Determinants of Calcium Infusion Rate During Continuous Veno-venous Hemofiltration with Regional Citrate Anticoagulation in Critically Ill Patients with Acute Kidney Injury / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>It is unclear that how to decide the calcium infusion rate during continuous veno-venous hemofiltration (CVVH) with regional citrate anticoagulation (RCA). This study aimed to assess the determinants of calcium infusion rate during CVVH with RCA in critically ill patients with acute kidney injury (AKI).</p><p><b>METHODS</b>A total of 18 patients with AKI requiring CVVH were prospectively analyzed. Postdilution CVVH was performed with a fixed blood flow rate of 150 ml/min and a replacement fluid flow rate of 2000 ml/h for each new circuit. The infusion of 4% trisodium citrate was started at a rate of 29.9 mmol/h prefilter and adjusted according to postfilter ionized calcium. The infusion of 10% calcium gluconate was initiated at a rate of 5.5 mmol/h and adjusted according to systemic ionized calcium. The infusion rate of trisodium citrate and calcium gluconate as well as ultrafiltrate flow rate were recorded at 1, 2, 4, 6, 12, and 24 h after starting CVVH, respectively. The calcium loss rate by CVVH was also calculated.</p><p><b>RESULTS</b>Fifty-seven sessions of CVVH were performed in 18 AKI patients. The citrate infusion rate, calcium loss rate by CVVH, and calcium infusion rate were 31.30 (interquartile range: 2.70), 4.60 ± 0.48, and 5.50 ± 0.35 mmol/h, respectively. The calcium infusion rate was significantly higher than that of calcium loss rate by CVVH (P < 0.01). The correlation coefficient between the calcium and citrate infusion rates, and calcium infusion and calcium loss rates by CVVH was -0.031 (P > 0.05) and 0.932 (P < 0.01), respectively. In addition, calcium infusion rate (mmol/h) = 1.77 + 0.8 × (calcium loss rate by CVVH, mmol/h).</p><p><b>CONCLUSIONS</b>The calcium infusion rate correlates significantly with the calcium loss rate by CVVH but not with the citrate infusion rate in a fixed blood flow rate during CVVH with RCA.</p>

Plasma gelsolin level and its relationship with the prognosis of patients with severe burns / 中华烧伤杂志

<p><b>OBJECTIVE</b>To observe the changes in plasma gelsolin (pGSN) level of patients with severe burn and to explore its relationship with sepsis and death of patients.</p><p><b>METHODS</b>One hundred and two patients with total burn area equal to or larger than 30% TBSA hospitalized from May 2010 to May 2012 were included as burn group. Twenty-five healthy volunteers were recruited as healthy control group. Peripheral venous blood of patients was harvested on post burn day (PBD) 1, 3, 7, 14, and 21 to determine the pGSN level with double antibody sandwich ELISA kits, and the same maneuver was carried out in healthy volunteers. (1) Patients in burn group were divided into three groups by burn size: small burn area group (30% - 49% TBSA, n = 39), medium burn area group (larger than 49% and smaller than or equal to 69% TBSA, n = 33), and large burn area group (larger than 69% and smaller than or equal to 99% TBSA, n = 30). (2) According to diagnostic criteria of burn sepsis, patients in burn group were divided into sepsis group (n = 43) and non-sepsis group (n = 59). (3) According to the prognosis of patients with sepsis, patients in sepsis group were further divided into non-survival sepsis group (n = 14) and survival sepsis group (n = 29). The levels of pGSN in above groups were compared, and their relationship with sepsis and death of patients was analyzed. Data were analyzed with analysis of variance, LSD test and one-way Logistic regressions.</p><p><b>RESULTS</b>(1) Levels of pGSN in burn group were obviously lower than those of healthy control group on PBD 1, 3, 7, 14, and 21 (with F values respectively 140.01, 369.52, 702.15, 360.14, 84.16, P values all below 0.01). (2) The mean levels of pGSN in large, medium, and small burn area groups at five time points were (43 ± 11), (85 ± 23), (124 ± 38) mg/L, showing statistically significant differences among them (F = 367.76, P < 0.01), and they were all lower than that of healthy control group [(326 ± 51) mg/L, P values all below 0.01]. (3) The mean levels of pGSN in sepsis group and non-sepsis group at the five time points were (77 ± 12), (122 ± 38) mg/L. Levels of pGSN in sepsis group were lower than those in non-sepsis group on PBD 3, 7, 14, and 21 (with F values respectively 30.35, 111.59, 209.36, 422.76, P values all below 0.01). (4) The mean levels of pGSN in non-survival sepsis group and survival sepsis group at the five time points were (53 ± 8) and (103 ± 25) mg/L. Levels of pGSN in non-survival sepsis group were lower than those in survival sepsis group on PBD 1, 3, 7, 14, and 21 (with F values respectively 9.05, 18.48, 41.34, 107.11, 180.48, P values all below 0.01). (5) Logistic regression analysis showed that the level of pGSN is the independent risk factor related to the complication of sepsis (odds ratio: 5.44, 95% confidence interval: 2.35 - 12.74, P < 0.01) and death (odds ratio: 5.52, 95% confidence interval: 2.34 - 12.19, P < 0.01) in burn patients.</p><p><b>CONCLUSIONS</b>Severe burn injury could down-regulate the pGSN level of patients, and it decreases along with the increase in the area and severity of burn trauma. pGSN level appears to be an early prognostic marker for patients suffering from severe burns.</p>

Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review / 世界急诊医学杂志（英文）

@#BACKGROUND: High mobility group box 1 protein (HMGB1) is a highly conserved, ubiquitous protein in the nuclei and cytoplasm of nearly all cell types. HMGB1 is secreted into the extracellular milieu and acts as a proinflammatory cytokine. In this article we reviewed briefly the cellular immune response mediated by HMGB1 in inflammation and sepsis. METHODS: This systemic review is mainly based on our own work and other related reports. RESULTS: HMGB1 can actively affect the immune functions of many types of cells including T lymphocytes, regulatory T cells (Tregs), dendritic cells (DCs), macrophages, and natural killer cells (NK cells). Various cellular responses can be mediated by HMGB1 which binds to cell-surface receptors [e.g., the receptor for advanced glycation end products (RAGE), Toll-like receptor (TLR)2, and TLR4]. Anti-HMGB1 treatment, such as anti-HMGB1 polyclonal or monoclonal antibodies, inhibitors (e.g., ethyl pyruvate) and antagonists (e.g., A box), can protect against sepsis lethality and give a wider window for the treatment opportunity. CONCLUSION: HMGB1 is an attractive target for the development of new therapeutic strategies in the treatment of patients with septic complications.

The potential role of regulatory T cells in postburn sepsis / 中华烧伤杂志

It has been demonstrated that severe burn per se may contribute to activation and proliferation of regulatory T cells (Treg). This characteristic phenomenon might allow Treg to function for a prolonged period of time to regulate immune response, and to induce suppression of T lymphocyte immune function. Different degrees of elevated levels of cytokines produced by Treg and activation markers on Treg surface could also be involved in the development of sepsis and fatal outcome in patients with severe burn. Thus, the regulation of Treg as a cellular therapeutic strategy might be important to the Th1/Th2 cytokine balance in burn patients complicated with sepsis.

Influence of splenic high mobility group box-1 protein on immune function of regulatory T lymphocytes in scald rats / 中华烧伤杂志

<p><b>OBJECTIVE</b>To observe the influence of high mobility group box-1 protein (HMGB1) derived from spleen on the phenotype of regulatory T lymphocytes (Treg) and HMGB1-mediated immune function in severely scalded rats after delayed resuscitation.</p><p><b>METHODS</b>One hundred and four Wistar rats were divided into normal control group (NC, n = 8), sham scald group (SS, n = 32), scald group (S, n = 32), and ethyl pyruvate (EP) treatment group (EPT, n = 32) according to the random comparison table. Rats in the latter 2 groups were subjected to 30%TBSA full-thickness scald, which were intraperitoneally injected with Ringer solution or EP solution at post scald hour (PSH) 6 (delayed antishock treatment) and administered with 4 mL Ringer solution or EP solution per 12 hours after PSH 12 till PSH 48. Rats in SS group were treated the same as that of S group except for sham scald with 37 degrees C water. Injured rats were sacrificed at post scald day (PSD) 1, 3, 5, 7 (rats in NC group were also sacrificed), and CD4(+)CD25(+)Treg were isolated from spleen with magnetic-activated cell sorting method. The content of HMGB1 in spleen and IL-2 level in supernatant were determined with ELISA. The expression of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on Treg was determined with flow cytometry, and the proliferation activity of T lymphocytes was also detected (recorded as absorbance value). Data were processed with analysis of variance among groups and independent samples t test.</p><p><b>RESULTS</b>(1) Compared with that of rats in SS group and EPT group, the expression of splenic HMGB1 in S group increased significantly on PSD 1 through PSD 7 [peaked on PSD 1: (46.7 +/- 8.3) ng/mg protein]. (2) Compared with that in SS group, the expression of CTLA-4 in S group was enhanced significantly on PSD 1 through PSD 5 (with t value respectively 10.459, 12.051, 4.029, P < 0.05 or P < 0.01); while that in EPT group decreased significantly on PSD 1 through PSD 7 as compared with that from S group (with t value respectively 2.796, 9.913, 9.581, 10.022, P < 0.05 or P < 0.01). (3) Compared with that of rats in SS group, the proliferation activity of T lymphocytes in S group was markedly suppressed on PSD 1 through PSD 7 (nadir on PSD1: 0.167 +/- 0.059), and release of IL-2 was decreased significantly [nadir on PSD 5: (44 +/- 24) pg/mL]. T lymphocytes proliferation activity was restored and excretion of IL-2 increased in EPT group as compared respectively with that of S group at each time point.</p><p><b>CONCLUSIONS</b>The release of HMGB1 may stimulate splenic Treg to mature, thereby induce suppression of proliferation activity of T lymphocytes and immune function. EP can ameliorate immune dysfunction in animals with delayed resuscitation through inhibiting the synthesis and release of HMGB1.</p>

The effect of hyperoxic Ringer's solution on the rabbits with inhalation injury at early postburn stage / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the effect of hyperoxic Ringer's solution on inhalation injury given at early postburn stage in rabbit.</p><p><b>METHODS</b>Seventy-seven rabbits were randomly divided into four groups, i.e. A (normal control, n = 5, without injury), B (n = 24, with Ringer's solution infusion for 10 days after injury), C (n = 24, with hyperoxic Ringer's solution infusion for 10 days after injury) and D (n = 24, without treatment after injury) groups. The rabbits in B, C and D groups were observed on 1 post injury day (PID), 2 PID, 3 PID, 5 PID, 7 PID and 10 PID, with 4 in each time points. The vital signs and survival rate were observed and the blood gas analysis, the WBC and PMN in the peripheral blood, ratio of wet/dry weight (W/D) of the lung tissue, the MDA, SOD contents in the pulmonary tissue, and the pulmonary pathomorphology were determined by corresponding methods.</p><p><b>RESULTS</b>The respiratory rate of the rabbits increased postburn, which was accompanied with gasping breath, flapping of nasal alae, frequent cough, and increased buccal and nasal secretion. Dry and wet rales were heard in the lungs after injury. The survival rate in D, B and C groups was 13.3%, 27.8% and 65.6%, respectively. Metabolic acidosis was identified in these groups by blood gas analysis. The indices of PaCO2, WBC, PMN, W/D, MDA in B, C and D groups were higher than those in A group in the order of D > B > C > A groups. While the pH, PaO2 value and SOD content in D group were lower than those in A group in the order of D < B < C < A groups (P < 0.05). Pathomorphological examination revealed that pulmonary volume increased after the injury with microscopic inflammatory changes in pulmonary tissue in B, C and D groups. While the extent and degree of injury in C group after the treatment of hyperoxic Ringer's solution were evidently less severe than those in other groups.</p><p><b>CONCLUSION</b>Early administration of hyperoxic Ringer's solution during the early postburn stage could be beneficial to the management of inhalation injury.</p>