TOPLINE:

Specific gastrointestinal (GI) manifestations in patients with early systemic sclerosis (SSc) were associated with distinct cardiac phenotypes, with upper GI symptoms such as dysphagia and peptic ulcers linked to conduction defects, and lower GI involvement, particularly malabsorption, associated with systolic dysfunction.

METHODOLOGY:

• Researchers analyzed patients with SSc from the prospective GENISOS cohort in the US to assess the association between GI and cardiac involvement.
• They included 459 adult patients with SSc (82% female) who had disease onset within 5 years before enrollment, with a median follow-up of 4.1 years.
• GI involvement at baseline was defined as the presence of one or more manifestations: dysphagia, gastroesophageal reflux disease, peptic ulcer, bloating, diarrhea, malabsorption, constipation, and pseudo-obstruction.
• Cardiac involvement was defined as having at least one of the two manifestations: conduction defects identified on resting or ambulatory electrocardiography and systolic dysfunction documented using echocardiography (ejection fraction < 40%) or nuclear imaging.

TAKEAWAY:

• At baseline, 88% of patients had GI involvement, and the median time to the onset of cardiac complications was 1.12 years. During follow-up, 27% of patients developed both cardiac and GI manifestations, and GI symptoms preceded cardiac complications in 65% of cases.
• Bloating and malabsorption at baseline were significant predictors of cardiac manifestations (adjusted hazard ratio [aHR], 2.78; 95% CI, 1.8-4.3 and aHR, 10.01; 95% CI, 3.7-26.9, respectively).
• Patients with cardiac involvement vs those without had higher rates of dysphagia (76% vs 61%; P = .005), peptic ulcers (19% vs 7%; P = .001), bloating (62% vs 40%; P < .001), diarrhea (55% vs 44%; P = .045), and malabsorption (17% vs 7%; P = .005).
• Peptic ulcers (adjusted odds ratio [aOR], 3.73; 95% CI, 1.67-8.52), dysphagia (aOR, 2.3; 95% CI, 1.23-4.28), and bloating (aOR, 2.2; 95% CI, 1.2-3.9) were associated with cardiac conduction defects, whereas malabsorption remained significantly associated with systolic dysfunction (aOR, 4.3; 95% CI, 1.4-13.4).

IN PRACTICE:

“Our findings not only support earlier cardiovascular risk stratification but also provide a framework for exploring shared pathophysiological mechanisms across organ systems. Importantly, they highlight the heterogeneous nature of the GI tract, suggesting that different segments may be affected independently through distinct mechanisms, each contributing uniquely to disease progression,” the authors of the study wrote.

SOURCE:

The study was led by Francesca R. Di Ciommo, MD, Sapienza University of Rome, Rome, Italy. It was published online on June 1, 2026, in Arthritis Care & Research.

LIMITATIONS:

Data for certain variables were missing, which may have affected the statistical power. Patient-reported outcome measures were not available. Some GI manifestations relied on physician reports and may be underrepresented.

DISCLOSURES:

The study received support from grants provided by the National Institutes of Health, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and other sources. Some authors reported receiving support for the present manuscript and reported receiving grants or contracts, consulting fees, payments or honoraria, or having other ties with various foundations, organizations, or companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.