Adrenal incidentaloma and the Janus Kinase 2 V617F mutation: A case-based review of the literature
An 81-year-old male patient had been undergoing treatment for 12 years after being diagnosed with ET. At the time of diagnosis, his platelet count was 1.700.000/mm3. Reactive thrombocytosis was ruled out. Two years previously, he had been checked for the JAK2 V617F mutation and was found to be homozygous positive. The patient had a 20-year history of type 2 diabetes mellitus (DM) and hypertension. He was taking metformin (2 g/day), irbesartan (150 mg/day), anagrelide (2 mg/day), and acetylsalicylic acid (80 mg/day). There was no family history of essential thrombocytosis or adrenal incidentaloma. The findings of the physical examination were as follows: Blood pressure, 130/80 mmHg; heart rate, 66 beats/min; and body mass index (BMI), 26.4 kg/m2. During patient follow-up, he underwent an upper abdomen MRI because of abdominal pain. An ovoid mass was detected and it was minimally enhancing with intravenous gadolinium. It was approximately 23 × 33mm at the suprarenal region and was compatible with a well-circumscribed adenoma. The patient was evaluated as having adrenal incidentaloma, and functional evaluations were carried out accordingly. After low-dose dexamethasone suppression cortisol was given, a level of 1 mcg/dl was determined to be normal. The levels of serum dehydroepiandrosterone sulfate (DHEA-S), testosterone, vanillylmandelic acid (VMA) at 24 hrs urine, metanephrine, normetanephrine, and the plasma aldosterone/rennin activity ratio were also normal. The patient was admitted for follow-up for non-functional adrenal incidentaloma, but he died at the 13th month due to myocardial infarction.