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肠道衰竭中的全身炎症介质与骨稳态

Systemic inflammatory mediators and bone homeostasis in intestinal failure.

作者信息

Compher Charlene, Pazianas Michael, Benedict Stephen, Brown John C, Kinosian Bruce P, Hise Mary

机构信息

University of Pennsylvania School of Nursing, Philadelphia, Pennsylvania 19104-6096, USA.

出版信息

JPEN J Parenter Enteral Nutr. 2007 Mar-Apr;31(2):142-7. doi: 10.1177/0148607107031002142.

DOI:10.1177/0148607107031002142
PMID:17308255
Abstract

BACKGROUND

A proinflammatory state has been described in patients with intestinal failure. The prevalence of metabolic bone disease in this group is considerable. It is not known whether this proinflammatory state is related to bone parameters, though bone disease is recognized as a proinflammatory process in postmenopausal women. The purpose of this study was to examine whether inflammation was related to bone disease.

METHODS

Eight patients with parenteral nutrition (PN)-dependent intestinal failure but no recent infections or immunosuppressive medications had serum assayed for interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, and its receptors (TNFR-I and TNFR-II), C-reactive protein, and whole blood for lymphocyte proliferation. Routine clinical laboratory measures of vitamin D, parathyroid hormone, serum calcium, and phosphorus within 3 months of the inflammatory measures were compared by Pearson's correlation to the inflammatory measures.

RESULTS

Mean values for calcium, phosphorus, and albumin were normal, but 25-hydroxy vitamin D was reduced and parathyroid hormone and alkaline phosphatase elevated. Serum total calcium was negatively related to TNFR-II, TNF-alpha and positively to T-helper cells. Longer PN dependence was associated with inflammation and negatively with T-helper cells.

CONCLUSIONS

These preliminary findings are hypothesis generating only but support an association of low calcium and longer duration of PN with inflammation in patients with intestinal failure. Whether the inflammation results from vitamin D deficiency or the vitamin D deficiency develops secondary to excessive use of activated vitamin D to modulate inflammation from some other cause, such as a component of PN or repeated infectious challenge, requires further study.

摘要

背景

肠衰竭患者存在促炎状态。该群体中代谢性骨病的患病率相当高。尽管骨病在绝经后女性中被认为是一个促炎过程,但尚不清楚这种促炎状态是否与骨参数有关。本研究的目的是探讨炎症是否与骨病相关。

方法

8例依赖肠外营养(PN)的肠衰竭患者,近期无感染或未使用免疫抑制药物,检测其血清白细胞介素-6(IL-6)、肿瘤坏死因子(TNF)-α及其受体(TNFR-I和TNFR-II)、C反应蛋白,并检测全血淋巴细胞增殖情况。将炎症指标检测后3个月内维生素D、甲状旁腺激素、血清钙和磷的常规临床实验室测量值与炎症指标进行Pearson相关性比较。

结果

钙、磷和白蛋白的平均值正常,但25-羟维生素D降低,甲状旁腺激素和碱性磷酸酶升高。血清总钙与TNFR-II、TNF-α呈负相关,与辅助性T细胞呈正相关。更长时间的PN依赖与炎症相关,与辅助性T细胞呈负相关。

结论

这些初步发现仅为提出假设,但支持低钙和较长时间的PN依赖与肠衰竭患者炎症之间存在关联。炎症是由维生素D缺乏引起,还是维生素D缺乏继发于过度使用活性维生素D来调节由其他原因(如PN的某种成分或反复感染挑战)引起的炎症,尚需进一步研究。

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