Timing of Levothyroxine in the Treatment of Primary Hypothyroidism.

Aim: Timing of levothyroxine (L-thyroxine) administration seems beneficial for early obtaining thyroid state. The present study aimed at investigating the best time of L-thyroxine administration that can achieve earlier normalization of thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels in patients with primary hypothyroidism. Study Design: Eighty two patients with primary hypothyroidism were recruited between November 2012 and July 2013 during their consultation to Al-Faiha Specialized Diabetes, Endocrine and Metabolism Center, Basrah, Iraq. The patients were divided into two equal groups; group A were receiving L-thyroxine daily, one hour before breakfast, group B: the dose of L-thyroxine was given at the evening. TSH, FT4, Body mass index (BMI), blood pressure, lipid profile were measured before, 30, 60 and 90 days after treatment with L-thyroxine. Results: The mean reduction in TSH from baseline for the evening treatment was 13.6±22.2 mIU/ml which was slightly and insignificantly higher than the value of the morning treatment (11.3±22.5 mIU/ml), P = .63, df = 80, 95% CI: -12.17, 7.5). The mean increase in FT4 from baseline for the evening treatment was 5.7±4.9 pmol/l which was lower than 7.6±6 pmol/l in the morning treatment, (P = .12, df = 80, 95% CI: - 0.5, 4.3). There was no effect of treatment timing on lipid profile, blood pressure, and BMI. Conclusions: There were no differences between the morning and evening treatment with L-thyroxine on early normalization of TSH and FT4.

A significant hepatotoxicity associated with paracetamol overdose in the absence of kidney injury in rabbits.

Background: Overdose of paracetamol (PCM) is reported to cause hepatotoxicity and nephrotoxicity, or nephrotoxicity in absence of hepatotoxicity. This study was planned to investigate hepatotoxicity or nephrotoxicity induced by PCM. Methods: Two groups of rabbits, six rabbits in each were used; control group were treated with normal saline, the second group was treated with PCM 1 g/kg/day orally for 9 days. Results: PCM lead to a significant rise in serum liver enzymes, aspartate aminotransferase, alanine transaminase, alkaline phosphatase and total bilirubin with an increase in serum level of malondialdehyde (MDA) and reduction in serum glutathione (GSH). MDA level in liver homogenate was also significantly increased. These findings were further confirmed by histopathological changes suggestive of severe liver damage. On the contrary, PCM slightly increased serum creatinine, without changing MDA and GSH in kidney homogenate. Lack of PCM nephrotoxicity was further confirmed by histopathological examination. Conclusion: PCM overdose produced severe hepatotoxicity without affecting the kidneys of the rabbits.