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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 5  |  Issue : 2  |  Page : 144-146

Study of ascorbic acid levels in hypothyroid patients


1 Junior Resident, Dept. of Biochemistry, IGIMS, Patna, Bihar, India
2 Associate Professor, Dept. of Biochemistry, IGIMS, Patna, Bihar, India

Date of Submission15-Jun-2019
Date of Acceptance18-Jul-2019
Date of Web Publication12-Aug-2019

Correspondence Address:
Ravi Shekhar
Associate Professor, Dept. of Biochemistry, IGIMS, Patna
India
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Source of Support: None, Conflict of Interest: None


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  Abstract 


Introduction : Ascorbic acid has role in wound healing, collagen formation, enzymatic action, anti-oxidants, hormone action, synthesis of neurotransmitters etc. Thyroid hormone regulates a wide range of genes and plays a crucial role in the regulation of mitochondrial oxidative metabolism. Disorders of thyroid hormones, overt hyperthyroidism and hypothyroidism represent opposite clinical conditions. Increased concentrations of thyroid hormones result in increased production of large quantities of reactive oxygen species which enhance oxidative stress, even low concentration of thyroid hormone ie hypothyroidism has been associated with increased oxidative stress, but is controversial. This study was aimed to correlate the ascorbic acid level in patients of thyroid disorder.
Material and methods : The blood samples of 150 patients were collected after the analysis of thyroid profile. The samples of the patients in the study were categorized in three groups- euthyroid, subclinical hypothyroid and overt hypothyroid based on free T3, free T4 and thyroid stimulating hormone (TSH). The ascorbic acid was estimated using 2,4-Dinitrophenyl hydrazine method.
Result : The ascorbic acid levels in the patients of hypothyroid disorder was ranging from 0.43-2.60 mg/dl
Conclusion : There was no correlation observed between ascorbic acid and hypothyroid disorders in the study. The dietary intake of ascorbic acid in the study group must be adequate.

Keywords: Ascorbic Acid, hypothyroidism, anti-oxidants


How to cite this article:
Kumari R, Sinha P, Shekhar R. Study of ascorbic acid levels in hypothyroid patients. J Indira Gandhi Inst Med Sci 2019;5:144-6

How to cite this URL:
Kumari R, Sinha P, Shekhar R. Study of ascorbic acid levels in hypothyroid patients. J Indira Gandhi Inst Med Sci [serial online] 2019 [cited 2022 Oct 2];5:144-6. Available from: http://www.jigims.co.in/text.asp?2019/5/2/144/301099




  Introduction : Top


Ascorbic acid is an essential vitamin for a variety of biological functions, like pro-oxidants, anti-oxidants, anti carcinogenic effect, activation of genes controlling several cellular transduction pathways in hypoxia, hydroxylation of amino acid residues in formation of collagen etc.[1] Oxidative stress plays a pivotal role in cellular injury. Weak defence system of the body becomes unable to counteract the enhanced reactive oxygen species generation.[2] Both hypo and hyperthyroidism promote cellular oxidative stress by influencing the intensity of oxygen reactions.[3],[4] Studies suggest that tissues may be protected from oxidant damage because of a hypo-metabolic state in hypothyroidism, but few report suggested increased oxidative stress in hypothyroidism.[5] Thus, the depletion or deficiency of anti-oxidants contributes to oxidative stress.[6]

Vitamin deficiencies are not common nowadays as these are most common food supplements. Despite the widespread availability of vitamins, their health impact knowledge, the role in the prevention and treatment of disease remain insufficiently understood.[3] Thus, the aim of the study was to evaluate ascorbic acid level and correlate it in hypothyroid patients.


  Materials and Methods : Top


The patients of both genders with age group 18 to 60 years requiring thyroid profile estimation attending biochemistry lab, IGIMS, Patna were included in the study. 4ml blood sample was collected in red vaccutainer. The patient’s serum was analyzed for total T3, total T4, FT3, FT4, TSH and ascorbic acid. Thyroid hormones were estimated by chemiluminescent immuno assay (CLIA) on Beckmann Coulter Access 2. The estimation of Ascorbic acid was done by 2,4-Dinitrophenyl hydrazine method (DNPH method). Ascorbic acid is oxidized by copper to form dehydroascorbic acid and diketogulonic acid. These products are treated with 2, 4, DNPH to form the derivative bis-2, 4-dinitrophenylhydrazone. This compound, in strong sulphuric acid, undergoes rearrangement to form a product with an absorption that is measured at 520 nm. The reaction is run in the presence of thiourea to provide a mildly reducing medium, which helps to prevent interference from non-ascorbic acid chromogen.[7]

The patients with TSH levels 0.35 to 5.49μIU/ml was considered as euthyroid, from 5.5μIU/ml to 10μIU/ml with free T3 & free T4 within normal range, were considered as subclinical hypothyroid patients. The patients with elevated TSH level (>10 μIU/ml) with decreased both free T3 & free T4 levels and either of the two were considered as overt hypothyroid patients. The history of patients with elevated TSH levels was taken individually to correlate the findings. Patients with infections, drug allergy, hepatic, renal, cardiac morbidity were not included in the study.


  Result Top


One hundred and fifty patients, comprising of 56 males and 94 females were included in the study. The male and female ratio was found to be 1:1.67. The mean age of patients in the study was 42.54 ± 13.61 years and mode was 60 years. The mean TSH value of the patients of euthyroid, sub-clinical hypothyroid and overt hypothyroid groups averaged 3.87μIU/ml, 6.88μIU/ml and 24.88μIU/ml respectively. The data was analyzed on MS excel 2007.

The serum ascorbic acid ranged from 0.6-2.0 mg/dl. In the study, the levels of ascorbic acid ranged from 0.43 - 2.60 mg/dl. The average value of ascorbic acid in euthyroid, subclinical hypothyroid and overt hypothyroid patients was 1.17 mg/dl, 1.27 mg/dl and 1.53 mg/dl respectively.
Figure 1: Correlation of Ascorbic acid and TSH in euthyroid patients

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Figure 2: Correlation of Ascorbic acid and TSH in subclinical hypothyroid patients

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Figure 3: Correlation of Ascorbic acid and TSH in overt hypothyroid patients

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  Discussion : Top


Ascorbic acid is a water soluble free radical scavenger act as non enzymatic anti-oxidants. It acts directly on O2 and OH-with the formation of semi dehydro-ascorbate (free radical) that is subsequently reduced by glutathione to generate dehydro-ascorbate and also neutralise several oxidants of blood.[4],[8] To reduce or control the delirious effect of free radicals, nature has provided human being with a set of anti oxidants. Anti-oxidant even at low concentration delays or inhibits the oxidation of substances. Thyroid hormones function by activating metabolism and promoting mitochondrial utilization of oxygen leading to excess generation of free radical. In hyperthyroid disorders, which are hyper-metabolic state, thyroid hormones promote mitochondrial oxygen utilization leading to excess generation of free radical. Hypothyroidism is a hypometabolic state with reduced utilisation of oxygen. There are multiple pathways for generation of oxidative stress like dyslipidemia, lipid peroxidation, protein glycation, autoimmunity and low grade inflammation.[9] The oxidative stress should be elevated in both hyperthyroid and hypothyroid disorders. Hypothyroidism influences the endothelial changes and it is predisposed by low level of ascorbic acid.[10] Decreased generation of oxidative stress was reported by many authors.[11],[12] All these reports strengthened the previous notion that hypothyroidism is associated with decreased oxidative stress.[9] but there is controversies regarding the presence of oxidative stress in hypothyroidism. Experiments on rats have proven that ascorbic acid has effect on thyroid activity, low dose stimulate and high dose inhibit the thyroid activity.[13] The level of anti-oxidant was mainly assessed in experimental hypothyroidism or in hyperthyroid patients. While comparing its levels with euthyroid and hypothyroid individuals, the report suggested a decreased antioxidant levels in hypothyroidism. The rise in anti oxidants in hyperthyroidism was deduced as a response to increase in oxidative stress. A lack of rise in anti-oxidant was implied as a consequence of reduced oxidative stress in hypothyroidism.[14]

Ascorbic acid is able to restore thyroid function by reducing the oxidative stress but, there is controversies regarding presence of oxidative stress in hypothyroidism. The treatment of hypothyroidism with antioxidant supplementation gives good result.

A study on benign thyroid disorder reported no association in the levels of ascorbic acid with TSH.[10] The mechanism of ascorbic acid in improvement of circulating levels of TSH and thyroid hormone is not known. But, study on hypothyroid patients associated with gastro intestinal pathology demonstrated it to help in the improving the management.[15] Ascorbic acid is able to restore thyroid function to normal in heavy metal intoxication, cadmium and lead , by preventing heavy metal induced decrease T3 and hepatic 5’ deiodination. Most of the studies suggest that Ascorbic acid has no association on hypothyroidism.[16]


  Conclusion : Top


Ascorbic acid has no relation on thyroid hormone levels in the study. This may be due to intake of sufficient amount of ascorbic acid in diet of the patients in the study group. The study should be conducted in larger sample size with different socio-economic strata for better result.



 
  References Top

1.
Grosso G, Bei R, Mistretta A, Marventano S, Calabrese G, Masuelli L, Giganti MG, Modesti A, Galvano F, Gazzolo D. Effects of vitamin C on health: a review of evidence. Front Biosci 2013; 18: 1017-29  Back to cited text no. 1
    
2.
Halliwell B, Gutteridge JM. Role of free radicals and catalytic metal ions in human disease: an overview. Methods Enzymol. 1990;186:1- 85.  Back to cited text no. 2
    
3.
Sworczak K, Wi?niewski P. The role of vitamins in the prevention and treatment of thyroid disorders. Endokrynol Pol. 2011;62(4):340-4.  Back to cited text no. 3
    
4.
Mancini A, Di Segni C, Raimondo S, Olivieri G, Silvestrini A, Meucci E, Curro D. Thyroid Hormones, Oxidative Stress, and Inflammation. Mediators Inflamm. 2016; 2016: 6757154.  Back to cited text no. 4
    
5.
Varun SK and Kshitiz K K. Study of oxidative stress and lipid profile in hypothyroid patients. Int. J. Curr. Res. Med. Sci. 2017; 3: 56-61.  Back to cited text no. 5
    
6.
Chakrabarti SK, Ghosh S, Banerjee S, Mukherjee S, and Chowdhury S. Oxidative stress in hypothyroid patients and the role of antioxidant supplementation. Indian J Endocrinol Metab. 2016 Sep-Oct; 20(5): 674-678.  Back to cited text no. 6
    
7.
Gunter Ew, Turner WE, Neese JW, Bayse DD. Laboratory Procedures used by the Clinical Chemistry Division, Centers for DiseaseControl, for the Second Health and Nutrition Examination Survey (HANES II) 1976-1980. Atlanta GA : Public Health Services centers for disease control.  Back to cited text no. 7
    
8.
Rai RR, Phadke MS. Plasma oxidant -antioxidant status in different Respiratory disorders. Indian J Clin Biochem. 2006; 21(2):161-164.  Back to cited text no. 8
    
9.
Nanda N. Oxidative stress in hypothyroidism. Int J Clin Exp Physiol 2016;3:4-9  Back to cited text no. 9
    
10.
Moncayo R, Kroiss A, Oberwinkler M, Karakolcu F, Starzinger M, Kapelari K, Talasz H, Moncayo H. The role of selenium, vitamin C, and zinc in benign thyroid diseases and of selenium in malignant thyroid diseases: Low selenium levels are found in subacute and silent thyroiditis and in papillary and follicular carcinoma. BMC Endocr Disord. 2008; 8: 2.  Back to cited text no. 10
    
11.
Bilgihan K, Bilgihan A, Diker S, Ataoglu O, Dolapci M, Akata F, Hasanreisoglu B, Turkozkan N. Effects of hyper- and hypo- thyroidism on oxidative stress of the eye in experimental acute anterior uveitis. Acta Ophthalmol Scand. 1996 ;74: 41-3.  Back to cited text no. 11
    
12.
Rastogi L, Godbole MM, Ray M, Rathore P, Pradhan S, Gupta SK, Pandey CM. Reduction in oxidative stress and cell death explains hypothyroidism induced neuroprotection subsequent to ischemia/perfusion insult. Exp Neurol 2006; 200: 290-300  Back to cited text no. 12
    
13.
Mallick N, Deb C. Effect of different doses of ascorbic acid on thyroid activity in rats at different levels of dietary protein intake. Endokrinologie 1975; 65: 333-9  Back to cited text no. 13
    
14.
Hubner G, Meng W, Meisel P, Ventz M, Hampel R, Bleyer H. Behavior of the erythrocyte glucose-6-phosphate dehydrogenase in patients with functional thyroid disorders and in hyperthyroxinemic rats. Z Gesamte Inn Med. 1979; 34:386-9.  Back to cited text no. 14
    
15.
Jubiz W, Ramirez M. Effect of vitamin C on the absorptionof levothyroxine in patients with hypothyroidism and gastritis. J Clin Endocrinol Metab 2014; 99: E1031-4  Back to cited text no. 15
    
16.
Kelly GS. Peripheral metabolism of thyroid hormones: a review. Altern Med Rev 2000; 5:306-33  Back to cited text no. 16
    


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