect gastric function are limited and often disappointing. The female predominance, the mostly idiopathic nature of the illness with a common history of abuse, and coexisting anxiety or depression show parallels with other functional disorders of the gastrointestinal tract. These parallels provided the rationale for some initial studies investigating alternative therapies that target the brain rather than the stomach. This emerging shift in medical therapy comes at a time when clinical studies suggest that gastric electrical stimulation may exert its effects by modulating visceral sensory processing rather than altering gastric motility. Physiologic and detailed anatomic investigations also support a more complex picture with different disease mechanisms, ranging from impaired accommodation to apparent visceral hypersensitivity or decreased interstitial cells of Cajal to inflammatory infiltration of myenteric ganglia. Delayed gastric emptying remains the endophenotype defining gastroparesis. However, our treatment options go beyond prokinetics and may allow us to improve the quality of life of affected individuals.
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PMID:Gastroparesis: concepts, controversies, and challenges. 2427 91

Patients with advanced pancreatic cancer (APC) require early and frequent palliative interventions to achieve optimal quality of life for the duration of illness. Evidence-based supportive treatments exist to maximize quality of life for any patient, whether receiving chemotherapy or not. This article provides a comprehensive review of symptoms with current treatment recommendations and directions for future development. Celiac plexus neurolysis improves pain in the majority of patients with APC and should be moved earlier in the analgesic paradigm. Malignant bowel obstruction can be palliated quickly with optimal management via gastric decompression, octreotide, parenteral opioids, and standing antiemetics. Recommendations are provided for best treatment of malignant gastroparesis, gastric outlet obstruction, and chemotherapy-induced nausea and vomiting in this population. Malignant ascites can be treated initially with diuretics and sodium-restriction in patients with an exudative process; however, an indwelling catheter is recommended for patients with recurrent ascites, particularly because of carcinomatosis or a refractory process. With exocrine insufficiency contributing to weight loss, pancreatic enzyme replacement is essential to improve nourishment in the majority of patients. Presently, megestrol acetate is the only U.S. Food and Drug Administration (FDA)-approved therapy for the anorexia-cachexia syndrome, although future developments are promising. Finally, patients with advanced pancreatic cancer should be screened and treated early for depression as a common comorbid diagnosis. Early palliative care consultation also helps address the existential and psychosocial concerns of patients facing death from pancreatic cancer in a holistic manner.
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PMID:A myriad of symptoms: new approaches to optimizing palliative care of patients with advanced pancreatic cancer. 2445 42

Rumination is a normal and common phenomenon among ruminant animals; but in humans, it is always regarded as symptom indicative of abnormal function of the upper gastrointestinal tract, and understanding of the mechanisms explaining this event are still evolving. Learning-based theories, organic factors such as gastroesophageal reflux disease and psychological disturbances (eg, depression, anxiety) and the role of life stresses have been postulated as potential mechanisms of rumination. In this review, we take the approach that rumination syndrome is a distinct and discrete functional gastroduodenal disorder. We review current concepts of the pathophysiology of this entity and diagnostic approaches, then detail the treatment paradigms that have been pursued in rumination syndrome in adults. Patients with rumination syndrome have a very distinct set of symptoms. It was focused on the immediate postprandial period, but recently, there is an awareness of an expanding spectrum of the clinical presentation. This includes the concept of "conditioned vomiting" occurring in the setting of delayed gastric emptying (gastroparesis). Physicians' awareness of rumination syndrome is essential in the diagnosis and management of this disorder. Stress and psychological aspects in rumination syndrome are invariably in the background and have to be addressed. The crucial steps in the treatment strategy for rumination syndrome rely on reassurance, education and a physiologic explanation to the patient and family that this is not a "disease," followed by behavioral and relaxation programs and addressing stress factors.
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PMID:Rumination syndrome: a review of current concepts and treatments. 2464 53


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