Infectious diseases of the central nervous system (CNS)—including bacterial meningitis, viral encephalitis, tuberculous meningitis, and neuroinvasive systemic infections—do not remain confined to the brain and meninges. They frequently trigger systemic inflammation, neuroendocrine stress responses, hemodynamic instability, and therapeutic exposures that collectively reshape hepatic physiology. The liver, as an immune-metabolic “gatekeeper,” responds to CNS infection through acute-phase signaling, altered bile acid transport, microcirculatory changes, mitochondrial stress, and immune-cell trafficking. Clinically, these processes can manifest as transient transaminase elevation, sepsis-associated cholestasis, mixed hepatocellular–cholestatic patterns, steatosis during prolonged critical illness, and drug-induced liver injury (notably during anti-tuberculous therapy). This article synthesizes current mechanistic evidence for the brain–liver axis, describes the most typical biochemical and morphological patterns of hepatic change after CNS infections, and proposes a practical IMRAD-style approach to evaluation and monitoring. The key message is that post-CNS-infection hepatic abnormalities are often multifactorial: inflammation-driven bile transporter dysfunction, hypoxic–ischemic stress, immune-mediated injury, and medication toxicity may co-occur. Recognizing these patterns can prevent unnecessary invasive procedures, improve antimicrobial/adjunctive therapy safety, and support early detection of clinically significant liver dysfunction.
O'ralova et al. (2026) studied this question.