Abstract. Аlcohol abuse is the most frequent cause of polyneuropathy in adults. This polyneuropathy is morphologically heterogeneous with a va-riable degree of lesion in axons or myelin. The pathogenesis is complex and it is not clear why in some patients the lesion is limited to axonal degeneration only while in others it develops into demyelinating polyneuropathy [3]. The main problem of the latter concerns the possible impact of immunological factors on this type of myelin lesion [2]. To elucidate these questions we evaluated the expression of some cytokines, i.e. tumour necrosis factor alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1) and growth-regulated oncogene alpha (GRO-α), known also under the term cytokine-induced neutrophil chemoattractant-1 (CXCL1) in the blood serum of patients with alcoholic polyneuropathy. TNF-α is a pleiotrophic cytokine that plays a crucial role in immunological and defence reactions [1]. It has an impact on cell infiltration by promoting adhesion molecules and chemokine agents. MCP-1, as a strong monocyte chemoattractant factor, exerts an effect on differentiation of ThO lymphocytes into Th2 cells, by playing the role of a key factor in inflammatory processes [7]. GRO-α is another chemokine acting as a growth stimulator involved in inflammatory reactions and tumorigenesis [4,6].