PATHOGENESIS OF AUTONOMIC AND PERIPHERAL NEUROPATHY IN PATIENTS WITH PSORIASIS

Abstract

There is enough data confirming the common mechanisms of damage to the nervous system and skin in psoriasis. Cardiac autonomic denervation is a mechanism of cardiovascular pathology in psoriasis. Thus, a simultaneous disturbance of sympathetic and parasympathetic impact on vascular tone and heart rhythm has been established. When performing an active orthotest in trial subjects, heart rate centralization and decreased autonomous circuit activity were found. In psoriasis, vegetative-vascular dystonia develops due to metabolic disorders that occur in diabetes mellitus. Inflammatory cytokines Th-1, adhesion molecules, and angiogenic factors are involved in pathological processes in obesity, diabetes, metabolic syndrome, and thrombotic complications. Microangiopathy, which develops in psoriasis, reduces the response of blood vessels to autonomic innervation. Such negative influences eventually lead to a persistent alteration of the autonomic nervous control. The authors resent the results of a few studies on the peripheral nervous system in patients with psoriasis. There is evidence of a symmetrical alteration of vibration, tactile, pain and temperature sensitivity in the distal regions of all four limbs. There are some histological studies of the sural nerve in patients with psoriasis, which indicate demyelination of nerve fibers. In this regard, the study of neuropathy pathogenesis in psoriasis is necessary to improve the disease course and the effectiveness of psoriasis therapy. Assessment of psoriatic lesion severity and timely detection of cardiac denervation will reduce the risk of fatal cardiovascular complications. Instrumental diagnostics of the peripheral nervous system will make it possible to differentiate damage to muscle and nerve fibers in psoriasis.