Amiodarone is an iodine-based, potent antiarrhythmic drug bearing a structural resemblance to thyroxine (T4). It is known to produce thyroid abnormalities ranging from abnormal thyroid function testing to overt hypothyroidism or hyperthyroidism. These adverse effects may occur in patients with or without preexisting thyroid disease. Amiodarone-induced thyrotoxicosis (AIT) is a clinically recognized condition commonly due to iodine-induced excessive synthesis of thyroid, also known as type 1 AIT. In rare instances, AIT is caused by amiodarone-induced inflammation of thyroid tissue, resulting in release of preformed thyroid hormones and a hyperthyroid state, known as type 2 AIT. Distinguishing between the two states is important, as both conditions have different treatment implications; however, a mixed presentation is not uncommon, posing diagnostic and treatment challenges. We describe a case of a patient with amiodarone-induced type 2 hyperthyroidism and review the current literature on the best practices for diagnostic and treatment approaches.

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Objective: Pituitary complications during delivery are relatively rare in developed countries. In this case report we describe a case of panhypopituitarism during pregnancy with concomitant acute liver failure.Methods: We present the case of a pregnant female with acute fatty liver of pregnancy (AFLP) complicated by panhypopituitarism. We also review the current literature on cases of anterior pituitary hormone deficiencies with AFLP, including presentation, management, and outcomes.Results: A 29 year-old female at 25-weeks gestation presented with subacute onset of headache accompanied by nausea and vomiting. She was diagnosed with acute liver failure and coagulopathy secondary to disseminated intravascular coagulation (DIC). Further workup revealed deficiencies of all anterior pituitary hormones, and magnetic resonance imaging (MRI) of the brain was compatible with pituitary hemorrhage/apoplexy from probable infarction.Conclusion: AFLP, especially in association with DIC, can lead to pituitary apoplexy and panhypopituitarism related to underlying coagulopathy. Given the high mortality rates associated with pituitary apoplexy, clinical awareness and a high index of suspicion are important for diagnosing this condition. Prompt initiation of hormone replacement therapy is essential to reduce morbidity and mortality risk. CASE REPORTA 29-year-old Caucasian female who had previously given birth to 4 children presented at 25-weeks gestation to a hospital external to our health care system with a 1-week history of bifrontal headache and profound fatigue, which she described as flu-like symptoms. She had associated persistent nausea and vomiting every other day but was able to carry out her daily activities and go to work. She reported the headaches being distinctly different from migraine episodes that she recalled as last occurring 1 year prior to her current presentation. Fatigue and generalized weakness accompanied her headaches, but she denied having hematemesis, abdominal pain, or bloating. Her headaches persisted despite using over-the-counter medications including acetaminophen, 1,000 mg, every 8 hours. During the next week she noticed reduced frequency of fetal movements, which prompted her to seek medical care at a nearby hospital. At that visit, the patient was noted to be confused, tachycardic, and jaundiced. Her laboratory workup was significant for hypoglycemia with blood glucose of 40 mg/dL (reference range 70-99) and elevated creatinine at 2.82 mg/dL (reference range 0.6-1.35). Her liver function tests were abnormal, including elevated aspartate aminotransferase (AST) at 205 U/L (reference range 10-40), alanine amino transferase (ALT) at 224 IU/L (reference range 9-46), alkaline phosphatase at 215 IU/L (reference range 40-115), and total bilirubin at 11.9