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Introduction Denosumab is a receptor activator of nuclear factor kappa-B (RANK) ligand inhibitor used for treatment of osteoporosis and bone metastases in patients with solid tumors. Denosumab induced hypophosphatemia has been reported in less than 1% of patients, and in most cases described as mild to moderate in severity. We present a case of severe hypophosphatemia after denosumab treatment for diffuse bone metastases due to prostate cancer. Case report A 78-year-old male patient with history of diffuse bone metastases due to prostate cancer, schizophrenia on treatment and intermittent alcohol use, presented to the hospital with suicidal ideation and worsening fatigue. Patient was found to have a phosphorus levels of Discussion In patients treated with denosumab, the primary concern is potential post-treatment hypocalcemia, however, our case brings attention to severe hypophosphatemia as a serious side effect to treatment with denosumab. Multiple specialties are involved in the treatment of osteoporosis and metastatic bone lesions, and each should be aware that denosumab can lead to lower serum phosphate levels due to its effects on bone resorption and reduction of proximal tubular reabsorption of the phosphate resulting in clinical symptoms of muscle weakness, bone pain, fractures and even stupor, coma and death. We therefore conclude that monitoring phosphate levels should be part of the pre- and post-treatment evaluation in patients who are candidates for treatment with denosumab, particularly high-dose denosumab. Presentation: No date and time listed

A 67-year-old male was admitted with shortness of breath and diarrhea. His COVID-19 polymerase chain reaction test was positive, and he was found to be in acute heart failure. Troponin levels were elevated, echocardiogram showed ejection fraction of 24%, and his electrocardiogram was normal. Inflammatory markers were elevated. Further testing revealed suppressed thyroid-stimulating hormone and elevated free thyroxine (T4). Differential diagnosis at this point included possible myocarditis from the viral illness, exacerbation of heart failure from the viral infection or from thyrotoxicosis was considered. Patient’s heart failure improved with initiation of heart failure therapies; however, biochemically, his thyroid function tests (TFTs) did not improve, despite empiric methimazole. Thyroid antibody tests were unremarkable. Thyroid ultrasound showed mildly enlarged thyroid gland with no increased vascularity and 5-mm bilateral cysts. Thyroid dysfunction was attributed to subacute thyroiditis from COVID-19, methimazole was tapered, and prednisone was initiated. The patient’s TFTs improved. With the ongoing COVID-19 pandemic, it is imperative that clinicians keep a broad differential in individuals presenting with heart failure, and obtaining baseline TFTs may be reasonable. Rapid treatment of the underlying thyroiditis is important in these patients to improve the cardiovascular outcomes. In our experience, steroid therapy showed a rapid improvement in the TFTs.

A 70-year-old female with unspecified diabetes presented to the emergency department complaining of nausea, dizziness, and anorexia for 4 days. She was diagnosed with diabetes at age 37 years. In her record, both type 1 diabetes and type 2 diabetes were listed as diagnoses. No prior C-peptide or serum antibodies were available. She had peripheral neuropathy and early stage 3 chronic kidney disease without proteinuria.

Introduction Adrenal glands are highly vascularized organs and can be the foci of metastatic disease. Incidentally discovered adrenal nodules should be evaluated with CT or MRI imaging and biochemical testing. Metastatic lesions do not have a specific clinical presentation or imaging features but are suspected when there is attenuation greater than 10 HU, presence of calcification, hemorrhage, or abnormal enhancement signals in CT scan or MRI. However, malignant lesions can be present along with benign ones as described here. Clinical Case A 74-year-old female initially presented with uncontrolled hypertension in 2002, at which time she was found to have a left adrenal incidentaloma. MRI/MRA of the abdomen with and without gadolinium contrast showed a 2.5 x 2.6 cm left adrenal nodule, described as a benign lipid rich adrenal adenoma. Biochemical testing revealed no evidence of pheochromocytoma, hyperaldosteronism, or hypercortisolism. Follow-up CT scan in 2003 showed the left adrenal nodule was slightly larger (3.0 x 2.5 cm) but remained lipid rich (

Introduction Primary adrenal lymphoma (PAL) is a very rare and aggressive form of Non-Hodgkin’s lymphoma originating from the adrenal glands and with no prior history of lymphoma. It can present with symptoms related to adrenal insufficiency due to tumoral destruction of normal adrenal tissue. Hypercalcemia has also been previously reported as a less common presentation of PAL. We describe here a case of PAL presenting with severe hypercalcemia and adrenal insufficiency. Clinical Case 75 year male presented with 50 pound weight loss, fatigue and anorexia for several months. On admission, patient had altered mental status. Further investigation revealed severe hypercalcemia (corrected calcium for albumin =15mg/dl) and AKI (serum creatine=3.45mg/dl, blood urea nitrogen=89). He was started on IV fluids for the hypercalcemia and AKI. Additional work up revealed suppressed parathyroid hormone (PTH) levels of 9 (12 - 88 pg/mL), high normal PTH-related peptide 22 (14-27), low 25-OHD 7.34 (20-120 ng/ml), high normal 1,25-(OH)2-D 63.0 (19.9-79 pg/mL). His ACTH level was elevated ~159 (7.2-63.3 pg/ml) with low normal morning cortisol levels ~10 mcg/dl. Patient was started on IV stress dose steroids for concerns of adrenal insufficiency and calcitonin was also initiated for the treatment of hypercalcemia. CT of the abdomen showed bilateral adrenal masses, measuring 9.8 x 6.4 x 10.8 cm on the right and 9.3 x 5.2 x 9.6 cm on the left with marked retroperitoneal lymphadenopathy. After ruling out pheochromocytoma with negative plasma and urine metanephrines, biopsy of the adrenal mass revealed a highly aggressive diffuse B large cell lymphoma, with BCL2 and MYC overexpression. Concurrent flow cytometric analysis also identified an abnormal population of medium to large B cells expressing bright CD20, CD19, CD38, CD45 without CD10, CD5, CD23 or overt kappa or lambda expression. His calcium levels improved with hydration and steroids. Chemotherapy was later initiated. Conclusion Primary adrenal lymphoma is rare and aggressive type of NHL. While adrenal insufficiency is expected in this clinical scenario, hypercalcemia from 1,25-(OH)2-D excess is a relatively uncommon presentation. Adrenal insufficiency should be ruled out in bilateral infiltrative adrenal masses. Likely etiologies for hypercalcemia in our case appeared to be secondary to elevated 1,25-(OH)2-D production, humoral hypercalcemia of malignancy and worsened by untreated clinically evident adrenal insufficiency. References (1) Laurent C, Casasnovas O, Martin L, et al. Adrenal lymphoma: presentation, management and prognosis. QJM. 2017 Feb 1;110(2):103-109. doi: 10.1093/qjmed/hcw174 (2) Masood A, Tumyan A, Nussenzveig D R., Wakefield D N., Barb D, Ghayee H K., Maalouf N M. The Diverse Clinical Presentations of Adrenal Lymphoma. AACE Clinical Case Reports: Autumn 2017, Vol. 3, No. 4, pp. e307-e312. doi: 10.4158/EP161595.CR

Introduction: About 20–40% of patients with Cushing’s syndrome present with cyclic Cushing’s Syndrome characterized by episodes of cortisol excess interspersed with periods of normal cortisol secretion. A high degree of suspicion is needed to identify patients with cyclical hypercortisolism. Fluctuations in cortisol levels can make this a diagnostic challenge. Rarely, hypocortisolemia and frank adrenal insufficiency can occur. Case Report: A 77-year-old female with history of Cushing’s syndrome and transsphenoidal surgery with no adenoma identified on pathology presented with fatigue and concern for recurrence with ACTH of 358 pg/mL (6–50 pg/mL) and morning serum cortisol of 41.4 mcg/dL. Brain MRI showed a possible 4 mm pituitary adenoma. However, when she was transferred to our hospital, there was no evidence of hypercortisolism with cortisol of 9.5 mcg/dL, ACTH of 33pg/mL, 24 hr urine free cortisol (UFC) of 4.4ug/d ( Discussion: Cyclic Cushing’s syndrome is diagnosed with three peaks and two troughs of cortisol production. Diagnosis and treatment are challenging since the cycles of hypercortisolism can occur sporadically and rapid fluctuations in cortisol makes it difficult to localize a source. Cortisol fluctuations can affect quality of life and result in complications such as diabetes, hypertension, and osteoporosis. Prompt identification of the source of the Cyclic Cushing’s syndrome is vital to pursue definitive therapy. However, in 9% of cases, there is no identifiable source. In such cases, medical therapy is warranted.

Introduction: Pseudopheochromocytoma presents as paroxysmal events of hypertension and other noradrenergic symptoms similar to pheochromocytoma (PCC) but do not meet tumoral diagnosis. Case Report: A 70-year-old Caucasian male with history of gastroesophageal reflux disease (GERD) and Barrett’s esophagus presented to the Emergency Department with fatigue, shortness of breath, palpitations, and fasciculations in the anterior chest wall. He reported recent diagnosis of PCC. Patient had episodes of non-exertional palpitations, diaphoresis, dizziness, facial flushing, and facial involuntary movement along with self-monitored average blood pressure (ABP) of 160/100 mmHg and heart rate (HR) of 90 beats per minute (bpm). Spells occurred 2 to 3 times per month at first, later increased. Between episodes self-monitored ABP was 120/70 mmHg and HR of 50 bpm and asymptomatic. He reported unintentional weight loss of 40 pounds in the same interval and newly muscle weakness that he attributed to weight loss and malnutrition. Patient had no remarkable past medical history. Medications included coq10 enzyme, glucosamine, flax seed oil, primrose oil and recently added doxazosin 1 mg tab per day. Evaluation revealed a cachectic patient (body mass index 17.46 k/m2) with normal vital signs, otherwise unremarkable physical exam except for diffuse fasciculations in chest and upper extremities. Outpatient work up included normal complete blood count, comprehensive metabolic panel, drug screening, thyroid function test. He had elevated free plasma metanephrine (FPM) of 73 pg/mL (< 57 pg/mL), free plasma normetanephrine (FPN) of 487 pg/mL (

Introduction: Pneumonia is defined as an infection of the parenchyma of the lung and is one of the most common causes of death from infectious diseases in the United States (US). Pneumonia is classified into two groups; community acquired pneumonia (CAP) and hospital acquired pneumonia (HAP). Most CAPs are secondary to bacterial pathogens. Methicillin resistant Staphylococcus aureus (MRSA) is identified as a potential pathogen in 8.9% of CAP cases. Community acquired methicillin resistant Staphylococcus aureus (CA-MRSA) produces a cytotoxin called Panton–Valentine leukocidin (PVL), which causes white blood cell destruction and necrosis, resulting in necrotizing pneumonia when it reaches the lungs. Vancomycin and linezolid are most common recommended antibiotics when treating MRSA necrotizing pneumonia. Ceftaroline fosamil, a fifth-generation cephalosporin, is approved for the treatment of skin and soft tissue infection caused by MRSA and pneumonia, but it has not been approved for MRSA pneumonia. Case Report: A 72-year-old Hispanic male presented with a medical history of hypertension, diabetes mellitus type 2, chronic kidney disease stage 3B, unspecified chronic thrombocytopenia and asthma developed an upper respiratory tract infection that manifested with fever and rhinorrhea and resolved without treatment. Ten days later, the patient arrived at the emergency room due to productive cough of rust colored sputum that started three days before admission. Associated symptoms included malaise, fever, chills and shortness of breath. The patient was admitted to medicine ward with diagnosis of CAP and was initially managed with azithromycin/ceftriaxone. However, persistent fever and tachypnea resulted in the need for reassessment. Sputum culture revealed MRSA and the patient was switched to ceftaroline fosamil for a 21-day course of treatment. Patient was discharged home and has been followed at the outpatient clinic with none of the aforementioned symptoms. Conclusion: Methicillin resistant Staphylococcus aureus necrotizing pneumonia is an uncommon cause of CAP, but its incidence has increased during the recent years. This type of CAP has gained notoriety due to the PVL cytotoxin, with its dire results. Vancomycin and linezolid are the most recommended antibiotics; vancomycin is recommended if the bacteria show a minimum inhibitory concentration (MIC) < 2. In this case, the S. aureus recovered at sputum culture showed a MIC >2 and since the patient presented with several additional comorbidities management was started with ceftaroline fosamil, a fifth-generation cephalosporin that has no hepatic adjustment and has no problem in thrombocytopenic patients. The ceftaroline fosamil was administered at 400 mg intravenously every 12 hours for 21 days. The patient improved clinically and was discharged home and followed the next week then monthly for two months.

Introduction: In patient with diabetes and refractory epilepsy requiring vagal nerve stimulator (VNS), glycemic management can be challenging. Clinical experience is limited in this scenario. Case Report: A 67-year-old male, BMI 30 kg/m2, with history of type 2 diabetes and hemispheric hemangioma complicated by seizure disorder is referred to our diabetes clinic for evaluation of persistent hyperglycemia. The patient reports 25-year history of seizures that have been difficult to control with antiepileptic drugs alone and eventually requiring VNS placement. Patient has normal kidney (eGFR > 60mL/min) and liver function. His antiepileptic drug regimen consisted of gabapentin and as needed lorazepam. He was never on glucocorticoids. Glycated hemoglobin (HgA1c) at our initial evaluation was 10.1%. His anti-glycemic regimen consisted of glipizide monotherapy. Fasting and pre-prandial blood glucose were in the 200-400mg/dL range with occasional values higher than 500mg/dL. This was confirmed with 14-day continuous glucose monitoring that showed average blood glucose of 287mg/dL with 100 percent above target (higher than 180 mg/dL). We optimized therapy by adding once daily glargine, pioglitazone and continued glipizide. At follow up visit, HgA1c still remained high at 10.5%, despite medication adherence. Patient emphasized that hyperglycemia was related to VNS use and given documented hyperglycemia with blood glucose range 500–600 mg/dL when on higher output current of 2 milliamps, his neurologist approved a trial off VNS for 4 weeks. His glucose improved to average less than 200 mg/dL and HgA1c decreased to 9.1% on the same anti-glycemic regimen. Device was re-started due to recurrence of seizures, however the output current and “on time” were reduced to minimal effective range for optimizing seizure therapy while avoiding hyperglycemia. Subsequent HgA1C improved to 8.7%. Discussion: VNS is a FDA approved device for epilepsy and depression. It works by intermittent stimulation or “on/off” periods. In animal studies, elevation of blood glucose was noted with afferent stimulation. Conversely, efferent activation lowers blood glucose. There are limited human studies on the effects of vagal nerve stimulation on glycemic control. The few available, showed variation in blood glucose based on output current and length of on/off period. This should be factored in during glycemic evaluation and management and close collaboration with neurology is essential. Reference: (1) Strauss H, et al. Cervical Vagal Nerve Stimulation Impairs Glucose Tolerance and Suppresses Insulin Release in Conscious Rats. Physiological Reports 2018; 6(24): 1–9 (2) Strauss H, et al. Effect of Vagus Nerve Stimulation on Blood Glucose Concentration in Epilepsy Patients - Importance of Stimulation Parameters. Physiological Reports 2019; 7(14): 1–10