Niloofar Chitsaz; Leila Dehghani; Amir Safi; Nazgol Esmalian-Afyouni; Vahid Shaygannejad; Majid Rezvani; Karim Sohrabi; Kaykhosro Moridi; Milad Moayednia
Volume 18, Issue 4 , December 2019, , Pages 150-153
Abstract
Background: Multiple sclerosis (MS) and neuromyelitis optica (NMO) are both demyelinating disorders and oxidative stress is suggested to have a role in their pathogenesis. Glucose-6-phosphate dehydrogenase (G6PD) produces nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. ...
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Background: Multiple sclerosis (MS) and neuromyelitis optica (NMO) are both demyelinating disorders and oxidative stress is suggested to have a role in their pathogenesis. Glucose-6-phosphate dehydrogenase (G6PD) produces nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. NADPH is not only involved in the synthesis of fatty acids necessary for myelination, but also it is involved in the defense against oxidative stress. Prescribing supplementary vitamin D as a part of the MS treatment plan can increase G6PD gene expression. The aim of this study was to determine the serum level of G6PD in patients with MS and NMO and its relationship with vitamin D, since it is yet to be explored thoroughly.Methods: In this case-control study, subjects were divided into three experimental and control groups. The experimental groups comprised 50 patients with relapsing-remitting MS (RRMS) who had a history of vitamin D consumption, 50 newly-diagnosed MS patients, and 50 patients with NMO. Control group included 65 healthy individuals. Serum level of G6PD was measured and compared among these groups.Results: No significant difference was seen between the G6PD level in patients with MS and NMO, but it should be noted that this level was significantly lower than the healthy group. G6PD serum level was significantly higher in patients with MS who had previously consumed supplementary vitamin D compared to those who had not.Conclusion: G6PD deficiency is observed in patients with MS and NMO. Also, supplementary vitamin D may induce favorable results on the G6PD level.
Ehsan Kheradmand; Shaghayegh Haghjooy-Javanmard; Leila Dehghani
Volume 16, Issue 1 , January 2017, , Pages 30-33
Abstract
Background: Activated protein C (APC) inactivates factor V (FV) by cleavage of its heavy chain at Arg306, Arg506, Arg679, and Lys994. Mutational changes, which abolish APC cleavage sites, may predispose thrombosis by altering the inactivation process of FV. FV Leiden (FVL) (Arg506Glu) has been demonstrated ...
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Background: Activated protein C (APC) inactivates factor V (FV) by cleavage of its heavy chain at Arg306, Arg506, Arg679, and Lys994. Mutational changes, which abolish APC cleavage sites, may predispose thrombosis by altering the inactivation process of FV. FV Leiden (FVL) (Arg506Glu) has been demonstrated as a strong risk factor for thrombosis. In the current study, we have studied whether mutations in the cleavage sites of FV for APC, not due to FVL, would have a role in presenting APC resistance (APCR) and initiation of a cerebral thrombotic event.Methods: A group of 22 patients with a history of cerebral venous thrombosis (CVT), who were not carriers of FVL enrolled in the study. The patients who had conditions associated with acquired APCR were excluded from the study. APCR test was performed on the remaining 16 patients, which showed APCR in 4 plasma samples. DNA sequencing was performed on four exons of FV of APCR patients, encoding Arg306, Arg506, Arg679, and Lys994.Results: Mutations were not found within nucleotides encoding the cleavage sites; neither was found within their close upstream and downstream sequences.Conclusion: Our results show that polymorphisms affecting cleavage sites of FV other than Arg506Glu it would be less likely to be the basis for APCR and its increased thrombosis susceptibility. In addition, it emphasizes on the importance of screening for APCR in the patients diagnosed with CVT.
Masoud Etemadifar; Noushin Mehrbod; Leila Dehghani; Aryan Golabbakhsh; Mahboobeh Fereidan-Esfahani; Mojtaba Akbari; Zahra Nasr
Volume 13, Issue 1 , March 2014, , Pages 50-51
Masoud Etemadifar; Leila Dehghani; Soheil Tahani; Nafiseh Toghianifar; Marzieh Rahaimi; Nahid Eskandari
Volume 12, Issue 4 , December 2013, , Pages 172-175
Abstract
Background: Anti-phospholipids syndrome (APS) is considered a non inflammatory auto-immune disease with a significant thrombophilic risk with varied clinical manifestations. The purpose of the current study was to investigate the frequency of thrombotic and non-thrombotic events in patients with APS.Methods: ...
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Background: Anti-phospholipids syndrome (APS) is considered a non inflammatory auto-immune disease with a significant thrombophilic risk with varied clinical manifestations. The purpose of the current study was to investigate the frequency of thrombotic and non-thrombotic events in patients with APS.Methods: In this retrospective study, 102 definite APS subjects were recruited (2007-2011) at Alzahra Hospital, Isfahan, Iran. The patients were referred to Multiple Sclerosis Clinic with the diagnosis of definite APS according to 2006 Sydney's criteria. Disorders associated with APS such as pregnancy complication, vascular thrombosis and livedo reticularis (LR) were assessed. Neurological signs and symptoms such as cognitive dysfunction were recorded. Data analyses were performed using SPSS software and P < 0.05 were considered to be statistically significant.Results: Our findings showed that majority of female gender, higher rate of ischemic thrombotic stroke and high miscarriage lied in a large number of APS patients.Conclusion:Overall recurrent miscarriage is a common complication among (antiphospholidpid antibody) aPL patients. Furthermore, ischemic stroke is the second common neurological manifestations of APS patients.
