MATERIALS AND METHODS: Randomised controlled trial was conducted on STEMI patients who undergo PCI in two hospitals in Jakarta, 104 patients enrolled to this study, and 77 patients completed the trial. 37 patients were randomly assigned to receive colchicines (2 mg loading dose; 0.5 mg thereafter every 12 hour for 48 hours) while 40 patients received placebo. NLRP3 level was measured from venous blood at baseline (BL), after procedure (AP), dan 24-hour post procedure (24H).
RESULTS: No NLRP3 difference was observed initially between colchicine arm and placebo arm 38,69 and 39,0138, respectively (p >0.05). Measurement conducted at 24H, patients received colchicine demonstrate reduction in NLRP3 level (37.67), while placebo arm results increase in NLRP3 level (42.89) despite not statistically significant (p >0,05).
CONCLUSION: Colchicine addition to standard treatment of STEMI patients undergo PCI reduce NLRP3 level despite statistically insignificant.
METHODS: We did a network meta-analysis based on a systematic review of randomised controlled trials comparing fibrinolytic drugs in patients with STEMI. Several databases were searched from inception up to Feb 28, 2017. We included only randomised controlled trials that compared fibrinolytic agents as a reperfusion therapy in adult patients with STEMI, whether given alone or in combination with adjunctive antithrombotic therapy, against other fibrinolytic agents, a placebo, or no treatment. Only trials investigating agents with an approved indication of reperfusion therapy in STEMI (streptokinase, tenecteplase, alteplase, and reteplase) were included. The primary efficacy outcome was all-cause mortality within 30-35 days and the primary safety outcome was major bleeding. This study is registered with PROSPERO (CRD42016042131).
FINDINGS: A total of 40 eligible studies involving 128 071 patients treated with 12 different fibrinolytic regimens were assessed. Compared with accelerated infusion of alteplase with parenteral anticoagulants as background therapy, streptokinase and non-accelerated infusion of alteplase were significantly associated with an increased risk of all-cause mortality (risk ratio [RR] 1·14 [95% CI 1·05-1·24] for streptokinase plus parenteral anticoagulants; RR 1·26 [1·10-1·45] for non-accelerated alteplase plus parenteral anticoagulants). No significant difference in mortality risk was recorded between accelerated infusion of alteplase, tenecteplase, and reteplase with parenteral anticoagulants as background therapy. For major bleeding, a tenecteplase-based regimen tended to be associated with lower risk of bleeding compared with other regimens (RR 0·79 [95% CI 0·63-1·00]). The addition of glycoprotein IIb or IIIa inhibitors to fibrinolytic therapy increased the risk of major bleeding by 1·27-8·82-times compared with accelerated infusion alteplase plus parenteral anticoagulants (RR 1·47 [95% CI 1·10-1·98] for tenecteplase plus parenteral anticoagulants plus glycoprotein inhibitors; RR 1·88 [1·24-2·86] for reteplase plus parenteral anticoagulants plus glycoprotein inhibitors).
INTERPRETATION: Significant differences exist among various fibrinolytic regimens as reperfusion therapy in STEMI and alteplase (accelerated infusion), tenecteplase, and reteplase should be considered over streptokinase and non-accelerated infusion of alteplase. The addition of glycoprotein IIb or IIIa inhibitors to fibrinolytic therapy should be discouraged.
FUNDING: None.
METHODS: Kidney IRI was performed with bilateral pediculus clamping in Swiss Background mice (3 months, 30-40g). Mice were euthanised on day one (I/R1, n=6), day eight (I/R8, n=6), and day twelve (I/R12, n=6) to exam acute and chronic episodes. Sham operation procedure was performed in the control. Tubular injury was assessed based on periodic acid- Schift (PAS) staining. Reverse transcriptase PCR (RT-PCR) was done to quantify mRNA expression of Bax, Bcl-2, and p16. Immunohistostaining (IHC) was performed to examine localisation of apoptosis (p53) and proliferation (Bcl-2).
RESULTS: RT-PCR analysis showed upregulation of mRNA expression of Bcl-2, Bax, and p16 (p<0.05). The data showed that ischemia/reperfusion induces upregulation of Bax (p=0.20), Bcl-2 (p=0.45), p16 (p=0.18). Apoptosis and proliferation occurred in the epithelial cells in acute episodes, but occurred in interstitial areas in chronic episodes.
CONCLUSIONS: Ischemia/reperfusion injury induces upregulation proliferation, apoptosis, and cellular senescence in acute kidney injury. Apoptosis reached its peak on day 1, proliferation on day 8, and cellular senescence on day 12.
Case Description: A patient with cervical stenosis secondary to metastatic tumor in the intradural and extradural compartments presented with lower limb paraparesis. She underwent an uneventful tumor excision accompanied by posterior cervical decompression and fusion. Postoperatively, she was quadriplegic and required ventilator support. The emergent postoperative MR scan revealed focal hyperintensity on the T2-weighted image consistent with spinal cord edema extending into the lower brain stem.
Conclusion: Very few cases of reperfusion injury of the cervical spinal cord or "white cord syndrome" are described in the literature. Here we present a patient who, following cervical laminectomy and fusion for excision of metastatic tumor, developed quadriplegia. Notably, postoperative MR showed only findings of upper cervical cord and lower brain stem edema consistent with a "white cord syndrome" without other compressive pathology.