BackgroundBlood loss warranting transfusion is a relatively rare requirement for degenerative cervical spine surgery. Despite this rarity, pretransfusion testing (blood typing, screening, and cross‐matching) has become routine in most parts of the world. We sought to determine if such routine testing is necessary for patients who undergo degenerative cervical spine surgery patients in specialty surgical hospitals by (1) measuring the current rate of intraoperative transfusions in degenerative cervical spine surgery and (2) identifying risk factors for transfusions.Study MethodsRetrospective review was performed on patients who underwent degenerative cervical spine surgery in two institutions. Demographic and baseline clinical and laboratory data were collected and analyzed to identify predictors of transfusion. Bivariate and multivariate logistic regression analysis was performed to identify perioperative transfusion risk factors.ResultsOverall transfusion rate was 1.9% (7/372), with no emergent transfusions. Decreases between preoperative and postoperative hemoglobin and hematocrit were 1.4 (SD 1.1) g/dL and 7.2 (SD 4.1) %, respectively. Multivariate logistic regression identified preoperative Hgb lower than 12 gr/dl (OR 27.62; 95% CI 4.31–176.96; p < 0.001) as significant independent transfusion risk factor. The receiver operating characteristic (ROC) curve for the model showed a very good discriminatory power with an area under the curve of 0.91.DiscussionOur study suggests that pretransfusion testing for all patients undergoing degenerative cervical spine surgery is unnecessary. We recommend that only patients with preoperative Hgb lower than 12 gr/dl would routinely need pretransfusion testing.
Background Apolipoprotein E (APOE)-4 isoform, Reelin and Clusterin share VLDLR and APOER2 receptors and are related to cognition in neuropsychiatric disorders. These proteins are expressed in plasma and brain but studies involving plasma expression and cognition are scarce. Methods We studied the peripheral expression (plasma and PBMCs) of these proteins in 24 Alcohol Use Disorder (AUD)-diagnosed middle-aged subjects at 4-12 weeks of abstinence (t=0) and 34 controls. Cognition was assessed using the 'Test of Detection of Cognitive Impairment in Alcoholism' (TEDCA). In a follow-up study (t=1), we measured Reelin levels and evaluated cognitive improvement at six months of abstinence. Results APOE4 isoform was present in 37.5% and 58.8% of patients and controls, respectively, reaching similar plasma levels in ε4 carriers, regardless of whether they were AUD subjects or controls. Plasma Reelin and Clusterin were higher in the AUD group, and Reelin levels peaked inpatients expressing APOE4 (p<0.05, ⴄ 2=0.09), who showed reduced VLDLR and ApoER2 expression in PBMCs. APOE4 had a negative effect on Memory/Learning mainly in the AUD group (p<0.01, ⴄ 2=0.15).Multivariate logistic regression analyses identified plasma Reelin as a good indicator of AUD cognitive impairment at t=0.At t=1, AUD subjects showed lower Reelin levels versus controls, along with some cognitive improvement. Conclusions Reelin plasma levels are elevated during early abstinence in AUD subjects who express the APOE4 isoform, identifying cognitive deterioration to a great extent, and it may participate as a homeostatic signal for cognitive recovery in the long-term.
Wernicke encephalopathy (WE) is a neurologic disease caused by vitamin B1 or thiamine deficiency (TD), being the alcohol use disorder (AUD) its main risk factor. WE patients present limiting motor, cognitive and emotional alterations related to a selective cerebral vulnerability. Neuroinflammation has been proposed as one of the phenomena contributing to brain damage. Our previous studies provide evidence for the involvement of the innate immune receptor Toll-like (TLR) 4 in the inflammatory response induced in the frontal cortex and cerebellum in TD animal models (animals fed with TD diet and receiving pyrithiamine). However, the effects of the combination of chronic alcohol consumption and TD on TLR4 and their specific contribution to the pathogenesis of WE are currently unknown. Additionally, no studies on TLR4 have been conducted on WE patients since brains from these patients are difficult to achieve. Here, we used rat models of chronic alcohol (CA; 9 months of forced consumption of 20% (w/v) alcohol), TD hit (TDD; TD diet + daily 0.25 mg/kg i.p. pyrithiamine during 12 days), or a combined treatment (CA+TDD) to check the activation of the proinflammatory TLR4/MyD88 pathway and related markers in the frontal cortex and the cerebellum. In addition, we characterized for the first time the TLR4 and its co-receptor MyD88 signature, along with other markers of this proinflammatory signaling such as phospo-NFkappaB; p65 and IkappaB, in the post-mortem human frontal cortex and cerebellum (gray and white matter) of an alcohol-induced WE patient, comparing it with negative (no disease) and positive (aged brain with Alzheimer disease) control subjects for neuroinflammation. We found an increase in the cortical TLR4 and its adaptor molecule MyD88, together with an upregulation of the proinflammatory signaling molecules p-NFkappaB and IkappaB in the CA+TDD animal model. In the patient diagnosed with alcohol-induced WE we observed cortical and cerebellar upregulation of the TLR4/MyD88 pathway. Thus, our findings provide evidence, both in the animal model and the human postmortem brain, of the upregulation of the TLR4/MyD88 proinflammatory pathway in WE related to alcohol consumption.
Wernicke’s encephalopathy (WE) is a neurologic disease caused by vitamin B1 or thiamine deficiency (TD), being the alcohol use disorder its main risk factor. WE patients present limiting motor, cognitive, and emotional alterations related to a selective cerebral vulnerability. Neuroinflammation has been proposed to be one of the phenomena that contribute to brain damage. Our previous studies provide evidence for the involvement of the innate immune receptor Toll-like (TLR)4 in the inflammatory response induced in the frontal cortex and cerebellum in TD animal models (animals fed with TD diet [TDD] and receiving pyrithiamine). Nevertheless, the effects of the combination of chronic alcohol consumption and TD on TLR4 and their specific contribution to the pathogenesis of WE are currently unknown. In addition, no studies on TLR4 have been conducted on WE patients since brains from these patients are difficult to achieve. Here, we used rat models of chronic alcohol (CA; 9 months of forced consumption of 20% (w/v) alcohol), TD hit (TDD + daily 0.25 mg/kg i.p. pyrithiamine during 12 days), or combined treatment (CA + TDD) to check the activation of the proinflammatory TLR4/MyD88 pathway and related markers in the frontal cortex and the cerebellum. In addition, we characterized for the first time the TLR4 and its coreceptor MyD88 signature, along with other markers of this proinflammatory signaling such as phospo-NFκB p65 and IκBα, in the postmortem human frontal cortex and cerebellum (gray and white matter) of an alcohol-induced WE patient, comparing it with negative (no disease) and positive (aged brain with Alzheimer’s disease) control subjects for neuroinflammation. We found an increase in the cortical TLR4 and its adaptor molecule MyD88, together with an upregulation of the proinflammatory signaling molecules p-NF-ĸB and IĸBα in the CA + TDD animal model. In the patient diagnosed with alcohol-induced WE, we observed cortical and cerebellar upregulation of the TLR4/MyD88 pathway. Hence, our findings provide evidence, both in the animal model and the human postmortem brain, of the upregulation of the TLR4/MyD88 proinflammatory pathway in alcohol consumption–related WE.
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