Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the respiratory tract, but gastrointestinal (GI) symptoms may obscure a secondary diagnosis. GI symptoms similar to the ones presented in acute pancreatitis (AP) have been reported. SARS-CoV-2 binds to angiotensin-converting enzyme 2 receptors, which have been identified in the lungs and pancreas. It has been discussed that systemic response to the infection prompts dysregulation in the affected organs. Hyperglycemia is an independent risk factor for increased mortality and thus a detailed assessment must be performed. A 47 year-old man with dyslipidemia arrived at the ER due to a severe constant epigastric pain of 1 day of evolution with back radiation associated with nauseas, emesis, and hyporexia. Upon examination he was tachycardic and in distress due to pain. Laboratories revealed normocytosis, normal hemoglobin, mild thrombocytopenia, hyperglycemia (150 mg/dL), corrected hyponatremia (130 mmol/L), and corrected hypocalcemia (7.4 mg/dL). Amylase (2,332 U/L) and lipase (2,990 U/L) were elevated. Triglycerides were 6,256 mg/dL and glycated hemoglobin was 6.1%. Abdominal CT scan revealed pancreatitis. He was admitted to the ICU due to severe AP due to hypertriglyceridemia with IV hydration and IV insulin infusion. During the first day of admission, he developed respiratory distress requiring intubation, marked abdominal distension, hemodynamic instability, and oliguria. Intra-abdominal pressure yielded 24 mmHg leading to the diagnosis of abdominal compartment syndrome. He underwent emergent abdominal decompressive laparotomy with Bogota Bag placement. COVID-19 PCR test was performed and reported positive. 72 hours later, triglycerides improved and IV insulin was discontinued, but hyperglycemic state prompted subcutaneous basal and correction boluses. Insulin requirement progressively decreased and was discontinued after 14 days. He continued to show clinical improvement and by day 40, the patient was successfully extubated and discharged after physical rehabilitation. SARS-CoV-2 infection has shown a complex multisystem involvement leading to variable presentations which can be fatal if not identified and addressed properly. Albeit, AP is a rare manifestation of COVID-19, clinicians should be aware and pay attention to the related complications. Proposed mechanisms for hyperglycemia and AP include β-cell damage. The pathogenetic role of COVID-19 in hypertriglyceridemia is unclear. Little attention has been paid to the extent of pancreatic injury caused by this virus. To our knowledge this is the second case presenting with hyperglycemia, hypertriglyceridemia, and AP in COVID-19 infection. As the global pandemic is still growing, elucidation of key pathways and mechanisms underlying these associations would aid in the treatment of patients with COVID-19 worldwide.

Introduction: Hyperthyroidism is a well-known non-parathyroid hormone-mediated cause of hypercalcemia. Hypercalcemia associated with thyrotoxicosis is usually asymptomatic. Increased osteoclastogenesis is one of the mechanisms underlying this etiology. Hyperthyroidism is associated with mild to moderate levels of hypercalcemia in approximately 20% of patients, but severe hypercalcemia is rare. We report a case of a male with Grave’s disease-induced symptomatic severe hypercalcemia. Clinical Case: A 36-year-old male with type 2 diabetes mellitus and arterial hypertension who was transferred from another institution to our Emergency Department due to suspected primary hyperparathyroidism for Endocrinology Services evaluation. Family history is non-contributory. Patient reports palpitations, irritability, and unintentional weight loss of approximately fifty pounds in nine months. One month ago, he started with constipation, anxiety, depression, abdominal discomfort, nausea, and vomiting for which decided to seek medical attention. Physical examination was remarkable for tachycardia, dry mucous membranes, and goiter. Laboratory tests showed lipase 69 U/L (13-60U/L), albumin-corrected calcium 14.3 mg/dL (8.8-10.3mg/dL), phosphorus 3.30 mg/dL (2.4-4.2mg/dL), magnesium 1.58 mg/dL (1.8-2.2mg/dL), creatinine 1.38 mg/dL (0.90-1.30 mg/dL), alkaline phosphatase 77 IU/L (43-115IU/L), iPTH 4 pg/mL (11-67pg/mL), PTHrp <0.4 pmol/L (≤4.2pmol/L), 25-OH vitamin D 32.1 ng/mL (30-100ng/mL), 1,25-dihydroxyvitamin D <5.0 pg/mL(19.9-79.3pg/mL), hemoglobin 11.6 g/dL (14-18g/dL), negative serum and urine protein electrophoresis, TSH 0.003 uIU/mL (0.45-5.33 uIU/mL), free T4 2.80 ng/dL (0.71-1.85ng/dL), total T3 2.57 ng/mL (0.80-2.00ng/mL), TSI: 486% (<140%), urine calcium 24hr 525mg/day (100-300mg/day). Thoracic and abdominopelvic CT scan without contrast was unremarkable for masses, adenopathies, osseous lesions, or acute abdominal processes. Patient was treated with IV isotonic saline and methimazole 10mg oral daily with resolution of symptoms. Finally, diagnosed with Graves’ disease as the cause of hypercalcemia after ruling out other etiologies. He was discharged home with calcium levels 10.8 mg/dL, normal renal function, methimazole, and follow up with Endocrinology Services. Conclusion: This is a case of an atypical presentation of hyperthyroidism-induced symptomatic hypercalcemia. It is important to consider hyperthyroidism in the differential diagnoses of severe hypercalcemia. Prompt suspicion is essential due to the effective treatments available for Graves’ disease. Early treatment of hypercalcemia is important for quick resolution of symptoms and decreased associated mortality.

Cushing’s syndrome (CS) is considered a rare disease. The most common cause is the exogenous use of glucocorticoids (GCs), which are often given within a controlled medical setting, but their factitious use is rare. Factitious CS is more common in females, young patients, those with psychiatric disorders, and those with contacts within the medical field. The diagnosis of CS is challenging because some features are non-specific and commonly present in the general population, such as obesity, depression, diabetes, hypertension (HTN), and low bone mineral density (BMD). A high suspicion is warranted. We present the case of a 47-year-old man with HTN, obesity, dyslipidemia, obstructive sleep apnea, and low BMD who complained of increased appetite, significant weight gain, fatigue, sleepiness, muscle weakness, and occasional facial flushing. Medications include Hydrochlorothiazide, Furosemide, Losartan, Atorvastatin, and Teriparatide. Vital signs were normal and body mass index was 41.9 kg/m2. He had a round face, central obesity, and wide purple striae in his abdomen. Dual-energy X-ray absorptiometry scan showed low BMD at spine. Laboratories revealed a glycated hemoglobin of 6.1%, late-night salivary cortisol of <0.03 mcg/dL, 24-hour urine free cortisol of 22.5 mcg/24hr, morning cortisol of 0.01 ug/mL, ACTH 23.5pg/mL, and dehydroepiandrosterone sulfate (DHEA-S) 35 mcg/dL. Our patient persistently denied use of exogenous GCs, but a urine synthetic GC screen disclosed a positive result for dexamethasone; levels at 1.1 mcg/dL. After an exhaustive conversation, our patient confessed to using over-the-counter dexamethasone 4mg to treat occasional muscle aches. ACTH is usually suppressed in factitious CS, but this was not our patient’s case, giving the appearance of ACTH-dependent hypercortisolism. This can lead to unnecessary diagnostic and therapeutic approaches. An unsuppressed ACTH could be due to an unreliable ACTH immunoassay or intermittent, instead of continuous, ingestion of GCs. A suppressed DHEA-S level, as seen in our patient, may provide the clue to exogenous GC use as the cause of CS. Our case is also rare because our patient is male, older, and not related to the medical field. Hypercortisolism must be detected and treated early due to its high morbidity and mortality. Several features may be reversed with treatment. The possibility of hypothalamic-pituitary-adrenal (HPA) axis suppression due to prolonged use of GCs, resulting in adrenal insufficiency (AI) should be considered. The prevalence of GC-induced AI ranges from 14–63%, with the highest risk in those with Cushingoid features and those receiving a dose equivalent to prednisone 20mg daily for more than three weeks. Sudden withdrawal of GCs should be avoided to prevent adrenal crisis. A tapering regimen should be adopted with subsequent biochemical testing of the HPA axis once GCs have been reduced to a physiologic dose.

Introduction: Isolated adrenocorticotropic hormone (ACTH) deficiency is a rare pituitary hormone deficiency defined by secondary adrenal insufficiency and normal secretion of all other pituitary hormones. Patients present with fatigue, weakness, weight loss, anorexia, nausea, low cortisol levels and low ACTH levels. Isolated ACTH deficiency is more common in males and usually presents in the fifth decade of life. Main mechanisms involved in the pathogenesis are genetics and autoimmune causes, traumatic brain injury and infarction of the pituitary postpartum, known as Sheehan’s syndrome. Sheehan’s syndrome is characterized by postpartum hemorrhage, failure to lactate and menstrual irregularities and it can occur from immediate postpartum period to years after delivery. The most common hormone deficiencies are prolactin and growth hormone. Empty sella is the most common finding on brain MRI. We are reporting a case of a woman in her third decade with isolated ACTH deficiency due to Sheehan’s syndrome two years postpartum, able to lactate, with normal menses and normal brain MRI. Clinical Case: A 33-year-old woman G3P3A0 with hypothyroidism who was referred to Endocrinology clinics due to tiredness, fatigue and weakness. She reported postpartum hemorrhage requiring 4 PRBC transfusions and IV steroids after last pregnancy 5 years ago. Patient was able to lactate after pregnancy and continued in her usual state of health until 3 years ago when she referred loss of consciousness with traumatic head injury due to hypoglycemia. At Endocrinology office physical examination and vital signs were unremarkable, including no blood pressure or heart rate variations with positional changes. Despite hypothyroidism being adequately controlled, she continued with extreme fatigue and weakness affecting her quality of life, for which cortisol and ACTH levels were ordered. Laboratories showed normal electrolytes, negative autoantibodies, cortisol 0.20 μg/dL (5-25 μg/dL) and ACTH 22 pg/mL (10-60 pg/mL) suggesting partial isolated ACTH deficiency. ACTH stimulation test was done and noted with suboptimal response. Evaluation of other anterior pituitary hormones was normal. Brain MRI showed normal pituitary gland. She was started on hydrocortisone in AM and PM and symptoms resolved. Conclusion: Immediate recognition of isolated ACTH deficiency due to Sheehan’s syndrome is necessary due to the availability of effective treatment and morbidity and mortality associated with this serious condition. To our knowledge isolated ACTH deficiency due to Sheehan’s syndrome in which the patient was able to lactate and normal findings on brain MRI has not previously been reported.References: Shivaprasad C. Sheehan’s Syndrome: Newer advances. Indian J Endocrinol Metab. 2011 Sep; 15(3): S203-207. DOI:10.4103/2230-8210.84869.

Background: Upon evaluation of patients with recurrent hypoglycemia, both exogenous and endogenous causes should be excluded. Among endogenous hyperinsulinemic hypoglycemia (EHH) pathologies, Insulin Autoimmune Syndrome (IAS), even though extremely rare, must be considered. Most cases of IAS have been reported in the Oriental population, mostly Japanese. No gold standard of care for this condition has been established. Clinical Case: This is the case of an 82 year-old obese female patient with dyslipidemia, obstructive sleep apnea, and osteoarthritis that comes to the Endocrinology clinics for evaluation due to recurrent episodes of hypoglycemia. She refers that for the last three years she had been presenting with multiple episodes of symptomatic hypoglycemia, even levels as low as 30 mg/dL, requiring multiple hospitalizations. Consequently, she refers a 15-pound weight gain because of multiple daily snacks. Home medications were simvastatin and diclofenac. She denies using insulin, sulfonylureas, other hypoglycemic agents, alcohol, or illicit substances. Abdominal MRI and PET CT scan were remarkable only for an atrophic pancreas without focal masses. Patient was hospitalized for a supervised 72-hour fast, resulting in severe hypoglycemia within 14 hours with elevated insulin levels at 46.3 uIU/mL (1.7-31.0 uIU/mL), elevated C-peptide levels at 5.79 ng/mL (0.9-4.3 ng/mL) and elevated insulin antibodies 53µU/mL (<5µU/mL). Patient showed sufficient hepatic reserve after glucagon administration as well as intact cortisol and growth hormone axis upon severe hypoglycemia. With these results, a diagnosis of IAS was made; not associated with other autoimmune diseases, or with medications with sulfhydryl groups, such as the cases already reported on literature. This condition represents a therapeutic challenge because there is no gold standard of care. Literature recognizes diverse treatment options that range from diet modification to more aggressive therapies, including plasmapheresis and immunosupressants. Our patient was managed with diet modification including frequent snacks and Diazoxide with the goal of decreasing insulin levels and inducing hyperglycemia. Diazoxide therapy achieved a steady euglycemic state and decreased insulin antibodies. Patient developed intolerable bilateral lower extremity edema and treatment was modified to complex carbohydrates, frequent snacks in the daytime and Diazoxide only at bedtime, which is the longer fasting period. Patient has remained without episodes of hypoglycemia and diabetes has not been diagnosed since starting treatment two years ago. Conclusion: Early recognition of IAS is essential in order to avoid unnecessary studies and procedures which could delay management. Although no gold standard therapy has been identified for this condition, our case report identifies Diazoxide as a compelling medical treatment.