Barak V, Schwartz A, Kalickman I, Nisman B, Gurman G, Shoenfeld Y
Immunology Laboratory for Tumor Diagnosis, Sharett Institute of Oncology, Hadassah University Hospital, Jerusalem, Israel.
Am J Med. 1998 Jan;104(1):40-7. doi: 10.1016/s0002-9343(97)00275-1.
Sepsis occurs following the presence of bacteria in the circulation and is associated with fever, hyperthermia, and hypotension. Hypophosphatemia develops in the early stages of sepsis. High levels of inflammatory cytokines also characterize early sepsis.
The aim of the present study was to correlate hypophosphatemia with cytokines and cytokine receptor levels during early sepsis. We aimed to reestablish the results obtained from patients in an in vivo experimental model, in order to understand the mechanism of hypophosphatemia induction in early sepsis.
Ninety-nine patients were enrolled in this study and their clinical condition was classified as the presence of infection, sepsis, and bacterial growth in blood cultures. Phosphate levels and cytokine levels were recorded. In order to determine whether hypophosphatemia is correlated to the increased inflammatory cytokines, we injected normal mice with recombinant cytokines and studied their effect on phosphate levels.
Our results revealed that 80% of the septic patients had hypophosphatemia associated with very high levels of tumor necrosis factor (TNF)alpha and interleukin (IL)-6 and of soluble IL receptor (sIL)-2R and IL-6R, especially in those patients with positive blood cultures. Injection of IL-6, TNFalpha and IL-1beta in mice markedly decreased the phosphate serum levels.
Significant associations were demonstrated between high levels of inflammatory cytokines and their receptors and between serum phosphate levels, especially in patients with positive blood culture. Our results point to a correlation between the high inflammatory cytokines levels and hypophosphatemia during early sepsis. Cytokine levels and hypophosphatemia may be included in sepsis evaluation and prognosis. Anticytokine strategies might, therefore, reverse hypophosphatemia and other parameters of sepsis.
脓毒症发生于循环系统中存在细菌之后，与发热、体温过高和低血压相关。低磷血症在脓毒症早期出现。高水平的炎性细胞因子也是早期脓毒症的特征。
本研究的目的是关联早期脓毒症期间低磷血症与细胞因子及细胞因子受体水平。我们旨在在体内实验模型中重现从患者获得的结果，以了解早期脓毒症中低磷血症诱导的机制。
99名患者纳入本研究，其临床状况分类为存在感染、脓毒症以及血培养中有细菌生长。记录磷酸盐水平和细胞因子水平。为了确定低磷血症是否与炎性细胞因子增加相关，我们给正常小鼠注射重组细胞因子并研究其对磷酸盐水平的影响。
我们的结果显示，80%的脓毒症患者存在低磷血症，与非常高水平的肿瘤坏死因子（TNF）α、白细胞介素（IL）-6、可溶性IL受体（sIL）-2R和IL-6R相关，尤其是在血培养阳性的患者中。给小鼠注射IL-6、TNFα和IL-1β显著降低血清磷酸盐水平。
炎性细胞因子及其受体的高水平与血清磷酸盐水平之间存在显著关联，尤其是在血培养阳性的患者中。我们的结果表明早期脓毒症期间炎性细胞因子高水平与低磷血症之间存在相关性。细胞因子水平和低磷血症可能纳入脓毒症评估和预后。因此，抗细胞因子策略可能逆转低磷血症和脓毒症的其他参数。
