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Introduction: Majority of children and adolescents diagnosed with Type 1 Diabetes Mellitus (T1D) present with the classic symptoms of polyuria, polydipsia and polyphagia, associated with hyperglycemia. Concurrent conditions at the time of T1D diagnosis may alter its presentation and potentially lead to challenges in diagnosis and management. Clinical Case: We present a 17-year-old male with worsening fatigue and unintentional weight loss for two months, then one week of emesis and abdominal pain. Initial work-up by his primary care provider showed sodium 125 mmol/L (133–145), potassium 5.7 mmol/L (3.5–5.1), HCO3 20 mmol/L (21–31), anion gap 13 mmol/L (9–18), random glucose 141 mg/dL (70–199). Due to hyponatremia and dehydration, he was sent to a local emergency room where he was found to be mildly hypotensive at 87/57 mmHg. He received intravenous fluids for hydration and was sent home. On out-patient follow up, he appeared well despite being hypotensive. His additional labs revealed a random glucose of 330 mg/dl and elevated HbA1C of 8.3% (4.4–5.6). His urine was positive for glucose but negative for ketones. He was admitted for further management of new onset diabetes. On admission, he was well appearing and in no acute distress. Blood pressure was 86/57 mmHg, heart rate was 109 bpm, and other physical exam findings were unremarkable. Although his hyperglycemia improved after initiation of insulin therapy, his electrolyte abnormalities persisted, raising suspicion for adrenal insufficiency. An ACTH stimulation test was performed, with both baseline and 60-minute cortisol levels low at 1 ug/dl and 0.9 ug/dl, respectively, confirming adrenal insufficiency. He responded well to glucocorticoid and mineralocorticoid replacement. His electrolytes and blood pressure normalized. Further testing confirmed elevated levels of Glutamic Acid Decarboxylase antibodies 0.19 nmol/L (less than 0.02), Islet Antigen 2 Antibodies: 3.38 nmol/L (less than 0.02), and 21-Hydroxylase antibodies, consistent with T1D with concomitant Addison’s disease (AD). Conclusion: About 0.5% of patients with T1D have AD, but the diagnosis of T1D typically precedes AD for several years, thus the coexistence of both autoimmune conditions at diagnosis is rare.

Introduction: Primary adrenal insufficiency (PAI), also known as Addison’s disease, is a disorder of the adrenal glands characterized by decreased levels of glucocorticoids and mineralocorticoids. It is a rare condition with a prevalence of 120 cases per million and is less frequently seen in the pediatric population. Here, we report a previously healthy 15-year-old patient with acute kidney injury (AKI) and PAI. Case Presentation: The patient was admitted to the hospital after findings of abnormal laboratory studies, which included an elevated BUN (53 mg/dL), creatinine (1.39 mg/dL), calcium (11.3 mg/dL), potassium (5.6 mmol/L), and hyponatremia (126 mmol/L). These were performed at an outpatient visit due to three-week history of back pain, fatigue and emesis. On admission, he had stable vital signs. Physical examination revealed generalized darkening of skin, more noticeable on the knuckles and palmar creases, with hyperpigmented patches in oral mucosa and both upper extremities. Although his renal function, serum potassium and calcium levels normalized after intravenous hydration with normal saline, hyponatremia (128 mmol/L) continued. His urine analysis and renal ultrasound were normal. Due to his hyperpigmentation and persistent hyponatremia, PAI was suspected. An ACTH stimulation test revealed that basal and stimulated serum cortisol levels were low, 2.6 mcg/dL and 2.9 mcg/dL, respectively. His plasma ACTH level was elevated at 1,625 pg/mL and serum aldosterone level was low at Discussion: PAI is well described in the literature, though reports in pediatrics vary. Patients may present with nonspecific symptoms such as unexplained weight loss, fatigue, diffuse abdominal pain, nausea, vomiting and muscular weakness. These symptoms may be of insidious onset, which often leads to delayed diagnosis. Physical signs include hypotension and hyperpigmentation. Characteristic biochemical findings are hyponatremia, hyperkalemia and hypoglycemia. Despite the electrolyte derangements, AKI is not a common presentation of PAI. There are only a few case reports associating these two diseases. In this case, his symptoms and abnormal electrolytes were initially considered to be the result of AKI of unknown origin. PAI only became a suspicion after a careful physical exam and persistent hyponatremia despite improvement of his AKI with fluid resuscitation. His low serum cortisol and aldosterone levels with elevated plasma ACTH confirmed the diagnosis of PAI. Conclusion: This case highlights a unique presentation of PAI in an adolescent. A timely diagnosis reduces the risk of unwanted and potentially life-threatening complications such as an Addisonian crisis.

Background: Hypercalcemia secondary to primary hyperparathyroidism (PHPT) is less common in children than adults. Single parathyroid adenoma is commonly the cause of primary hyperparathyroidism in children. Clinical Case: We present a 15-year-old female with one-week history of abdominal pain despite taking over the counter antacids. Her initial work up by her primary care provider revealed serum calcium of 11.8 mg/dL (9.0–11.5) and creatinine of 0.8 mg/dL (0.4–1.2). A week later, she presented to the emergency department with same complaint. In ED, she was found to have hypercalcemia (12.8 mg/dl) with elevated parathyroid hormone (PTH) at 78.5 pg/mL (15–65). Her random urine calcium creatinine ratio was high at 2.1. Her 25OHD was 25 ng/mL (30–100). She had negative urine pregnancy test but had trace ketones, leukocyte esterase, blood and bacteria. CBC and CMP were otherwise unremarkable. She continued to complain abdominal pain with nausea, decrease appetite, fatigue, and general muscle weakness. There was no known family history of calcium or metabolic bone disorders. Her vital signs and physical exam were normal. Subsequent labs showed mild improvement of calcium between (11–12.3 mg/dL), PTH between 54.5 and 77 pg/mL, normal thyroid function. Ionized calcium was mildly elevated 6.0 mg/dL (4.5–5.3) but her repeat 25OHD was low at18 ng/mL. Serum phosphorus levels were relatively normal with lowest level of 2.5 mg/dL (2.7–4.5). Gliadin Deamidated IgA was detectable 15 U/mL (< 15.0 U/). Ultrasound of abdomen was significant for nonspecific mild hepatomegaly; kidneys were normal in size and appearance. Ultrasound of thyroid was significant for probably intrathyroid parathyroid, measuring 6 x 8 x 8 mm. Tc-Sestamibi scan did not confirm a parathyroid adenoma. Genetic testing for MEN-1 was negative. FHH- related genes (i.e. CASR) was positive for p.R990G variant resulting in a mild gain of function of the calcium-sensing receptor. Although previous Tc-Sestamibi scan was unremarkable, an over read of it raised a concern for questionable uptake in the left superior lobe. SPEC-CT demonstrated possible abnormal parathyroid tissue in the upper pole of the left thyroid. FNA of the left thyroid nodule confirmed likely intrathyroidal parathyroid adenoma. Subsequent follow up and treatment, including parathyroidectomy, was done by another institution. She underwent a left parathyroidectomy with normalization of serum calcium and PTH levels post operatively (10.1 mg/dl and 8 pg/mL, respectively) and has complete resolution of her previous abdominal and gastrointestinal symptoms. Conclusion: PHPT is uncommon in children and adolescents and is typically associated with a single parathyroid adenoma. High index of suspicion is key for early diagnosis of PHPT despite a negative Tc-Sestamibi initially.