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Amylin serum levels are upregulated in patients with systemic lupus erythematosus


1, 2, 3, 4, 5, 6, 7, 8, 9

 

  1. Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
  2. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
  3. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
  4. Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
  5. Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
  6. Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
  7. Division of Health Sciences, Universidad Europea de Canarias, Tenerife, Spain.
  8. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, and Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain; and Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. miguelaggay@hotmail.com
  9. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain. iferrazamaro@hotmail.com

CER14959
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PMID: 34596033 [PubMed]

Received: 02/07/2021
Accepted : 30/08/2021
In Press: 28/09/2021

Abstract

OBJECTIVES:
Amylin is a pancreatic hormone that participates in glucose homeostasis. We aimed to investigate how serum amylin levels are expressed in patients with systemic lupus erythematosus (SLE) compared to matched controls, and their possible relationship to disease-related characteristics, such as activity or damage.
METHODS:
144 SLE patients and 96 non-diabetic sex- (female 96% vs. 91%, p=0.43) and age-matched controls (49±11 vs. 51±8 years, p=0.09) were included. Amylin, insulin and C-peptide serum levels, as well as insulin resistance indexes were assessed in both groups. Multivariable regression analysis was performed to compare amylin between groups and to explore its interrelations with SLE features. The analyses were adjusted for glucocorticoids intake and for insulin resistance classic risk factors.
RESULTS:
Patients with SLE exhibited significant higher serum levels of amylin when compared to controls after multivariable analysis (beta coef. 1.56 [95%CI 1.01–2.11], p=0.000). Moreover, SLE patients not on prednisone (beat coef. 1.54 [95%CI 0.98–2.10] ng/ml, p=0.000) and those on prednisone (beta coef. 1.51 [95%CI 0.96–2.07] ng/ml, p=0.000) disclosed higher amylin serum levels compared to controls in the fully multivariable analysis. Hyperamylinaemia in SLE patients remained significant even adjusting for differences in the insulin resistance and beta cell production rates between patients and controls. The damage produced by the disease and its severity were independently and positively associated with amylin serum levels. CONCLUSIOINS: Amylin is upregulated in SLE patients compared to controls, regardless of the insulin resistance that SLE may present. The damage produced by the disease and its severity independently explains this upregulation.

Rheumatology Article