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An event is serious (based on the ICH definition) when the patient outcome is:

  • * death

  • * life-threatening

  • * hospitalisation

  • * disability

  • * congenital anomaly

  • * other medically important event

A 20-year-old woman developed acute liver injury and cholestasis syndrome during treatment with thiamazole and hypothyroidism during treatment with iodine 131 for Basedow Graves' disease (GD) [routes not stated; not all dosages and outcomes stated].

The woman was admitted to hospital with symptoms of vomiting, jaundice, nausea and urinary hyperchromia. On admission, she was diagnosed with acute viral hepatitis A. She started receiving glucose and unspecified hepatoprotective agents. Her general status and hepatic panel tests improved. During hospitalisation, she had an enlargement of the anterior cervical region. Two weeks following the discharge, a thyroid ultrasound was performed and an autoimmune thyroid disease was suggested. Blood parameters and imaging studies confirmed basedow GD. She started receiving thiamazole [methimazole] 30mg along with propranolol. After three weeks of treatment with thiamazole, she was admitted to hospital with complaints of fatigue, jaundice, tiredness and urinary hyperchromia. Physical examination showed icteric sclera and skin. The liver blood panel showed hepatic cytolysis and cholestatic syndrome.

The woman started receiving treatment with unspecified hepatoprotective drugs on admission. Thiamazole was discontinued. However, her general state did not improve. An autoimmune cholangiohepatitis was suspected. She was transferred to the gastroenterology department for further medical investigations. Physical examination showed hepatosplenomegaly with normal HR and BP. Liver tests revealed severe cholestasis and cytolysis. Abdominal ultrasound showed splenomegaly, hepatomegaly, lymphadenopathy in the hepatic hilum and gallbladder wall thickening. She continued to receive treatment with unspecified hepatoprotective agents, gastroprotective agents, cardioactive agents along with tapered dose of prednisone and ursodeoxycholic acid; which were discontinued eventually. Liver biopsy revealed hepatitis with minimum necrotic inflammatory activity and inflammatory infiltrate at the portal space with neutrophils, lymphocytes and oeosinophilic granulocytes. Her liver condition had progressively improved. She was re-transferred to the endocrinology department. Her thyroid function tests were normal, however the hepatic panel showed mild cytolysis and cholestatic syndrome. On re-evaluation after five months, her thyroid function tests showed a relapse of the hyperthyroidism associated with Basedow GD, but the liver function tests were normal. Given the medical history and acute liver injury (ALI) due to the thiamazole, definitive treatment with iodine-131 [I-131] was recommended. One month later, she was started on a therapeutic dose of 11.72 mCi of iodine-131 concomitantly with unspecified cardioactive agent and hepatoprotective agent. She was reevaluated three weeks later, and only mild thyrotoxicosis was noted. She was discharged without any additional anti-thyroid drugs. Three months later, she presented with severe hypothyroidism, with low thyroid volume and normalised liver functions tests. She received treatment with levothyroxine sodium [levothyroxine].