Since the start of the COVID-19 pandemic, there have been multiple reports of related thyroid dysfunction, most commonly, thyroiditis. The exact mechanism for this has not been elucidated, but it is known that thyroid gland cells have both angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) receptors, which the SARS-CoV-2 virus uses to enter cells. While SARS-CoV-2 has also been shown to precipitate other autoimmune diseases, there are only a few reported cases of new onset Graves’ disease in the setting of SARS-CoV-2 infection. We report 2 patients who presented with severe thyrotoxicosis (thyroid storm and impending storm) that was likely precipitated by SARS-CoV-2 infection. Both patients had no previous history of hyperthyroidism, and potentially also developed Graves’ disease after getting COVID-19. The addition of these cases to the medical literature will further highlight the fact that SARS-CoV-2 infection should be considered a causative agent for thyrotoxicosis when no other cause can be found, and that SARS-CoV-2 may be a potential trigger for autoimmune thyroid disease. It is important to know the SARS-CoV-2 status of such patients for infection control purposes, and to identify patients who may have their hospital course complicated by this disease. These cases may also help further our understanding of the etiology of autoimmune thyroid disease following a viral infection.
Objective: To present a case of recurrent hypoglycemia following Roux-en-Y gastric bypass (RYGB) surgery whose etiology was determined to be a proinsulin-predominant pancreatic neuroendocrine tumor (a proinsulinoma). Methods: A case report along with a brief discussion and review of the pertinent literature is presented. Results: The patient is a 62-year-old female who presented with symptomatic hypoglycemia 11 years after RYGB surgery. Initial workup revealed low insulin levels with elevated proinsulin levels. A 72-hour fast confirmed the presence of proinsulin-induced hypoglycemia secondary to a pancreatic neuroendocrine tumor (PNET). She underwent distal pancreatectomy with splenectomy and a PNET tumor was successfully removed with resolution of her symptoms. Conclusion: Hypoglycemia after RYGB surgery is a well-established syndrome. While there are several etiologies for this, PNETs (including proinsulinomas) should be considered in the differential diagnosis in this population. Proinsulinomas are an increasingly recognized cause of hypoglycemia. Proinsulin levels must always be included as part of the workup of hypoglycemia in an adult.
Dabrafenib, a BRAF selective tyrosine kinase inhibitor (TKI) has been associated with pancreatitis alone, and in combination with trametinib (a MEK pathway inhibitor). We report a case of dabrafenib induced acute pancreatitis in a patient undergoing treatment for metastatic papillary thyroid cancer (PTC). This adverse event has not been previously reported in thyroid cancer patients using dabrafenib. Case: A 61-year-old female with papillary thyroid cancer status post total thyroidectomy with pathology revealing right 7.6cm PTC with extrathyroidal extension and 13/72 metastatic lymph nodes. She received 100mCi of radioactive iodine (RAI). Ten months post-surgery, she underwent revision neck dissection with 3/36 nodes positive for metastatic disease and neck muscle invasion by PTC. Molecular testing demonstrated AKT1 and BRAFV600E mutations. Due to progressive neck and mediastinal tumors, recommendation was to proceed with systemic therapy. Initially started dabrafenib monotherapy; after 3 doses patient developed burning epigastric pain and fever. Examination revealed abdominal tenderness, elevated lipase at 2266 U/L (8-76U/L), mild hyperbilirubinemia and leukocytosis. CT abdomen/pelvis revealed peripancreatic fat stranding consistent with focal acute pancreatitis. No history of alcohol use. Dabrafenib was assessed to be culprit of pancreatitis; with immediate discontinuation of TKI and supportive management patient improved. At present patient is tolerating Lenvatinib therapy. BRAFV600E mutation occurs in 29-83% of thyroid cancers affecting growth, proliferation, survival, migration, and loss of tissue-specific differentiation via the intracellular MEK/ERK pathway1. RAI offers an important treatment modality for thyroid cancer patients, however patients with BRAFV600E are often poor responders or refractory to RAI1. Dabrafenib, a specific BRAFV600E tyrosine kinase inhibitor in combination with trametinib (a MEK inhibitor) is FDA approved for treatment BRAFV600E mutated anaplastic thyroid cancer; furthermore there is evidence on PTC responses including redifferentiation 2. Pancreatitis has been reported in <1% of dabrafenib treated patients as monotherapy and in combination with trametinib in unresectable or metastatic melanoma clinical trials. It was reported in 4% of patients in a NSCLC when used in combination with trametinib. Recurrent pancreatitis when dabrafenib was re-introduced at a lower dose has also been reported3. Furthermore, it was the cause of pancreatitis in a patient with metastatic melanoma 4 months into the treatment in combination with trametinib4. As this treatment option becomes increasingly utilized for metastatic or locally advanced anaplastic/papillary thyroid cancers, endocrinologists should be aware of the potential for dabrafenib induced pancreatitis during monotherapy use or in combination with trametinib.
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