A 35-year-old gentleman presented with epigastric pain and bilious emesis. He also endorsed urinary frequency, non-bloody diarrhea and diffuse bone pain. On physical examination he had epigastric tenderness and multiple hyperpigmented skin lesions. An abdominal computed tomography (CT) scan revealed multiple diverticula with peri-colonic fat stranding in the descending and sigmoid colon, concerning for diverticulitis. He was started on a course of metronidazole and ciprofloxacin. A 3.1 cm mass was incidentally noted in the uncinate process of the pancreas. Bilateral adrenal nodules were also appreciated. An endoscopic ultrasound (EUS) guided trans-gastric fine needle aspiration biopsy was performed, revealing a well differentiated pancreatic neuroendocrine tumor (pNET - pT3N1Mx, intermediate risk). Chromogranin A was elevated to 108 ng/ml (reference range <93 ng/ml). Serum and urine metanephrine, V-peptide, gastrin, glucagon and parathyroid hormone related peptide were all normal; indicating a nonfunctioning neuroendocrine tumor. He underwent a pancreaticoduodenectomy. Octreotide scan was unrevealing for residual uptake. Adrenal biopsy revealed adrenal adenomas. Three years later, he presented with severe abdominal pain and a new pancreatic mass was noted on CT. Chromogranin A was elevated to 227 ng/mL. EUS revealed a 0.35 cm mass in the bed of the pancreatic head, encasing the superior mesenteric artery. Pathology was positive for recurrence of the neuroendocrine tumor. He was hypercalcemic to 11.4 mg/dL and parathyroid hormone was elevated to 319 pg/mL. CT neck revealed a 0.1 cm nodule concerning for parathyroid adenoma. He underwent a subtotal parathyroidectomy. Genetic testing confirmed Multiple Endocrine Neoplasia Type 1 (MEN1) with a heterozygous mutation of the menin1 gene. MEN1 is a rare genetic syndrome with affected individuals at increased risk of developing pancreatic, pituitary, parathyroid gland and cutaneous tumors. With a kaleidoscope of presentations, clinicians must maintain a high index of suspicion for MEN1, particularly for cases with nonfunctioning pNETs which present insidiously and are the foremost cause of mortality in MEN1 patients.1 Further clarity is needed on MEN1 associated pNET prognostic risk stratification, surveillance and targeted immunochemotherapy.2 Timely and algorithmic screening for MEN 1 syndrome in patients with pancreatic incidentalomas is essential to improving patient outcomes. 1. Kamilaris CDC, Stratakis CA. Multiple Endocrine Neoplasia Type 1 (MEN1): An Update and the Significance of Early Genetic and Clinical Diagnosis. Front Endocrinol. 2019;10:339. doi:10.3389/fendo.2019.00339 2. Yates CJ, Newey PJ, Thakker RV. Challenges and controversies in management of pancreatic neuroendocrine tumours in patients with MEN1. Lancet Diabetes Endocrinol. 2015;3(11):895-905. doi:10.1016/S2213-8587(15)00043-1
The FreeStyle Libre flash glucose monitor (FGM) has made the use of continuous glucose monitors more accessible to the typical diabetes patient in an outpatient setting given the significantly lower cost and ease of use of FGM as compared to other systems. However, FGM is not labeled for use in a critically ill population. The critical care department at our institution queried the endocrine department about studying the use of FGM in critically ill patients. The interest of the critical care department was due to the potential of decrease in patient discomfort and decrease in time and effort of nursing and support staff related to the performance of fingerstick capillary glucoses if FGM was an adequate replacement measure. As of yet, there has been only minimal study of flash glucose monitoring in critically ill patients. One Australian study evaluated 8 patients in an ICU setting and determined that as compared with arterial blood glucose monitoring, flash glucose monitoring provided acceptable numerical and clinical accuracy.1 A Swedish study evaluated a total of 26 patients undergoing cardiac surgery and compared the use of FGM to use of a microdialysis intravascular system and concluded that the microdialysis system was more accurate, though in this study, only 25% of patients had diabetes. 2 To further investigate use of FGM in a critically ill population, we plan to undertake a single center, prospective, single arm study enrolling at least 20 and up to 40 patients. Inclusion criteria include a known diagnosis of type 1 or type 2 diabetes, age of 18 or older, and admission to the medical intensive care unit (MICU) with expected MICU stay of at least 48 hours. Participating subjects will have a sensor applied by a study investigator. After confirmation that the sensor is operational, the investigator will place opaque tape over the monitor to blind the monitor data. Nurses or medical assistants will conduct the standard of care fingerstick glucose monitoring per hospital protocol but will also have been notified of request to also pass FGM reader over the sensor at time of fingerstick glucose data collection. The primary objectives are to determine numerical accuracy in a critical care setting using the mean absolute relative difference and to determine clinical accuracy in a critical care setting using the surveillance error grid and the clarke error grid analyses. Preliminary data should be available by March, 2020. 1. Ancona P, Eastwood GM, Lucchetta L, Ekinci EI, Bellomo R, Martensson J. The performance of flash glucose monitoring in critically ill patients with diabetes. Crit Care Resusc 2017; 19: 167-174, June 2017. 2. Schierenbeck F, Franco-Cereceda A, Liska J. Accuracy of 2 Different Continuous Glucose Monitoring Systems in Patients Undergoing Cardiac Surgery: Intravascular Microdialysis Versus Subcutaneous Tissue Monitoring. Journal of Diabetes Science and Technology 2017, Vol. 11(1) 108–116
A 21-year-old Ethiopian female with a five-year history of hypertension presented to medicine clinic with headaches and fatigue for two weeks. She was hypertensive to 163/113 mmHg. She had recently moved to the US and no prior medical records were available. She had been taking an unknown antihypertensive until three weeks prior. She was found to have a creatinine of 3.49 mg/dL. Renal ultrasound revealed bilateral, small echogenic kidneys without any evidence of renal artery stenosis. An intrauterine pregnancy was also incidentally discovered. Her aldosterone level was elevated to 486 ng/dL and her renin activity was 1.3 ng/ml/hr, with a ratio of 373, diagnostic of primary aldosteronism. Due to the markedly high ratio, a saline suppression test was deemed unnecessary for confirmation. Her serum potassium was normal at 3.6 mEq, likely due to poor renal clearance. Given renal failure, a CT non-contrast of the adrenal glands was performed with normal findings. She elected to terminate the high-risk pregnancy. Based upon her young age at presentation, family history of early onset hypertension, grossly elevated aldosterone: renin ratio and unrevealing workup for a primary tumor or hyperplastic adrenals, a diagnosis of familial hyperaldosteronism was considered. She failed a month-long trial of dexamethasone therapy, therefore glucocorticoid remediable aldosteronism was excluded. She was subsequently started on spironolactone with good response. Adrenal vein sampling was considered to find a surgical target for adrenalectomy but could not be performed given worsening kidney function. After discussion with Nephrology she opted for a pre-emptive renal transplant evaluation, rather than pursuing dialysis. Genetic testing for subclassification has been negative for mutations in KCNJ5 and CACNA1H with ongoing testing for novel mutations. Primary aldosteronism (PA) usually presents with recalcitrant hypertension, hypokalemia and an elevated aldosterone: renin ratio. It is commonly attributed to adrenal adenomas or hyperplasia with familial hyperaldosteronism (FH) remaining a rare etiology. FH is sub-divided into glucocorticoid remediable, type I, and non- glucocorticoid remediable, types II – IV. The initial diagnosis of such a condition during pregnancy and in the setting of worsening kidney disease presents a diagnostic and management challenge as this precludes adrenal vein sampling and contrast imaging. Our case highlights the importance of early screening for PA and illustrates the need for updated guidelines on aldosteronism workup in the setting of ESRD and pregnancy.
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