Diagnostic complexity in the older patient: an unusual presentation of advanced biliary disease.

Biliary disease is common in the older population, and gallbladder dysfunction and increased bile lithogenicity predispose to calculi formation. This case demonstrates an unusual presentation of gallbladder empyema. A 90-year-old male with metastatic prostate cancer presented with hypoactive delirium. With no localising features, normal liver function tests but persistently raised inflammatory markers, he was initially managed as a urinary tract infection. Chest wall discomfort and swelling over the right costal margin later developed. Abdominal imaging demonstrated a massive gallbladder empyema invaginating through the lower right rib cage, causing the superficial swelling. Pre-morbid status prevented cholecystectomy and he was managed conservatively with percutaneous cholecystostomy and antibiotics. He was discharged to 24-h care 2 weeks after diagnosis with a long-term drain.

Heterogeneity of cellular inflammatory responses in ageing white matter and relationship to Alzheimer's and small vessel disease pathologies.

White matter lesions (WML) are common in the ageing brain, often arising in a field effect of diffuse white matter abnormality. Although WML are associated with cerebral small vessel disease (SVD) and Alzheimer's disease (AD), their cause and pathogenesis remain unclear. The current study tested the hypothesis that different patterns of neuroinflammation are associated with SVD compared to AD neuropathology by assessing the immunoreactive profile of the microglial (CD68, IBA1 and MHC-II) and astrocyte (GFAP) markers in ageing parietal white matter (PARWM) obtained from the Cognitive Function and Ageing Study (CFAS), an ageing population-representative neuropathology cohort. Glial responses varied extensively across the PARWM with microglial markers significantly higher in the subventricular region compared to either the middle-zone (CD68 p = 0.028, IBA1 p < 0.001, MHC-II p < 0.001) or subcortical region (CD68 p = 0.002, IBA1 p < 0.001, MHC-II p < 0.001). Clasmatodendritic (CD) GFAP+ astrocytes significantly increased from the subcortical to the subventricular region (p < 0.001), whilst GFAP+ stellate astrocytes significantly decreased (p < 0.001). Cellular reactions could be grouped into two distinct patterns: an immune response associated with MHC-II/IBA1 expression and CD astrocytes; and a more innate response characterised by CD68 expression associated with WML. White matter neuroinflammation showed weak relationships to the measures of SVD, but not to the measures of AD neuropathology. In conclusion, glial responses vary extensively across the PARWM with diverse patterns of white matter neuroinflammation. Although these findings support a role for vascular factors in the pathogenesis of age-related white matter neuroinflammation, additional factors other than SVD and AD pathology may drive this. Understanding the heterogeneity in white matter neuroinflammation will be important for the therapeutic targeting of age-associated white matter damage.