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      Levothyroxine improves Paraoxonase (PON-1) serum levels in patients with primary hypothyroidism: Case–control study

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          Abstract

          Primary hypothyroidism is associated with oxidative stress and insufficient antioxidant capacity. This study was conducted to evaluate the effects of levothyroxine replacement therapy on paraoxonase 1 (PON-1) serum levels in a patients with primary hypothyroidism. Thirty-one patients with primary hypothyroidism compared to 20 healthy controls were recruited from. A venous blood sample were taken after an overnight fasting for biochemical parameters, before and after starting levothyroxine therapy (100 μ g/day) for 3 months duration. The biochemical variables were PON-1 serum levels, lipid profiles, triiodothyronine (T3), thyroxin (T4), and thyroid stimulating hormone (TSH) serum levels. Levothyroxine replacement therapy leads to a significant amelioration of thyroid functions, lipid profile, cardiometabolic measures P < 0.05 in patients with primary hypothyroidism. Levothyroxine leads to significant elevation in PON-1 serum levels from 188.42 ± 19.81 (U/mL) to 361.23 ± 33.62 (U/mL) P < 0.0001. This study concluded that levothyroxine replacement therapy significantly increases PON-1 serum levels in patients with primary hypothyroidism and attenuating hypothyroidism-induced oxidative stress.

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          Most cited references 33

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          Declaration of Helsinki, 2008: implications for stakeholders in research.

           K Puri,  K R Suresh,  N Gogtay (2015)
          The Declaration of Helsinki (DoH) was adopted by the World Medical Association (WMA) in 1964, as a statement of ethical principles, to provide guidance to physicians and other participants in medical research involving human subjects. Having undergone several amendments, the most recent version was approved on 18 October 2008, by the WMA General Assembly at Seoul, South Korea, replacing all previous versions. This version highlights issues such as, participant safety, the need to include participants from otherwise underrepresented groups, clinical trial registration, post-study access, usage of data and human tissues, compensating participants with research-related injury, and usage of placebo. In this article, we discuss the major aspects of the 2008 version, including the impact of this version on all stakeholders in research, including, investigators, ethics committee members, sponsors, authors, editors, and reviewers.
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            Serum total antioxidant status and lipid peroxidation marker malondialdehyde levels in overt and subclinical hypothyroidism.

            Mitochondria are the main production site of free oxygen radicals, which can cause organ dysfunction by oxidation of cellular macromolecules such as carbohydrates, lipids and proteins. Oxidative stress may result from either overproduction of these species or from failure of the antioxidant defence systems. Thyroid hormones have well-known effects on mitochondrial oxygen consumption, but data about how hypothyroidism affects oxidative stress are controversial, and little is known about oxidative stress in subclinical hypothyroidism. Total antioxidant status (TAS) gives information about all of the antioxidants in the organism, while malondialdehyde (MDA) is a lipid peroxidation marker used to assess lipid peroxidation due to increased oxidative stress. We aimed to determine how hypothyroidism and subclinical hypothyroidism affect serum MDA and TAS. Serum TAS, MDA, C-reactive protein levels and lipid compositions were studied in 20 hypothyroid, 40 subclinical hypothyroid and 40 healthy subjects. MDA was elevated in both hypothyroid and subclinical hypothyroid patients compared with controls, while TAS levels show no significant differences between groups. Low-density lipoprotein (LDL) cholesterol levels were significantly high in both hypothyroid and subclinical hypothyroid patients. Triglyceride levels were high only in hypothyroid patients when compared with the controls. MDA showed a correlation with LDL cholesterol, total cholesterol and triglyceride. These results suggest an increased oxidative stress in both hypothyroid and subclinical hypothyroidism states, which can be explained by both the insufficient increase in the antioxidant status and the altered lipid metabolism in these cases.
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              Management of primary hypothyroidism: statement by the British Thyroid Association Executive Committee

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                Author and article information

                Affiliations
                Department of Clinical Pharmacology, College of Medicine, Al-Mustansiriya University, Baghdad, Iraq
                [1 ]Department of Clinical Pharmacology and Therapeutic, Medical Faculty, College of Medicine, Al-Mustansiriya University, Baghdad, Iraq
                Author notes
                Address for correspondence: Dr. Hayder M. Alkuraishy, Department of Clinical Pharmacology and Therapeutic, Medical Faculty College of Medicine, Al-Mustansiriya University, Baghdad, Iraq. E-mail: hayderm36@ 123456yahoo.com
                Journal
                J Adv Pharm Technol Res
                J Adv Pharm Technol Res
                JAPTR
                Journal of Advanced Pharmaceutical Technology & Research
                Medknow Publications & Media Pvt Ltd (India )
                2231-4040
                0976-2094
                Jul-Sep 2018
                : 9
                : 3
                : 113-118
                6174702 JAPTR-9-113 10.4103/japtr.JAPTR_298_18
                Copyright: © 2018 Journal of Advanced Pharmaceutical Technology & Research

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                Categories
                Original Article

                Pharmacology & Pharmaceutical medicine

                hypothyroidism, levothyroxine, pon-1

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