Research Paper Sample on the Levels of Vitamin D in Patients with Graves Disease

The purpose of the research was to make a comparison between the levels of vitamin D in patients with Graves disease and correlate the findings with the clinical and laboratory parameters of Graves disease. The research also focused on the variation that exists in the genes that cause vitamin D metabolism and how they are associated with the occurrence of GD (Graves Disease). The vitamin D levels of two hundred and ninety-two patients who had newly acquired the GD was compared. The research used 2,305 controls. There were 708 GD patients and 1,178 controls used during the examination of vitamin D binding protein (DBP), 1-Alpha-hydroxylase and the single nucleotide polymorphisms (SNPs). The research concluded that patients that had Graves disease had a lower vitamin D level about the controls (55.0 vs87.2 nmol/L, p<0.001). 219 patients were used during the genes examination. The free thyroxine(fT4), thyrotropin receptor antibodies (TRAb), the free triiodothyronine (fT3), Graves ophthalmopathy(GO) were examined, and the findings show no correlation between them and the levels of vitamin D when the treatment with antithyroid drugs was terminated. There was two single nucleotide polymorphism ad vitamin D receptor (VDR) that were associated with Graves Disease. The genotype Of the patients did not affect the vitamin D levels. The conclusion was that Graves disease affected reduced the level of vitamin D in patients but it did not affect the laboratory and clinical parameters of the disease. The SNP and VDR only affected the mechanisms of Graves disease but not the levels of vitamin D.

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Introduction

Graves disease is an autoimmune illness the affects the thyroid. When it is in an acute stage, it results in weak muscles sleeping problems, irritability and an enlarged thyroid, diarrhea, and loss of weight and other minor symptoms. It is believed that graves disease is caused by environmental and genetic factors. Graves disease can be treated in three ways: medications, radioiodine therapy and through a thyroid surgery. Vitamin D variation was examined in the research because studies show that it associates with many autoimmune disorders. Earlier studies indicate that graves disease lowers vitamin D in patients. However, the correlation between the vitamin D levels and the clinical parameters is scarce. The following research was conducted to ascertain the effect the Grave disease has on the production of vitamin D on patients and also the variations of genes that ensure vitamin D is metabolized.

Methodology

The study involved 295 patients and was the one who had been newly diagnosed with Grave disease from the Skane University Hospital. The analysis was carried out by an endocrinologist. At the time of the research, none of the patients had started taking any form of thyrotoxicosis treatment. The Controls for the study were recruited from the Malmo Diet and Cance Study. Those patients that had started to take treatments on thyroid and parathyroid disease used supplements rich in calcium and vitamin D were excluded from the research, hence leaving 2,305 controls and 292 patients. Vitamin D level was determined using the high-performance liquid chromatography for the controls and liquid chromatography-tandem mass spectrometry.

Vitamin D correlation with laboratory and clinical parameters for patients with GD

Some of the clinical and laboratory parameters used were the level of free thyroxine (fT4), thyroid peroxidase antibodies (TPOAb), free triiodothyronine (fT3), presence of GO, thyrotropin receptor antibodies (TRAb) and relapse when the treatment had ended. These parameters were correlated with the vitamin D levels. There were 139 patients who were on relapse analysis and were under anti-thyroid drugs.

The presence of GO was examined an endocrinologist. An electrochemiluminescence immunoassay was used to measure Ft3, fT4, TPOAb, TRAb and thyroid-stimulating hormone (TGH).

Association between vitamin D metabolism and SNPs in genes

Genetic relation with vitamin D metabolism was examined in 708 patients (245 patients had ophthalmopathy, and 459 didn't have). There were 1,178 controls for this examination. Based on the associations the SNPs have with the autoimmune thyroid, the following genes were chosen. Rs731236 (Taql), rs10735810 (Fokl), rs1544410 (Bsml) in VDR, rs7975232 (Apal) and rs4588 in DBP.The allele frequency was greater than 0.05 for all SNPs, and the genotyping success was greater than 95 percent. Statistical analysis was carried out using SPPSS software, version 22 to correlate the genotype and the vitamin D levels of GD. Genetic analyses were performed by the PLINK tool. All participants engaged in the study willingly.

Results

The research found out that the level of vitamin D in patients was low than that of the subjects (55.0 23.2 vs. 87.2 27.6 nmol/L, p < 0.0001). There was a high probability for the patients with GD to have a vitamin D deficiency was less than 25 nmol/L of its inadequacy was less than50 nmol/L. Thebe using supplements but did not report it to the researchers of this study. Therefore the subjects included were only those that had a vitamin level ranging between 150-100nmol/L. Despite excluding those with very high level, the patients of GD still had low vitamin (patients (n = 292): 55.0 23.2 nmol/L vs. controls (n = 2248): 85.1 24.2 nmol/L, p < 0.0001). For those subjects that had a vitamin level of less than 150nmol/L, the deficiency was 7.5% in cases while the controls had 0.4%. While the insufficiency was 38.4% in cases and 8.9% in controls. To eliminate the difference between the cases and the controls, logistic regression on confounders was done. The difference remained significantly high. The logistic regression adjusted for gender, lifestyle habits such as smoking and ethnicity, indicated that vitamin D had a negative correlation with GD.

Vitamin D and clinical and laboratory parameters

There was no correlation between the levels of fT4, fT3, TRAb, relapse within one year, and TPOAb with vitamin D. The comparison between subjects with a vitamin level of less than 25nmol/L to those with higher levels, indicated no variation in the levels of fT4, fT3, TRAb, and TPOAb. The patients with GO and without had the same vitamin level; (n = 254, 55.5 22.9 nmol/L vs. n = 37, 52.1 24.6 nmol/L, p = non-significant, ns). The logistic regression adjusted for age, sex, ethnicity, and smoking it did not show a correlation between the GO diagnosis and the vitamin D levels. For those subjects that had a relapse of GD within one year, the vitamin D level had no impact on them. The logistic regression did not show any relationship between the relapse after thyroid drugs and the vitamin D levels.

Association of SNPs and vitamin D

The rs10735810 and rs1544410 are two SNPs in VDR that have been associated with Graves disease. There was no variation in the levels of vitamin D in rs1544410 (AA 56.6 nmol/L, AG 57.5 nmol/L, GG 54.8 nmol/L, p = ns or rs10735810 (AA 55.9 nmol/L, AG 56.1 nmol/L, GG 54.1 nmol/L, p = ns). The regression analysis also showed no relation between the two genes and the vitamin D level.

Discussion

This study revealed that the patient of Graves disease had a low level of vitamin in their body when compared to levels of the controls. Our finding matched studies of other studies previously done. One core aspect of the study is that a large sample was used for both patients and controls. However, its drawback is that both samples were collected at different times. The vitamin level did not affect the levels of thyroid hormones and indicated that it did not have an influence on the severity of the disease at diagnosis.

Earlier studies on from different parts of the world indicate that certain genes are related with the metabolism of vitamin D. for instance, a stud conducted on the Asian population, the Apal, BsmI, AND FokI were identified to be associated with GD, while European studies included the TaqI. In our research, BsmI and FokI influenced the nature of GD. However, they never altered the metabolism of vitamin D. the GC genes were the once that affected the vitamin D levels in other studies, but in our research, it was the rs4588. The rs4588 affected the ability of the DBP to bind with the and plasma vitamin D. There was also a correlation of the gene with TRAb level in our study. However, the results about TRAb ought to be treated with caution because there were few subjects with data on TRAb.

Understanding the influence of vitamin D on the development of Graves disease is very crucial. There are studies done on mice that were vitamin D deficient had a low T4 preimmunization level and a high chance of developing hyperthyroidism. The TRAb levels showed no change. That indicates that suggest that vitamin D affected the functionality of the thyroid in animals. Due to limited data that can conclusively prove that there is a relationship between the level of vitamin D and TRAb, this paper hypothesizes that vitamin D affects the thyroid gland in human beings. However, our clinical studies together with the one from other researchers address the association of vitamin D level and GD in a cross-sectional design. Therefore it is difficult to conclude that vitamin D level is a result of the disease or it is involved in its parthenogenesis.

The paper investigated the relationship between the level of vitamin D in Grave disease. The research took place at Skane University Hospital in Sweden, and the diagnosis was carried out by endocrinologists. The researchers did a correlation between the levels of vitamin D and SNPs genes and clinical and laboratory parameters such as Ft3, fT4, TPOAb, TRAb and thyroid-stimulating hormone (TGH). The research found out that the level of vitamin D was low in the patients than in the control subjects. The logistic regression indicated that there is no correlation between the laboratory and clinical parameters with vitamin D. Other related studies coincide with our findings.