7 research outputs found

    Vascular Endothelial Growth Factor Level as A Predictor of Hepatocellular Carcinoma in Liver Cirrhosis Patients

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    BACKGROUND: Alpha-fetoprotein (AFP) has been used for hepatocellular carcinoma (HCC) diagnosis and screening, however, AFP has poor specificity. The extensive hypervascularity associated with HCC could be driven in part by the pro-angiogenic factor known as vascular endothelial growth factor (VEGF). Furthermore, invasiveness of certain HCC lesions has recently been linked to high levels of VEGF. Therefore, circulating VEGF levels of patients with liver cirrhosis (LC) and HCC were investigated and analysed.METHODS: An analytical cross sectional study was designed. Diagnosis of HCC and LC was performed using clinical criteria and findings obtained from B-mode ultrasonography (USG), computed tomography (CT) angiography, or magnetic resonance imaging (MRI). Blood were collected intravenously from all subjects. Obtained serum and plasma were stored in -80°C for following analyses: hepatitis B surface antigen (HBSAg), hepatitis C virus (HCV), alanine aminotransferase (ALT), total bilirubin, albumin, VEGF and AFP.RESULTS: Levels of VEGF and AFP were significantly higher in HCC group compared with LC group with p = 3.05 x 10-6 and p = 8.74 x 10-5, respectively. There was a significant positive correlation (p=0.029, r=0.309) between VEGF level and tumor size in HCC group. The area under curve (AUC) for VEGF level in HCC and LC groups was 0.771. In the level of median 435.6 pg/mL VEGF, the sensitivity was 50% and specificity was 86%. In the level of 199.99 pg/mL VEGF the sensitivity was 74% and specificity was 76%.CONCLUSION: The present findings suggested that VEGF level could be a useful marker for the presence of HCC in patients with LC.KEYWORDS: hepatocellular carcinoma, HCC, liver cirrhosis, LC, vascular endothelial growth factor, VEGF, alpha-fetoprotein, AFP

    LABORATORIUM KLINIK PELUANG DAN TANTANGANNYA SUATU TINJAUAN DARI SEGI MANAJEMEN

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    Keberhasilan atau bahkan kelangsungan hidup suatu organisasi pelayanan kesehatan tergantung dari kemampuan organisasi tersebut dalam meningkatkan kualitas pelayanan dan produktivitasnya. Peningkatan kualitas dan produktivitas ini hanya dapat dicapai melalui peningkatan manajemen. Dalam membenahi struktur dan manajemennya, Laboratorium/Instalasi Patologi Klinik berpedoman pada konsep dari Mc. Kinsey dalam upaya menuju sukses. Konsep ini dikenal sebagai McKinsey 7-S Framework yang terdapat dalam buku In Search of Excellence karangan Thomas J. Peter & Robert H. Waterman Jr. Dalam konsep tersebut Mc-Kinsey menguraikan unsur-unsur penting yang menjadi inti konsep. Agar konsep ini mudah diingat, Anthony Athos dari Harvard Business School menganjurkan agar dari ketujuh unsur tersebut dibentuk suatu framework

    The association between cortisol dynamics and the course of aneurysmal subarachnoid hemorrhage

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    -Context; One of aneurysmal subarachnoid hemorrhage complication is delayed ischemic neurological deficits (DIND). It is postulated that Cortisol dynamics might be associated with the severity of this complication.\ud Aims: The goal of the study is to investigate whether the peak of morning serum Cortisol levels are associated with the severity of its complication during the course of the disease.\ud Settings and Design: This is a prospective cohort study conducted from January 2009 to June 2011, at our institution.\ud Materials and Methods: The study follows a consecutive cohort of patients for 14 days after the aneurysmal subarachnoid hemorrhage. Serum Cortisols, Cortisol binding globulin, adenocorticotrophic hormone (ACTH) were measured pre operatively and then on post operative days (POD) 2, 4, 7, and 10. Blood was drawn to coincide with peak Cortisol levels between 08.00-09.00 hours. Neurological examinations were conducted at least twice daily and patient outcome were graded according to modified Ranklin Scale. DIND was defined by a decrease in the Glasgow Coma Scale of two or more points compared to the status on POD 1.\ud Statistical Analysis Used: All the results were analyzed using statistical software, Statistical Package for Social Sciences (SPSS v61; SPSS, Inc., Chicago, IL). Logistic regression analysis was used to compare the relationship between the variables.\ud Results: Thirty six consecutive patients are collected, but only 28 patients (12 M and 16 F) were eligible for the cohort analysis. Average patient age is 50.75 years old (50.75 ?? 12.27), and more than 50% (15/28) arrived with World Federation of Neurologic Surgeons grade 3 or better. Elevated total Cortisol levels of more than 24 jig/dl on day 2, 4, and 10 were associated with DIND, and the most significant being on day 4 (P=0.011). These patients also had a higher grade on the modified Ranklin scale of disability.\ud Conclusions: This study shows that the elevated levels of morning total Cortisol in the serum are associated with the onset of DIND during the disease course, and it's also associated with bad outcomes

    Cortisol dynamics and endothelin-1/nitric oxide ratio are associated with clinical vasospasme

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    Background: Cortisol dynamics in serum might be related to clinical vasospasm, also known as delayed ischemic neurological deficits (DIND). Two vasoactive substances that play a role in pathophysiology of DIND are endothelin-1 (ET1) and nitric oxide (NO), both are proved associated with cortisol. This study aimed to know how cortisol play a role on ET1/NO ratio and its relationship to DIND.Methods: This was a prospective cohort study for the first 14 days after aneurysmal subarachnoid hemorrhage (SAH). Patients with inclusion criteria will be enrolled for blood test before surgery, and post-operative day 2, 4, 7, and 10 (between 8:00-9:00 AM). The blood tests were performed for cortisol, ACTH, CBG, NO, and ET1. Free cortisol is calculated with Coolens equation. Logistic regression was used to see the interaction model and its scale. Bivariate analysis (corelation) was used to see the relationship between total cortisol, free cortisol, NO, ET1, and clinical vasospasm (DIND).Results: Forty-four patients are enrolled into this study (20 male; 24 females). Mean age is 52.02 years (52.02 ± 11.23). There were 29 patients (66%) within  DIND group and 15 patients Non-DIND as the control group. The mean of cortisol level shown is significantly higher in DIND group (35.99 ± 14.24) µg/dL compared to Non-DIND group (19.57 ± 6.19) µg/dL, p &lt; 0.001. The mean of free cortisol level was significantly higher in DIND group (2.06 ± 1.094) µg/dL compared to non-DIND group (0.838 ± 0.365 µg/dL; p &lt; 0.001). The Scatter Plot graph show that correlation of cortisol with ET1/NO ratio started increasing on day 4 and became stronger on day 10.Conclusion: Cortisol is associated with DIND following aneurysmal SAH,  probably through its role in keeping the balance between ET1 and NO level. (Med J Indones. 2013;22:161-6. doi: 10.13181/mji.v22i3.585) Keywords: Cortisol dynamics, delayed ischemic neurological deficits, endothelin-1, nitric oxide</p

    Serum vascular endothelial growth factor as a predictor of clinical outcomes in anterior circulation ischemic stroke

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    Background: Inflammatory response in the acute phase of ischemic stroke will trigger the process of neuroplasticity and determine the clinical outcomes. Angiogenesis and neurogenesis are induced by expression of vascular endothelial growth factor (VEGF) in the acute phase of stroke. The purpose of this study was to determine the association between VEGF serum level in acute phase of stroke with the clinical outcomes.Methods: This longitudinal cohort study was conducted on 64 patients suffering from first-attack of anterior circulation blockage as evidenced by cephalic diffusion-weighted magnetic resonance imaging (DWI). VEGF serum level was measured at 72 hours and 7 days after stroke and the clinical outcomes were assessed on day 30 post-stroke using the National Institutes of Health Stroke Scale (NIHSS).Results: VEGF level at hour-72 and on day-7 were 5.84 ± 0.736 ng/mL and 5.797 ± 0.96 ng/mL, respectively (p &gt; 0.05). High VEGF levels at hour-72 can be used to predict poor clinical outcome 30 days after stroke (OR = 6.5; 95% CI = 1.15-36.61; p = 0.034). Subjects who have increasing levels of VEGF on day-7 compared to hour-72 tend to have better clinical outcomes on day-30. (NIHSS score = 1.33 ± 1.22 vs 3 ± 3.78; p = 0.232).Conclusion: VEGF levels in the acute phase of ischemic stroke reflect the degree of brain damage, the dynamic of the increase in VEGF levels after a stroke was associated with better clinical outcomes.</p

    Genetic risk factor APOEε4 associates with plasma amyloid beta in amnestic mild cognitive impairment and alzheimer’s disease

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    Background: APOEε4 is a strong genetic risk factor for Alzheimer’s disease (AD). AD itself has been associated with reduced Aβ clearance from the brain and plasma. Understanding the potential pathogenic link between APOEε4 and plasma Aβ might allow for earlier identification of people at risk of developing AD. The aim of this study is to find out the correlation between APOEε4 and plasma Aβ in amnestic mild cognitive impairment (aMCI) and AD patients. Methods: This is a comparative cross-sectional study of patients attending a memory clinic in Siloam Hospital Lippo Karawaci, Tangerang, during the period of 2013-2014. Subjects were categorized into three categories: normal aging, aMCI, and AD. We performed blood test to examine APOEε4, plasma Aβ4o level, and plasma Aβ42 level. All data analyses were performed using correlation test and logistic regression. Results: Sixty subjects (normal aging = 23, aMCI = 17, AD = 20) were included. There were 19 (31.7%) subjects with APOEε4 positive. Subjects carrying ε4 allele were more likely to have AD by 3.9-fold than subjects with APOE ε4 allele negative. There is a significant difference between the mean of plasma Aβ40 in aMCI group and AD group. We also found correlation between APOEε4 (+) and higher plasma Aβ42 (p<0.05). Conclusion: There is a correlation between APOEε4 and plasma Aβ42 level, which supports the hypothesis that this genetic isoform accelerates the rate and progression of AD through Aβ-dependent pathways
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