Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Several serotonin (5-HT) receptor subtypes have been defined by pharmacological responses to selective agonists and antagonists and by pathways of receptor-effector coupling. Using molecular techniques, additional receptor subtypes have been described. 5-HT receptors are prevalent in the central nervous system and gut and participate in induction of emesis. 5-HT3 antagonists are used to prevent emesis from cancer chemotherapy and also demonstrate efficacy in radiation-induced nausea, postoperative nausea, hyperemesis gravidarum, and nausea and vomiting with the acquired immunodeficiency syndrome. 5-HT4 agonists exhibit prokinetic properties in nauseated patients with gastroparesis and functional dyspepsia. Conversely, 5-HT4 antagonists have antiemetic activity in some experimental models. The 5-HT1D receptor agonist sumatriptan reduces emesis with migraine headaches and in cyclic vomiting syndrome, most likely via action on central nervous system sites. In other models, 5-HT1A and 5-HT2A/5-HT2C agonists exhibit antiemetic properties. The utility of 5-HT receptor ligands in treating emesis is the subject of active investigation.
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PMID:Serotonin receptor physiology: relation to emesis. 1049 49

A kidney transplant patient with diabetic gastroparesis was effectively treated by jejunal feeding. The patient, a 31-year-old woman, has a complicated medical history, with insulin-dependent diabetes mellitus. Complications include kidney failure followed by transplantation, bilateral knee amputations, and being registered blind. She was admitted with nausea and vomiting for the previous 6 days; the provisional diagnosis was diabetic gastroparesis. Various treatments were tried, including several prokinetic drugs and total parenteral nutrition. The total parenteral nutrition provided most of the patient's nutritional requirements, and, only slight weight loss was observed. Nothing seemed to improve the symptoms of vomiting. An endoscopic retrograde cholangiopancreatography, a radiographic examination of the bile and pancreatic ducts, was performed to exclude obstruction. At the same time, having found nothing, a gastrostomy was placed with a jejunal extension. Feeding was established within 3 days. Her weight remained stable after 7 weeks of jejunal feeding. She had started to increase her oral intake of solid foods and fluids. By 8 weeks, she was taking a full oral diet and fluids. Now, 14 weeks after the placement of the gastrostomy tube with the jejunal extension, she is doing well. Her weight remains stable and her oral intake is excellent. Her diabetes is under control. After 22 weeks, the gastrostomy was removed. After this success with jejunal feeding when all other treatments had failed, this treatment could be used to treat future diabetic gastroparesis. Slow introduction of the feed seems to help toleration.
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PMID:Gastroparesis and jejunal feeding. 1052 53

Nausea and vomiting are debilitating symptoms complicating many clinical conditions. Conventional antiemetic agents act as muscarinic, histamine, and dopamine receptor antagonists in the central nervous system. In a retrospective analysis, tricyclic antidepressant drugs demonstrated efficacy in long-term treatment of functional nausea. Some cases of vomiting result from impaired gastrointestinal motor activity. Agents which act on gastric serotonin (5-HT4), dopamine, and motilin receptors accelerate gastric emptying and relieve symptoms in gastroparesis. Recent investigations suggest that some patients with refractory gastroparesis may benefit from gastric electrical pacing. The treatment of acute chemotherapy-induced emesis was revolutionized by 5-HT3 receptor antagonists; however, these agents are less efficacious in delayed vomiting. Neurokinin (NK-1) receptor antagonists show promise in treating delayed chemotherapy-evoked emesis. Furthermore, animal studies indicate a broad spectrum of action for NK-1 antagonists in treating diverse causes of nausea and vomiting. The cyclic vomiting syndrome is characterized by discrete episodes of relentless vomiting separated by asymptomatic intervals and is associated with migraine headaches. Antimigraine therapies including the 5-HT1D receptor agonists sumatriptan reduce the severity of cyclic vomiting attacks. Investigations into these and other novel treatments may provide important advances in the care of difficult cases of nausea and vomiting resulting from disparate illnesses.
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PMID:Novel approaches to the treatment of nausea and vomiting. 1069 61

Gastroparesis-or delayed gastric emptying--is associated with upper gastrointestinal symptoms that include early satiety, nausea, vomiting, regurgitation, fullness, and bloating. Gastroparesis should be considered in the diagnosis of a patient with these symptoms after mechanical and structural lesions have been ruled out. This review briefly summarizes gastric motor physiology and discusses the etiology and diagnostic approach to the treatment of a patient with possible gastroparesis. We highlight the methods available to measure gastric motility and describe their relative advantages and disadvantages.
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PMID:The diagnosis and work-up of the patient with gastroparesis. 1073 Sep 17

Paraduodenal hernia (PDH) is an unusual condition that is caused by congenital intestinal malrotation. Noncatastrophic presenting symptoms and their responses to surgery have not been well-characterized. Barium upper gastrointestinal (UGI) series and small bowel follow-up x-rays, performed from December 1995 to September 1996, were sequentially reviewed by one radiologist (J.M.) to identify patients with small bowel series compatible with a PDH. Case histories were reviewed for symptomatic presentation, associated evaluation, and treatment. Based on the 294 UGIs and small bowel follow-throughs performed during this 10-month period, 6 cases were suspected to have a PDH. A right PDH was confirmed in the three patients who underwent surgical exploration (prevalence 1%). Preoperative patient symptoms included nausea, bilious vomiting, and right upper quadrant pain. Repair of the hernia defect resulted in complete resolution of chronic symptoms. Preoperative upper endoscopy, performed in three patients, was not helpful in identifying the disorder. Preoperative computerized tomography obtained in two patients was diagnostic for a right PDH. One symptomatic patient with vomiting and gastric stasis did not have surgery because of a terminal illness. The remaining two patients had no symptoms attributable to PDH. Patients with PDH frequently have chronic UGI symptoms. An upper endoscopy cannot be used to exclude this entity. After surgery, UGI symptoms from PDH are likely to resolve.
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PMID:Paraduodenal hernia: a treatable cause of upper gastrointestinal tract symptoms. 1103 2

Hemodialysis patients frequently experience such dyspeptic symptoms as nausea, vomiting, abdominal distension, early satiety, and anorexia. Gastroparesis might be a cause of malnutrition, and parameters of gastric emptying are inversely correlated with serum albumin levels. The aim of the present study is to determine whether delayed gastric emptying is related to dyspeptic symptoms. In 54 hemodialysis patients, a standardized history for dyspeptic symptoms was taken. In addition, gastric emptying for solids was measured in 26 patients, using the (13)C-octanoic acid breath test. There was a high prevalence of dysmotility-like dyspepsia in the hemodialyzed population. A significant difference in gastric emptying between dyspeptic hemodialysis patients and healthy volunteers and between dyspeptic and nondyspeptic hemodialysis patients was shown. There was a significant correlation between gastric emptying and dysmotility-like dyspepsia. Serum albumin level inversely correlated with gastric emptying. In conclusion, there is a high prevalence of dysmotility-like dyspepsia in hemodialysis patients. Dyspeptic patients have significantly delayed gastric emptying compared with both healthy volunteers and nondyspeptic patients.
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PMID:Delayed gastric emptying in dyspeptic chronic hemodialysis patients. 1105 52

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

Nutritional support is essential in treating patients with gastroparesis. Initially, dietary changes should be instituted to reduce extra fat and bulk, and patients should be encouraged to eat frequent small meals with liquid supplementation. Enteral feeding should be introduced in the event of weight loss or persistent vomiting. Medical therapy is usually necessary early in treatment. Cisapride is the initial agent of choice and may be combined with an antiemetic agent, such as promethazine or chlorpromazine or, if side effects occur, ondansetron and granesitron. If cisapride is ineffective or contraindicated, metoclopramide is a reasonable option, though limited by side effects. Erythromycin is useful in the acute treatment of postoperative ileus and hospitalized gastroparetic patients, but its role is limited based on concerns about poor long-term effectiveness and antimicrobial resistance. Once domperidone becomes available in the United States, it will be useful for its promotility and antiemetic qualities. Combination therapy should be considered if monotherapy with cisapride or metoclopramide alone is ineffective. While not yet well studied, combination therapy has the potential to offer dramatic benefit for patients with refractory gastroparesis. Metoclopramide may be added to cisapride for patients with breakthrough symptoms or refractory chronic symptoms. Other combinations include metoclopramide with erythromycin, domperidone with cisapride, and domperidone with erythromycin. In the future, gastric pacing may become an effective option for patients not responding to medical therapy. Total gastrectomy should be performed only for end-stage gastroparesis when all other therapy has failed. Both procedures should be reserved for centers that specialize in severe gastric motility disorders.
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PMID:Diabetic and Nondiabetic Gastroparesis. 1109 57


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