Amyloid plaques and tau tangles are the hallmark pathologic features of Alzheimer’s disease (AD). Traditionally, these changes are identified in vivo via cerebrospinal fluid (CSF) analysis or positron emission tomography (PET) scans. However, these methods are invasive, expensive, and resource-intensive. To address these limitations, there has been ongoing research over the past decade to identify blood-based markers for AD. Despite the challenges posed by their extremely low concentrations, recent advances in mass spectrometry and immunoassay techniques have made it feasible to detect these blood markers of amyloid and tau deposition. Phosphorylated tau (p-tau) has shown greater promise in reflecting amyloid pathology as evidenced by CSF and PET positivity. Various isoforms of p-tau, distinguished by their differential phosphorylation sites, have been recognized for their ability to identify amyloid-positive individuals. Notable examples include p-tau181, p-tau217, and p-tau235. Among these, p-tau217 has emerged as a superior and reliable marker of amyloid positivity and, thus, AD in terms of accuracy of diagnosis and ability for early prognosis. In this narrative review, we aim to elucidate the utility of p-tau217 as an AD marker, exploring its underlying basis, clinical diagnostic potential, and relevance in clinical care and trials.
Radiation induced cholecystitis is a known but rare complication of Yttrium90 (Y90) radioembolization of hepatic tumors due to nontarget embolization. Many documented cases of radiation induced cholecystitis have been treated with cholecystectomy, which is significant given the typical patient population undergoing radioembolization tends to be of higher surgical risk. Here, we present a case of a 68 year old male who developed radiation induced cholecystitis status post hepatic radioembolization that resolved with conservative management alone. This case highlights that radiation induced cholecystitis may be successfully and safely treated conservatively.
Solitary plasmacytoma of bone (SPB) is a rare plasma cell malignancy that most often presents with localized pain. This case describes a 70-year-old female with a pathologic humeral fracture due to a large, hypervascular SPB. The tumor was assumed to be a metastatic lesion, and preoperative embolization was performed to minimize intraoperative blood loss, followed by tumor debulking and total shoulder arthroplasty. The total estimated blood loss was limited to 100cc, and the patient was returned to baseline functional status with full shoulder range of motion at 6 months postop. Literature on embolization of appendicular plasmacytomas is sparse; however, this case supports its efficacy. We recommend considering preoperative embolization as an adjunctive therapy for all hypervascular bone tumors requiring surgical management, regardless of origin.