School of Medicine, University of Auckland, Auckland, New Zealand.
Auckland City Hospital, Room 12.085A, Level 12, Auckland, 1023, New Zealand.
Eur Radiol. 2020 May;30(5):2902-2911. doi: 10.1007/s00330-019-06633-7. Epub 2020 Feb 10.
Pancreatitis often represents a continuous inflammatory process, from the first episode of acute pancreatitis (FAP) to recurrent acute pancreatitis (RAP) to chronic pancreatitis (CP). Psoas muscle size is a validated surrogate for global skeletal mass, changes in which are associated with inflammation. The objective was to investigate psoas muscle size in individuals following FAP, RAP, and CP, as well as its associations with pro-inflammatory cytokines.
Individuals following pancreatitis and healthy individuals were recruited. All participants underwent magnetic resonance imaging, from which psoas muscle volume was derived independently by two raters in a blinded fashion. Circulating levels of four major cytokines (interleukin-6, tumour necrosis factor-α, C-C motif chemokine ligand 2, and leptin) were measured. Five linear regression additive models were built to adjust for possible confounders (age, sex, body composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and endocrine and exocrine pancreatic functions).
A total of 145 participants were enrolled. A significant downward trend in psoas muscle volume was observed between healthy controls and individuals following FAP, RAP, and CP in all adjusted models (p = 0.047, 0.005, 0.004, and < 0.001). Leptin was significantly associated with psoas muscle volume in all models (β = - 0.16, p = 0.030 in the most adjusted model). The other studied cytokines were not significantly associated with psoas muscle volume.
Psoas muscle size is significantly reduced along the continuum from FAP to RAP to CP. Leptin appears to be one of the factors implicated in this. Further studies are warranted to investigate the relationship between skeletal muscle and inflammation of the pancreas.
• First acute pancreatitis, recurrent acute pancreatitis, and chronic pancreatitis were associated with progressively reduced psoas muscle size. • The findings were independent of age, sex, body fat composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and exocrine and endocrine functions of the pancreas. • The mechanism underlying the observed findings may involve hyperleptinaemia.
胰腺炎通常代表一个连续的炎症过程,从首次急性胰腺炎(FAP)发作到复发性急性胰腺炎(RAP)再到慢性胰腺炎(CP)。腰大肌大小是全身骨骼质量的有效替代指标,其变化与炎症有关。本研究旨在探讨 FAP、RAP 和 CP 后个体的腰大肌大小及其与促炎细胞因子的关系。
招募了胰腺炎患者和健康个体。所有参与者均接受磁共振成像检查,由两名盲法独立的评分者从磁共振图像中得出腰大肌体积。测量了四种主要细胞因子(白细胞介素 6、肿瘤坏死因子-α、C 型趋化因子配体 2 和瘦素)的循环水平。建立了五个线性回归加性模型,以调整可能的混杂因素(年龄、性别、身体成分、体力活动、吸烟、饮酒、合并症以及内分泌和外分泌胰腺功能)。
共纳入 145 名参与者。在所有调整后的模型中,健康对照组与 FAP、RAP 和 CP 患者的腰大肌体积均呈显著下降趋势(p=0.047、0.005、0.004 和<0.001)。在所有模型中,瘦素与腰大肌体积显著相关(最调整模型中β=-0.16,p=0.030)。其他研究的细胞因子与腰大肌体积无显著相关性。
FAP 到 RAP 再到 CP 的连续过程中,腰大肌大小显著减小。瘦素似乎是其中一个涉及的因素。需要进一步研究以探讨胰腺炎症与骨骼肌之间的关系。
首次急性胰腺炎、复发性急性胰腺炎和慢性胰腺炎与腰大肌逐渐减小有关。
这些发现独立于年龄、性别、体脂肪成分、体力活动、吸烟、饮酒、合并症以及胰腺内外分泌功能。
观察到的结果的机制可能涉及高瘦素血症。