Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During disease, infection, or trauma, the cytokine tumor necrosis factor alpha (TNF alpha) causes fever, fatigue, malaise, allodynia, anorexia, gastric stasis associated with nausea, and emesis via interactions with the central nervous system. Our studies have focused on how TNF alpha produces a profound gastric stasis by acting on vago-vagal reflex circuits in the brainstem. Sensory elements of this circuit (i.e., nucleus of the solitary tract [NST] and area postrema) are activated by TNF alpha. In response, the efferent elements (i.e., dorsal motor neurons of the vagus) cause gastroinhibition via their action on the gastric enteric plexus. We find that TNF alpha presynaptically modulates the release of glutamate from primary vagal afferents to the NST and can amplify vagal afferent responsiveness by sensitizing presynaptic intracellular calcium-release mechanisms. The constitutive presence of TNF alpha receptors on these afferents and their ability to amplify afferent signals may explain how TNF alpha can completely disrupt autonomic control of the gut.
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PMID:TNFalpha: a trigger of autonomic dysfunction. 1791 Dec 24

Gastroparesis is a disorder of the stomach caused by delayed gastric emptying in the absence of mechanical obstruction. Symptoms of gastroparesis include nausea, vomiting, early satiety, bloating, and abdominal discomfort. Gastroparesis has been described as a complication of several malignancies, including gastric, pancreatic, gallbladder, esophageal, and lung cancers, as well as leiomyosarcoma. The prevalence of malignant gastroparesis (MG) is unknown, and this entity is widely underrecognized and undertreated. Diabetes mellitus is the most common identifiable cause of benign gastroparesis, ie, gastroparesis occurring in the absence of an underlying malignant pathology. In the setting of malignancy, gastroparesis may result from the cancer itself or may be a complication of its treatment with such modalities as surgery, radiation therapy, or chemotherapy. Coexisting conditions, including diabetes, hypothyroidism, and neurologic diseases, may further exacerbate MG. The pathogenesis of MG is not clearly understood at present. However, mechanisms suggested in the literature include postvagotomy syndrome, malignant infiltration of the autonomic nervous system, and paraneoplastic dysmotility with autoantibody-mediated destruction of the enteric nervous system (the interstitial cells of Cajal, also called the intrinsic pacemaker of the gastrointestinal tract, or the myenteric plexus). Appropriate treatment of MG may help to avoid serious consequences, such as cancer cachexia, intolerance of oral anticancer agents, dehydration, and hospitalization. In this article, we will describe our institutional experience with MG and will provide a concise review of the literature. Guidelines for management will be suggested.
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PMID:Malignant gastroparesis: pathogenesis and management of an underrecognized disorder. 1794 45

This review addresses the current concepts in our understanding of the epidemiology, mechanisms, symptoms, clinical consequences, diagnosis and treatment of delayed gastric emptying in patients with diabetes. Upper gastrointestinal symptoms, particularly postprandial fullness, nausea, vomiting and abdominal bloating, occur in 30-50% of patients with diabetes. The use of scintigraphic techniques, and more recently breath test, has shown that as many as 50% of diabetic patients have gastroparesis. Diabetic gastroparesis comprises a decrease in fundic and antral motor activity, a reduction or a lack of the interdigestive migrating motor complex, gastric dysrhythmias, and pylorospasms. The mechanisms involved include: autonomic neuropathy, acute hyperglycaemia, and abnormalities in gastrointestinal hormones and neuropeptides. Other possible contributing factors such as hypothyroidism and H. pylori infection are discussed as well. Because treatment is possible by means of dietary advise, prokinetics or surgical procedures, it is important to identify risk factors for and to diagnose gastroparesis to prevent morbidity by controlling gastrointestinal symptoms, and to enhance glucoregulation. Understanding the current advances is key to the development of novel therapeutic strategies and for making rational choices in the management of diabetic gastroparesis.
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PMID:Current concepts in gastric motility in diabetes mellitus. 1822 Jun 21

Gastroparesis is a disorder of gastric emptying that occurs in the absence of mechanical obstruction. Its cardinal features include nausea, vomiting, bloating, early satiety and discomfort. Weight loss, dehydration, electrolyte disturbances and malnutrition may develop in severe cases. The majority of cases is idiopathic, long standing diabetes mellitus is responsible for about 25-30% of cases. Diabetic gastroparesis may render glucose control extremely difficult, its treatment represents a major challenge. Besides frequent, small meals and psychological support, several drug options are available, however, their efficacy is limited and only a few randomized studies have been performed to date. Prokinetic agents (erythromycin, domperidone, metoclopramide) and antiemetics (phenothiazines, serotonin antagonists, butyrophenones) are the most wide-spread medicaments. Among the novel, recently developed agents, 5-HT4 serotonin receptor agonists and dopamine D2 receptor antagonists are the most promising. Injection of botulinum toxin into the pyloric sphincter resulted in faster gastric emptying and symptom alleviation in some studies. Gastric electric stimulation appears to be one of the most effective options, both low and high-frequency stimulation may alleviate symptoms. Gastrostomy/jejunostomy and other surgical interventions are considered as "last resort".
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PMID:[Gastroparesis and its treatment options]. 1829 33

The concept of the gut forming the centre of an integrated gut-brain-energy axis - modulating appetite, metabolism and digestion - opens up new paradigms for drugs that can tackle multiple symptoms in complex upper gastrointestinal disorders. These include eating disorders, nausea and vomiting, gastroesophageal reflux disease, gastroparesis, dyspepsia and irritable bowel syndrome. The hormones that modulate gastric motility represent targets for gastric prokinetic drugs, and peptides that modify eating behaviours may be targeted to develop drugs that reduce nausea, a currently poorly treated condition. The gut-brain axis may therefore provide a range of therapeutic opportunities that deliver a more holistic treatment of upper gastrointestinal disorders.
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PMID:Hormones of the gut-brain axis as targets for the treatment of upper gastrointestinal disorders. 1830 13

A case of synchronous adrenocortical carcinoma (ACC) and renal cell carcinoma (RCC) has not yet been described in the English medical literature, to our knowledge. We report a first such case of adrenocortical and renal cell carcinomas occurring simultaneously in a 53-year-old male. He presented with history of vague abdominal pain. Ultrasound followed by a computed tomography (CT) scan and a magnetic resonance imaging (MRI) examination revealed a 6.4 cm left adrenal mass and a 3.5 cm right renal mass. The patient had complaints of gastroparesis manifesting with constant nausea as well as intermittent abdominal bloating and abdominal pain. He also had history of profuse intermittent sweating. There was no history of palpitations or fluctuations in blood pressure. The patient's urinary vanillylmandelic acid (VMA) levels and serum cortisol levels were normal. His 24-hour urine metanephrine levels were slightly elevated. Left adrenalectomy and right partial nephrectomy were performed. In this case, it is important to determine whether these tumors represent metastases or two synchronous tumors, as this has implications on the patient's management and prognosis. Clinical and pathological clues that led to the diagnosis are discussed in detail.
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PMID:Synchronous renal cell carcinoma and adrenocortical carcinoma: a rare case report and clinicopathologic approach. 1840 53

Gastrointestinal complications of diabetes include gastroparesis, intestinal enteropathy (which can cause diarrhea, constipation, and fecal incontinence), and nonalcoholic fatty liver disease. Patients with gastroparesis may present with early satiety, nausea, vomiting, bloating, postprandial fullness, or upper abdominal pain. The diagnosis of diabetic gastroparesis is made when other causes are excluded and postprandial gastric stasis is confirmed by gastric emptying scintigraphy. Whenever possible, patients should discontinue medications that exacerbate gastric dysmotility; control blood glucose levels; increase the liquid content of their diet; eat smaller meals more often; discontinue the use of tobacco products; and reduce the intake of insoluble dietary fiber, foods high in fat, and alcohol. Prokinetic agents (e.g., metoclopramide, erythromycin) may be helpful in controlling symptoms of gastroparesis. Treatment of diabetes-related constipation and diarrhea is aimed at supportive measures and symptom control. Nonalcoholic fatty liver disease is common in persons who are obese and who have diabetes. In persons with diabetes who have elevated hepatic transaminase levels, it is important to search for other causes of liver disease, including hepatitis and hemochromatosis. Gradual weight loss, control of blood glucose levels, and use of medications (e.g., pioglitazone, metformin) may normalize hepatic transaminase levels, but the clinical benefit of aggressively treating nonalcoholic fatty liver disease is unknown. Controlling blood glucose levels is important for managing most gastrointestinal complications.
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PMID:Gastrointestinal complications of diabetes. 1861 80

Superior mesenteric artery (SMA) syndrome is a rare acquired disorder in which acute angulation of SMA causes compression of the third part of the duodenum between the SMA and the aorta, leading to obstruction. Loss of fatty tissue as a result of a variety of debilitating conditions is believed to be the etiologic factor causing the acute angulation. We report a case of 30 years old lady who presented with postprandial abdominal pain at the epigastric region, colic type without radiation accompanied by nausea, postprandial vomiting and weight loss. Esophageal gastric series revealed an abrupt interruption in the contrast medium flow at the level of the junction of third portion (midpart) of the duodenum in barium studies. Adiverticula is noted just proximal to the site of obstruction. High resolution ultrasound and color Doppler sonography showed narrowing of the aortomesenteric angle to 220. Duodenojejunostomy was performed in the patient. Unfortunately the patient later was admitted in the hospital for refractory gastroparesis associated with superior mesenteric artery syndrome. Although open and laparoscopic duodenojejunostomy have been described as the best surgical treatment options for Wilkie's syndrome, but further attention is needed to the management of patients with refractory symptoms of gastroparesis after corrective surgery.
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PMID:Superior mesenteric artery syndrome: case report. 1882 43

A 45-year-old female with a background of poorly differentiated ovarian adenocarcinoma treated with bilateral salpingo-oophorectomy presented with one week history of nausea, vomiting and decreased urine output. On examination, she was mildly dehydrated but haemodynamically stable. Abdominal examination revealed tender swelling in upper abdomen. Biochemistry revealed that she had acute renal failure and interestingly the acute renal failure was out of proportion to the degree of dehydration. Abdominal ultrasound showed marked distension of the stomach without any evidence of renal tract obstruction. She was aggressively treated with volume replacement and careful monitoring of input and output. She responded very well to fluid replacement and her renal failure resolved within four days of treatment. This case illustrates a case of acute renal failure secondary to gastroparesis which resolved after treatment of renal failure. Patients with chronic renal failure are prone to develop gastroparesis but it is extremely rare to have gastric stasis following acute renal failure. This case also illustrates the importance of aggressive treatment of a reversible but potentially fatal medical condition which could have been easily overlooked in view of patient's poorly differentiated ovarian cancer.
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PMID:A case report of gastroparesis secondary to acute renal failure. 1902 8

Gastroparesis presents with nausea, vomiting, early satiety and abdominal discomfort, as well as a range of nongastrointestinal manifestations in association with delays in gastric emptying. The disorder may be a consequence of systemic illnesses, such as diabetes mellitus, occur as a complication of gastroesophageal surgery or develop in an idiopathic fashion and may mimic other disorders with normal gastric emptying. Some cases of idiopathic gastroparesis present after a viral infection. Management relies primarily on therapies that accelerate gastric emptying or reduce vomiting, although endoscopic or surgical options are available for refractory cases. Current research is focusing on the cellular and molecular mechanisms underlying development of delayed gastric emptying, as well as factors unrelated to motor dysfunction that may elicit some symptoms. Future pharmaceuticals will target the contractile and nonmotor defects via novel pathways. Novel electrical stimulation techniques will be employed either alone or in combination with medications.
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PMID:Management of gastroparesis. 1907 89


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