The theoretical generalization of research results is presented in the thesis and the solution of the scientific problem is reached. The objective of the study was to improve quality of early diagnosis, to determine new link in pathogenetic construction and to develop prognostic criteria of peripheral neuropathy in patients with rheumatoid arthritis (RA), chlamydia urogenital reactive arthritis (ReA) and psoriatic arthritis (PA). Peripheral nervous system disorders such as PN (polyneuropathy and mononeuropathy in 5:1 ratio) were observed in 13% of patients with RA with motorial, sensor, mixed and vegetative disorders in ratio 1:2:3:3, in ¼ of events carpal tunnel syndrome and/or acute form of PNP were revealed which correlate to patient gender (more often in male patients), presence of tendovaginitis, digital arteritis, ophthalmopathy (uveitis, sclerite, keratitis), myositis, spondylopathy, hypothyroidism and Sjogren syndrome. The severity of PN is influenced by arthritis of elbow joint and presence of joint calcification. With that said prognostic criteria were index Lansbury levels and arthritis activity measured by DAS. Changes in vertebral column (osteochondrosis, spondylarthrosis) were observed in ½ of patients with RA, clinical manifestation of spondylopathy was observed in 35% of events which directly correlate to patients age, involvement of wrist, elbow, hip and sacroiliac joints, evidence of osteoporosis and tendovaginitis, sensor and motorial disorders as a result of PNP. Spondylopathy also influences on cardiac dysfunction (violation in heart electrical conduction, volume of chambers, left ventricle diastolic dysfunction), vegetative disorders and severity of neuropathy although prognostic criteria were blood level of rheumatoid factor and C-reactive protein. Patients experienced ReA had symptoms of PN in 19% of events as mononeuropathy/polyneuropathy in 1:1 ratio with motorial, sensor and mixed disorders in 1:3:6 ratio, evidence of vegetative disorders had every second patient and more frequent distal localization of the process which correlate to severity of articular syndrome, high blood level of antichlamydial antibodies, axonal and demyelinating indicators of electroneuromyography - to activity of urogenital process and the presence of acute form of PNP. The pathogenetic construction involves the inflammatory immune proteins, disturbances of vascular endothelial function and physicochemical surface rheological properties of the serum where level of cyclic citrullinated peptide has prognostic significance. The incidence of PN in patients with RA<ReA>PA, although severity RA<ReA<PA where all inflammatory joint diseases have similar ratio of motor, sensor and mixed disorders, trophic, visceral and vascular vegetative changes, association with male gender, activity of arthritis and presence of tendovaginitis, participation in PN pathogenesis of immune disorders, endothelial vascular dysfunction and changes in physic-chemical absorption-rheological viscoelastic and relaxation properties of blood. ReA and PA differ by incidence of distal localization of the process in hands and legs, PA influenced by digital arteritis, ophthalmopathy, myositis and Sjogren syndrome, ReA – sacroiliitis, RA - exudative form of cutaneous psoriasis, risk factor for severe course of neuropathy in patients with RA is considered changes in elbow joints, ReA – intervertebral and lumbar facet, PA – radiocarpal. Acute form of PNP develops in 3%, 4% and 5% of patients with RA, PA and PeA or in 24%, 17% and 26% of these patients with PN that is closely related to the presence of tendovaginitis in all inflammatory joint diseases and severity of articular syndrome, in RA depends on digital arteritis, hypothyroidism and Sjogren syndrome, in ReA – nephropathy and violations in heart electrical conduction, in PA – on exudative form of cutaneous psoriasis. The processes of endothelial dysfunction and vascular changes in physic-chemical absorption-rheological viscoelastic and relaxation properties of blood participate in the pathogenesis of acute form of PNP.