Functional Dyspepsia and Gastroparesis

2016 ◽  
Vol 34 (5) ◽  
pp. 491-499 ◽  
Author(s):  
Michael Camilleri

Background: Upper gastrointestinal disorders typically present with common symptoms. The most relevant non-mucosal diseases are gastroparesis, functional dyspepsia and rumination syndrome. The literature pertaining to these 3 conditions was reviewed. Key Messages: Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction of the stomach. The cardinal symptoms include postprandial fullness (early satiety), nausea, vomiting and bloating. The most frequently encountered causes of these symptoms are mechanical obstruction (pyloric stenosis), iatrogenic disease, gastroparesis, functional dyspepsia, cyclical vomiting and rumination syndrome. The most common causes of gastroparesis are neuropathic disorders such as diabetes, idiopathic, post-vagotomy and scleroderma among myopathic disorders. Principles of management of gastroparesis include exclusion of mechanical obstruction with imaging and iatrogenic causes with careful medication and past surgical history. Prokinetics and anti-emetics are the mainstays of treatment. Functional dyspepsia is characterized by the same symptoms as gastroparesis; in addition to delayed gastric emptying, pathophysiological abnormalities include accelerated gastric emptying, impaired gastric accommodation and gastric or duodenal hypersensitivity to distension and nutrients. Novel treatments include tricyclic antidepressants in patients with normal gastric emptying, acotiamide (acetyl cholinesterase inhibitor) and 5-HT1A receptor agonists such as buspirone. Rumination syndrome is characterized by repetitive regurgitation of gastric contents occurring within minutes after a meal. Episodes often persist for 1-2 h after the meal, and the regurgitant consists of partially digested food that is recognizable in its taste. Regurgitation is typically effortless or preceded by a sensation of belching. This has been summarized as a ‘meal in, meal out, day in, day out' behavior for weeks or months, differentiating rumination from gastroparesis. Patients often have a background of psychological disorder or a prior eating disorder. Treatment is based on behavioral modification. Conclusion: Precise identification of the cause and pathophysiology of upper gastrointestinal symptoms is essential for optimal management.

2019 ◽  
Vol 1 (4) ◽  
pp. 391-402 ◽  
Author(s):  
Asad Jehangir ◽  
Henry P. Parkman

The symptoms of gastroparesis, such as nausea, vomiting, postprandial fullness, early satiety and abdominal pain, frequently impair the quality of life of the affected individuals. The diagnosis of gastroparesis is made after structural etiologies are ruled out and an assessment of gastric function shows delayed gastric emptying. The role of the delay in gastric emptying in the pathogenesis of symptoms of gastroparesis has been debated, with some studies suggesting an association between delayed gastric emptying and the upper gastrointestinal symptoms, while others do not. The recent literature supports the importance of using reliable methods to assess gastric emptying, as delay in gastric emptying measured on a reliable test (4-h scintigraphy or breath test) is associated with the severity of upper gastrointestinal symptoms. In addition to measuring total gastric emptying, evaluation of regional gastric retention in the proximal and distal stomach and whole gut transit to assess small intestinal and colonic transit may provide additional useful information in patients with more generalized symptoms of gastrointestinal dysmotility.


2020 ◽  
Vol 318 (4) ◽  
pp. G635-G645 ◽  
Author(s):  
Justin Brandler ◽  
Laurence J. Miller ◽  
Xiao Jing Wang ◽  
Duane Burton ◽  
Irene Busciglio ◽  
...  

Abnormal gastric accommodation (GA) and gastric emptying contribute to pathophysiology in functional dyspepsia (FD). Secretin is a key regulator of GA in animal studies. Our aim was to study the effects of secretin on gastric motility, satiation, postprandial symptoms, and key hormones. We performed two double-blind, randomized, saline-controlled crossover trials in 10 healthy volunteers and 10 patients with FD by Rome IV criteria. We used measured GA (by validated SPECT method) after a 111In radiolabeled Ensure 300-mL meal and quantified gastric emptying for 30 min by scintigraphy. Satiation was measured by volume to fullness (VTF) and maximum tolerated volume (MTV) on an Ensure nutrient drink test and postprandial symptoms 30 min post-MTV. Fasting and postprandial GLP-1, GIP, and HPP were measured. The ages and sex distribution of healthy controls and patients with FD were similar. Compared with placebo, secretin delayed gastric emptying at 30 min in both health [−11% (−16, −4), P = 0.004]; and FD [−8% (−9, 0), P = 0.03]. Satiation (VTF and MTV), GA, and plasma levels of GLP-1, GIP, and HPP did not differ between treatment arms in health or FD. On ANCOVA analysis (adjusting for age and sex), secretin did not consistently increase postprandial symptoms in health or FD. Secretin delayed gastric emptying in both health and FD without significantly altering GA, VTF, or MTV or selected hormones. Thus, secretin receptor activation may provide a novel therapeutic mechanism for patients with FD and rapid gastric emptying. NEW & NOTEWORTHY The naturally occurring hormone secretin retards gastric emptying of solids without deleteriously affecting gastric accommodation, satiation, other upper gastrointestinal hormones, or postprandial symptoms. Given these findings, a subset of patients with rapid gastric emptying (e.g., the estimated 20% of patients with functional dyspepsia) could be candidates for treatments that stimulate a secretin receptor such as sacubitril, which inhibits neprilysin, an enzyme that degrades secretin.


2021 ◽  
Vol 11 (7) ◽  
pp. 831
Author(s):  
Heithem Soliman ◽  
Benoit Coffin ◽  
Guillaume Gourcerol

Patients with Parkinson disease (PD) experience a range of non-motor symptoms, including gastrointestinal symptoms. These symptoms can be present in the prodromal phase of the disease. Recent advances in pathophysiology reveal that α-synuclein aggregates that form Lewy bodies and neurites, the hallmark of PD, are present in the enteric nervous system and may precede motor symptoms. Gastroparesis is one of the gastrointestinal involvements of PD and is characterized by delayed gastric emptying of solid food in the absence of mechanical obstruction. Gastroparesis has been reported in nearly 45% of PD. The cardinal symptoms include early satiety, postprandial fullness, nausea, and vomiting. The diagnosis requires an appropriate test to confirm delayed gastric emptying, such as gastric scintigraphy, or breath test. Gastroparesis can lead to malnutrition and impairment of quality of life. Moreover, it might interfere with the absorption of antiparkinsonian drugs. The treatment includes dietary modifications, and pharmacologic agents both to accelerate gastric emptying and relieve symptoms. Alternative treatments have been recently developed in the management of gastroparesis, and their use in patients with PD will be reported in this review.


2017 ◽  
Vol 46 (2) ◽  
pp. 792-801 ◽  
Author(s):  
W-J Guo ◽  
S-K Yao ◽  
Y-L Zhang ◽  
S-Y Du ◽  
H-F Wang ◽  
...  

Objective This study was performed to investigate impaired vagal activity to meal in patients with functional dyspepsia (FD) with delayed gastric emptying (GE). Methods Eighty-five patients were studied. GE parameters, including those in the overall and proximal stomach, were measured by GE functional tests at the Department of Nuclear Medicine. Autonomic nervous function was tested by spectral analysis of heart rate variability (HRV). The vagal activity and sympathetic activity were analyzed by recording the power in the high-frequency component (HF), low-frequency component (LF), and LF/HF ratio. Results Overall and proximal GE were delayed in 47.2% and 50.9% of the patients, respectively. Spectral analysis of HRV showed that the HF in patients with delayed proximal GE was significantly lower and that the LF/HF ratio was significantly higher than those in patients with normal proximal GE after a meal. Conclusion Delayed proximal GE might be caused by disrupted sympathovagal balance as a result of decreased vagal activity after a meal. Improvement in vagal activity may constitute an effective treatment method for patients with FD.


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