J-LSMS | Abstracts | 2023

involvement of genetic predisposition compounded with an infectious or environmental stimulus.

such as CRP and ESR are within normal ranges, and rheumatoid factor and anti-CCP antibody is negative. Testing revealed the HLA-B27 phenotype. Discussion: Behcet’s disease is a clinical diagnosis without pathognomonic laboratory findings. Although the combination of recurrent uveitis, joint pain, and mucosal ulcers increases clinical suspicion for Behcet’s disease, more common autoimmune and infectious diagnoses such as lupus, rheumatoid arthritis, and HSV should be ruled out first. It is noteworthy that psoriasis and psoriatic arthritis is twice as likely in individuals with Behcet’s disease compared to the general population. Through a combination of daily 60 mg apremilast, and lifestyle modifications such as the avoidance of food triggers, this patient was able to drastically limit the frequency and duration of symptomatic recurrences.

Case: A 52-year-old woman with a history of pheochromocytoma status post resection and stroke presents with fatigue and severe, progressive, and chronic polyarthritis in her hips, knees, elbows, and toes of 2 years. Her joint pain is now dramatically reducing her mobility, often waking her from sleep. She was previously prescribed certolizumab and adalimumab with little to no relief. CT and MRI have shown mild degenerative arthritis in her bilateral 1st metatarsal joints. On further investigation, she also reports flare-ups of bilateral anterior uveitis up to 6 times a year as well as recurrent genital ulcers and aphthous stomatitis, despite repeatedly testing negative for HSV. Additionally, she has a 20-year history of psoriasis. Inflammatory markers

CASE OF VIABLE INTRAPARENCHYMAL NEUROCYSTICERCOSIS David Szarvas, Logan Ledet, MD, and Victoria Burke, MD; LSUHSC School of Medicine, New Orleans, LA.

Introduction: We describe a case of biopsy-proven viable intraparenchymal neurocysticercosis (VPN), highlighting the importance of considering this diagnosis in patients presenting with new-onset seizures and risk factors for tapeworm infection. Case: A previously healthy 20-year-old Guatemalan man presented following new-onset seizures. He denied fever/chills, sweats, weight loss, head trauma, new medications, or substance abuse. On presentation, his vital signs were unremarkable, and his examination was without focal neurologic deficits. He was discharged with levetiracetam but had another witnessed seizure. Readmission evaluation noted a leukocytosis of 14,000 and an area of decreased attenuation on head CT. A lumbar puncture revealed a minimal lymphocytic pleocytosis attributed to his postictal state, given his unremarkable spinal fluid. He received empiric coverage for possible meningitis with vancomycin, ceftriaxone, and acyclovir. Subsequent brain MRI revealed a temporoparietal, heterogeneously enhancing lesion. Given non-diagnostic studies from minimally invasive testing (including bacterial/ fungal/AFB cultures, CSF multiplex PCR assay, cryptococcal antigen, HSV PCR, and MRA brain), he underwent brain biopsy, which found a nodular mass whose pathology revealed a cysticercal lesion. He was transferred to our facility where MRI

showed no lesions and fundoscopic examination without ocular involvement. Screening for tuberculosis and Strongyloides was negative, and he was started on a 14-day course of albendazole concurrent with a prolonged prednisone taper. Follow-up showed no residual disease. Discussion: The presentation of neurocysticercosis (NCC) depends upon the location and number of cysticerci, and each variant can present with focal or generalized seizures with hydrocephalus, meningitis, or stroke symptoms. A thorough history includes inquiring about country of origin/travel, sanitation, exposure to pigs, consumption of undercooked pork, and exposure to known tapeworm carriers. Both CT and MRI are recommended for radiographic diagnosis of NCC. Definitive diagnosis can also be made by histopathology of lesion biopsy or cysticercal lesions on fundoscopic examination. Management of NCC requires addressing significant hydrocephalus, cerebral edema, or increased intracranial pressure prior to initiation of anti-parasitic therapy. All patients should undergo fundoscopic examination and screening to exclude ocular cysticercosis, tuberculosis, and Strongyloidiasis prior to treatment initiation, to prevent vision loss and unmasking of infections during steroid treatment.

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