ABSTRACT
Neurodegenerative illnesses are notorious for paucity of treatments and relentless clinical progression. Illness may follow a relatively acute presentation, as is seen with primary brain tumors such as glioblastoma or have a more insidious onset with a slower yet unyielding course, such as that seen in Parkinson's disease. Though disparate in presentation, these neurodegenerative illnesses are universally terminal, and both the patients and their families benefit from the intervention of supportive care in conjunction with primary disease management. Supportive palliative care has been shown to improve quality of life, enhance patient outcomes, and often extend patient life-but such care needs to be tailored. This clinical commentary examines the role of supportive palliative care in the management of neurologic patients, comparing and contrasting glioblastoma patients with idiopathic Parkinson's disease patients. Both patient populations are high utilizers of healthcare resources, require active management of multiple symptoms, and have high caregiver burden which underscores the need for supportive services in conjunction with disease management provided by the primary care team. Review of prognostication, patient and family communication, trust and relationship building, and complementary medicinal approaches are explored for these two diseases which broadly represent two differing poles of incurable neurological illness.
ABSTRACT
Hepcidin inhibits ferroportin-mediated iron efflux, leading to intracellular macrophage iron retention, possibly favoring Mycobacterium tuberculosis iron acquisition and tuberculosis (TB) pathogenesis. Plasma hepcidin was measured at human immunodeficiency virus (HIV) diagnosis in a retrospective HIV-prevalent, antiretroviral-naïve African cohort to investigate the association with incident pulmonary and/or extra-pulmonary TB. One hundred ninety-six participants were followed between 5 August 1992 and 1 June 2002, with 32 incident TB cases identified. Greater hepcidin was associated with significantly increased likelihood of TB after a median time to TB of 6 months. Elucidation of iron-related causal mechanisms and time-sensitive biomarkers that identify individual changes in TB risk are needed.
