Association between lipid accumulation product index and chronic kidney disease: A systematic review and meta-analysis.

Diabetes mellitus and lipid metabolism disorders are increasingly recognized as key contributors to the development of chronic kidney disease (CKD). The lipid accumulation product (LAP) index, a novel marker of lipid accumulation, has potential implications for CKD risk assessment. The present meta-analysis aimed to assess the association between LAP index and CKD, with an emphasis on varying impacts in diabetic and non-diabetic populations. A comprehensive search for relevant publications was performed using PubMed/MEDLINE, Scopus, Cochrane Library, ScienceDirect and Google Scholar databases, and a meta-analysis of 17 studies was performed to investigate the relationship between LAP index and CKD. The random-effects inverse-variance model employing the DerSimonian-Laird estimator for τ² was utilized to calculate pooled odds ratios (ORs). Diagnostic accuracy was assessed using summary receiver operating characteristic (ROC) curves, with calculations of the area under the ROC curve (AUROC), sensitivity, specificity, likelihood ratios and diagnostic OR. The pooled OR for the association between higher quintiles or tertiles of LAP index and CKD was 1.098 (95% CI: 1.043-1.152), with substantial heterogeneity (I²=91.2%) and evidence of publication bias. Subgroup analysis revealed a stronger association in non-diabetic (OR=2.422, 95% CI: 1.802-3.042) compared with diabetic patients (OR=1.018, 95% CI: 0.993-1.043). The diagnostic accuracy of LAP index for CKD was moderate (AUROC=0.64), with sensitivity and specificity estimates of 0.58 and 0.63, respectively. In conclusion, in the present study, LAP index demonstrated a modest but significant association with CKD, particularly in non-diabetic patients. Despite its moderate diagnostic accuracy, the LAP index could serve as a valuable tool in CKD risk stratification, particularly when integrated with other clinical markers.

Outcomes of percutaneous coronary intervention for chronic total occlusions in the elderly: A systematic review and meta-analysis.

OBJECTIVE: This study aimed to compare outcomes of percutaneous coronary intervention (PCI) for chronic total occlusions (CTO) in the elderly (≥75 years) versus nonelderly and assess the impact of successful CTO-PCI in the elderly. METHODS: PubMed, Embase, ScienceDirect, CENTRAL, and Google Scholar databases were searched up to October 1, 2020. Mortality rates and major adverse cardiac events (MACE) were compared between elderly and nonelderly patients and successful versus failed CTO-PCI in the elderly. RESULTS: Eight studies were included. Meta-analysis indicated no statistically significant difference in the risk of in-hospital mortality (RR: 1.97 95% CI: 0.78, 4.96 I2 = 0% p = .15) but higher tendency of in-hospital MACE (RR: 2.30 95% CI: 0.99, 5.35 I2 = 49% p = .05) in the elderly group. Risk of long-term mortality (RR: 3.79 95% CI: 2.84, 5.04 I2 = 41% p < .00001) and long-term MACE (RR: 1.53 95% CI: 1.14, 2.04 I2 = 80% p = .004) were significantly increased in the elderly versus nonelderly. Elderly patients had a significantly reduced odds of successful PCI as compared to nonelderly patients (OR: 0.63 95% CI: 0.54, 0.73 I2 = 1% p < .00001). Successful CTO-PCI was associated with reduction in long-term mortality (HR: 0.51 95% CI: 0.34, 0.77 I2 = 27% p = .001) and MACE (HR: 0.60 95% CI: 0.37, 0.97 I2 = 53% p = .04) as compared to failed PCI in elderly. CONCLUSIONS: Elderly patients may have a tendency of higher in-hospital MACE with significantly increased long-term mortality and MACE after CTO-PCI. The success of PCI is significantly lower in the elderly. In elderly patients with successful PCI, the risk of long-term mortality and MACE is significantly reduced.

Delayed cerebellar infarction after a slight electric injury.

Electrical injury causes direct damage to nerves. It may manifest as peripheral nerve injury, spinal cord damage, cerebellar ataxia, hypoxic encephalopathy, or intracerebral hemorrhage. Various factors determine the severity of electric injury, including type of current, amperage, voltage, tissue resistance, pathway of the current, and duration of contact with the body. However, the severity of the electrical injury is not proportional to the source voltage, visible burns, loss of consciousness, or neuroimaging findings. While most neurologic aftereffects due to electric injuries are immediate and transient, delayed and permanent manifestations are also known. We report a case of a middle-aged man who accidentally sustained cerebellar infarction without burns, which occurred 4 days after a slight electrical injury. Magnetic resonance imaging of the brain showed an acute infarct in the bilateral cerebellar and left occipital regions. The exact mechanism of the delayed cerebellar infarction after a slight electric injury still remains unknown. The initial electrical injury might result in a transient neurapraxia-like situation, but progressive cellular damage and death accounts for the evolution of delayed-onset symptoms. We learned from this case that we should not underestimate any potential risk of electrical injury; continuous observation should be made in case of subsequent neurologic dysfunction.