Corneal biomechanical properties in patients with Hashimoto's thyroiditis.

BACKGROUND: Hashimoto's thyroiditis (HT) is an autoimmune endocrine disorder that results from a dysregulation of the immune system leading to an immune attack on the thyroid gland. It has potential effects on different organs and tissues. OBJECTIVES: The aim of the study was to investigate the effect of HT on corneal biomechanical properties using the ocular response analyzer (ORA). MATERIAL AND METHODS: A total of 48 patients with HT and 49 healthy subjects were enrolled in the study. The mean age of the patients and healthy subjects was 42.33 ±11.96 and 40.20 ±12.60 years, respectively (p = 0.39). All of the subjects underwent a full ophthalmological examination, including visual acuity, corneal pachymetry with topography, biomicroscopy, and funduscopy. Corneal biomechanical properties, including corneal hysteresis (CH) and corneal resistance factor (CRF), Goldmann-correlated intraocular pressure (IOPg) and corneal compensated IOP (IOPcc) were measured with the ORA. RESULTS: Central corneal thickness (CCT) in the patient group and the control group were not significantly different (p = 0.65). Corneal hysteresis of the HT patients was significantly lower than that of the control group (p = 0.005). There were no statistically significant differences in CRF between the 2 groups (p = 0.53). Goldmann-correlated IOP and IOPcc were higher in the HT patients, but only IOPcc showed a statistically significant difference (p = 0.001). CONCLUSIONS: In conclusion, our data shows that HT affects corneal biomechanical properties by decreasing CH. Thus, IOPcc measured with the ORA should be taken into account when determining accurate IOP values in patients with HT.

Effects of Vitamin D treatment on thyroid autoimmunity.

BACKGROUND: Vitamin D was shown to be related to autoimmune thyroid diseases (AITDs) in the previous studies. We aimed to investigate the relationship between Vitamin D and thyroid autoimmunity. MATERIALS AND METHODS: Eighty-two patients, diagnosed with AITD by the endocrinology outpatient clinic, were included in this prospective study. All of the patients had both AITD and Vitamin D deficiency, defined as serum values <20 ng/mL. They were randomly assigned into two groups. The first group included 46 patients and the second one included 36 patients. The first group was treated with Vitamin D for 1 month at 1000 IU/day. The second group served as the control group and was not treated with Vitamin D replacement. Serum thyroid-stimulating hormone, free T4 (fT4), thyroid peroxidase antibody (TPO-Ab), thyroglobulin antibody (TgAb), and Vitamin D levels were measured at the initiation of the study and again at 1 month in all patients. RESULTS: Two groups were similar with regard to age, sex, and type of thyroid disease. Whereas TPO-Ab (before; 278.3 ± 218.4 IU/ml and after; 267.9 ± 200.7 IU/ml) and TgAb (before; 331.9 ± 268.1 IU/ml and after; 275.4 ± 187.3 IU/ml) levels were significantly decreased by the Vitamin D replacement therapy in group 1 (P = 0.02, P = 0.03, respectively), the evaluated parameters in the control group did not significantly change (P = 0.869, P = 0.530, respectively). In addition, thyroid function tests did not significantly change with Vitamin D replacement in two groups. CONCLUSION: Vitamin D deficiency may contribute to the pathogenesis of AITDs. Since supplementation of the Vitamin D decreased thyroid antibody titers in this study in Vitamin D deficient subjects, in the future Vitamin D may become a part of AITDs' treatment, especially in those with Vitamin D insufficiency. Further clinical and experimental studies are required to understand the effect of Vitamin D on AITD.

Prevalence of gluten sensitive enteropathy antibodies in restless legs syndrome.

The prevalence of restless legs syndrome (RLS) is increased in gluten sensitive enteropathy (GSE); but prevalence of GSE is not known in RLS. 96 RLS patients and 97 healthy controls, both with or without iron deficiency were enrolled. All secondary RLS patients except iron deficiency were excluded. Subjects underwent a thorough biochemistry and routine blood analyses, and tissue transglutaminase antibodies (TTGA), endomysium antibodies (EMA) and gliadin antibodies (AGA) were also tested. In RLS patients positivity rates of all GSE antibodies were similar to those in controls. The rate of iron deficiency anaemia in RLS patients with at least one positive GSE antibody was significantly higher than that of RLS patients whose GSE antibodies were all negative. The prevalence of GSE antibodies in RLS patients is not increased. GSE might have a role in the aetiology of RLS in association with iron deficiency anaemia. Since the prevalence of GSE antibodies is not increased in RLS, it seems unlikely that GSE is involved in the aetiology of RLS through different mechanisms (e.g. immunological mechanisms) other than iron deficiency as proposed in some published papers.