Bipolar i disorder in a patient with selective IgA deficiency and iatrogenic hepatitis C infection. A complex neuroimmunological and affective intersection

Bipolar I Disorder (BD-I) is a severe, recurrent psychiatric condition arising from intricate interactions between genetic, environmental, and biological factors. Immune dysfunction and neuroinflammation are increasingly recognized as contributors to its pathogenesis. We present the case of a 51-year-old male with BD-I, selective immunoglobulin A deficiency (SIgAD), and iatrogenic hepatitis C infection, whose clinical course highlights the complex neuroimmune and affective interplay underlying mood disorders. His psychiatric history includes recurrent manic episodes with psychotic features, initially triggered by interferon-alpha therapy, a known immune activator. Early life adversity, including paternal loss and the psychosocial burden of premature caregiving, intersected with chronic immune dysregulation from SIgAD and iatrogenic hepatitis C, potentially fostering neuroinflammatory priming. The trajectory of his illness is consistent with the affective sensitization (kindling) model, where initial episodes were stress-linked, but subsequent recurrences emerged autonomously. Additionally, a traumatic brain injury during a manic state likely added neuroanatomical vulnerability without altering the primary affective phenotype. This case underscores the relevance of immune-inflammatory mechanisms in BD-I and highlights the importance of integrative, biopsychosocial approaches to both diagnosis and management, especially in medically complex patients.