Background. Analysis of clinical symptoms in patients has an important diagnostic and prognostic value; for HIV-infected patients, the role of clinical symptoms is difficult to overestimate. At the same time, dermatological symptoms and their dynamic changes are a key component of many clinical symptoms and often indicate the features of the course of both somatic and infectious pathology. Evaluation of homeostasis parameters on modern laboratory equipment allows to accurately determine many metabolic disorders, deviations in the functioning of the immune system, as well as other changes in the stability of the patient’s state, while the process is time consuming and requires material costs. Many researchers believe that skin symptoms in HIV-infected patients suffering from psoriasis are a common pathology and are not used enough to assess the condition of these patients. At the same time, studies on the involvement of the immune directions Th1, Th2 and others in the development of psoriasis and the activity of these directions at various stages of the pathogenesis of HIV infection have shown that these diseases have a large number of intersecting pathogenetic links. This fact allows to compare clinical and laboratory parameters for a more complete understanding of the mutual influence of these diseases and the widespread use of dermatological symptoms to assess the condition of HIV-infected patients.
Objective. Evaluation of the role of psoriasis in HIV-infected patients in the development of systemic inflammation, using the indicators of the systemic immune inflammation index (SII) and acute phase proteins (CRP) against the background of genetic engineering biological therapy.
Methods. The study included 180 HIV-infected patients aged 20 to 45 years, of whom 90 had a verified diagnosis HIV infection and psoriasis (group 1). Depending on the severity of psoriasis (Psoriasis Area and Severity Index – PASI), patients in group 1 were divided into subgroups: 1a (n=30) – mild psoriasis – PASI ≤10 points; 1b (n=30) – moderate-to-severe psoriasis – PASI 11 to 20 points; 1c (n=30) – severe psoriasis – PASI >20 points. In order to control the indicators of systemic inflammation, comparison group 2 was selected. This group included 90 people only with HIV infection, without psoriasis. Group 2 was selected using the «pair selection method» (paired groups) to group 1 (taking into account gender characteristics, age, HIV stage, antiretroviral therapy [ART] regimen). The group was divided into subgroups of 30 patients – 2a, 2b, 2c. In total, there were 106 men (58.9%) and 74 women (41.1%) in both groups. All patients in both groups had been receiving ART for at least 3 months at the time of inclusion in the study. Systemic immune inflammation (systemic immune-inflammation index – SII) was assessed using the formula: SII = P × N / L. Where: P is the absolute value of the platelet count, N is the absolute number of neutrophils, and L is the number of lymphocytes in the peripheral blood. C-reactive protein (CRP) levels were determined by generally accepted laboratory methods, with a value of 5 mg/L taken as the norm. To assess the correlation coefficient in subgroups 1a, 1b, 1c of psoriasis severity with the values of systemic immune inflammation indices (SII) and CRP levels, the Pearson correlation coefficient was used, with the calculation of the covariance ratios of two variables and the product of their standard deviations. Therapy for psoriasis in patients with its mild course consisted of topical use of an ointment containing, per 100 g: betamethasone dipropionate – 0.05; salicylic acid – 3.0; patients with moderate and severe psoriasis additionally received the drug netakimab subcutaneously according to the scheme attached to the instructions for the drug.
Conclusion. Psoriasis in HIV-infected patients, depending on its severity, had a pronounced effect on the parameters of systemic inflammation, as indicated by the levels of the median SII index (Me SII1a=362.8 U; Me SII1b=638.2 U) and acute phase proteins CRP (Me CRP1a=15.6 mg/l; Me CRP1b=241.3 mg/l). The SII levels in these patients were linearly associated with the psoriasis severity and significantly improved against the background of biological therapy with Netakimab (Me 0week1b=638.2 U; Me 5week1b=394.7 U; p<0.01). The increase in CRP levels depended on the severity of psoriasis and was significantly reduced by the use of genetically engineered biological therapy (Me 0week 1v=241.3 mg/l; Me 5week 1v=32.9 mg/l; p<0.001).

Keywords: systemic immune inflammation index, psoriasis, HIV infection