Background Idiopathic intracranial hypertension (IIH) is typically seen in females of childbearing period; therefore, it is possible that female sex hormones have a pathogenic role in IIH. Obesity is considered as a strong risk factor for IIH, Leptin levels in the serum and CSF were found to be positively correlated with anthropological measures of obesity. The role of leptin and sex hormones in the pathogenesis of idiopathic intracranial hypertension is not fully understood. The aim of this work was to assess CSF leptin, serum leptin, estradiol, testosterone, Dehydroepiandrosterone sulfate (DHEAS) levels in idiopathic intracranial hypertension (IIH) patients. Results This is a case control study which was conducted on 38 IIH female patients and 38 females as controls. IIH patients had significantly higher levels of serum Leptin, CSF Leptin, serum estradiol and serum testosterone than controls (P value < 0.001, < 0.001, 0.005 and < 0.001, respectively), whereas there was no statistically significant difference between IIH patients and controls in serum DHEAS (P value = 0.142). IIH patients with body mass index (BMI) ≥ 30 kg/m2 had significantly higher levels of serum Leptin, CSF Leptin, serum estradiol, serum testosterone, and serum DHEAS than IIH patients with BMI < 30 kg/m2 (P value < 0.001, < 0.001, 0.009, < 0.001, and < 0.001, respectively). Conclusions Patients with IIH express a characteristic elevation in CSF leptin, serum leptin, estradiol and testosterone levels. These hormones are significantly elevated in patients with high BMI.
Breast cancer is the most common cancer among females with increasing incidence and death rates. Resistin is pro-inflammatory molecule which shares in diverse cellular signaling pathways. This study aimed to evaluate resistin and RETN rs3219175 gene polymorphism and their relevance to diagnostic susceptibility, prognostic value, and genetic risk among Egyptian female patients with breast cancer. Eighty female patients with breast cancer were recruited from the Oncology Department, Faculty of Medicine, Beni-Suef University. Breast cancer staging and grading were determined. Eighty age-matched normal females participated as controls. Quantitative determination of serum resistin was assayed by an enzyme-linked immunosorbent assay (ELISA). RETN rs3219175 gene polymorphism was determined by real time polymerase chain reaction (RT-PCR) TaqMan allelic discrimination assay. Serum resistin showed statistically significantly higher level among females with breast cancer when compared to controls (p <0.001). Resistin showed sensitivity of 80% and specificity of 67.5% at cut off value of 1.27 ng/mL for diagnosis of breast cancer (p =0.001). RETN rs3219175 gene polymorphism showed significantly higher frequency of AG, AA genotypes, and A allele among cases when compared to controls (p <0.001). No statistical difference was found in resistin level or RETN rs3219175 gene polymorphism regarding tumor characteristics including size, lymph nodes or distant metastasis. Resistin showed significantly higher level among carriers of AG followed by AA genotypes and among A allele (p <0.001). In conclusion, resistin could be proposed as a possible potential diagnostic marker and A allele of RETN rs3219175 gene might be suggested as a genetic risk allele among female patients with breast cancer.
Background The potential impact of insulin resistance on stroke prognosis after IV thrombolysis is poorly understood. This study aimed to assess the effect of insulin resistance and metabolic syndrome on the outcome of IV thrombolysis in non-diabetic patients with acute ischaemic stroke. Methods This prospective observational study was conducted on 70 non-diabetic acute ischaemic stroke patients who received rt-PA within 3 h of stroke onset. Patients were subjected to baseline and follow-up NIHSS measurements at 24 h and 3 months post-treatment. Stroke outcome was assessed after 3 months using the Modified Rankin Scale (mRS). The homeostasis model assessment–insulin resistance (HOMA-IR) was calculated for the included patients at stroke onset. Results The mean age of included patients was 57.04 ± 14.39 years. Patients with unfavourable outcome had a significantly higher frequency of insulin resistance and metabolic syndrome, higher values of baseline NIHSS, insulin, HOMA-IR, uric acid and lower levels of HDL than those with favourable outcome (P value = 0.035, 0.007, ≤ 0.001, 0.001, ≤ 0.001, 0.002, 0.033, respectively). Each point increase in NIHSS before rt-PA increased the odds of an unfavourable outcome by 2.06 times (95% CI 1.22 − 3.478). Also, insulin resistance increased the odds of the unfavourable outcome by 11.046 times (95% CI 1.394–87.518). There was a statistically significant improvement in NIHSS 3 months after receiving rt-PA in all patients, significantly higher in patients who did not have insulin resistance or metabolic syndrome. Conclusion Insulin resistance and metabolic syndrome were associated with worse functional outcomes in non-diabetic stroke patients after receiving rt-PA.
Background and aim HCV infection is associated with increased risk of ischemic cerebral stroke. HCV stroked patients are younger with a lower burden of classical risk factors and higher levels of systemic inflammation. The present study aimed to discover the association between HCV infection functional outcome of stroke. Patients and methods The present prospective study included 60 patients with acute ischemic stroke. All patients were subjected to careful history taking and through clinical and neurological examination. Stroke severity at presentation was assessed using National Institute of Health Stroke Scale (NIHSS). Quantitative HCV RNA test was used to diagnose HCV infection. The prognosis of the studied patients was 3 months after treatment using modified Rankin scale (mRS) for neurologic disability. Results The present study was conducted on 60 patients with ischemic stroke. They comprised 13 patients (21.7%) with HCV and 47 patients without. Stroke patients with HCV had significantly higher frequency of carotid artery stenosis, higher NIHSS (17.9 ± 6.9 versus 9.9 ± 5.3, p < 0.001) and higher frequency of severe stroke (46.1% versus 4.3%, p = 0.001) when compared with patients without HCV. Logistic regression analysis identified patients’ sex, NIHSS and HCV as significant predictors of outcome in univariate analysis. However, in multivariate analysis, only NIHSS proved to be significant. Conclusions The present study suggests a significant link between chronic HCV infection and ischemic stroke severity and poor outcome. This is probably related to the pathogenic effects of the chronic inflammatory state induced by HCV infection on the cerebral microvasculature.
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