Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Our understanding of gastric motility disorder--diabetic gastroparesis has advanced in the last ten to fifteen years, but the published data regarding pathogenesis are confusing and show conflicting results. The pathogenesis is sometimes linked with hyperglycemia, autonomic neuropathy, gastrointestinal hormone or myogenic mechanism. Antral hypomotility is often associated with hyperglycemia which is often accompanied by reduction in duodenal waves. Varying level of motilin, a gastrokinetic hormone has been reported. However none of the mechanism could explain the exact pathogenesis. The relationship of this mortality disorder with clinical symptoms is not always established, however nausea and vomiting lasting for days or weeks are the prominent symptoms. Other symptoms are post-prandial fullness, early satiety, bloating, belching, and vague abdominal discomfort. In a few cases, it may be the cause of poor nutrition, uncontrolled diabetes and recurrent ketoacidosis. Last one or two decades have seen some advancement in the investigational procedures like scintigraphy, radio-opaque markers, breath test, electrogastrography and MRI. Which can lead to a proper diagnosis. Such objective assessment is all the more important as nearly half of the patients do not have any symptom. Symptomatic improvement of gastroparetic patients should be the aim and in asymptomatic patients, treatment is often not recommended. Some dietary advice and prokinetic agents like metoclopramide, cisapride etc. are often prescribed but much needs to be further known as management is not always uniformly rewarding.
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PMID:Diabetic gastroparesis. 1122 21

Gastric emptying scintigraphy (GES) is usually performed for up to 2 hr to measure the gastric emptying (GE) of solids. Symptomatic patients, however, may have borderline results at 2 hr, making it difficult to determine whether a gastric motor disorder is present. The aim of this study was to assess whether extending GES to 4 hr is useful in evaluating patients for gastroparesis and to correlate the results of GES with patient symptoms. We studied 129 patients undergoing GES at Temple University Hospital between July 1998 and March 1999. Solid-phase GE was measured at 0, 0.5, 1, 2, 3, and 4 hr after ingestion of a 99mTc sulfur colloid-labeled egg meal. Dyspeptic symptoms of upper abdominal discomfort, early satiety, postprandial abdominal bloating, nausea, vomiting, and anorexia were graded as none, mild, moderate and severe (0, 1, 2 and 3, respectively) with the sum representing a total symptom score. Of 129 patients, 86 had normal GE at 2 hr; 26 of the 86 normal scans at 2 hr were delayed at 3 hr. Six of the 60 scans normal at 2 and 3 hr were delayed at 4 hr. Of 43 patients with delayed GE at 2 hr, 39 were delayed at 3 hr and 35 were delayed at 4 hr. Overall, the percentage of patients with delayed GE increased from 33% at 2 hr only to 58% using the results of the 2-, 3-, and 4-hr scans (P < 0.05). There was a significantly greater symptom score in patients with delayed GE compared to patients with normal GE (8.4 +/- 0.5 vs 7.1 +/- 0.5; P < 0.05). Conclusion, prolonging GES after ingestion of a 99mTc-labeled egg meal from 2 to 4 hr increased the number of symptomatic patients found to have delayed GE. These results suggest that GES should be performed for up to 4 hrs when the 2-hr result is normal.
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PMID:Extending gastric emptying scintigraphy from two to four hours detects more patients with gastroparesis. 1127 Jul 90

Patients often develop nausea, vomiting and bloating after bone marrow transplantation (BMT). These symptoms may interfere with nutrition and the ability to take oral medications. Gastroparesis is a recognized cause of these symptoms in non-transplant patients but less is known about patients who undergo BMT. Between January 1996 and March 1997, a total of 151 patients underwent BMT. Eighteen patients (12%) developed persistent symptoms suggestive of gastroparesis (persistent nausea, vomiting or bloating). Scintigraphic gastric emptying studies were performed to assess for gastroparesis. Prokinetic agents were administered at the time of study. The records on these patients were compared with those of all other patients undergoing BMT during the same time period without these symptoms. Nine patients who demonstrated delayed gastric emptying were further evaluated with esophagastroduodenoscopy and biopsy. Biopsy samples were reviewed for evidence of graft-versus-host disease (GVHD). Fourteen of 18 patients demonstrated delayed gastric emptying and most responded to prokinetic agents given at the time of study. Age, conditioning regimen, cytomegalovirus antigenemia and acute GVHD did not appear to be associated with the development of gastroparesis. Allogeneic BMT recipients were at higher risk than autologous BMT patients (26% vs 0%, P < 0.0001). of allogeneic bmt recipients, there was a nonsignificant trend of patients receiving tacrolimus to be less likely to experience gastroparesis than those receiving cyclosporine (27% vs 48%, P = 0.08). For the nine patients undergoing upper endoscopy, GVHD on gastric biopsy was an uncommon finding and was mild when present. Gastroparesis appears to be a common cause of nausea, vomiting and bloating following allogeneic BMT. This may occur less often with tacrolimus than cyclosporine because of the former agent's prokinetic properties. Patients usually respond to prokinetic drugs at the time of scintigraphy. GVHD and CMV infection do not appear to be major contributing factors.
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PMID:Gastroparesis following bone marrow transplantation. 1149 45

Gastroparesis may be related to a variety of underlying disorders, but diabetes mellitus is by far the most common cause. Symptoms of gastroparesis include early satiety, postprandial bloating, nausea and vomiting. Gastric scintigraphy with 99-technetium-labeled low-fat meal is the gold standard method of diagnosing delayed gastric emptying. Dietary measures and prokinetic drugs bring symptomatic relief in most patients. Some patients with severe nausea and vomiting will require antiemetic medications. Few patients will fail medical therapy and will continue to have debilitating symptoms of gastroparesis; such patients may benefit from a venting gastrostomy or a jejunostomy placed surgically, endoscopically, or fluoroscopically. Gastric electrical stimulation is an exiting new approach in the management of gastroparesis. As the treatment of gastroparesis is far from ideal, nonconventional approaches and nonstandard medications are presented.
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PMID:Gastroparesis and its management. 1209 72

Diabetic gastroparesis is a common and debilitating condition affecting millions of patients with diabetes mellitus worldwide. Although gastroparesis in diabetes has been known clinically for more than 50 years, treatment options remain very limited. Until recently, the scientific literature has offered few clues regarding the precise aetiology of gastric dysfunction in diabetes.Up to 50% of patients with diabetes may experience postprandial abdominal pain, nausea, vomiting and bloating secondary to gastric dysfunction. There is no clear association between length of disease and the onset of delayed gastric emptying. Gastroparesis affects both type 1 (insulin dependent) and type 2 (non- insulin dependent) forms of diabetes. Diagnosis requires identifying the proper symptom complex, while excluding other entities (peptic ulcer disease, rheumatological diseases, medication effects). The diagnosis of gastroparesis may be confirmed by demonstrating gastric emptying delay during a 4-hour scintigraphic study. Treatment options are limited and rely on dietary modifications, judicious use of available pharmacological agents, and occasionally surgical or endoscopic placement of gastrostomies or jejunostomies. Gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation. Current pharmacological agents for treating gastroparesis include metoclopramide, erythromycin, cisapride (only available via a company-sponsored programme) and domperidone (not US FDA approved). All of these drugs act as promotility agents that increase the number or the intensity of gastric contractions. These medications are not uniformly effective and all have adverse effects that limit their use. Cisapride has been removed from the open market as a result of over 200 reported cases of cardiac toxicity attributed to its use. Unfortunately, there is a paucity of clinical studies that clearly define the efficacy of these agents in diabetic gastroparesis and there are no studies that compare these drugs to each other. The molecular pathophysiology of diabetic gastroparesis is unknown, limiting the development of rational therapies. New studies, primarily in animals, point to a defect in the enteric nervous system as a major molecular cause of abnormal gastric motility in diabetes. This defect is characterised by a loss of nitric oxide signals from nerves to muscles in the gut resulting in delayed gastric emptying. Novel therapies designed to augment nitric oxide signalling are being studied.
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PMID:Current concepts in diabetic gastroparesis. 1282 60

Gastric neuromuscular disorders encompass a spectrum of dysfunction in nerve and smooth muscle that includes gastric visceral hypersensitivity, gastric dysrhythmias, fundic dysfunction, antral hypomotility, and gastroparesis. Patients with each disorder may present with such vague dyspepsia symptoms as early satiety, upper abdominal discomfort, bloating, or nausea with or without vomiting. A careful history and physical examination may suggest a gastric neuromuscular disorder, but symptoms are nonspecific. Gastroparesis is the most severe form of neuromuscular dysfunction. Such reversible causes of gastroparesis as mechanical obstruction of the stomach and chronic mesenteric ischemia must be excluded. Gastroparesis, gastric dysrhythmias, and hypersensitivity may follow viral infection or be due to degenerative processes that affect the gastric enteric neurons, smooth muscle, or interstitial cells of Cajal. Commonly, the cause of these gastric neuromuscular disorders is unknown. An approach to the diagnosis and treatment of gastric neuromuscular disorders is reviewed, including dietary counseling, drugs, and medical devices.
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PMID:Diagnosis and treatment of neuromuscular disorders of the stomach. 1286 63

Gastroparesis is a condition of abnormal gastric motility characterised by delayed gastric emptying in the absence of mechanical outlet obstruction. It is seen commonly in people with diabetes but is idiopathic in a third of patients. Symptoms include nausea and vomiting, post-prandial fullness and early satiety, and abdominal bloating and discomfort. Investigations fall into three categories: gastric emptying studies, intraluminal pressure measurements and recording of gastric myoelectrical activity. Nuclear scintigraphy is considered the gold standard for diagnosing and quantifying delayed gastric emptying. Treatment options include diet and behavioural changes, prokinetic drugs and surgical interventions. New advances in drug therapy and gastric electrical stimulation techniques hold considerable promise.
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PMID:Current perspectives on the management of gastroparesis. 1579 44

Diabetic gastroparesis is a long term complication of diabetes mellitus which could basically be defined as dysregulated gastric emptying leading to various pathological, biochemical and clinical changes in absence of any structural changes. Symptoms include nausea, vomiting, bloating, epigastric pain, anorexia, weight loss and so on. For symptomatic gastroparesis prokinetic drugs like metoclopramide, domperidone, cisapride, erythromycin and itcopride are used. Itopride is currently emerging as a prokinetic drug of choice. There is also scope of surgery.
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PMID:Management of diabetic gastroparesis. 1617 96

Several weeks or even months after heart-lung transplantation, gastroparesis-or delayed gastric emptying-commonly presents with cough, early satiety, and bloating. As it progresses, gastroparesis can cause substantial malnutrition and impair drug absorption. Gastroparesis after heart-lung transplantation can be attributed to bilateral vagus nerve injury, which probably occurs just above the level of the carina, where the recipient's trachea is resected. We report a highly unusual case wherein gastroparesis presented early after heart-lung transplantation and was managed conservatively. However, 19 days postoperatively, the patient developed acute abdominal pain and hypotension. Laparotomy revealed a massively dilated stomach and total avulsion of the splenic capsule with hemorrhage. The patient was fed via jejunostomy tubes until the gastroparesis resolved spontaneously. This case illustrates an important sequela of heart-lung transplantation. In order to decrease the morbidity from gastroparesis in these fragile patients, a drainage procedure should be considered as an adjunct to heart-lung transplantation.
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PMID:Severe gastroparesis causing splenic rupture: a unique, early complication after heart-lung transplantation. 1721 83


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