PERSISTENT HYPERFERRITINEMIA AS A POTENTIAL BIOMARKER AND PATHOGENETIC COFACTOR IN THE PROGRESSION OF MILD COGNITIVE IMPAIRMENT IN DYSCIRCULATORY ENCEPHALOPATHY (a clinical case with comprehensive laboratory-clinical analysis and literature review)

Abstract

The article presents a clinical case of persistent inflammatory hyperferritinemia in a patient with dyscirculatory encephalopathy (DE) and mild cognitive impairment (MCI), together with a review of the literature on the relationship between iron homeostasis disturbances and cognitive decline. The role of persistent hyperferritinemia in the progression of MCI in DE under conditions of polyetiological chronic inflammatory burden remains insufficiently described in the literature. Comprehensive neuropsychological testing (MMSE, MoCA), an extended laboratory work-up, and neuroimaging were performed in a 72-year-old female patient. Serum ferritin was 490 µg/L (×3.6 the upper reference limit) and remained stable over 24 months; MoCA and MMSE scores of 25/30 and 27/30 objectively confirmed MCI. Normal transferrin, liver enzymes, rheumatoid factor, and thyroid hormone levels verified an inflammatory rather than a true iron-overload origin of the hyperferritinemia. An original five-factor pathogenetic model is proposed, integrating chronic stress, implant-associated inflammation, neurogenic inflammation due to sciatica, ferritin as an acute-phase protein, and anxiety disorder. Serum ferritin is substantiated as a biologically plausible biomarker and potential therapeutic target in DE with MCI; its inclusion in the standard laboratory screening of this patient category is pathogenetically and clinically justified.