Abstract
Background & Aims:
Gastroparesis is a chronic disorder of the stomach characterized by nausea, vomiting, early satiety, postprandial fullness, and abdominal pain. There is limited information on gastroparesis in minority populations. We assessed ethnic, racial, and sex variations in the etiology, symptoms, quality of life, gastric emptying, treatments, and symptom outcomes of patients with gastroparesis.
Methods:
We collected information from the National Institutes of Health Gastroparesis Consortium on 718 adult patients, from September 2007 through December 2017. Patients were followed every 4 or 6 months, when data were collected on medical histories, symptoms (based on answers to the PAGI-SYM questionnaires), and quality of life (based on SF-36). Follow-up information collected at 1 year (48 week) was used in this analysis. Comparisons were made between patients of self-reported non-Hispanic white, non-Hispanic black, and Hispanic ethnicities, as well as and between male and female patients.
Results:
Our final analysis included 552 non-Hispanic whites (77%), 83 persons of Hispanic ethnicity (12%), 62 non-Hispanic blacks (9%), 603 women (84%), and 115 men (16%). A significantly higher proportion of non-Hispanic blacks (60%) had gastroparesis of diabetic etiology than of non-Hispanic whites (28%); non-Hispanic blacks also had more severe retching (2.5 vs 1.7 score) and vomiting (2.9 vs 1.8 score) and a higher percentage were hospitalized in the past year (66% vs 38%). A significantly higher proportion of Hispanics had gastroparesis of diabetic etiology (59%) than non-Hispanic whites (28%), but Hispanics had less-severe nausea (2.7 vs 3.3 score), less early satiety (3.0 vs 3.5 score), and a lower proportion used domperidone (8% vs 21%) or had a peripherally inserted central catheter (1% vs 7%). A higher proportion of women had gastroparesis of idiopathic etiology (69%) than men (46%); women had more severe symptoms of stomach fullness (3.6 vs 3.1 score), early satiety (3.5 vs 2.9 score), postprandial fullness (3.7 vs 3.1 score), bloating (3.3 vs 2.6 score), stomach visibly larger (3.0 vs 2.1 score), and upper abdominal pain (2.9 vs 2.4 score). A lower proportion of women were hospitalized in past year (39% vs 53% of men).
Conclusion:
In patients with gastroparesis, etiologies, symptom severity, and treatments vary among races and ethnicities and between sexes.
Keywords: PICC, gender, QoL, causes
Introduction
The morbidity and mortality of many diseases, including coronary artery disease and stroke, is higher in African-Americans as compared to whites. Race was often a surrogate for many social and economic factors that influence health status and healthcare delivery. However, racial differences are also present in the prevalence and treatment outcomes for hypertension (1).
The prevalence of some gastrointestinal disorders varies depending on race and ethnicity. For instance, uninvestigated dyspepsia and irritable bowel syndrome occur less frequently among African Americans (2,3,4). Hispanic persons have been reported to have a higher risk of dyspepsia (5). In inflammatory bowel disease, there are variations in disease phenotype, symptoms, quality of life, health care utilization, and clinical outcomes among different racial and ethnic groups (6,7). Genetic, environmental and socioeconomic factors have been suggested to play a role.
Gastroparesis is a chronic disorder of the stomach with diabetes and idiopathic the most common etiologies. Symptoms include nausea, vomiting, early satiety, postprandial fullness, and abdominal pain. Gastroparesis has a significant impact on patient’s quality of life (8). The prevalence of gastroparesis is unknown, but it has been estimated that up to 4% of the population may have gastroparesis. The majority (up to 80%) of gastroparetic patients are women (9). Few studies have looked at differential presentations of gastroparesis by gender; in one study, the response to treatment with metoclopramide for diabetic gastroparesis was better in females than in males (10).
Most series of patients with gastroparesis have been primarily in white patients (9). There is little data assessing clinical characteristics, symptom severity, or impact on quality of life of gastroparesis in minority populations. In a small study, non-white gastroparesis patients had more severe symptoms and worse quality of life despite similar delays in gastric emptying (11). The reasons for this were not clear.
The aim of this study was to assess racial/ethnic and gender variations in the etiology of gastroparesis, the type and severity of gastroparetic symptoms, quality of life, and gastric emptying in patients with gastroparesis as well as clinical outcomes.
Methods
Patient Enrollment
The National Institutes of Health Gastroparesis Consortium (NIH GpC) registries were used with patients from the initial Gastroparesis Registry (ClinicalTrials.gov Identifier: NCT00398801) and Gastroparesis Registry 2 (ClinicalTrials.gov Identifier: NCT01696747) implemented as observational studies of patients with gastroparesis (9,12). Enrolled patients met entry criteria: 18 years or older with symptoms of at least 12 weeks duration, delayed gastric emptying scintigraphy (GES) within 6 months of enrollment, and no structural abnormality as seen by upper endoscopy. Gastroparetic patients were enrolled at 7 centers from September 2007 to December 2017.
This report focuses on patients with either idiopathic or diabetic gastroparesis. The diabetic patients could have either Type 1 diabetes mellitus (T1DM) or type 2 diabetes mellitus (T2DM) as defined by the physician. Diagnosis of patients with idiopathic etiology was based on no previous gastric surgery, no diabetes history, a normal hemoglobin A1C, and no other known etiologies. Comparisons were made between patients with self-reported non-Hispanic white, non-Hispanic black, Hispanic, and others, as well as by gender comparing males to females.
All studies were approved by the Institutional Review Board at each Clinical Center and the Data Coordinating Center. All authors had access to the study data and also reviewed and approved the final manuscript.
Study Protocol
During interviews with each subject, study physicians or coordinators at each Clinical Center completed case report forms capturing gastroparesis disease onset, symptoms, disease profile, associated medical and surgical conditions, including diabetes, and medication and supplemental therapies. Clinical severity of gastroparesis was graded on a scale (13); grade 1: mild gastroparesis; grade 2: compensated gastroparesis; grade 3: gastroparesis with gastric failure. Laboratory measures were obtained, including hemoglobin A1C (HbA1c), erythrocyte sedimentation rate (ESR), and C-reactive peptide (CRP).
Patients filled out the 20 item Patient Assessment of Upper GI Symptoms (PAGI-SYM) questionnaire which assesses symptoms of gastroparesis, dyspepsia, and gastroesophageal reflux disease (14); it includes the nine symptoms of the Gastroparesis Cardinal Symptom Index (GCSI) (15).
Disease-specific quality of life was assessed by the Patient Assessment of Upper Gastrointestinal Disorders Quality of Life (PAGI-QOL) survey (16). The Medical Outcomes Study 36-Item Short-Form Health Survey version 2 (SF-36v2) was used to assess the patients’ views of overall physical and mental health in the past 4 weeks (17). Depression was assessed with the Beck Depression Index (BDI) (18) and anxiety with the State-Trait Anxiety Inventory (STAI) (19).
Gastric emptying scintigraphy was performed using a low-fat, egg white meal with imaging at 0, 1, 2, 4 hours after meal ingestion (20,21). This protocol ensures standardized information about gastric emptying across sites.
Patients were followed in the registries with changes in clinical care prescribed by their physician recorded at follow up visits every 4 months for GpR1 and every 6 months for GpR2. At these follow up visits, patients filled out the PAGI-SYM and information recorded about their treatment (22,23). For this study, the follow up information at the 1 year (48 week) visit was used.
Statistical Methods
Baseline patient characteristics were compared by ethnicity and race (non-Hispanic whites, non-Hispanic blacks, Hispanics, and other) as well as by gender comparing males and females. Data are presented as means±SD or N (%) and p-values determined by Fisher’s exact test for categorical measures and by ANOVA for continuous measures (24). Two types of p-values were calculated. Overall p-values were calculated to assess the difference in characteristics across 4 ethnicity/race groups; three pairwise p-values were calculated to assess the difference between non-Hispanic black and non-Hispanic white, between Hispanic and non-Hispanic white, and between Hispanic and non-Hispanic black. The assessed baseline characteristics included age, gender, ethnicity, race, diabetes status, gastroparesis etiology, acute vs. insidious symptom onset, presence of initial infectious prodrome, hospitalization for gastroparesis in the year prior to enrollment, 2 and 4 hour gastric emptying retention (%), GCSI, PAGI-QOL, SF-36 physical and mental scores. Multiple linear regression analysis was used to determine whether race and ethnicity associated with selected clinical factors after adjustment (25). The assessed outcomes were: GCSI total score and three subscores; SF-36 physical composite score, mental composite score and body pain score. The covariates included: race/ethnicity; age; gender; education; annual household income; occupation; marital status; BMI; and etiology of gastroparesis.
As a second part of the analyses, we assessed race/ethnic difference in change in selected patient characteristics between baseline and 48-week visits. For continuous measures (GCSI total and subscores, PAGI-SYM items), we used ANOVA to assess the difference in change in these scores. For binary measures (improvement in GCSI total score by ≥ 1-point, use of medical devices and medication), we used Fisher’s exact test to assess difference in proportion of new users.
We performed a similar analysis looking at the effects of gender on gastroparesis comparing females to males in the baseline patient characteristics and outcomes. We also looked at differences in female patient characteristics by menopausal status and by use of hormone supplements.
Associations were considered significant if P<0.05. We assessed the overall p- value first, and then, the pairwise or individual p-values if the overall p-value was significant. Analyses were performed using Stata (Release 15.1, Stata Corporation, College Station, TX) (26).
Results
Patients
718 patients with gastroparesis were studied: 552 (77%) reported non-Hispanic whites, 83 (12%) reported Hispanic ethnicity, 62 (9%) reported non-Hispanic black race, and 21 (3%) were non-Hispanic other racial groups (Asian, Native American, Pacific Islander, or multiracial) (Table 1 and Supplemental Table 1 containing extended data). Of the 83 Hispanics, 74 were Hispanic whites, 2 were Hispanic blacks, 1 Hispanic Native American, 1 Hispanic Pacific Islander. There were 603 (84%) females and 115 (16%) males (Table 4).
Table 1.
Patient Characteristics by Ethnicity and Race
| Patient characteristics | Non-Hispanic white (N =552) |
Non-Hispanic black (N = 62) |
Hispanic (N = 83) |
Overall P* |
|---|---|---|---|---|
| Gastroparesis | ||||
| Etiology (%) | <0.001 | |||
| Diabetic | 153 (28%) | 37 (60%) | 49 (59%) | |
| Idiopathic | 399 (72%) | 25 (40%) | 34 (41%) | |
| Demographic & behavioral | ||||
| Gender (%female) | 468 (85%) | 52 (84%) | 66 (80%) | 0.60 |
| Age (mean) | 43.0 (±13.7) | 39.4 (±12.4) | 45.9 (±12.4) | 0.004 |
| Marital status (% married) | 324 (59%) | 27 (44%) | 49 (59%) | 0.04 |
| Education (%) | <0.001 | |||
| High school or less | 114 (21%) | 21 (34%) | 39 (47%) | |
| Bachelor’s degree or higher | 199 (36%) | 11 (18%) | 15 (18%) | |
| Annual household income (% ≥$50k) | 315 (57%) | 18 (29%) | 16 (19%) | <0.001 |
| Medical history | ||||
| BMI (mean) | 27.0 (±7.5) | 30.3 (±7.9) | 27.7 (±6.7) | 0.008 |
| Post-menopausal (natural or surgical)‡ | 196 (42%) | 16 (31%) | 36 (55%) | 0.05 |
| Hormone therapy if post-menopausal§ | 49 (26%) | 5 (31%) | 9 (25%) | 0.79 |
| Gastric emptying test (mean) | ||||
| 2-hr retention | 64.9 (±17.7) | 63.1 (±19.8) | 67.5 (±18.6) | 0.38 |
| 4-hr retention | 31.3 (±21.8) | 34.5 (±23.1) | 37.3 (±24.3) | 0.11 |
| Hospitalization last year (%) | 211 (38%) | 41 (66%) | 40 (48%) | <0.001 |
| Use of TPN (%) | 37 (7%) | 10 (16%) | 4 (5%) | 0.07 |
| Use of J tube (%) | 13 (2%) | 1 (2%) | 0 (0%) | 0.65 |
| Use of G tube (%) | 5 (1%) | 1 (2%) | 1 (1%) | 0.55 |
| Use of PICC (%) | 40 (7%) | 8 (13%) | 1 (1%) | 0.02 |
| Use of GES (%) | 36 (7%) | 3 (5%) | 4 (5%) | 0.96 |
| Use of narcotic pain medication (%) | 208 (38%) | 29 (47%) | 28 (34%) | 0.21 |
| Use of domperidone (%) | 118 (21%) | 8 (13%) | 7 (8%) | 0.02 |
| Laboratory measures | ||||
| Erythrocyte sedimentation rate (mm/hr) | 16 (±16) | 33 (±26) | 32 (±29) | <0.001 |
| C-reactive protein (mg/dL) | 1.7 (±4.5) | 1.6 (±3.3) | 2.3 (±5.1) | 0.007 |
| HbA1c (among diabetics)† (%) | 7.8 (±1.9) | 8.2 (±2.4) | 8.9 (±2.2) | 0.006 |
| PAGI-SYM (0–5; mean) | ||||
| Total GCSI score | 2.9 (±1.0) | 3.0 (±1.3) | 2.8 (±1.2) | 0.51 |
| Nausea/vomiting subscore | 2.3 (±1.4) | 3.0 (±1.5) | 2.1 (±1.6) | <0.001 |
| Bloating subscore | 3.0 (±1.6) | 2.9 (±1.9) | 3.2 (±1.5) | 0.79 |
| Postprandial fullness subscore | 3.4 (±1.1) | 3.2 (±1.3) | 3.1 (±1.3) | 0.07 |
| Nausea | 3.3 (±1.4) | 3.5 (±1.4) | 2.7 (±1.7) | 0.003 |
| Retching | 1.7 (±1.7) | 2.5 (±1.7) | 1.8 (±1.8) | 0.004 |
| Vomiting | 1.8 (±1.8) | 2.9 (±1.8) | 1.8 (±1.9) | <0.001 |
| Stomach fullness | 3.6 (±1.2) | 3.4 (±1.6) | 3.3 (±1.4) | 0.17 |
| Unable to finish meal | 3.5 (±1.4) | 3.1 (±1.6) | 3.0 (±1.7) | 0.01 |
| Feel full after meals | 3.6 (±1.3) | 3.6 (±1.5) | 3.4 (±1.4) | 0.53 |
| Loss of appetite | 2.9 (±1.5) | 2.9 (±1.5) | 2.6 (±1.7) | 0.35 |
| Bloating | 3.2 (±1.6) | 3.0 (±1.9) | 3.3 (±1.5) | 0.59 |
| Stomach visibly larger | 2.8 (±1.7) | 2.8 (±2.0) | 3.0 (±1.6) | 0.88 |
| Upper abdominal pain | 2.9 (±1.7) | 2.9 (±1.9) | 2.6 (±1.7) | 0.49 |
| Upper abdominal discomfort | 3.1 (±1.5) | 3.1 (±1.9) | 2.8 (±1.6) | 0.37 |
| PAGI-QoL (0–5; mean) | ||||
| Total score | 2.6 (±1.1) | 2.5 (±1.3) | 2.5 (±1.3) | 0.77 |
| SF-36v2ǁ (mean) | ||||
| Physical summary score | 33.2 (±10.5) | 31.9 (±10.5) | 34.6 (±10.4) | 0.47 |
| Mental summary score | 39.1 (±12.9) | 40.0 (±12.9) | 37.1 (±13.8) | 0.53 |
Data are means ± standard deviations or number (percents). BMI, body mass index; GCSI, Gastroparesis Cardinal Symptom Index; GES, Gastric Electrical Stimulator; PAGI-QoL, Patient Assessment of Upper Gastrointestinal Disorders – Quality of Life; PAGI-SYM, Patient Assessment of Upper Gastrointestinal Disorders - Symptom Severity Index; PICC, peripherally inserted central catheter; SF-36v2, SF-36v2 Health Survey.
P-values were calculated using ANOVA for continuous variables and Fisher’s exact test for categorical variables.
Scores were normalized to the 1998 U.S. general population with a mean (±SD) of 50±10.
Table 4.
Unadjusted and adjusted associations of gender with selected outcomes (N = 718)
| Outcome | Unadjusted model* |
Adjusted model† |
||||
|---|---|---|---|---|---|---|
| Estimated difference (female vs. male) |
95% CI | P | Estimated difference (female vs. male) |
95% CI | P | |
| PAGI-SYM | ||||||
| GCSI total score | 0.4 | (0.2,0.6) | <0.001 | 0.4 | (0.2,0.6) | <0.001 |
| GCSI nausea subscore | −0.0 | (−0.3,0.3) | 0.89 | 0.0 | (−0.3,0.3) | 0.90 |
| GCSI bloating subscore | 0.7 | (0.4,1.1) | <0.001 | 0.7 | (0.4,1.1) | <0.001 |
| GCSI postprandial fullness subscore | 0.5 | (0.3,0.7) | <0.001 | 0.4 | (0.2,0.7) | <0.001 |
| SF-36v2 | ||||||
| Physical composite score | −1.2 | (−3.3,0.9) | 0.27 | −1.8 | (−3.9,0.3) | 0.10 |
| Mental composite score | 2.8 | (0.2,5.4) | 0.03 | 2.4 | (−0.2,5.1) | 0.07 |
| Body pain score | −1.3 | (−3.4,0.9) | 0.24 | −1.7 | (−3.9,0.5) | 0.13 |
Notes: Results of linear regression.
Unadjusted model based on the logistic regression. The included covariate was the variable for gender only (female vs. male).
Adjusted model based on the logistic regression. The used regression models were the same as those in Table 2.
Race and Ethnicity
Baseline Enrollment
Table 1 depicts the patient characteristics by self-reported ethnicity and race.Non-Hispanic blacks (n=62), compared to non-Hispanic whites (n=552), were younger (39.4 vs. 43.0 years; p=0.05) and had higher body mass index (30.3 vs. 27.0 kg/m2; p<0.001). They were less likely to have a college education (18% vs 36%) and less likely to have annual income ≥$50,000 (29% vs 57%; p<0.001). Non-Hispanic blacks were more likely to have diabetic etiology of gastroparesis (60% vs. 28%; p<0.001). Of the non-Hispanic blacks with diabetes, 54% had T1DM, compared to 49% for non-Hispanic whites (p=0.42). Similar HgbA1c levels were present on average (8.2% vs 7.8%). Non-Hispanic blacks had more severe retching, vomiting with a significant greater nausea/vomiting subscore (3.0 vs 2.3; p<0.001). There were no differences in gastric emptying. Non-Hispanic blacks were more likely to have a hospitalization in past year (66% vs. 38%; p<0.001) (Table 1) with more admissions related in part to hyperglycemia (34 vs 14%; p=0.006) and dehydration (85 vs 62%; p=0.004) (Supplemental Table 1). Using multiple linear regression adjusting for demographic characteristics and etiology of gastroparesis, non-Hispanic blacks, compared to non-Hispanic whites tended to have higher mean nausea/vomiting GCSI subscores [difference=0.4 (95% CI=0.0, 0.7); p=0.06] (Table 2).
Table 2.
Unadjusted and adjusted associations of ethnicity and race with selected outcomes (N = 718)
| Outcome / Association of race with outcome* |
Unadjusted model† |
Adjusted model‡ |
||||
|---|---|---|---|---|---|---|
| Estimated difference |
95% CI | P | Estimated difference |
95% CI | P | |
| PAGI-SYM | ||||||
| GCSI total score | 0.51§ | 0.38§ | ||||
| Non-Hispanic black vs. white | 0.2 | (−0.1,0.4) | 0.29 | 0.0 | (−0.3,0.3) | 0.89 |
| Hispanic vs. non-Hispanic white | −0.1 | (−0.4,0.1) | 0.39 | −0.2 | (−0.5,0.0) | 0.09 |
| Hispanic vs. non-Hispanic black | −0.3 | (−0.6,0.1) | 0.15 | −0.2 | (−0.6,0.1) | 0.18 |
| GCSI nausea subscore | <0.001§ | 0.02§ | ||||
| Non-Hispanic black vs. white | 0.7 | (0.3,1.1) | <0.001 | 0.4 | (−0.0,0.7) | 0.06 |
| Hispanic vs. non-Hispanic white | −0.1 | (−0.5,0.2) | 0.43 | −0.4 | (−0.7,−0.0) | 0.04 |
| Hispanic vs. non-Hispanic black | −0.8 | (−1.3,−0.4) | <0.001 | −0.7 | (−1.2,−0.3) | 0.002 |
| GCSI bloating subscore | 0.79§ | 0.75§ | ||||
| Non-Hispanic black vs. white | −0.1 | (−0.5,0.3) | 0.62 | −0.2 | (−0.6,0.2) | 0.41 |
| Hispanic vs. non-Hispanic white | 0.1 | (−0.2,0.5) | 0.45 | 0.1 | (−0.3,0.4) | 0.76 |
| Hispanic vs. non-Hispanic black | 0.2 | (−0.3,0.8) | 0.36 | 0.2 | (−0.3,0.8) | 0.37 |
| GCSI postprandial fullness subscore | 0.07§ | 0.09§ | ||||
| Non-Hispanic black vs. white | −0.2 | (−0.5,0.1) | 0.32 | −0.1 | (−0.4,0.2) | 0.42 |
| Hispanic vs. non-Hispanic white | −0.3 | (−0.6,−0.1) | 0.01 | −0.3 | (−0.6,−0.1) | 0.01 |
| Hispanic vs. non-Hispanic black | −0.2 | (−0.6,0.2) | 0.35 | −0.2 | (−0.6,0.2) | 0.26 |
| SF-36v2 | ||||||
| Physical composite score | 0.47§ | 0.12§ | ||||
| Non-Hispanic black vs. white | −1.3 | (−4.1,1.5) | 0.36 | −0.7 | (−3.5,2.2) | 0.65 |
| Hispanic vs. non-Hispanic white | 1.4 | (−1.0,3.8) | 0.26 | 2.9 | (0.3,5.4) | 0.03 |
| Hispanic vs. non-Hispanic black | 2.7 | (−0.8,6.2) | 0.13 | 3.5 | (0.1,7.0) | 0.05 |
| Mental composite score | 0.53§ | 0.52§ | ||||
| Non-Hispanic black vs. white | 0.9 | (−2.5,4.4) | 0.59 | 2.6 | (−1.0,6.1) | 0.15 |
| Hispanic vs. non-Hispanic white | −2.0 | (−5.0,1.0) | 0.20 | −0.3 | (−3.5,2.8) | 0.84 |
| Hispanic vs. non-Hispanic black | −2.9 | (−7.2,1.4) | 0.18 | −2.9 | (−7.2,1.4) | 0.19 |
Notes: Results of linear regression.
Results for 3 comparisons are presented.
Unadjusted model based on the logistic regression. The included covariate was the variable for ethnicity/race only (4 categories; non-Hispanic white, non-Hispanic black, Hispanic, other).
Adjusted model based on the logistic regression. The included covariates were, ethnicity/race variable (4 categories), age (4 categories; <30, 30–44, 45–59, 60+), gender (female vs. male), marital status (married vs. other), education (3 categories; high school or less, post high school, bachelor’s degree or higher), annual household income (≥ $50,000 vs. < $50,000), occupation (3 categories; professional, clerical, other), BMI (4 categories; underweight, normal, overweight, obese); etiology of gastroparesis (idiopathic vs. diabetic).
Global test for ethnicity/race (Wald test, df = 3). The null hypothesis is: means are different across 4 ethnicity/race groups.
Hispanics (n=83) were more likely to have, compared to non-Hispanic whites (n=552), diabetic etiology of gastroparesis (59% vs. 28%; p<0.001). Of the Hispanics with diabetes, 37% had T1DM, compared to 49% for Non-Hispanic whites (p=0.21).There was an increase in HgbA1c in Hispanics (8.9±2.4) compared to non-Hispanic whites (7.8±1.9; p<0.001). Hispanics were less likely to have a college degree (18% vs. 36%; p<0.001) and less likely annual income ≥$50,000 (19% vs. 57%; p<0.001).Gastric emptying showed similar retention at 2 hours with trend to more retention at 4 hours (37.3±24.3 vs 31.1±21.7; p=0.02) in Hispanics than non-Hispanic whites.Hispanics had less nausea and early satiety with a significant less postprandial fullness subscore (3.1 vs 3.4; p=0.01). There were no significant differences in quality of life measures using SF36v2 or depression and anxiety measures using BDI and STAI. Hispanics were less likely to use of domperidone (8% vs 21%; p=0.005), and fewer had a PICC line (1% vs 7%; p=0.03) (Table 1). Using multiple linear regression adjusting for demographic characteristics and etiology of gastroparesis, Hispanics had lower mean nausea/vomiting GCSI subscore [difference=−0.4 (95% CI=−0.7, −0.0); p=0.04] (Table 2).
Table 1 also compares the 83 Hispanic patients to the 62 non-Hispanic black patients. The etiology of gastroparesis was similar: 60% diabetic in non-Hispanic blacks and 59% in Hispanics (p=1.00). Of the diabetics, the non-Hispanic blacks tended to be more T1DM (54%) than in the Hispanics (37%; p=0.07). The non-Hispanic blacks had a significantly higher nausea/vomiting subscore (3.0 vs 2.1; p=0.001) with increases in nausea, retching vomiting. The non-Hispanic blacks had more hospitalizations in the last year (66% vs 48%; p=0.04) with a trend for more admissions related to abdominal pain (80 vs 63%; p=0.09) (Supplementary Table 1). Using multiple linear regression adjusting for demographic characteristics and etiology of gastroparesis, Hispanics, compared to non-Hispanic blacks had lower mean nausea/vomiting GCSI subscores [difference=−0.7 (95% CI=−1.2, −0.3); p=0.002] (Table 2).
Follow up information
Follow up data at 1 year is available in 397 of the 718 patients. Patients with follow-up data included more non-Hispanic white, older, more married persons, higher income, less diabetic, more idiopathic gastroparesis patients, more using domperidone, but less using marijuana and alternative medicines (Supplemental Table 2).
Of the 397 total patients, there were 323 Non-Hispanic whites, 29 Non-Hispanic blacks, 36 Hispanics that had outcome data over a one year follow up period (Supplemental Table 3). The improvement in GCSI total score was similar (p=0.87) in the four groups: non-Hispanic whites (2.9 to 2.5), non-Hispanic blacks (3.1 to 2.7), and Hispanics (3.1 to 2.9). However, the improvement in vomiting over one year tended (p=0.07) to improve with differences among the different ethnic/racial groups with better improvement in non-Hispanic blacks (2.8 to 1.8) compared to non-Hispanic whites (1.7 to 1.4; p=0.02), and Hispanics (2.0 to 2.1; p=0.02). We assessed the possibility of regression to the mean by use of a regression model in which we adjusted for the initial symptom severity values of the outcome variable. The differences observed were attenuated with higher p values that were not significant after adjustment suggesting the differences may be in part due to differences in the initial symptom severity scores.
In this patient cohort of gastroparesis patients, 98 of the 379 patients with baseline GCSI≥1 (26%) had a reduction of total GCSI of ≥1.0. An improvement in total GCSI by ≥1 was seen in 27% of non-Hispanic whites, 21% of non-Hispanic blacks, and 21% of Hispanics (p=0.91) (Supplemental Table 4). There was not a significant differential use of starting different ethnic/racial groups on TPN, J tube, gastric stimulator, or domperidone (Supplementary Table 4).
Gender
Baseline Enrollment
We also looked at the effects of gender on gastroparesis presentation (Table 3) and Supplemental Table 5 containing extended data). Racial and ethnic backgrounds were similar for the males and the females (p=0.60). Females were more likely to have idiopathic gastroparesis than the males (69% vs 46%; p<0.001). T1DM was present in 61% of the diabetic males compared to 43% of diabetic females (p=0.04). Males were more likely to be smokers (51% vs 28%; p<0.001) and more likely to have alcohol consumption ≥2/month (22% vs 12%; p=0.007). Females had greater symptom severity for stomach fullness, early satiety, postprandial fullness, bloating, stomach visibly larger, and upper abdominal pain with greater total GCSI total score (3.0 vs 2.6; p<0.001), bloating subscore (3.1 vs 2.4; p<0.001), and postprandial fullness subscore (3.4 vs 2.9; p<0.001). Females tended to have lower QOL on PAGI-QOL (2.5 vs 2.8; p=0.07) with similar SF-36v2 physical summary QOL scores but higher mental summary score (p=0.03). More males had hospitalizations in the last year (53% vs 39%; p=0.007). However, gastric emptying was not different amongst genders. Using multivariable analysis, females had a greater GCSI total symptom score than males [difference=0.4 (95% CI=0.2, 0.6); p<0.001] with higher bloating subscore (p<0.001) and higher postprandial fullness subscore (p<0.001), but not nausea/vomiting subscore (p=0.90) (Table 4).
Table 3.
Patients Characteristics by Gender (N = 718)
| Patient characteristics | Male (N =115) |
Female (N = 603) |
P* |
|---|---|---|---|
| Gastroparesis | |||
| Etiology (%) | <0.001 | ||
| Diabetic | 62 (54%) | 184 (31%) | |
| Idiopathic | 53 (46%) | 419 (69%) | |
| Demographic & behavioral | |||
| Age (mean) | 43.7 (±13.7) | 42.7 (±13.5) | 0.44 |
| Race (%) | 0.60 | ||
| Non-Hispanic white | 84 (73%) | 468 (78%) | |
| Non-Hispanic black | 10 (9%) | 52 (9%) | |
| Hispanic | 17 (15%) | 66 (11%) | |
| Marital status (% married) | 68 (59%) | 340 (56%) | 0.61 |
| Education (%) | 0.49 | ||
| High school or less | 31 (27%) | 147 (24%) | |
| Bachelor’s degree or higher | 32 (28%) | 202 (33%) | |
| Annual household income (% ≥$50k) | 55 (48%) | 302 (50%) | 0.68 |
| Regular smoker (%) | 59 (51%) | 166 (28%) | <0.001 |
| Alcohol intake (% ≥2/month) | 25 (22%) | 72 (12%) | 0.007 |
| Medical history | |||
| BMI (mean) | 27.5 (±6.3) | 27.3 (±7.7) | 0.75 |
| Gastric emptying test (mean) | |||
| 2-hr retention | 65.3 (±19.6) | 65.2 (±17.8) | 0.93 |
| 4-hr retention | 33.2(±23.0) | 32.2 (±22.0) | 0.64 |
| Hospitalization last year (%) | 61 (53%) | 238 (39%) | 0.007 |
| Use of TPN (%) | 5 (4%) | 47 (8%) | 0.24 |
| Use of J tube (%) | 2 (2%) | 12 (2%) | 1.00 |
| Use of G tube (%) | 1 (1%) | 6 (1%) | 1.00 |
| Use of PICC (%) | 7 (6%) | 42 (7%) | 0.84 |
| Use of GES (%) | 10 (9%) | 34 (6%) | 0.21 |
| Use of narcotic pain medication (%) | 40 (35%) | 236 (39%) | 0.40 |
| Use of domperidone (%) | 17 (15%) | 119 (20%) | 0.24 |
| Laboratory measures (0–5; mean) | |||
| Erythrocyte sedimentation rate (mm/hr) | 16 (±21) | 20 (±20) | 0.04 |
| C-reactive protein (mg/dL) | 2.5 (±11.8) | 1.8 (±4.5) | 0.27 |
| HbA1c (among diabetics only) (%) | 8.0 (±1.9) | 8.1 (±2.2) | 0.84 |
| PAGI-SYM (0–5; mean) | |||
| Total GCSI score | 2.6 (±1.1) | 3.0 (±1.1) | <0.001 |
| Nausea/vomiting subscore | 2.3 (±1.5) | 2.3 (±1.4) | 0.89 |
| Bloating subscore | 2.4 (±1.6) | 3.1 (±1.6) | <0.001 |
| Postprandial fullness subscore | 2.9 (±1.2) | 3.4 (±1.1) | <0.001 |
| Nausea | 3.1 (±1.4) | 3.3 (±1.5) | 0.11 |
| Retching | 1.9 (±1.7) | 1.8 (±1.7) | 0.65 |
| Vomiting | 2.1 (±1.8) | 1.9 (±1.9) | 0.25 |
| Stomach fullness | 3.1 (±1.3) | 3.6 (±1.3) | <0.001 |
| Unable to finish meal | 2.9 (±1.7) | 3.5 (±1.4) | <0.001 |
| Feel full after meals | 3.1 (±1.5) | 3.7 (±1.3) | <0.001 |
| Loss of appetite | 2.7 (±1.6) | 2.9 (±1.5) | 0.17 |
| Bloating | 2.6 (±1.6) | 3.3 (±1.6) | <0.001 |
| Stomach visibly larger | 2.1 (±1.8) | 3.0 (±1.7) | <0.001 |
| Upper abdominal pain | 2.4 (±1.8) | 2.9 (±1.7) | 0.002 |
| Upper abdominal discomfort | 2.7 (±1.6) | 3.2 (±1.5) | 0.006 |
| PAGI-QoL (0–5; mean) | |||
| Total score | 2.8 (±1.1) | 2.5 (±1.1) | 0.07 |
| SF-36v2ǁ (mean) | |||
| Physical summary score | 34.2 (±11.0) | 33.0 (±10.4) | 0.27 |
| Mental summary score | 36.6 (±13.3) | 39.4 (±12.9) | 0.03 |
Data are means ± standard deviations or number (percents). BMI, body mass index; GCSI, Gastroparesis Cardinal Symptom Index; GES, Gastric Electrical Stimulator; PAGI-QoL, Patient Assessment of Upper Gastrointestinal Disorders – Quality of Life; PAGI-SYM, Patient Assessment of Upper Gastrointestinal Disorders - Symptom Severity Index; PICC, peripherally inserted central catheter; SF-36v2, SF-36v2 Health Survey.
P-values were calculated using ANOVA for continuous variables and Fisher’s exact test for categorical variables.
Scores were normalized to the 1998 U.S. general population with a mean (±SD) of 50±10.
Overall, 253 of the 803 females were postmenopausal (42%). Hispanics were more likely to be postmenopausal (55%; p=0.05) as they were more likely to be older (Table 1). Postmenopausal women had less severe nausea (p<0.001), retching (p=0.04), and vomiting (p=0.01) compared to premenopausal women (Table 5). There were 65 women on hormone replacement therapy among the 253 postmenopausal women (26%). Postmenopausal women taking hormone replacement therapy had greater upper abdominal pain (p=0.02) and discomfort (p=0.03) than those not taking hormone replacement therapy (Table 6).
Table 5.
PAGI symptom severity by menopausal status among all female patients (N = 603)
| Mean (±SD) or N (%) |
P* | ||
|---|---|---|---|
| Premenopausal (N = 350) |
Postmenopausal (N = 253) |
||
| Race | 0.05 | ||
| Non-Hispanic white | 272 (78%) | 196 (77%) | |
| Non-Hispanic black | 36 (10%) | 16 (6%) | |
| Hispanic | 30 (9%) | 36 (14%) | |
| Other | 12 (3%) | 5 (2%) | |
| Age (years) | 34.4 (±9.3) | 54.1 (±9.4) | <0.001 |
| BMI (kg/m2) | 26.6 (±8.1) | 28.2 (±7.0) | 0.01 |
| Gastric retention at 2 hours (%) | 64.8 (±18.0) | 65.7 (±17.5) | 0.56 |
| Gastric retention at 4 hours (%) | 32.0 (±22.4) | 32.4 (±21.6) | 0.79 |
| Total GCSI score | 3.0 (±1.0) | 2.9 (±1.1) | 0.20 |
| Nausea/vomiting subscore | 2.5 (±1.5) | 2.1 (±1.4) | 0.002 |
| Bloating subscore | 3.1 (±1.5) | 3.2 (±1.6) | 0.32 |
| Postprandial fullness subscore | 3.5 (±1.1) | 3.4 (±1.2 ) | 0.29 |
| Nausea | 3.5 (±1.4) | 3.0 (±1.5) | <0.001 |
| Retching | 1.9 (±1.8) | 1.6 (±1.7) | 0.04 |
| Vomiting | 2.0 (±1.9) | 1.6 (±1.8) | 0.01 |
| Stomach fullness | 3.6 (±1.3) | 3.6 (±1.3) | 0.47 |
| Unable to finish meal | 3.5 (±1.4) | 3.4 (±1.5) | 0.59 |
| Feel full after meals | 3.7 (±1.3) | 3.6 (±1.3) | 0.41 |
| Loss of appetite | 3.0(±1.5) | 2.8 (±1.6) | 0.19 |
| Bloating | 3.3 (±1.5) | 3.3 (±1.6) | 0.47 |
| Stomach visibly larger | 2.9 (±1.7) | 3.1 (±1.7) | 0.25 |
| Upper abdominal pain | 3.0 (±1.6) | 2.8 (±1.7) | 0.14 |
| Upper abdominal discomfort | 3.2 (±1.5) | 3.2 (±1.5) | 0. 99 |
P-values were calculated using t-test for continuous variables and Fisher’s exact test for categorical variables.
Table 6.
PAGI symptom severity by use of hormone supplement among postmenopausal female patients (N = 253)
| Mean (±SD) or N (%) |
P* | ||
|---|---|---|---|
| Without hormone supplement (N = 188) |
With hormone supplement (N = 65) |
||
| Race | 0.79 | ||
| Non-Hispanic white | 147 (78%) | 49 (75%) | |
| Non-Hispanic black | 11 (6%) | 5 (8%) | |
| Hispanic | 27 (14%) | 9 (14%) | |
| Other | 3 (2%) | 2 (3%) | |
| Age (years) | 54.9 (±9.6) | 51.9 (±8.5) | 0.03 |
| BMI (kg/m2) | 28.4 (±6.9) | 27.5 (±7.1) | 0.35 |
| Gastric retention at 2 hours (%) | 64.9 (±17.5) | 67.9 (±17.4) | 0.23 |
| Gastric retention at 4 hours (%) | 32.7 (±21.5) | 31.7(±22.0) | 0.74 |
| Total GCSI score | 2.9 (±1.1) | 3.0 (±1.1) | 0.45 |
| Nausea/vomiting subscore | 2.1 (±1.4) | 2.1 (±1.4) | 0.85 |
| Bloating subscore | 3.2 (±1.6) | 3.4 (±1.5) | 0.39 |
| Postprandial fullness subscore | 3.3 (±1.2) | 3.4 (±1.1) | 0.48 |
| Nausea | 3.0 (±1.5) | 3.2 (±1.5) | 0.46 |
| Retching | 1.6 (±1.7) | 1.6 (±1.7) | 0.81 |
| Vomiting | 1.6 (±1.8) | 1.6 (±1.7) | 0.96 |
| Stomach fullness | 3.5 (±1.3) | 3.6 (±1.2) | 0.53 |
| Unable to finish meal | 3.4 (±1.5) | 3.6 (±1.4) | 0.43 |
| Feel full after meals | 3.6 (±1.4) | 3.7 (±1.2) | 0.80 |
| Loss of appetite | 2.8 (±1.6) | 2.9 (±1.6) | 0.56 |
| Bloating | 3.3 (±1.6) | 3.4 (±1.6) | 0.55 |
| Stomach visibly larger | 3.0 (±1.7) | 3.3 (±1.7) | 0.29 |
| Upper abdominal pain | 2.7 (±1.7) | 3.3 (±1.6) | 0.02 |
| Upper abdominal discomfort | 3.1 (±1.6) | 3.5(±1.3) | 0.03 |
P-values were calculated using t-test for continuous variables and Fisher’s exact test for categorical variables
Followup information
There were 337 females and 60 males that had outcome data over a one year follow up (Supplemental Table 6). The improvement in total GSCI score was not significantly different in females (3.0 to 2.6) compared to males (2.6 to 2.4; p=0.22). However, females had better improvement than males in stomach visibly larger (3.0 to 2.8 for females compared to 2.0 to 2.4 for males; p=0.03) and upper abdominal pain (3.0 to 2.4 for females compared to 2.4 to 2.3 for males; p=0.03). An improvement in total GCSI by ≥1 was seen in 26% of females and 24% of males (p=0.68). There was not a significant differential use between males and females starting TPN, J tube, gastric stimulator, or domperidone (Supplementary Table 7).
Discussion
This study shows that the etiology, symptom severity, and treatments for gastroparesis vary according to race, ethnicity, and gender of patients. Non-Hispanic blacks were more likely to have diabetic etiology with higher severity of nausea/vomiting and more likely to require hospitalization. Hispanics were also more likely to have diabetic etiology but had lower severity of nausea/vomiting. Non-Hispanic whites were more likely to have idiopathic gastroparesis. Females were more likely to have idiopathic gastroparesis with higher symptom severity of total GCSI total score, bloating and postprandial fullness subscore.
Effects of race, ethnicity, and gender in gastroparesis presentation have not been well studied; most studies enroll primarily white female patients. Whether this is due to lower prevalence of gastroparesis in nonwhite populations, difference in severity of symptoms leading to presentation to health care providers, or access in seeking health care seeking is not clear. We accessed NHANES data, finding 0.6% prevalence of gastroparesis (defined by taking prescription medication in the past month due to either gastroparesis or nausea and vomiting) with higher percentages of non-Hispanic whites and females compared to individuals without gastroparesis, although this was not significant possibly due to small numbers (27). One prior study involving a smaller number of subjects found non-white patients with gastroparesis had more severe symptoms (primarily nausea/vomiting), poorer quality of life, and utilized more health care resources than whites (11). Non-whites were more likely to have diabetes as the etiology. This small single center study came from one of the GpC centers; some of the patients might have been in this current multicenter study. In this multicenter GpC study, the larger sample size provided comparison of non-Hispanic blacks to Hispanics and the study design allowed collection of treatment and outcome data.
Non-Hispanic blacks, compared to non-Hispanic whites, were more likely to have diabetic etiology of gastroparesis with more severe retching, vomiting with a significant greater nausea/vomiting subscore. These patients with more severe retching/vomiting also had more Grade 3 severity and hospitalizations; these factors that might be related to each other. A recent study by Gibbons et al found the presence of longer poly GT repeat alleles in the HMOX1 genes of black/African American subjects with gastroparesis compared to non-black subjects with gastroparesis (28). HMOX1 encodes for the enzyme heme oxygenase 1 (HO1). Loss of HO1 expression and/or loss of HO1-containing macrophages leads to loss of pacemaker cells (interstitial cells of Cajal) in the stomach (29). Subjects with diabetic gastroparesis with one or two long polyGT repeat alleles had more severe nausea symptoms when compared to subjects without repeat alleles. In addition, black individuals with gastroparesis, nausea subscores were worse than scores in non-blacks with gastroparesis. This study suggests a potential genetic basis for the observed differences in disease severity.
One of the interesting findings was that non-Hispanic blacks and Hispanics were more likely to have diabetic gastroparesis and lower income, less education than whites but blacks had more severe symptoms whereas Hispanics had less severe symptoms. Further studies are needed to look at Hispanic ethnicity in gastric pathophysiology.
Differences in treatments for gastroparesis were present by race/ethnicity, specifically in the use of treatment with domperidone and use of PICC. Domperidone was used less in Hispanics than non-Hispanic whites. This could be in part due to decreased symptom severity of nausea, early satiety, and stomach fullness. There were also differences in the etiology of gastroparesis with Hispanics having more diabetic gastroparesis; domperidone has been studied mainly in diabetic gastroparesis (30). Alternatively, since the income of the Hispanics was lower; perhaps they could not afford domperidone, a medication the patient needs to purchase. In our cohort, the levels of Beck Depression Inventory score and State-Trait Anxiety Inventory scores were similar, suggesting these are not playing differential role in health care seeking for their GI distress. A possibility entertained was that patients entered the registry at different stage of the disease and the average level of the disease differed by race/ethnicity. However, the duration of gastroparesis symptoms did not differ by race/ethnicity. Socioeconomic factors and healthcare access to specific therapeutic services may be playing a role. We do not have information on the type of medical insurance the patients have; medical insurance can influence treatments used, specifically the use of gastric electric stimulation.
The impact of race and ethnicity in many gastrointestinal diseases has not been well studied; however, it may well be a relevant issue. For example, certain symptoms of IBS, particularly constipation, are more common in African American patients (31,32,33). Racial differences have also been noted in IBD with respect to disease location, presenting symptoms, family and surgical history, and extraintestinal manifestations (34,35). In GI cancers, esophageal squamous cell carcinoma and colorectal cancer show highest rates among blacks; the explanations for this disparity are likely multifactorial, including socioeconomic and health care access, treatment, and prevention differences, dietary and composition of the gut microbiome, as well as biologic and genetic influences (36). When substantiated in larger epidemiologic studies, the racial aspects of gastroparesis might need to be taken into account in treatment trials—stratifying for ethnic/racial background of patients.
We also looked at the effects of gender on the presentation of gastroparesis. In this study, the vast majority (84%) of patients with gastroparesis were females. Females were more likely to have idiopathic gastroparesis than the males. Females had greater symptom severity for stomach fullness, early satiety, postprandial fullness, bloating, stomach visibly larger, and upper abdominal pain. However, more males had hospitalizations in the last year. Among females, postmenopausal women had less severe nausea, retching, and vomiting compared to premenopausal women. Interestingly, postmenopausal women taking hormone replacement therapy had greater upper abdominal pain and discomfort than those not taking hormone replacement therapy. Various mechanisms have been suggested for the gender differences observed in GI disorders, including slower transit time in women, the effects of menstrual cycle, hormones, and nitric oxide (9). Females have slower gastric emptying than males, an effect postulated to be due to female sex hormones, estrogen and progesterone (37). There are also gender-related differences in neural pathways and neurotransmitter action (38). There appear to be gender differences in response to treatment for gastroparesis; metoclopramide may have more efficacy in females than males (10).
In this study, we also looked at symptom outcome and procedures performed over a one year follow up period in the different ethnic, racial, gender groups. In the first registry of the Gastroparesis Research Consortium, we found that only a minority of patients had symptomatic improvement over time (22): 28% of the 262 patients had reductions in GCSI scores of 1 or more at 48 weeks. In this study, which contains the patients in our previously reported outcomes studies (22,23) as well as patients in our second registry study, the improvement in GCSI total score was similar in the three ethnic/racial groups. However, vomiting improved more in non-Hispanic blacks compared to non-Hispanic whites and for Hispanics. Females had a greater improvement in nausea, stomach visibly larger, and upper abdominal pain.
Limitations to this study exist. We recruited patients from 7 clinical centers that are spread geographically; however, this does not guarantee that our patients represent the target population of all the gastroparesis patients. In addition, recruited patients may differ from other patients. The participating centers are academic medical centers which might lend to patients that are more symptomatic than seen in less specialized environments, and the centers might provide treatments not available in the community, e.g., domperidone, gastric electric stimulation. Each center enrolled patients from the patients seen at their centers and enrolled patients from varied locals and socioeconomic backgrounds. There was differential recruiting of minorities in different regions with the El Paso, Texas site recruiting more Hispanics probably due to their geographic location. Nevertheless, the group numbers are not balanced with a relatively small numbers of Hispanics, non-Hispanic blacks, and men which were a major focus of this study. Our study population for gastroparesis comprised 77% non-Hispanic white (general US population being 61%), 9% non-Hispanic blacks (general population 13%), and 12% Hispanic (general population 18%). There is the potential that socioeconomic factors (e.g., income, education, insurance) may play a role in the management of some of patients (domperidone, PICC lines for TPN). Patients had to be symptomatic to be entered into the registry; all findings in this study related to symptomatic gastroparesis. Gastroparesis can be asymptomatic and there is not a good correlation between emptying and symptoms.
In conclusion, the etiology, symptom severity, and treatments for gastroparesis vary according to the race, ethnicity, and gender of patients. Hispanics and Blacks were more likely to have diabetic etiology for gastroparesis than whites who more often had idiopathic gastroparesis. Blacks had higher severity of nausea/vomiting and were more likely to require hospitalization than Hispanics and Whites. Females were more likely to have idiopathic gastroparesis with higher symptom severity of bloating subscore and postprandial fullness subscore. Females had better improvement over time than males. Thus, this study demonstrates that race, ethnicity, and gender impacts on the presentation and treatments of gastroparesis.
Supplementary Material
What You Need to Know.
Background:
There is limited information on gastroparesis in minority populations.
Findings:
Hispanics and blacks are more likely to have diabetic etiology for gastroparesis than whites, who more often have idiopathic gastroparesis. Blacks have more severe nausea and vomiting and are more likely to require hospitalization and use total parenteral nutrition than Hispanics and whites. Women are more likely than men to have idiopathic gastroparesis, with higher symptom severity of bloating subscores and postprandial fullness subscores. Women have better improvement over time than men.
Implications for patient care:
The etiology, clinical presentation, treatment, and progression of gastroparesis vary with patient race, ethnicity, and sex. Race, ethnicity, and sex might directly or indirectly affect treatment and outcomes of patients with gastroparesis.
Acknowledgments
The NIH/NIDDK Gastroparesis Clinical Research Consortium (GpCRC) is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (grants U01DK073983, U01DK073975, U01DK073985, U01DK074007, U01DK073974, U01DK074008).
Footnotes
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No conflicts of interest exist.
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