Acromegaly is an uncommon clinical syndrome that results from excessive secretion of growth hormone with an annual incidence of 6 to 8 cases per 1 million of individuals with a mean age of diagnosis between 40-45 years. Pituitary adenomas can be the principal reason for an overgrowth of the anterior pituitary somatotroph cells, and account for approximately one-third of all hormone-secreting pituitary adenomas with a prevalence of about 38-69 cases per 1 million and an incidence of 3-4 cases per 1 million individuals. The onset of acromegaly is insidious, and its progression is usually very slow. At the moment of diagnosis, approximately 75% of patients have presence of macro adenomas, but most cases are diagnosed after several laboratory workups and incidental brain imaging. A characteristic clinical presentation of pituitary adenomas could be secondary to mass effect. Metabolic presentation such as diabetes is one of the most common related conditions preceding the diagnosis of acromegaly. Clinical presentation with abrupt onset of DKA could be a determining factor on disease progression due to higher GH levels correlating with an increased prevalence of insulin resistance. We present a rare case of a 28y/o female G5P3A2 without previous PMHx who presented to ER with abdominal pain, general malaise, slurred speech, headache and gait difficulty of 3 days of evolution. Upon initial evaluation at ER patient was found with hyperglycemia of 317mg/dL, low central bicarbonate, high anion gap and positive serum ketones suggestive of DKA de novo. Based on neurological complaints, head CT performed showed an incidental parasellar/suprasellar/temporal hyperdense mass measuring 2.5cm x 2.6cm with optic chiasm compression features. Upon further specific questioning patient referred amenorrhea for the past 3 years, bitemporal hemianopsia, galactorrhea and marked facial feature changes, frontal bossing, weight gain, and acanthosis nigricans, for the past year. Pituitary adenoma workup revealed low prolactin levels (1.38), markedly increased growth hormone (501) and IGF-1 (893) suggesting diagnosis of acromegaly, most likely secondary to a functioning macroadenoma. Patient initially treated with Cabergoline, uncontrolled diabetes was managed and was referred to Neurosurgery service for further evaluation and tumor removal. Based on current literature, the incidence of acromegaly cases is low, more specifically when presenting with new onset diabetic ketoacidosis, insulin resistance and secondary to functioning macroadenomas. Medical awareness should be promoted to assess for careful consideration of signs and symptoms, workup, management and treatment to assess and minimize further health complications and physical burdens acromegaly and pituitary adenomas could pose for affected individuals.
Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.
Sjögren's syndrome is an autoimmune disease characterized by exocrine glands lymphocytic infi ltration. However, some manifestations can happen outside the secretory glands affecting multiple organs. We report a 63-year-old man without previous history of any rheumatologic disease and negative arthralgias, mucosal or ocular dryness, in which fi ndings of chest CT scan were consistent with interstitial lung disease prompting further diagnostic workup. Given the serological results, Sjögren's syndrome was highly suspicious in our diagnosis for which a lip biopsy was performed revealing the etiology of our patient's interstitial lung changes. To our knowledge, respiratory symptoms are rarely the initial presentation of this disease, heightening a more thorough workup for a patient with interstitial lung disease with an unclear clinical association requiring a biopsy.
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.
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