Oxidative stress as a result of disequilibrium between free radical generation and antioxidant status has been implicated in several pathologies including thyroid diseases. Studies on antioxidant status in overt (OHT) and subclinical hypothyroidism (SHT) are controversial and limited. The aim of this study was to determine the effect of OHT and SHT on antioxidant status. Thirty-six patients with OHT, 36 patients with SHT, and 39 healthy euthyroid subjects as the control group were included in the study. Plasma levels of malondialdehyde (MDA), reduced glutathione (GSH) and total antioxidant capacity (TAC) as ferric reducing ability of plasma (FRAP), and erythrocyte antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), SOD/GPx ratios, catalase (CAT), and glutathione reductase (GR) were analyzed in all groups. MDA and GPx values were elevated, while GSH, FRAP, SOD, and SOD/GPx ratio were decreased in both patient groups compared with controls. No change in activities of CAT and GR were observed in both the patient groups. Significant differences were observed between OHT and SHT groups with high MDA, GPX and low GSH, FRAP, SOD, and SOD/GPx ratio in OHT group. Thus, hypothyroid patients have a deficient antioxidant defense in the form of decreased activity of SOD, decreased levels of FRAP and GSH along with an increase in GPx activity. The severity of the disease appears to decide the degree of deficiency and our findings also point to this, in the form of decrease in SOD, FRAP, and GSH observed being more in OHT than in SHT patients. Hormonal changes and increased lipid peroxidation, which also vary with severity of disease, appear to contribute to the antioxidant deficiency.

Several cardiovascular disease (CVD) risk factors have been identified among patients with chronic kidney disease (CKD). Gut-derived uremic toxins (GDUT) are important modifiable contributors in this respect. There are very few Indian studies on GDUT changes in CKD. One hundred and twenty patients older than 18 years diagnosed with CKD were enrolled along with forty healthy subjects. The patients were classified into three groups of forty patients based on stage of CKD. Indoxyl sulfate (IS), para cresyl sulfate (p-CS), indole acetic acid (IAA), and phenol were estimated along with the assessment of oxidative stress (OS), inflammatory state, and bone mineral disturbance. All the GDUT increased across the three groups of CKD. All patients had higher levels of malondialdehyde (MDA), ferric reducing ability of plasma (FRAP), high-sensitivity C-reactive protein (hsCRP), and interleukin-6 (IL-6) as compared to controls. IS and IAA showed positive association with MDA/FRAP corrected for uric acid, whereas IS and p-CS showed positive association with IL-6. IS, IAA, and phenol showed a positive association with calcium × phosphorus product. GDUT increase OS and inflammatory state in CKD and may contribute to CVD risk.

The present study demonstrates that adipokine levels are altered from initial to final stages of CKD due to renal dysfunction which in association with an exaggerated inflammation may contribute to the ED and CV events.