Background Artifactual Hypoglycemia (AH), is defined as a discrepancy between the measured and actual blood glucose level. The absence of classical symptoms of hypoglycemia in patients with low measured glucose levels should raise the suspicion of AH. Here we describe a case of AH in a patient with chronic myeloid leukemia (CML). Clinical Case A 47-year-old woman was hospitalized for the evaluation of a four-month history of headache, anorexia, and weight loss. After further workup, she was diagnosed with CML; and upon evaluation, she was found to have a very low serum glucose level of 22 mg/dL. She reported no symptoms of hypoglycemia at the time and no personal or family history of diabetes. She was not using any glucose-lowering medication. Physical examination findings, including vital signs, were unremarkable. Laboratory studies revealed a serum glucose of 22 mg/dL with a simultaneous point-of-care (POC) capillary glucose level of 81 mg/dL. This discrepancy in glucose levels raised the suspicion of artifactual hypoglycemia. To further explore this, we drew three simultaneous venous blood samples and processed them differently to examine the impact of sample processing on serum glucose level in this patient. Two samples were drawn in tubes with no antiglycolytic agent (one sample was centrifuged immediately after the blood draw, and the second one was processed 5 hours after the blood draw). Whereas, the third sample was drawn in a tube containing sodium fluoride, an inhibitor of aerobic glycolysis, and was processed after one hour of the blood draw. Glucose concentrations in the three samples were as follows: 79 mg/dl, 41.4 mg/dl, and 77.4 mg/dl, respectively. The diagnosis of artifactual hypoglycemia due to excessive glucose consumption by leukocytes was established based on the findings of normal capillary blood glucose and normal plasma glucose levels when a tube prefilled with a glycolysis inhibitor is used. Conclusion Artifactual hypoglycemia should be considered in patients with asymptomatic hypoglycemia, especially when there is a discrepancy between the capillary and venous glucose levels. Patients with marked leukocytosis can have artifactually low serum glucose, an erroneous finding that can be mitigated by a) rapid processing of the blood sample or b) utilization of tubes pre-filled with a glycolysis inhibitor. Presentation: No date and time listed

Brown tumor (BT) is a rare non-neoplastic skeletal manifestation of untreated tertiary hyperparathyroidism (THPT) that is associated with renal osteodystrophy in patients with End-Stage Renal Disease (ESRD). Nearly half of patients with ESRD have Osteitis Fibrosa Cystica (OFC) of varying severity, which is the most common form of renal osteodystrophy. BT represents the extreme form of OFC. As a result of frequent monitoring of bone profile and the expansion of pharmacological therapy, the disease is increasingly being diagnosed in its early stages; however, some are still seen at an advanced stage. Depending on the tumor size, the management will range from a conservative approach with supportive parathyroidectomy to a comprehensive surgical removal. Here, we report a rare case of an extensive BT of the pelvis in a patient with ESRD and THPT who was also found to have coincidental papillary thyroid cancer following total thyroidectomy and parathyroidectomy with a postoperative complication of hungry bone syndrome. She then underwent prophylactic intramedullary nail fixation for an impending fracture in the right femur. This case report highlights the importance of considering BT as a differential diagnosis of lytic bone lesions and that measuring serum calcium, phosphorus, and parathyroid hormone as part of the initial evaluation is essential to identify the correct diagnosis. Multidisciplinary team approach with frequent follow-up is crucial to allow early diagnosis and prevent unnecessary surgical interventions. Presentation: No date and time listed

Thyroid hormones and thyroid-stimulating hormone (TSH) laboratory tests are widely utilized worldwide, and their results have a significant impact on treatment decisions and subsequent diagnostic processes. In order to avoid misdiagnosis and inappropriate therapy, any differences between symptoms and laboratory findings should be thoroughly investigated. Many factors can cause discrepancies between thyroid function test and the patients’ clinical picture such as physiological changes, severe illness, drugs, or laboratory interference. Thyroid hormone autoantibodies, anti-streptavidin, and anti-ruthenium antibodies are the major thyroid function test interferers. Here, we present a case of a 70-year-old woman who is known to have hashimoto's thyroiditis maintained on Levothyroxine (LT4) for more than 10 years, but was stopped by her primary care physician due to abnormal thyroid panel results (high TSH and high fT4). She was referred to the endocrinology clinic for further evaluation. The patient complained of generalized fatigue and weakness. She had no hyperthyroid symptoms. She was not on any supplements. Testing thyroid hormones with the 2-step assay revealed severe hypothyroidism, so LT4 was resumed, and patient symptoms improved. This case aims to direct clinicians’ attention to the importance of considering the patient's clinical status in the diagnostic process and not replacing it with the laboratory diagnosis, given the possibility of many laboratories’ interference. Also, to underline the available methods to minimize false results and misleading diagnoses to avoid unnecessary investigations and interventions. Presentation: No date and time listed