Abstract
To the Editor, We have read the critics of Reddy et al. [1] with a great interest. We are grateful for the inspiring comments on our manuscript reported in the April 2013 issue of the Endocrine [2]. The patients in our study were divided into three groups: hypothyroid, subclinical hypothyroid and control. No significant difference was determined among these three groups in terms of the parameters hyperlipidemia and metabolic syndrome. Hypothyroidism can give rise to hypercholesterolemia, and this has been shown to be reversible with thyroid hormone replacement [3]. The data concerning the relation between subclinical hypothyroidism and hyperlipidemia are inconsistent. There are studies reporting no significant difference in plasma lipid levels in patients with subclinical hypothyroidism compared to controls [4, 5]. While in our study low-density lipoprotein (LDL) cholesterol levels were slightly higher in patients with evident hypothyroidism compared to those with subclinical hypothyroidism and the control group, no statistically significant difference was determined. We already have highlighted that as our groups did not differ for lipid levels on contrary to Ma and colleaugues’ study [6] we think that the possible effect that may arise from different lipid levels have been excluded in our study. The relatively low patient numbers in our study may have been involved in this. While a relation is reported between total cholesterol levels and ischaemic-modified albumin (IMA), this was not evaluated in our study since it is not a component of metabolic syndrome. While metabolic syndrome was slightly higher in evidently hypothyroid patients in our study, no statistically significant difference was determined among the three groups in terms of metabolic syndrome. There was no significant difference between the metabolic patient and control groups in terms of IMA levels. The authors pointed the study by Gottlieb and colleagues in which IMA levels were found to be higher than control group among patients with metabolic syndrome; however, in that study also similar to Ma and colleagues’ study [6] body mass index (BMI), waist circumference, blood pressure (systolic and diastolic), glucose levels and lipid levels (total cholesterol, LDL and HDL) were higher among patients with metabolic syndrome [7]. Although they have performed multivariate analysis for BMI and lipids they do not ignore the potential effect of these parameters on IMA levels in the discussion section [7]. It has been reported that hypothyroidism and subclinical hypothyroidism may be associated with an atherosclerotic process and chronic ischaemia [8]. In addition, a rise in metabolic rate as a result of the biological effect of thyroid hormones and a rise in oxygen radicals with calorigenesis has been reported [9]. It has also been reported that metabolic processes decelerating in hypothyroidism and decreasing oxygen radical production may have a protective effect against ischaemia [10]. The authors emphasised that the level of albumin is correlated with IMA levels and the absence of albumin levels of our patients. They are completely right, but our study group had no other diseases, other than thyroid disease; patients with abnormal albumin levels were not included in the study. Testing the binding of albumin to cobalt is a technique that measures IMA levels indirectly, and low albumin levels have been reported to be capable of affecting IMA levels. Gaze et al. reported a negative correlation between serum albumin levels and IMA levels, but I. Anaforoglu (&) K. Ersoy E. Algun Department of Endocrinology and Metabolism, Trabzon Kanuni Education and Research Hospital, 61000 Trabzon, Turkey e-mail: ianaforoglu@hotmail.com
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