Campylobacter is a gram negative bacterium that exhibits tissue tropism. We report a case of Campylobacter fetus bacteremia associated with infra-renal abdominal aortitis. The patient was a poor surgical candidate so she was initially treated only medically. Her course was complicated by the development of a pseudoaneurysm. An endovascular stent was placed and the patient was given 4 more weeks of antibiotics. The patient continues to do well several months after stent placement. This case illustrates the success of medical treatment combined with stent placement in a patient who could not undergo surgery for an infected abdominal aortic pseudoaneurysm.
Background Diabetes insipidus (DI) occurs in 1/30,000 pregnancies and can be difficult to recognize due to normal peripartum physiology. The most common etiology is excess production of placental vasopressinase, which degrades maternal anti-diuretic hormone. Although rare, hypothalamic and pituitary disorders must also be considered in pregnant patients presenting with DI. We present the case of a pregnant woman presenting with diabetes insipidus and pituitary apoplexy. Clinical case We were called to see a 33 year old female with polyuria and polydipsia on post-partum day #2. She had presented to the ED at 29.4 weeks of her 5th pregnancy (G5P4) with an unrelenting headache, nausea, and vomiting for 12 hours. She was tachycardic, hypertensive, and had no focal neurologic deficits. Fetal evaluation was reassuring. Admission labs included serum sodium of 147 mEq/L (n 136-145), serum potassium 2.8 mEq/L (n 3.4-4.4), and urine specific gravity of 1.003 (n 1.005-1.030). Glycemic parameters, renal function, and hepatic function were normal. She remained tachycardic despite vigorous IV fluid administration. Overnight into hospital day #3 she began to have uterine contractions with fetal decelerations, and betamethasone was given. It was noted that she had produced 8L of urine over the preceding 24 hours. Serum sodium was 159 mEq/L with urine osmolality of 78 mOsmol/kg (n 300-900). A presumptive diagnosis of gestational DI was made and 2 mcg of subcutaneous DDAVP was given. Shortly thereafter she delivered a healthy infant. Maternal blood loss was minimal. Over the next 12 hours her urine became concentrated and her serum sodium decreased, but by the next morning she re-developed dilute polyuria. At the time of our evaluation, her headache had resolved and she had no focal neurologic deficits. She had no apparent signs of glucocorticoid or thyroxine deficiency but had not begun to lactate. Biochemical evaluation included early morning cortisol of 4.6 ug/dL (n 3.5-18.3), TSH 0.46 uIU/mL (n 0.35-4.94), free T4 0.76 ng/dL (n 0.70-1.48), and prolactin 26.6 ng/mL (n 5.2-26.5). Pituitary MRI showed a mildly enlarged gland with central T1 hyperintensity, consistent with apoplexy. A regimen of hydrocortisone and DDAVP was initiated. Conclusion Pituitary apoplexy is uncommon during pregnancy but is potentially life-threatening for the mother and fetus if it goes unrecognized. The significant physiologic growth of the pituitary during pregnancy may increase the risk of apoplexy. A severe headache is the most common symptom and may be accompanied by signs of pituitary dysfunction. Although diabetes insipidus is more often caused by placental physiology, pituitary apoplexy must also be considered in a pregnant woman who has concurrent neurologic symptoms.
Background: Pheochromocytomas are rare catecholamine secreting tumors that arise from chromaffin cells of the adrenal medulla and sympathetic ganglia. Typical symptoms include paroxysmal hypertension, headache, and palpitations. Hyperglycemia is seen in 35-50% of these patients. There are a few case reports depicting the rare presentation of diabetic ketoacidosis (DKA) precipitated by a catecholamine-secreting tumor. We present a patient with recurrent DKA in the setting of a pheochromocytoma. Clinical Case: A 57-year-old woman with a history of breast cancer, hypertension, adrenal mass, and uncontrolled diabetes mellitus presented with severe DKA after taking oral steroids. Her review of systems noted intermittent pounding headaches, blurred vision, dizziness, unintentional weight loss, palpitations, and fluctuating blood pressure (BP). She had an episode of DKA 6 months prior. She was treated in the ICU with intravenous fluid and insulin with resolution of DKA. Subsequently, she acutely became severely hypertensive. BP was uncontrolled despite aggressive intravenous anti-hypertensive medication. Pertinent labs included hemoglobin A1c (HbA1c) 9.1%, GAD-65 Ab <5 IU/mL, fasting C-peptide 0.81 ng/mL, plasma free total metanephrines 29073 pg/mL(<205) and 24 hour urine total metanephrines 34633 mcg (149-603). A CT scan of the abdomen showed a 7.8 cm right adrenal mass with heterogeneous internal enhancement. Her BP was stabilized with clonidine and doxazosin and she was discharged on these medications and insulin. After appropriate alpha and beta blockade, she underwent right adrenalectomy at another hospital. Postoperatively her BP has been controlled off alpha-blockade and her diabetes has been controlled on metformin alone. Conclusion : This case illustrates the causative role of a pheochromocytoma in a patient with hyperglycemia and severe ketoacidosis. Epinephrine secreted by a pheochromocytoma inhibits insulin secretion by stimulation of alpha-adrenergic receptors and induces glucagon secretion by stimulation of beta and alpha-adrenergic receptors in the pancreas. In addition, stimulation of these receptors promotes glycogenolysis and gluconeogenesis in the liver and activates lipolysis contributing to insulin resistance. In a predisposed patient, these factors may lead to DKA. In a patient who presents with DKA and paroxysmal or uncontrolled hypertension, the diagnosis of pheochromocytoma should be considered. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.
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