Inflammation of the meningeal linings of the central nervous system (CNS), also known as meningitis, is one of the serious presentations in the emergency because it carries high morbidity and mortality. The most common cause is pus-producing organisms. However, non-suppurative meningitis, termed aseptic meningitis, is another cause of meningeal inflammation. Many etiologies stand behind aseptic meningitis. Those etiologies include viral and non-viral, drug-induced, malignancy, and systemic inflammation. Druginduced aseptic meningitis is a rare type of meningitis. Although it is easily treated, it can be a challenging disease if not present in the differential diagnosis. It is commonly associated with nonsteroidal antiinflammatory drugs (NSAIDs). Nonetheless, other medications have been also reported to cause aseptic meningitis, including antibiotics. Trimethoprim-sulfamethoxazole (TMP-SMX) is one of the most prescribed antibiotics as a prophylactic and therapeutic drug due to its effectiveness and low cost. Although immunocompromised patients are at a higher risk to develop aseptic meningitis, immunocompetent patients are also at risk. Unrelated to the source of the infection, TMP-SMX carries a risk of aseptic meningitis and should be considered as an etiology in patients presenting with meningeal signs and symptoms. Hereby, we report a young immunocompetent patient who developed aseptic meningitis eight days after being prescribed TMP-SMX. Like all drug-induced aseptic meningitis, all his symptoms resolved two days after stopping the medication.

Moyamoya disease is an arterial disorder causing stroke in a young patient. This is a chronic condition causing progressive cerebrovascular disease due to bilateral stenosis and occlusion of the arteries around the circle of Willis, with prominent arterial collateral circulation. It was first described in Japan and subsequently reported in other Asian countries, but infrequently found in the Western world. Interestingly, there may be racial differences in the presentation and subsequent prognostication of treatment of moyamoya. It is diagnosed with classic angiographic findings of stenosis or occlusion of the circle of Willis vessels. Here, we describe a 28-year-old Caucasian female who was initially diagnosed with anxiety when she presented with symptoms of impaired concentration and fatigue. After the development of remitting slurred speech and facial droop, magnetic resonance imaging and cerebral angiogram yielded the discovery of high-grade stenosis of the origin of the left middle cerebral artery with associated thrombosis in that area. She did well after getting surgery and rehabilitation. This demonstrates a unique presentation of prominent psychiatric symptoms initially thought to be anxiety and culminated in the finding of ischemic stroke in an adult patient with moyamoya.

Background: Hypophosphatasia is a rare metabolic bone disease caused by mutations in the tissue-nonspecific alkaline (TNSALP) phosphatase gene. The disease is typically diagnosed in children but may be seen in adults with premature loss of adult teeth, poor bone healing, recurrent bone fractures, and limited mobility due to chronic pain. Clinical case: A 48-year-old female with Juvenile Onset hypophosphatasia and diabetes mellitus type 2 who presented to the endocrine clinic for diabetes mellitus. She had a telemedicine visit because she was not able to come to the office due to her recent rib fracture and pain. She had multiple fractures since she was 16-years-old with multiple fractures in her toes. She later developed a femur fracture when 20 years old and second at 28-years-old in the other femur. She was tested for juvenile hypophosphatasia and the diagnosis was confirmed. She received no treatment at that time. She subsequently had recurrent non-traumatic rib fractures that interfered with daily life. She is unable to exercise due to her frequent fractures and consequently having poor diabetic control. She has family history of brother with femur fracture. Labs showed decreased alkaline phosphatase (<5 normal: 38–126 U/L), elevated vitamin B6 levels (2296.2: normal 20–125 nmol/L) normal vitamin D (33: normal 30–100 ng/mL) and calcium levels. Chest x-ray showed multiple rib fractures with different healing stages. Dexa scan was also done and was normal to age with lowest Z-score being 8.2. Patient was started on Asfotase Alfa (an enzyme replacement therapy that contains the active site of TNSALP). Conclusion: This case illustrates the debilitating effects of hypophosphatasia and importance of recognizing previously untreated adult patients with hypophosphatasia. Many patients have very late diagnosis and suffer severe complications in their adulthood. Although this disease is rare, recognizing the symptoms of juvenile onset hypophosphatasia can help initiate early treatment to decrease these complications. Hypophosphatasia should be considered as a differential diagnosis in adults with multiple fractures and decreased alkaline phosphatase.

months later. Contrast was injected into the residual cyst cavity and contrast filling was noted of what appeared to be a splenic vessel without active bleeding (Figure A). CT angiogram showed no PA but proximity of the splenic hilar vasculature to the LAMS (Figure B). The LAMS was successfully removed 2 months later without complication. On presentation, she was tachycardic but normotensive. Laboratory studies were notable for hemoglobin 8.8 g/dL (baseline 14 g/dL). Upper endoscopy showed brisk bleeding in the proximal gastric body near the area of prior LAMS. Her bleeding was refractory to endoscopic hemostatic maneuvers, and she underwent emergent mesenteric angiography. Angiography revealed active arterial extravasation arising from the inferior segmental branch of the splenic artery ( Figure C) which was successfully embolized with no further bleeding. Discussion: Visceral artery PA development after LAMS placement is thought to occur due to friction of the inner flange against regional vasculature surrounding the necrotic cavity as it collapses. Close anatomical proximity of LAMS to regional vasculature increases the risk of PA development. In our case, the LAMS was placed near the rich vascular supply of the splenic hilum. Most reported bleeding events related to LAMS have occurred within 8 weeks of placement. Our case is notable for the prolonged delay between LAMS removal and bleeding presentation. Adherent scar tissue between the gastric wall and vasculature could potentially cause delayed PA development after LAMS removal. This case reinforces that high clinical suspicion for PA bleeding is necessary for patients who have previously undergone distant LAMS removal who present with massive GIB.[1718] Figure 1. (A) Fluoroscopic image of contrast injection into residual cyst cavity demonstrating opacification of likely splenic vasculature; (B) Coronal images demonstrating the proximity of the LAMS to the vasculature of the splenic hilum (yellow arrow); (C) Super-selective angiography demonstrating active extravasation into the lateral aspect of the stomach from a pseudoaneurysm (White arrow) involving an inferior segmental branch of the splenic artery.