Association of hepatitis C infection and risk of kidney cancer: A systematic review and meta-analysis of observational studies.

Although some epidemiological studies have investigated the association between Hepatitis C virus (HCV) infection and the development of kidney cancer, the results are far from consistent. We conducted a systematic review and meta-analysis of observational studies to determine the association. PubMed, EMBASE and Cochrane database were searched from 1 January 1975 to 7 January 2020. Study selection, data extraction and bias assessment (using the Newcastle-Ottawa scale) were performed independently by 2 authors. Pooled odds ratios (ORs) with corresponding confidence intervals (CIs) were calculated using a random-effects model. In all, 16 studies (11 cohort studies and 5 case-control studies) involving a total of 391,071 HCV patients and 38,333,839 non-HCV controls were included. The overall analysis showed a 47% higher risk to develop kidney cancer among the patients with HCV infection (pooled OR 1.47; 95% CI 1.14-1.91), despite significant heterogeneity (I2  = 87.6%). The multivariable meta-regression showed that study design, age, sample size and HIV co-infection were significant sources of variance, and totally accounted for 82% of the I2 . The risk of KC in HCV patients was further increased in studies without HCV/HBV- and HCV/HIV- co-infection (pooled OR 1.66; 95%CI 1.23-2.24). Multiple sensitivity analyses did not change the significant association. The present meta-analysis indicated that HCV-infected patients have a significantly higher risk of developing kidney cancer. Our results highlighted the rationale for improved renal surveillance in HCV patients for the early diagnosis of kidney cancer. Further investigations for the mechanisms underlying HCV-induced kidney cancer are warranted.

Efficacy and safety of epidural block with lidocaine for refractory severe plaque psoriasis: An open-label pilot study in real world setting.

Epidural block using lidocaine, a non-selective blocker of voltage-gated sodium channels (Nav), has demonstrated efficacy in the treatment of severe plaque psoriasis in a limited number of cases. This study aimed to evaluate the effectiveness and safety of epidural lidocaine block in adult patients with severe, treatment-resistant plaque psoriasis. This was an open-label pilot study. Patients with severe plaque-type psoriasis unresponsive to at least one systemic treatment were enrolled for a 1-week epidural lidocaine block and followed up for 48 weeks. Thirty-six patients participated, with 32 completing the study. At the 12-week mark, there was a remarkable 59% improvement in the mean Psoriasis Area Severity Index (PASI) score (P < 0.001). By week 48, 28 out of 32 patients (87%) achieved PASI 75, while 18 out of 32 (56%) reached PASI 90. Within 7 days, 20 out of 21 patients (95%) reported a reduction in itch, with a mean itch reduction of 82% at day 1 and 94% at day 7. Notably, no severe side effects were observed. Epidural lidocaine block proved to be an effective and safe long-term treatment option for individuals with refractory severe plaque psoriasis.

Epidural block with lidocaine ameliorates kidney function deterioration and fibrosis of chronic kidney disease in rats.

BACKGROUND: According to evidences from clinical practices and experiments, renal denervation achieved by removing both the afferent and sympathetic nerves has therapeutic impacts on poor renal function and hypertension in chronic kidney disease (CKD). Epidural anesthesia is presumed to function on the target spine segments with a complete sympathetic block. Based on this perspective, we hypothesized that epidural block with lidocaine could ameliorate renal injury in CKD rats. METHOD AND RESULTS: Male Sprague-Dawley rats weighing 250-300 g were randomized into four groups: control, CKD, CKD + sham, and CKD + epidural block with lidocaine groups. CKD was induced by resection of the lower and upper thirds of the left kidney followed by right nephrectomy one week later. Significant differences in renal function, sympathetic activation as well as renal fibrosis parameters were observed between CKD and control rats. These parameters corresponded with typical phenotypes of CKD rats. Epidural block with lidocaine improved renal function as well as renal fibrosis, and reversed the abnormalities of the renal function and cardiovascular parameters either fully or partially. CONCLUSION: Epidural block with lidocaine confers renal protection, which is presumably mediated by decreasing sympathetic nerve activities in the renal region and other target organs in CKD.

Involvement of the nitric oxide-cyclic GMP-protein kinase G-K+ channel pathway in the antihyperalgesic effects of bovine lactoferrin in a model of neuropathic pain.

The possible involvement of the nitric oxide (NO)-cyclic GMP (cGMP)-protein kinase G (PKG) pathway on bovine lactoferrin (BLF)-induced spinal antihyperalgesic activity was elucidated in sciatic nerve injured rats. Intrathecal BLF reduced thermal hyperalgesia in a dose-dependent manner. Pretreatment with NG-L-nitro-arginine methyl ester (L-NAME, non-specific inhibitor of NO synthase), 7-nitroindazole (7-NI, neuronal NO synthase inhibitor), 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, guanylyl-cyclase inhibitor), (9S, 10R, 12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2, 9-dimethyl-1-oxo-9, 12-epoxy-1H-diindolo-[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester (KT-5823, specific PKG inhibitor) or glybenclamide (ATP-sensitive K+ channel blocker), but not NG-D-nitro-arginine methyl ester (D-NAME, an inactive enantiomer of l-NAME), d-Phe-Cys-Tyr-d-Trp-Orn-Thr-NH2 (CTOP, selective mu-opioid receptor antagonist) or naloxone (nonselective opioid receptor antagonist) prevented BLF-induced antihyperalgesia. Data suggest that BLF-induced spinal antihyperalgesia could be due to activation of the NO-cGMP-PKG-K+ channel pathway and it is not mediated by mu-opioid receptor in a model of neuropathic pain.