Objective: To report a case of linagliptin-induced acute pancreatitis and remind clinicians about risks with incretin-based drugs. Patients at risk for pancreatitis should be switched to another type of hypoglycemic treatment. Methods: We present the case of a 74-year-old Latina who presented to the emergency department with sudden onset of epigastric pain radiating to her back. Medical history, physical exam, laboratory tests, and medical images were compatible with acute pancreatitis. Upon further investigation, common causes for her pathology were excluded. Ten weeks prior to presentation she had changed her medications for diabetes mellitus type 2 to linagliptin. Results: Using the Naranjo algorithm of adverse drug reactions, we concluded that linagliptin was the most likely culprit. Conclusion: Incretin-based drugs, including dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 receptor agonists, have been shown to be relatively safe for the management of type 2 diabetes mellitus. Since their introduction to the market, conflicting data regarding pancreatic side effects have been published, including a small risk of developing acute pancreatitis with dipeptidyl peptidase-4 inhibitors like sitagliptin and saxagliptin. To date there has been only 1 case report associating linagliptin with acute pancreatitis in the English medical literature. Ours is the first case report in the United States associating linagliptin with acute pancreatitis. It is worth warning both patients and prescribers about this serious adverse effect, as it might affect the choice of antiglycemic agent.

Background Since their recent discovery of zinc transporter 8 antibodies (ZnT8A) by Wenzlau et al. in 2007, the relevance and clinical utility of this marker has been in question. Some recent reports have shown a wide potential for both diagnostic as well as prognostic clinical applications in T1DM as they can be found years before clinical symptoms appear. Understanding the timing of the seropositivity of antibodies such as ZnT8A can help us understand how to utilize this marker for the diagnosis and prognosis of T1DM. Up to 20% of T1DM patients are reported to have ZnT8A positive with negative GAD-65 and IAA autoantibodies. The duration of seropositivity of ZnT8A is unclear. We describe 2 cases from our endocrine clinic with significant zinc 8 transporter antibody titers over 8 - 26 years after their initial diagnosis. Clinical Cases CASE 1: 34-year-old man diagnosed initially with T2DM 9 years prior and later re-classified as T1DM. He was treated initially with oral agents and switched over to Multiple Daily Injection (MDI) insulin about 3-4 years later. He has no family history of diabetes. Approximately 8 years after his initial diagnosis, his autoantibodies profile showed a positive zinc transporter 8 antibody of 28 U/mL (reference of < 15 U/mL), but negative GAD-65 antibodies (reference <5 IU/mL) and negative Islet cell antibodies. CASE 2: 47-year-old man diagnosed with T2DM in 1995 and was initially started on oral hypoglycemic medications. He was later evaluated at our endocrinology clinic and reclassified as type 1 DM after his serologic testing showed a low C peptide < 0.1 ng/mL, positive zinc transporter 8 antibody of 32 U/mL (reference of < 15 U/mL), and negative islet cell antibody screen negative, and negative GAD-65 antibodies (reference <5 IU/mL). He was transitioned to continuous glucose monitoring and an insulin pump, but was too difficult for the patient to manage. He was ultimately transitioned to a basal-bolus regimen of insulin with MDI. His latest serologic testing showed a HgA1C of 9.2%. Conclusions Zinc 8 transporter antibody can help differentiate type 1 from type 2 diabetes and initiate insulin therapy for better glycemic control as well as aid in prognosis and stratification strategies. The duration of seropositivity of ZnT8A has not been clearly established. Previous reports have shown that ZnT8A can be detected at an age around 3 years of age, but peaks around late adolescence and does not have a significant decline in seropositivity rates in older adults, as does IAA. This emphasizes the use of ZnT8A as a useful marker in adult and elderly patients. We describe 2 case reports which indicate that ZnT8 antibodies can remain positive for at least 8 - 26 years in the absence of other autoantibodies. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

SUMMARYThis case report describes a patient who presented with pyrexia of unknown origin allied with hypertriglyceridaemia (16.2 mmol/l) but not hypercholesterolemia (4.1 mmol/l). Investigations identified the cause of the pyrexia as an adult T‐cell lymphoma of natural killer cell phenotype (CD3[+], CD7[+], anti‐TCR alpha/beta[+], CD8[+], CD56[+]). Hypertriglyceridaemia has been reported with non‐Hodgkins lymphoma, and an animal model suggests that antilipoprotein lipase antibodies may be made as an immunological response to the tumour. Lymphomas should be considered as part of the differential diagnosis in type IV‐V hyperlipidaemia.

Background: Pheochromocytomas (PHEOs) are enterochromaffin tumors arising from the adrenal gland. Their diagnosis and preoperative preparation is crucial due to high morbidity and mortality rates with unrecognized, undiagnosed PHEOs. Case 1: 62-year-old male with a medical history of HCC, noted to have right adrenal adenoma measuring 1.7 x 1.6 cm. Denied any symptoms and normotensive on exam. A PET scan done showed a hypermetabolic right adrenal nodule concerning for malignancy. Serum metanephrines were 45 pg/ml (nl <57 pg/ml) and total plasma metanephrines were 172 pg/ml (nl <205 pg/ml). A CT guided biopsy was consistent with a PHEO. Other labs included: 24 hour urine metanephrines: 155 mcg (nl 90–315), total metanephrines: 520 (nl 224–832) and vanillylmandelic acid was 3.6 (nl <6.0). 24-hour urine epinephrine: 10 mcg (nl 2–24), norepinephrine:57 mcg (nl 15–100) and dopamine: 421 (normal 52–480). Case 2: 55 year old male with UTI and flank discomfort, noted to have incidental 8cm Right adrenal mass noted concerning for malignancy. Also denied any symptoms and normotensive. Plasma fractionated metanephrines 938 (ref <206), metanephrine 279,Normetanephrine 659(ref <148), 24 hr urine metanephrines=1176mcg/24 hr (90–315), Normetanephrines 1487 (122–676), 24 hr urine total metanephrines 2663 (224–832). He is refusing α and β blockade due to normotension in preparation for surgery. Discussion: It is important to suspect, confirm, localize, treat, and PHEOs for several reasons. Most of these tumors hypersecrete catecholamines, and if untreated, cardiovascular morbidity and mortality are high. Another reason to encourage case detection is that, for familial disease, detection of a tumor in the proband may result in earlier diagnosis and treatment in other family members. Alpha-blockade is usually used prior to resection of Pheochromocytomas. However, the data available in the literature regarding alpha blockade for “truly asymptomatic” functioning or non functioning Pheochromocytomas is scarce. However what is unique to our cases is that they both are normotensive and asymptomatic and refusing preoperative preparation. Conclusion: Asymptomatic PHEO are becoming more common presentation given Pheochromocytomas are rare. Are the genetics and biochemical nature any different than classic pheos? Are we supposed to manage them the same way? Would we rethink current guidelines for managing normotensive or nonfunctioning pheochromocytomas pre operatively? We also would like guidelines on how to prepare such truly asymptomatic patients prior to surgery. We refer to Endocrine Society guidelines for management of such tumors.