Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cisapride induces acetylcholine release in cells of the myenteric plexus, thus promoting gastrointestinal motility. We studied the effects of cisapride on 11 patients with idiopathic gastroparesis. All had negative gastrointestinal endoscopy, normal glucose, and took no drugs capable of influencing motility. Most (9/11) were prior metoclopramide treatment failures. Patients' symptoms were scored (0-60) for pain, satiety, bloating, nausea, vomiting, and heartburn. All underwent a solid gastric emptying study using a Technetium-99-labeled egg meal and received placebo prior to cisapride. There were 10 females and one male with a mean (+/- SE) age of 37.8 +/- 2.6 years. Disease duration was 7.9 +/- 2.8 years. The dose of cisapride was 30-60 mg/day and the duration of therapy was 12.6 +/- 2.6 months (range 2.5-25 months). The symptom score improved on cisapride from 30.9 +/- 3.6 to 14.4 +/- 2.7 (P < 0.002 signed rank test). Emptying half-time improved from 113 +/- 4 min to 94 +/- 6 min, and 46.9 +/- 2.4% food remaining at 120 min decreased to 35.5 +/- 3.6% (both P < 0.05). Emptying half-time in normals was 68 +/- 5 min with 16.9 +/- 2.9% remaining at 120 min. Nine of 11 patients gained weight, with a mean increase of 6.7 +/- 1.6 lb (range 2-12 lb). We conclude that cisapride significantly reduces gastrointestinal symptoms and promotes weight gain in patients with idiopathic gastroparesis and is associated with improvement in solid gastric emptying. The drug is useful in patients who previously failed metoclopramide.
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PMID:Open label study of long-term effectiveness of cisapride in patients with idiopathic gastroparesis. 802 48

Diabetic neuropathy is the most frequent complication of diabetes and the leading cause of polyneuropathy in the Western world. A distal symmetric predominantly sensory polyneuropathy is the most common of the diverse neuropathies that occur secondary to diabetes. Pain is often the most bothersome and difficult to treat symptom of diabetic neuropathy. Autonomic neuropathy is a frequent feature of diabetic neuropathy and the source of many significant problems including postural hypotension, gastroparesis, diarrhea, constipation, neurogenic bladder, and male impotence. Physicians need to be familiar with the multiple, less common forms of diabetic neuropathy, as these often mimic other medical or neurologic conditions. The cause of diabetic neuropathy is not determined, but abundant evidence suggests that both metabolic and ischemic nerve injury are likely factors. These should not be considered mutually exclusive causes of diabetic neuropathy as both factors likely operate to different degrees to produce the clinical spectrum of neuropathies that are seen in diabetes. Although no effective treatment exists to cure diabetic neuropathy, improvement is possible with glycemic control and symptomatic therapy.
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PMID:Neuropathies associated with diabetes. 841 16

The objective of the study was to assess the efficacy of sucralfate in promoting duodenal ulcer healing and to assess the value of some variables in predicting outcome of such therapy. Following variables were tested for predicting the outcome: age at onset, age at presentation, duration of symptoms, sex, periodicity, smoking, nocturnal pain, relief by food, relief by antacid, gastric stasis like symptoms, associated irritable bowel syndrome, site, size and number of ulcers and degree of deformity of bulb. Sixty patients with uncomplicated DU confirmed at endoscopy were treated with sucralfate one gram before three major meals and 1 g at bedtime for two months. Endoscopy was repeated at the end of the trial. There were four drop-outs. Complete, partial and no healing occurred in 45 (80.36)%, 3 (5.36%) and 8 (14.28%) subjects. Ulcer healing rate was higher in those without gross bulbar deformity (41/46) than in those with gross deformity (4/10), (Odd's ratio 12.3, 95% ci 1.98 to 78.44). Other variables were not found to be associated with ulcer healing.
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PMID:Predictors of duodenal ulcer healing in sucralfate treated patients. 910 58

The effect of long-term cisapride therapy (20 mg orally three times daily for 2 years) on gastric emptying and gastrointestinal symptoms was investigated in 30 patients with severe gastroparesis (24 idiopathic, 6 diabetic). Symptoms were assessed every 2 months, using an overall symptom score based on six symptoms (anorexia, nausea, vomiting, pain, early satiety and bloating), and a 2-year mean overall symptom score was used for analysis. Gastric emptying was measured at 0, 6, 12, 18 and 24 months. Of the 24 patients who completed the study, 10 showed a significant improvement in gastric emptying (P < 0.05) and felt improved on therapy, seven patients showing a > 20% improvement in overall symptom score compared to baseline. Results for 15 patients who underwent at least one follow-up gastric-emptying test showed only a weak correlation between individual symptom score and gastric emptying (r = 0.40). Thus long-term cisapride therapy at the study dose produced long-term symptomatic improvement in 42% of patients with severe gastroparesis, with sustained acceleration of gastric emptying for up to 2 years.
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PMID:Cisapride in the long-term treatment of chronic gastroparesis: a 2-year open-label study. 928 90

Gastroparesis, defined as delayed gastric emptying because of abnormal gastric motility in the absence of mechanical outlet obstruction, is a common problem causing significant morbidity. Although many cases are caused by diabetes, more than 90 different conditions are known to interfere with normal gastric motor function (Scand J Gastroenterol 1995;30[suppl]:7-16). Patients may present with nausea, vomiting, heartburn, early satiety, or postprandial pain. The current gold standard for quantifying gastric emptying is nuclear scintigraphy. The main goal of treatment is to improve patient comfort by accelerating the rate of gastric emptying, which may be achieved through dietary changes and the use of prokinetic agents. In rare instances, relief can only be obtained with surgical intervention. This report reviews the pathophysiology, clinical presentation, evaluation, and treatment of patients with gastroparesis, an understanding of which will lead to more effective patient care.
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PMID:University of Miami Division of Clinical Pharmacology therapeutic rounds: update on diagnosis and treatment of gastroparesis. 1042 52

The aim of this study was to evaluate results of completion gastrectomy for severe postgastrectomy gastric stasis. A total of 51 women and 11 men underwent completion gastrectomy for gastric stasis between 1985 and 1996; follow-up was complete in 98% at 5.4 +/- 5 years. All patients had modified Visick scores preoperatively of grade III (37%) or IV (63%). Presentation included combinations of nausea, vomiting, postprandial pain, chronic abdominal pain, and chronic narcotic use. All had undergone prior vagotomy and had a median of four previous gastric operations. Hospital mortality was zero. Complications occurred in 25 patients (40%) and included the following: narcotic withdrawal syndrome (18%), ileus (10%), wound infection (5%), intestinal obstruction (2%), and anastomotic leak (5%). All or most symptoms were relieved in 43% (Visick grade I or II), but 57% of the patients remained in Visick grade III or IV. Nausea, vomiting, and postprandial pain were reduced from 93% to 50%, 79% to 30%, and 58% to 30%, respectively (P<0.05), but chronic pain, diarrhea, and dumping syndrome were not significantly affected. Univariate analysis revealed no preoperative characteristic to be predictive of good outcome. Logistic regression analysis suggested that the combination of nausea, need for total parenteral nutrition, and retained food in the stomach predicted a poor outcome (P<0.05). Completion gastrectomy is successful in 43% of patients. The combination of nausea, need for total parenteral nutrition, and retained food at endoscopy are negative prognostic factors.
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PMID:Near-total completion gastrectomy for severe postvagotomy gastric stasis: analysis of early and long-term results in 62 patients. 1045 19

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

Postoperative nausea and vomiting (PONV) are unpleasent for patients and increase the risk of aspiration pneumonia. PONV is the leading cause of unexpected admission following planned day surgery. Despite new anaesthetic drugs and antiemetics, the incidence of PONV remains high. The incidence of PONV depends numerous factors including age, gender, obesity, anxiety, gastroparesis, history of motion sickness, previous PONV, and the duration and type of surgery. Anaesthesia related factors include premedication, ventilation techniques, and postoperative pain management. Recently, the intraoperative inspired oxygen concentration was identified as a factor that influences PONV. Among the three studies that evaluated intraoperative supplemental O2 for prevention of PONV, two found that it halves PONV while the third failed to identify any benefit. Since supplemental O2 is inexpensive and essentially risk-free, it appears preferable to pharmacologic anti-emetics for prevention of PONV in abdominal surgery.
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PMID:Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. 1202 76

The purpose of this study was to define the place of endovascular treatment in chronic intestinal ischemia (CII). We report here a series of 19 consecutive patients treated with percutaneous angioplasty of the intestinal arteries. We excluded patients with acute ischemia, from the study. From January 1, 1989 to December 31, 2001, 19 patients with symptomatic CII were treated by endovascular techniques. This study group included 11 men and 8 women with a mean age of 59 years (range 30 to 90 years). The clinical presentation included postprandial pain in 16 patients, weight loss in 14 patients, with a mean weight loss of 7.4 kg (range 0 to 30 kg); and gastroparesis in 2 patients. Stenoses were significant in the single superior mesenteric artery (SMA) in 2 patients and in two arteries in 17 patients, including the celiac artery (CA) and SMA (n = 13), CA and inferior mesenteric artery (IMA) (n = 1), and SMA and IMA (n = 3). Balloon angioplasty was performed in only one of the arteries in each patient, 15 times in the SMA and 4 times in the CA. In 7 patients, angioplasty required stenting because of recoil (n = 5) or dissection (n = 1). In one patient the lesion was stented primarily, because of adjacent thrombus on the stenosis. Our results showed that initial treatment of CII can be endovascular. Focus on one artery only, seems to be reasonable and efficient in the short and long term.
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PMID:Endovascular treatment as first choice in chronic intestinal ischemia. 1239 8

Currently, electrical stimulation is utilized to treat morbid obesity, gastroparesis, and diaphragmatic paralysis. Although this technology is in its infancy, numerous case reports and small series appear throughout the literature. Furthermore, electrical stimulation is not relegated to only academic centers and tertiary referral centers. As these technologies continue to evolve and alter the treatment of several different pathophysiologic processes, the general surgeon needs to understand the technical aspects of these devices and their potential complications. This paper presents the management of a gastroparetic patient with chronic abdominal pain following the successful placement of gastric pacing wires. A 45-year-old female with idiopathic gastroparesis underwent laparoscopic placement of gastric pacing wires without complications. Four months postoperatively, she presented with chronic left upper quadrant abdominal pain. Her nausea and vomiting had dissipated and she was tolerating a regular diet. Abdominal and pelvic computed tomography (CT) was normal except for the presence of a generator and pacing wires. Ultimately, she required a diagnostic laparoscopy and an upper endoscopy. The upper endoscopy was normal. The diagnostic laparoscopy showed a wide adhesive band from the seromuscular tunnel of the pacing wires to the abdominal wall in the left upper quadrant. The band was lysed and an omental patch was sutured over the insertion site of the wires. On postoperative day 1, the patient was pain-free and discharged home on a regular diet. This case presents an unusual complication of electrical pacing wires. This patient experienced somatic pain due to an adhesive band from her pacing wires to the abdominal wall. Based on the findings of this case, an omental patch was placed on top of the seromuscular electrode tunnel in order to prevent adhesions and potentially persistent abdominal wall pain.
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PMID:Laparoscopic revision of gastric pacing wires. 1524 74


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