Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. Idiopathic gastroparesis refers to gastroparesis of unknown cause not from diabetes; not from prior gastric surgery; not related to other endocrine, neurologic, rheumatologic causes of gastroparesis; and not related to medications that can delay gastric emptying. There is overlap in the symptoms of idiopathic gastroparesis and functional dyspepsia. Patients with idiopathic gastroparesis often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. Current treatment options of dietary management, prokinetics agents, antiemetic agents, and symptom modulators do not adequately address clinical need for idiopathic gastroparesis.
Key points
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Idiopathic gastroparesis is a common form of gastroparesis, being among the three main causes of gastroparesis: diabetic, postsurgical, and idiopathic gastroparesis.
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Patients with idiopathic gastroparesis have a constellation of symptoms including nausea; vomiting; early satiety; postprandial fullness; and in some patients, upper abdominal pain.
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The presentation of idiopathic gastroparesis is similar to diabetic gastroparesis, although abdominal pain occurs more often in idiopathic gastroparesis, whereas nausea and vomiting are more severe in diabetic gastroparesis.
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Treatment of the symptoms may use agents used for diabetic gastroparesis and functional dyspepsia.
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Idiopathic gastroparesis significantly impacts on the quality of life of patients and development of new effective therapies for symptomatic control is needed.
Introduction
Gastroparesis is a chronic symptomatic disorder of the stomach manifested by delayed emptying without evidence of mechanical obstruction. The common causes of gastroparesis include diabetic, postsurgical, and idiopathic. Idiopathic gastroparesis (IG) refers to gastroparesis of unknown cause; that is, not from diabetes, not from prior gastric surgery, and not related to other endocrine, neurologic, or rheumatologic causes of gastroparesis. In addition, it is not related to medications that can delay gastric emptying, such as opiate narcotic analgesics and anticholinergics.
In most series, IG is the most common category for gastroparesis. In the series reported by Soykan and colleagues the causes in 146 patients were 36% idiopathic, 29% diabetic, 13% postgastric surgery, 7.5% Parkinson disease, 4.8% collagen vascular disorders, 4.1% intestinal pseudo-obstruction, and 6% miscellaneous causes. Miscellaneous causes of gastroparesis include other neurologic diseases, eating disorders, other metabolic or endocrine conditions (hypothyroidism), and critical illness.
This article discusses IG, symptomatic gastroparesis not from other known etiologies. This article updates the present status of the understanding of this disorder and reviews recent studies from the National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Gastroparesis Consortium.
Introduction
Gastroparesis is a chronic symptomatic disorder of the stomach manifested by delayed emptying without evidence of mechanical obstruction. The common causes of gastroparesis include diabetic, postsurgical, and idiopathic. Idiopathic gastroparesis (IG) refers to gastroparesis of unknown cause; that is, not from diabetes, not from prior gastric surgery, and not related to other endocrine, neurologic, or rheumatologic causes of gastroparesis. In addition, it is not related to medications that can delay gastric emptying, such as opiate narcotic analgesics and anticholinergics.
In most series, IG is the most common category for gastroparesis. In the series reported by Soykan and colleagues the causes in 146 patients were 36% idiopathic, 29% diabetic, 13% postgastric surgery, 7.5% Parkinson disease, 4.8% collagen vascular disorders, 4.1% intestinal pseudo-obstruction, and 6% miscellaneous causes. Miscellaneous causes of gastroparesis include other neurologic diseases, eating disorders, other metabolic or endocrine conditions (hypothyroidism), and critical illness.
This article discusses IG, symptomatic gastroparesis not from other known etiologies. This article updates the present status of the understanding of this disorder and reviews recent studies from the National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Gastroparesis Consortium.
Epidemiology
Gastroparesis occurs more often in women than men, often by a 3:1 margin. This is true not only for IG, but also for the other main causes of gastroparesis (diabetic and postsurgical). Patients with IG are typically young or middle-aged women. Even after adjusting for gender differences in gastric emptying, because females in general have slower gastric emptying than males, gastroparesis occurs more commonly in women.
Outside of gender issues and cause, the epidemiology of gastroparesis has not been systematically studied. This is because for proper diagnosis, a gastric emptying test is needed, one that presently cannot be done in population studies. Data from the Rochester Epidemiology Project, a database of linked medical records of residents of Olmsted County, Minnesota, showed that the age-adjusted incidence of definite gastroparesis per 100,000 person-years for the years 1996 to 2006 was 9.8 for women and 2.4 for men. Definite gastroparesis was defined as diagnosis of delayed gastric emptying by standard scintigraphy and symptoms of nausea and/or vomiting, postprandial fullness, early satiety, bloating, or epigastric pain for more than 3 months. The age-adjusted prevalence of definite gastroparesis per 100,000 persons was 37.8 for women and 9.6 for men. More recent estimates have suggested that the prevalence of gastroparesis was an underestimation and the prevalence is greater, approaching 2% of the general population.
Symptoms
Common symptoms of gastroparesis include nausea (>90% of patients), vomiting (84% of patients), and early satiety (60% of patients). Other symptoms include postprandial fullness and upper abdominal pain. There is slight variation in symptoms depending on the cause of gastroparesis: abdominal pain occurs more often in IG than in diabetic gastroparesis (DG), whereas nausea and vomiting are more severe in DG than in IG. In patients with gastroparesis, weight loss, malnutrition, and dehydration may be prominent in severe cases.
There is overlap in the symptoms of IG and functional dyspepsia. Abdominal pain or discomfort may be present to varying degrees in patients with gastroparesis, but it is not usually the predominant symptom, as it can be in functional dyspepsia. A substantial minority of patients (20%–40%) with functional dyspepsia can have delayed gastric emptying, blurring the distinction between IG and functional dyspepsia. Patients with IG often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain.
Symptoms may fluctuate, with episodes of pronounced symptoms interspersed with relatively symptom-free intervals. Thus it can be difficult to differentiate IG from cyclic vomiting syndrome, especially in the latter when there can be a “coalescence of symptoms,” such that they can occur nearly daily rather than as typical for cyclic vomiting syndrome with the vomiting episodes more sporadic on a monthly or less frequent basis. In cyclic vomiting syndrome, gastric emptying is normal or often, it can be rapid
The symptom profile and symptom severity of gastroparesis can be assessed with the Gastroparesis Cardinal Symptom Index (GCSI), a subset of the Patient Assessment of Upper Gastrointestinal Symptoms. The GCSI comprises three subscales (nausea and vomiting, postprandial fullness and early satiety, and bloating) that the patient scores with reference to the preceding 2 weeks. The GCSI daily diary can be used to record symptoms on a daily basis and may be more accurate in recording symptoms. This daily diary of symptoms captures symptoms of early satiety, nausea, vomiting, postprandial fullness, and upper abdominal pain. This questionnaire has been shown to capture relevant symptoms of gastroparesis in patients with DG and IG.
Although it has been a common assumption that the gastrointestinal symptoms can be attributed to the delay in gastric emptying characteristic of the disorder, most investigations have observed only weak correlations between symptom severity and the degree of gastric stasis. In general, the symptoms that seem to be best correlated (significant, but low correlation coefficients of 0.2–0.3) with a delay in gastric emptying include nausea, vomiting, early satiety, and postprandial fullness. Some symptoms present in patients with gastroparesis, such as bloating and upper abdominal pain, are not correlated with delayed gastric emptying and might be related to sensory alterations that might also be present in patients with gastroparesis.
Most patients with gastroparesis are underweight, probably because of frequently experienced early satiety, nausea, and vomiting. Some patients with gastroparesis, however, are overweight, for reasons that are not well understood. In a recent study, the factors that influence bodyweight in patients with IG and in healthy control subjects were investigated. Thirty-nine healthy control subjects and 29 subjects with IG underwent resting energy expenditure (indirect calorimetry), body composition (bioelectrical impedance), dietary intake (Block Food Frequency Questionnaire), symptoms (Patient Assessment of Upper GI Symptoms), and physical activity (Paffenbarger exercise survey) assessment. Both median caloric intake (1242 vs 1804 kcal; P = .005) and caloric expenditure (486 vs 2172 kcal; P <.01) were significantly lower in patients with gastroparesis as compared with control subjects, although body mass index (25.8 ± 5.8 vs 24.3 ± 4.0 kg/m 2 ) and resting energy expenditure (1327 ± 293 vs 1422 ± 243 kcal) were similar. Interestingly, the 12 patients with gastroparesis who had gained weight since diagnosis had lower symptom severity (12.9 ± 4.4 vs 19.3 ± 6.3; P <.05), consumed more calories (1342 vs 1134 kcal; P = .08), and expended fewer calories for activity per week (406 vs 644 median kcal; P = .45) compared with the 17 patients with gastroparesis who had lost weight or remained weight neutral. Thus, patients with gastroparesis consumed and expended fewer calories than healthy control subjects. A subgroup of patients with gastroparesis who were less symptomatic gained weight because of increased caloric intake and reduced energy expenditure.
National Institutes of Health Gastroparesis Consortium Registry Studies in Idiopathic Gastroparesis
The NIDDK Gastroparesis Clinical Research Consortium is a cooperative network of seven clinical centers and one Data Coordinating Center funded through the NIDDK of the NIH. The Gastroparesis Clinical Research Consortium Gastroparesis (GpC) Registry was implemented as an observational study of patients with gastroparesis enrolled prospectively at seven centers. Several of the published studies have addressed IG.
The characteristics of 243 patients with IG enrolled in the GpC Registry were recently described. This study is the largest study of patients with IG. Patients’ mean age was 41 years, and most (88%) were female. The most common presenting symptoms were nausea (34%), vomiting (19%), and abdominal pain (23%). Severe delay in gastric emptying (>35% retention at 4 hours) was present in 28% of patients and was associated with more severe symptoms of nausea and vomiting and loss of appetite compared with patients with mild or moderate delay. Of these patients with IG, 86% met criteria for functional dyspepsia, predominately postprandial distress syndrome. Of interest, 46% of the patients were overweight. Thus, this study shows that IG is a heterogeneous syndrome that primarily affects young women and can also affect overweight or obese individuals.
Although gastroparesis can be diabetic or idiopathic, little is known about differences in their presentation. The GpC compared clinical characteristics, symptoms, and gastric emptying in patients with IG with patients with type 1 or type 2 diabetes mellitus DG. A total of 416 patients with gastroparesis were analyzed; 254 had IG, and 137 had DG (78 had type 1 and 59 had type 2 diabetes mellitus). Symptoms that prompted evaluation more often included vomiting for DG and abdominal pain for IG. Patients with DG had more severe retching and vomiting than those with IG, whereas patients with IG had more severe early satiety and postprandial fullness subscores. Compared with IG, gastric retention was greater in patients with type 1 diabetes mellitus. Thus, there are many similarities and some differences in clinical characteristics of DG and IG. Gastroparesis is a heterogeneous disorder; the cause of the gastroparesis impacts symptoms and severity.
Abdominal pain can be present in patients with IG. Factors associated with abdominal pain in gastroparesis have not been well studied. The NIH GpC studied the symptom of abdominal pain and how it relates to other clinical factors in 393 patients with gastroparesis. Upper abdominal pain was moderate-severe in 261 (66%) patients. Pain and discomfort were predominant in 81 (21%); nausea and vomiting were predominant in 172 (44%). Moderate-severe pain was more prevalent with IG than in DG and correlated with scores for nausea and vomiting and opiate use, but not gastric emptying. Gastroparesis severity, quality of life, and depression and anxiety were worse with moderate-severe pain. Predominant pain and discomfort were associated with impaired quality of life. Thus, moderate-severe abdominal pain is prevalent in gastroparesis, impairs quality of life, and is associated with idiopathic etiology and opiate use. Pain was predominant in one-fifth of gastroparetics. Predominant pain has at least as great an impact on disease severity and quality of life as compared with the more classic symptoms of predominant nausea and vomiting.
Bloating is commonly reported in gastroparesis, but is an underappreciated symptom of gastroparesis. The prevalence of bloating in gastroparesis and its severity was assessed in 335 patients with gastroparesis. Bloating severity of at least severe (GCSI ≥4) grades was reported by 41% of patients. Bloating severity related to female gender and overweight status and correlated with intensity of nausea, postprandial fullness, visible distention, abdominal pain, and altered bowel function. Antiemetics, probiotics, and antidepressants with significant norepinephrine reuptake inhibitor activity may affect reports of bloating. Disease-specific quality of life and general measures of well-being were progressively impaired with increasing bloating severity. Thus, the symptom of bloating impairs quality of life but is not influenced by gastric emptying rates.
Many patients with gastroparesis have had their gallbladders removed; how this impacts on gastroparesis is not known. The clinical presentations of patients with gastroparesis were compared in those with prior cholecystectomy with patients who have not had their gallbladder removed. Of 391 subjects with DG or IG, 142 (36%) had a prior cholecystectomy. Patients with prior cholecystectomy were more often female, older, and overweight or obese. Cholecystectomy had been performed in 46% of type 2 diabetes mellitus compared with 24% of type 1 diabetes mellitus and 38% of IG. Patients with cholecystectomy had more comorbidities, particularly chronic fatigue syndrome, fibromyalgia, depression, and anxiety. Postcholecystectomy patients with gastroparesis had increased health care use and had a worse quality of life. Etiology was not independently associated with a prior cholecystectomy. Thus, symptom profiles in patients with and without cholecystectomy differ: postcholecystectomy patients with gastroparesis had more severe upper abdominal pain and retching and less severe constipation. These data suggest that prior cholecystectomy is associated with selected manifestations of gastroparesis.
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