THE OCCURRENCE OF ACUTE PANCREATITIS AFTER IODINE 131 TREATMENT OF HYPERTHYROIDISM

Abstract

Acute pancreatitis is a common and potentially fatal gastrointestinal disease. We report a case of acute pancreatitis induced by iodine-131 therapy for hyperthyroidism. Iodine 131 is distributed through the blood, so it can accumulate and damage normal tissues in other parts of the body that are involved in thyroid hormone metabolis.

Dear Editor,

Acute pancreatitis is a common and potentially fatal gastrointestinal disease; we report a case of acute pancreatitis induced by iodine-131 therapy for hyperthyroidism. Iodine 131 is distributed through the blood, so it can accumulate and damage normal tissues in other parts of the body that are involved in thyroid hormone metabolis (1). It has been reported that post-treatment scans often reveal diffuse uptake of iodine-131 in the pancreas and increased uptake during total thyroidectomy (2).

A 52-year-old woman presented with palpitation and shakiness diagnosed as hyperthyroidism and detectable anti-thyroid autoantibodies. Her TSH was suppressed at < 0.01 (0.49-4.91mIU/L), free T3 was raised to 1.29(3.09-7.42pmol/L), and free T4 was raised to 32.5(7.64-16.03 pg/mL). Her liver function, kidney function, triglyceride and blood amylase were in the normal range. The abdominal computed tomography (CT) of the whole abdomen showed no obvious abnormality before iodine-131 treatment. She underwent iodine-131 therapy with 7 mCi, 2 days later, she was admitted with nausea, abdominal pain and fever. Her laboratory investigation showed serum amylase and serum lipase higher obviously, low level of serum calcium and normal triglyceride levels. There was no other significant past medical history and other comorbidities. Full abdominal CT showed interstitial edematous pancreas revealed acute pancreatitis. The Ranson score for acute pancreatitis was evaluation suggested the presence of moderate to severe pancreatitis. WBC count >18000 cells/mm, serum LDH >400IU/L, serum calcium <2.0mmol/L and hypoxaemia PaO₂ <60mmHg, more than 3 scores were labelled as SAP (3). She has good living habits that there is no history of daily intake of alcohol, she denied any use of alcohol and any other factor that could contribute to acute pancreatitis such as a history of hypertriglyceridemia, gall-stone, hyperparathyroidism, diabetes, obesity, or recent infections and so on. To our knowledge, there have been no previous reports of iodine-131 therapy for hyperthyroidism-induced acute pancreatitis. This case suggests a possible association between iodine-131 induced thyroid hormone release and acute pancreatitis. The patient began to improve after symptomatic treatment with small doses of thyroxine and somatostatin.

Clearly there is a direct cause-and-effect relationship between iodine-131 therapy for hyperthyroidism and pancreatitis in our patient that hasn’t been proven yet, but it’s supported by similar findings, including reports of a relationship between thyroid hormone and pancreatic regeneration in inflammatory injury (4). Therefore, although we cannot prove a direct link between iodine-131 and acute pancreatitis, we believe that this event is quite possible, since this patient did not have any risk factors that ruled out pancreatitis; we believe that a possible causal relationship is reasonable, which provides further knowledge of the pathogenesis of acute pancreatitis.

Conflict of interest

The authors declare that they have no conflict of interest.