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Exocrine pancreatic function is preserved in systemic sclerosis

Artikel i vetenskaplig tidskrift
Författare G. Bozovic
Rille Pullerits
A. Stahl
K. Ydstrom
D. Wenger
J. Marsal
P. Thulin
K. Andreasson
Publicerad i Arthritis Research & Therapy
Volym 21
ISSN 1478-6354
Publiceringsår 2019
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Språk en
Länkar dx.doi.org/10.1186/s13075-019-1840-...
Ämnesord Pancreas, Systemic sclerosis, Fecal elastase, Malnutrition, fecal elastase-1, scleroderma, classification, involvement, criteria, disease, Rheumatology, udamore hh, 1968, american journal of gastroenterology, v49, p193
Ämneskategorier Reumatologi och inflammation, Invärtesmedicin

Sammanfattning

Background: Systemic sclerosis (SSc) has been suggested to cause exocrine pancreatic dysfunction. However, a case-control-based autopsy study failed to associate systemic sclerosis with any pancreatic histopathology. The primary objective of this study was to examine the exocrine pancreatic function in consecutive SSc patients in relation to an age- and sex-matched control group. A secondary objective was to relate exocrine pancreatic function to radiological, laboratory, and clinical SSc characteristics. Methods: One hundred twelve consecutive patients fulfilling the 2013 American Congress of Rheumatology/European League Against Rheumatism criteria for SSc and 52 control subjects were matched for sex and age. Exocrine pancreatic function was assessed by ELISA-based measurement of fecal elastase, and levels <= 200g/g were considered pathological, i.e., representing exocrine pancreatic insufficiency. Patients were characterized regarding SSc manifestations including gastrointestinal and hepatobiliary function, by use of laboratory and clinical examinations. Pancreas parenchyma characteristics were evaluated by high-resolution computer tomography (HRCT). Results: A similar proportion of subjects exhibited pathological levels of fecal elastase among SSc patients (6/112; 5.4%) and control subjects (3/52; 5.8%). Patients with fecal elastase <= 200g/g did not differ from other SSc patients with respect to laboratory and clinical characteristics, including malnutrition. SSc subjects with low levels of fecal elastase displayed significantly lower pancreas attenuation on HRCT examinations compared to the control subjects. Conclusions: In this study encompassing 112 consecutive SSc patients and 52 matched control subjects, we were unable to associate systemic sclerosis with clinically significant exocrine pancreatic dysfunction.

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