Objective: Pituitary adenomas have a population prevalence of less than 0.1%. They can rarely present with serious complications, such as pituitary tumor apoplexy with symptoms of sudden severe headache, vision impairment, nausea, and vomiting. Methods: To date, there has been no proven underlying mechanism for the development of pituitary apoplexy. We report a novel association between pituitary tumor apoplexy and influenza A, indicating an inflammatory pathology underlying influenza infection contributing to hemorrhage. Results: Our patient is a 44-year-old female with past medical history of hypertension and diabetes mellitus type 2 who presented with a 2-day history of visual deficits, progressively worsening headache, and dizziness. She reported fever, chills, myalgia, and cough and tested positive for influenza A. Magnetic resonance imaging of the brain revealed a large suprasellar macroadenoma with internal hemorrhage. She underwent emergent transsphenoidal excision of pathology-proven pituitary adenoma with apoplexy. Signs of the syndrome of inappropriate antidiuretic hormone and diabetes insipidus were frequent
Drug rash with eosinophilia and systemic symptoms (DRESS) is a severe drug-induced hypersensitivity reaction associated with 10% mortality rate with an incidence ranging from 1/1,000 to 1/10,000 drug exposures. Symptoms include fever, rash, eosinophilia and multi-organ failure. DRESS has been most commonly reported with anticonvulsants, allopurinol, sulfonamides and less commonly with vancomycin. This is a case of a 34-year-old female with history of osteomyelitis being treated with vancomycin in a rehabilitation facility. After 3 weeks on vancomycin, patient started to have fever and generalized rash and was still continued on vancomycin. One week thereafter, patient was noted to be hypoxic and tachycardic, and initially admitted and treated as severe sepsis. Initial laboratory studies were remarkable for WBC 21.6 × 10 3 /μL, eosinophils 2.2 × 10 3 /μL, creatinine 1.51 mg/dL, AST 710 unit/L, ALT 659 unit/L and lactic acid 2.8 mg/dL. CMV and HHV-6 were detected in serum. Chest CT showed ground glass opacities and lymphadenopathies. Liver ultrasound showed mild hepatosplenomegaly. Patient continued to be on broad spectrum antibiotics and showed no improvement. Due to worsening liver function tests and kidney injury, all antibiotics were withdrawn, after which she showed significant improvement of symptoms. During her 4 weeks of prolonged clinical course she had one relapse of symptoms with fever, rash and leukocytosis. Eventually, patient slowly recovered with supportive treatment. DRESS syndrome usually has a delayed onset with known relapse of symptoms throughout its clinical course. Addition of new drugs and herpesvirus reactivation have both been shown to cause relapse of symptoms. The mainstay of treatment remains to be withdrawal of drug and treatment with steroids. This case demonstrates DRESS syndrome secondary to vancomycin exposure with relapse of symptoms most likely associated with addition of new drugs, herpes viral reactivation and absence of steroid therapy. Vancomycin, as a commonly used drug especially with increasing MRSA, warrants increased awareness of its association with DRESS for prompt early recognition of symptoms and withdrawal of offending drug.
Objective: Autoimmune polyglandular syndrome (APS) involves autoantibodies against multiple endocrine glands causing either hormonal excess or insufficiency. APS type 2, or Schmidt syndrome, is rare and usually seen in middle-aged females and is characterized by the presence of at least 2 of the following: Addison disease, autoimmune thyroid disease, and type 1 diabetes mellitus. In 2008, there were 3 case reports of APS type 2 presenting as pericarditis with cardiac tamponade, 2 of which had recurrent pericarditis. Methods: We present a rare case of APS type 2 presenting as acute pericarditis leading to cardiac tamponade in a young male. Results: A 21-year-old male who presented with chest pain was found to have acute pericarditis. He developed cardiac tamponade with an ejection fraction of 20% and he underwent emergent pericardiocentesis. Clinical tests revealed low sodium (131 mmol/L), normal potassium (4.5 mmol/L), high thyroid-stimulating hormone (17.9 μU/ mL), and normal free thyroid hormones. His cortisol was low (0.5 μg/dL). Thyroid peroxidase antibodies were positive (985 U/mL), as was his anti-thyroglobulin antibody (27.2 U/mL). He also had positive 21-hydroxylase antibodies (11.8). His cardiac status responded well to high-dose intravenous steroids and intravenous immunoglobulin. He was discharged stable, however 5 weeks after discharge the patient experienced recurrent pericarditis with pericardial effusion that developed into cardiac tamponade. This time the patient underwent placement of a pericardial window. Conclusion: The patient has APS type 2 as he has Addison disease and Hashimoto thyroiditis. Although rare, it has been reported that acute pericarditis leading to cardiac tamponade can be the initial presentation of APS type 2.
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