1 Introduction

Gastroparesis is a disorder of upper gastrointestinal motility characterized by symptoms suggestive of, and objective evidence of delayed gastric emptying. It is typically associated with symptoms such as nausea, vomiting, upper abdominal pain, early satiety, fullness, or bloating, occurring in the absence of any mechanical obstruction of the stomach or duodenum [1-3]. To date, we categorize the causes of gastroparesis into three domains: diabetic gastroparesis, iatrogenic gastroparesis (resulting from upper gastrointestinal surgery or medications), and idiopathic gastroparesis [4]. However, in the largest group of patients, no identifiable underlying cause is found, and these cases are categorized as idiopathic gastroparesis [5, 6].

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by immune-mediated injury and chronic inflammation affecting multiple organ systems [7, 8]. Gastrointestinal involvement in patients with SLE is reported in up to 50% of cases [9]. Among the most common manifestations are nausea, anorexia, and vomiting [9]. Regarding clinical manifestations, abdominal pain and weight loss are reported in up to two-thirds of cases. Gastroparesis associated with substantial health care costs thus, prompt diagnosis of gastroparesis in SLE patients is crucial to improve long-term outcomes and quality of life. However, gastroparesis is often underdiagnosed due to the limited availability of the gold standard diagnostic tool, gastric emptying scintigraphy [10, 11].

While gastrointestinal involvement is a common manifestation of SLE, association between gastroparesis and SLE remains unclear. The majority of the data utilized were derived from a small cohort of patients treated at a single center [6]. While these findings provide valuable insights, the limited sample size and single-center nature of the study may affect the generalizability of the results to broader populations. To address these evidence gaps, the current study aimed to estimate the prevalence of gastroparesis in adults, describe patient demographics, explore disease etiology and treatments received following diagnosis, and treatment outcomes in a large, national administrative insurance claims database.

2 Methods

3 Results

A total of 12 538 228 patients were included from the NIS database. Of these, 1 165 925 patients (9.3%) were diagnosed with gastroparesis during intrahospitalization, and 11 372 303 patients (90.7%) did not have gastroparesis. In the gastroparesis group, 18 765 (1.6%) patients were SLE patients while 1 147 160 (98.4%) patients were non-SLE patients. In the nongastroparesis group, 0.7% of patients had SLE, while the remaining 99.3% did not have SLE.

4 Discussion

Our study is the first to utilize a large database to demonstrate that gastroparesis is associated with SLE. It also demonstrated a marked difference in clinical characteristics of patients with SLE who develop gastroparesis compared to the general gastroparesis patient population.

It is unsurprising that patients with SLE in our study had higher steroid usage and a greater prevalence of chronic kidney disease, as these are inherent to the disease's natural course. One might assume that SLE is linked to steroid use, which in turn leads to diabetes and eventually gastroparesis. However, our findings suggest otherwise, as SLE patients in our cohort had a lower prevalence of diabetes—a well-established major risk factor for gastroparesis. Additionally, SLE patients were younger and had lower smoking rates, both of which are also recognized risk factors. Although causality cannot be inferred due to the observational nature of our study, a more plausible explanation is that SLE itself, as a distinct disease entity, may contribute to the pathophysiology of gastroparesis. This hypothesis is further supported by a previous study demonstrating that SLE is associated with gastroparesis even in a nondiabetic population [12].

The mechanisms underlying the development of gastroparesis in SLE remain poorly understood. However, autonomic dysfunction is well-documented in SLE patients [13]. Autonomic neuropathy secondary to SLE, particularly its impact on the regulation of the enteric nervous system, may play a significant role. Additionally, intrinsic smooth muscle dysmotility due to immune complex deposition or vasculitis-related chronic ischemia, as observed in SLE patients with intestinal pseudo-obstruction, could also play a role [14].

In our study, patients with SLE and gastroparesis had significantly longer hospital stays and higher hospital costs, which may reflect that gastroparesis in the context of SLE is more difficult to manage and potentially associated with worse clinical outcomes. This may be due to the complex interplay between autoimmunity, autonomic dysfunction, and gastrointestinal dysmotility, making treatment less straightforward compared to idiopathic gastroparesis. Nutritional management is a key consideration in these patients, as malnutrition can exacerbate disease severity and increase hospitalization risks. The choice of nutrition depends on the severity of gastroparesis, with enteral nutrition generally preferred to maintain gut integrity, while parenteral nutrition is reserved for severe cases where enteral feeding is not tolerated [6]. Notably, patients with SLE in our study were more likely to receive TPN, and weight loss was more pronounced in this group, underscoring the critical role of early nutritional assessment and intervention. Although our study assessed the odds of SLE patients receiving gastric or jejunal feeding device placement, the association was not statistically significant. However, there was a significant increase in the likelihood of overall interventions, which likely contributed to the higher costs and longer hospital stays observed. This suggests that while gastroparesis in SLE may not always necessitate invasive nutritional support, the overall burden of disease often requires aggressive inpatient management.

Previous studies have shown that improving SLE disease control can lead to symptom relief in gastroparesis [10]. Given the potential for immune-mediated damage to the autonomic nervous system and smooth muscle, optimizing SLE management may be crucial not only for controlling systemic inflammation but also for improving gastrointestinal motility. A multidisciplinary approach involving rheumatologists, gastroenterologists, and nutritionists may be essential in reducing the need for interventions, ultimately leading to shorter hospital stays, lower healthcare costs, and improved patient outcomes.

This study has a few limitations. The administrative and cross-sectional nature of the NIS database restricted access to detailed patient-level data, such as clinical characteristics, endoscopic findings, gastric emptying study results, and laboratory values, which are critical for stratifying disease severity and accurately characterizing gastroparesis in SLE patients. Misclassification bias may be present, as the identification of gastroparesis was based solely on ICD-10-CM coding without confirmation through objective diagnostic testing. Additionally, the database lacks information on medication use, including specific prokinetics, immunosuppressive therapies, opioids, or steroid regimens, as well as SLE disease activity and duration, which could provide insights into treatment effects and potential confounding factors. The absence of data on the duration, frequency, and severity of symptoms such as nausea, vomiting, and weight loss limits our ability to assess the clinical burden of gastroparesis in this population. Furthermore, the database focuses exclusively on in-hospital occurrences, potentially overlooking significant postdischarge outcomes such as long-term nutritional status, quality of life, and subsequent hospital readmissions. It also may not fully represent the broader SLE population affected by gastroparesis, as a significant proportion of SLE patients are managed in the outpatient setting and were therefore not included in our analysis. Finally, the observational nature of this study precludes the establishment of definitive causal relationships between SLE and gastroparesis. Moreover, while we conducted multivariable analyses and age-stratified subgroup analysis to address confounding and assess robustness, we did not perform additional subgroup or sensitivity analyses (e.g., stratified by comorbidity burden) due to limitations in dataset granularity and statistical power. Future studies may explore these subgroup effects in more targeted cohorts or with prospectively collected data. While our findings suggest an association, further prospective studies are needed to confirm these relationships and explore underlying mechanisms. Despite these limitations, our study is the first to utilize a large database population to provide important insights into the prevalence, clinical impact, and treatment outcomes of gastroparesis in SLE patients. These findings underscore the need for heightened clinical awareness and further research to improve diagnosis, management, and outcomes in the SLE population.

In conclusion, gastroparesis is increasingly recognized as a significant gastrointestinal manifestation in SLE, with its presence contributing to longer hospital stays, higher healthcare costs, and an increased requirement for invasive interventions. These findings highlight the critical need for early identification and management of gastroparesis in SLE patients to mitigate its impact on morbidity, improve patient outcomes, and reduce healthcare burdens. The observed association emphasizes the importance of routine evaluation for gastrointestinal symptoms in SLE patients, particularly in those with risk factors for gastroparesis. Future research should prioritize elucidating the complex pathophysiological mechanisms linking SLE to gastroparesis, including the roles of autoimmunity, neural dysfunction, and comorbid conditions. Additionally, validating these findings in diverse populations and through well-designed prospective cohort studies will be essential to better understand this relationship and inform tailored therapeutic strategies.

Ethics Statement

As the NIS database does not include patient or hospital-specific identifiers, Institutional Review Board (IRB) approval was not required for this study. Nevertheless, we ensured compliance with ethical standards for research involving human subjects.

Conflicts of Interest

The authors declare no conflicts of interest.