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Ossie F Uzoigwe, Student University of Leeds
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Dear Editor, Icterus in the context of thyrotoxicosis is an interesting phenomenon. Given that jaundice is such a rare feature of hyperthyroidism it is unlikely that there exists a direct causal link. It is more probable that there is an underlying hepatic dysfunction which is unmasked and potentially exacerbated by the thyrotoxic state1. The most likely cause is Gilbert’s syndrome. Its prevalence may be as high as 12.4% in Caucasian men2. The disease is generally latent but becomes evident during times of illness. In the present case it is worth considering this possibility. If the true mechanism was thyroxine-induced oxidative damage, one would suspect considerable hepatocellular injury with a significant irreversible element if the bilirubin rose to levels of 581umol/l, as in the instant case. Indeed 300umol/l is the threshold for liver transplantation in cases of paracetamol overdose. This is notable given that oxidative stress is also the mechanism of paracetamol’s hepatotoxicity3. Such injury would not be consistent with such a radical recovery. The rapid resolution of symptoms, seen in this case, once euthyroidism was established would be classical of the Gilbert’s syndrome. 1. Greenberger NJ, Milligan FD, Degroot LJ, Isselbacher KJ. Jaundice and thyrotoxicosis in the absence of congestive cardiac failure. Am J Med. 1964; 36:840-6. 2. Sieg A, Arab L, Schlierf G, Stiehl A, Kommerell B. Prevalence of Gilbert's syndrome in Germany. Dtsch Med Wochenschr. 1987 31;112:1206-8. 3. Jaeschke H, Knight TR, Bajt ML. The role of oxidant stress and reactive nitrogen species in acetaminophen hepatotoxicity. Toxicol Lett. 2003; 144:279-88. Competing interests: None declared |