High prevalence of gastrointestinal symptoms in patients with primary Sjögren’s syndrome cannot be attributed to pancreatic exocrine insufficiency

Abstract

Introduction

Pancreatic exocrine insufficiency (PEI) results in maldigestion of fat, leading to steatorrhea, malabsorption and weight loss. Sjögren’s syndrome (SS) is a chronic autoimmune rheumatic disease with unknown etiology. The exocrine pancreas and the salivary glands are functionally and histologically comparable, and pancreatic dysfunction in SS has been hypothesized.

Methods

Patients were recruited from the Department for Rheumatology at the Karolinska University Hospital in Stockholm, Sweden, between June and December 2019. PEI was assessed by fecal elastase-1 (FE-1) and ¹³C-mixed triglyceride breath test (¹³C-MTG-BT). The presence and severity of gastrointestinal symptoms were assessed by a well-established and validated survey based on a seven-point Likert scale.

Results

Fifty-seven patients with primary SS were included in the study, comprising 92% females with a median age of 63 years. In total, 87% of SS patients were tested for FE-1 and all had normal results. All patients who underwent a ¹³C-MTG-BT had a normal cumulative ¹³C-exhalation. Compared to the control group, significantly more patients suffered from gastrointestinal (GI) symptoms (p < .01). The same number of patients noted moderate to severe loose bowel movements or constipation (38%). Eleven GI symptom parameters were compared to controls and the highest odd ratios were noted for the following moderate to severe symptoms: bloating, feeling of incompletely emptied bowel after defecation and abdominal pain relieved by bowel action.

Conclusion

In our study, most SS patients suffered from irritable bowel syndrome (IBS)-like GI symptoms that could not be attributed to PEI.

Keywords:

• Pancreatic exocrine insufficiency
• gastrointestinal symptoms
• chronic pancreatitis
• Sjögren’s syndrome

Acknowledgements

We thank our colleague Dr. Jutta Keller from Hamburg, Germany, for her kind support. This study is part of the PhD thesis of AH.

Disclosure statement

JML received lecture fees from Mylan (Viatris) and Abbott and was supported by Reumatikerförbundet, Sweden.

SLH was supported by ‘Centrum för innovativ medicin’ (CIMED), Region Stockholm.

AH received lecture fees from Mylan (Viatris).

SHL received lecture fees from Mylan (Viatris) and reimbursements for teaching at the workshops.

MV received lecture fees from Mylan (Viatris) and Abbott.

Additional information

Funding

This study was supported by Reumatikerfonden stipendium.