AB0548 Antibody to purinnucleosoid phosphililase can be used as an additional marker of infectious complications with systemic lupus erythromatosis
Authors: A.V. Aleksandrov, E.V. Benedickaya, I.Y. Alekhina, N.V. Aleksandrova
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Purine nucleoside phosphorylase (PNP, EC 2.4.2.1) plays a leading role in the assimilation of nucleosides and nucleotides by the cell, as well as in maintaining the immune status of the organism. Patients with PNP deficiency are highly susceptible to various infections, in view of the fact that the decreased activity of PNP is closely related to the insufficiency of cellular immunity. <h3>Objectives</h3> Study of the possibility of using the level antibodies to purine nucleoside phosphorylase as an additional marker of infectious complications in patients with systemic lupus erythematosus (SLE). <h3>Methods</h3> The study included 60 patients with SLE (women – 91.7%, mean age 36.32±15.27 years, average duration of the disease 7.96±7.35 years) with different clinical manifestations (SLEDAI activity 8.93±5,74, ECLAM activity 5.30±2.79, damage index SLICC/ACR 1.95±1.71). Antibodies to PNP (anti-PNP) were determined in our indirect ELISA test using the immobilised form of the enzyme as an antigenic matrix. The presence of infectious complications in SLE patients was assessed by characteristic clinical manifestations and was considered to be confirmed when the causative agent was recognised and/or the serological analyses are positive. Infections were diagnosed in 38.3% of patients, the most frequent localization was the urinary system (n=12; 52.2%) and female genitalia (n=5; 21.7%). <h3>Results</h3> In the presence anti-PNP in the blood serum of patients with SLE we have often noted infectious complications (p=0.025, criterion χ<sup>2</sup>) and less often lung damage (p=0.17) (when compared with a group of patients with SLE seronegative for the presence of anti-PNP). Statistically significant differences (Mann-Whitney U-criterion) were detected only for pyuria (p&lt;0.0005), C-reactive protein level (p=0.048) and the number of ceruloplasmin (p=0.008), while comparing the groups of SLE patients with the presence of infectious complications and without it; differences in the level of antibodies to CP (p=0.052) did not reach statistical significance. Other clinical and laboratory parameters do not have statistically significant differences between the two sessions. This fact complicates the recognition and differential diagnosis of infectious complications in SLE significantly. The analysis of the characteristic curve of antibodies to PNP in the diagnosis of infectious pathology in SLE shows limited possibilities for using this parameter. The square under the curve was 0.687 (95% confidence interval 0.523–0.804, p=0.008), the separation point was 0.386 U/ml with a sensitivity of 55% and a specificity of 83%. Taking into account that the typical clinical manifestations of infection with SLE can be erased as a result of the actual activity of SLE, and due to the use of immunosuppressive drugs, timely diagnosis and treatment become especially relevant. This study indicates the possibility of using the level of antibodies to PNP as an additional marker of infection, but the balance between specificity and sensitivity of this test does not allow to recommend it as a single study. <h3>Conclusions</h3> A high level of anti-PNP in the serum, especially combined with the C-reactive protein increase and in the absence of other markers of SLE activation allows to suspect the presence of infection and points to the need for in-depth research directed to identify the pathogen. <h3>Disclosure of Interest</h3> None declared