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Journal : Universa Medicina

High ferritin in homozygous and heterozygous β-thalassemia tends to decrease oxidative stress levels Maskoen, Ani Melani; Reniarti, Lelani; Sumantri, Nur Imaniati; Sahiratmadja, Edhyana
Universa Medicina Vol 37, No 2 (2018)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2018.v37.97-104

Abstract

BackgroundIneffective erythropoiesis and multiple blood transfusions may cause iron overload, leading to high level of ferritin in β-thalassemia patients. Iron has the ability to catalyze the production of reactive oxygen species (ROS), which can be prevented by an adequate activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). The aim of this study was to explore the association between high ferritin levels and oxidative stress among β-thalassemia patients by measuring SOD and GPx levels. MethodsThis was a cross sectional study among β-thalassemia major patients. Ferritin, SOD, and GPx were measured and compared between β-thalassemia patients with homozygous IVS1nt5 and heterozygous IVS1nt5/HbE mutations, which were the most prevalent mutations found in our previous study. The Spearman correlation test was used to analyze the data. ResultsThe ferritin levels in all β-thalassemia major patients were very high (range: 791-12,340 µg/L). However, no significant differences were observed (p=0.318) between homozygous IVS1nt5 (n=45) compared to heterozygous IVS1nt5/HbE (n=13). The oxidative stress markers SOD and GPx were not significantly different between homozygous IVS1nt5 and heterozygous IVS1nt5/HbE (p=0.450 and p=0.323, respectively). The correlations between ferritin and SOD and GPx oxidative stress levels were not significant in both homozygous IVS1nt5 and heterozygous IVS1nt5/HbE mutations. ConclusionHigh ferritin levels in β-thalassemia patients tend to decrease the GPx level in all thalassemia patients and SOD level in half of the patients, indicating that GPx and SOD may play a role in the occurrence of oxidative stress among thalassemia patients. The mechanism of oxidative stress in thalassemia needs to be further explored.
IFNG Polymorphism (+874 T>A) is not a risk factor for cervical cancer Ani Melani Maskoen; Herman Susanto; Samsudin Surialaga; Edhyana Sahiratmadja
Universa Medicina Vol. 32 No. 1 (2013)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2013.v32.29 - 36

Abstract

INTRODUCTION Cervical cancer cases are rising and many women are infected with human papillomavirus (HPV). Interferon gamma (IFN-ã) is one of the key regulatory cytokines that influence the HPV clearance. The production and the function of IFN-ã may impaired by the defect of the IFNG gene leading to the cervical malignant progression. This study aimed to examine the association between IFNG+874 T>A polymorphism and cervical cancer in women METHODS In a case-control study design, consecutive untreated women with cervical cancer who showed for the first time in Hasan Sadikin Hospital Bandung were enrolled (n=98) and for controls women who came for PAP smear (n = 81). Controls were not matched in ages and ethnicities. DNA extracted from blood was amplified by amplification refractory mutation system - polymerase chain reaction method (ARMS – PCR) to detect IFNG+874 T>A polymorphism. RESULTS The distribution of IFNG genotypes TT, TA and AA for women with cervical cancer who met the inclusion criteria (n= 64) and with negative intraepithelial lesion or malignancy (n=42) were 14.1%, 50.0%, 35.9% and 7.1%, 52.4%, 40.5%, respectively. No significant differences could be observed between both groups (p=0.64). Stratifying the cervical cancer women into a group of squamous cell carcinoma (n = 54) revealed no statistical different. CONCLUSION IFNG +874 T>A polymorphismseems not to contribute in susceptibility to cervical cancer. Identification of other variants in IFNG gene signaling and its role in the development of cervical cancer diseases need to be further examined.
Co-Authors Afandi Charles, Afandi Agnes Rengga Indrati Alvinsyah Adhityo Pramono Anggraini Widjajakusuma Anugrah Aulia Ulil Amri, Anugrah Aulia Ulil Artilia, Ira Atia Nurul Sidiqa Attamimi, Fathimah Azzahra Bethy S. Hernowo Budi Setiabudiawan Choirunnisa, Tias Cissy B. Kartasasmita Cynthia Kurniawan Dany Hilmanto Darwis, Rudi Satria Dewantoro, Julius Broto Dias Aryani Edhyana Sahiratmadja Edhyana Sahiratmadja Edhyana Sahiratmadja Edhyana Sahiratmadja Edhyana Sahiratmadja Efendi, Sjarief Hidajat Eky Setiawan Soeria Soemantri Eriska Riyanti Fitri Rahmi Fadhilah Florence Meliawaty Hardisiswo Soedjana Hendro Hendro Herman Susanto Herman Susanto Herry Garna I Made Joni Ida Parwati Indah Puti Rahmayani S. Kamisah, Yusof Khan, Muhammad Salman Lelani Reniarti Lelani Reniarti Maulia Putri, Maulia Mohammad Ghozali Muqdas, Faza Annisa Myrna Nurlatifah Zakaria, Myrna Nurlatifah Nasroen, Saskia Lenggogeni Nita Susanti Nurul Setia Rahayu Penggoam, Simeon Prasdiaz, Putri Indriani Prima Nanda Fauziah R. Agus Nurwiadh Rachman, Levina Azzahra Rahaju, Asih Rahayu, Nurul Setia Ramdan Panigoro Ratna Indriyanti, Ratna Ratu Safitri Reni Ghrahani Rovina Ruslami, Rovina Rusdianto Rusdianto, Rusdianto Samsudin Surialaga Sari Puspa Dewi Sarilita, Erli Saskia L. Nasroen, Saskia L. Simeon Penggoam Sulaksono, Haura Labibah Salsabil Sumantri, Nur Imaniati Syarief Hidayat Tichvy Tammama, Tichvy Tri Hanggono Achmad Ullah, Irfan Widiarsih, Erlina Widiarsih, Erlina Wijaya, Michelle Angelica Youngest, Racy Yuliati, Tri Yuliati, Tri Zannah, Putry Nurul