Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
Clin Exp Rheumatol. 2022 Jul;40(7):1378-1384. doi: 10.55563/clinexprheumatol/h5cidq. Epub 2021 Sep 28.
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.
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.
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.
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.
胰岛淀粉样多肽是一种参与葡萄糖稳态的胰腺激素。我们旨在研究系统性红斑狼疮（SLE）患者的血清胰岛淀粉样多肽水平与匹配对照组相比有何差异，并探讨其与疾病相关特征（如活动或损伤）的可能关系。
纳入 144 例 SLE 患者和 96 例非糖尿病性别匹配（女性 96%比 91%，p=0.43）和年龄匹配（49±11 比 51±8 岁，p=0.09）的对照组。评估两组患者的血清胰岛淀粉样多肽、胰岛素和 C 肽水平以及胰岛素抵抗指数。进行多变量回归分析以比较两组间的胰岛淀粉样多肽水平，并探讨其与 SLE 特征的相互关系。分析调整了糖皮质激素的摄入和胰岛素抵抗的经典危险因素。
经多变量分析后，SLE 患者的血清胰岛淀粉样多肽水平明显高于对照组（β系数 1.56 [95%CI 1.01-2.11]，p=0.000）。此外，未服用泼尼松的 SLE 患者（β系数 1.54 [95%CI 0.98-2.10]ng/ml，p=0.000）和服用泼尼松的 SLE 患者（β系数 1.51 [95%CI 0.96-2.07]ng/ml，p=0.000）与对照组相比，血清胰岛淀粉样多肽水平也更高。即使在调整了患者和对照组之间的胰岛素抵抗和β细胞产生率差异后，SLE 患者的高胰岛淀粉样多肽血症仍然显著。疾病引起的损伤及其严重程度与血清胰岛淀粉样多肽水平独立且呈正相关。
无论 SLE 是否存在胰岛素抵抗，SLE 患者的血清胰岛淀粉样多肽水平均高于对照组。疾病引起的损伤及其严重程度独立解释了这种上调。
