Atopicheskij dermatit (AtD) — shiroko rasprostranennoe mul'tifaktornoe geneticheski determinirovannoe vospalitel'noe zabolevanie kozhi, obuslovlennoe sredi prochih prichin narusheniem funkcij epidermal'nogo bar'era. Nulevye mutacii gena filaggrina — vazhnogo komponenta sistemy natural'nogo uvlazhnyayushchego faktora, privodyashchie k otsutstviyu vyrabotki polnocennogo belka-predshestvennika, associirovany s AtD. Cel' issledovaniya — ocenit' chastotu naibolee rasprostranennyh v evropejskih populyaciyah nulevyh mutacij gena filaggrina 2282delACTG (rs558269137), R501X (rs61816761), S3247X (rs150597413), R2447X (rs138726443) u vzroslyh pacientov so srednetyazheloj i tyazheloj stepen'yu AtD. Analiz proveden u 99 vzroslyh pacientov oboih polov v vozraste 18–68 let, so srednetyazhelym i tyazhelym AtD. Identifikaciyu mutacij osushchestvlyali s pomoshch'yu razrabotannogo metoda mul'tipleksnogo analiza chetyrekh odnonukleotidnyh polimorfizmov pri ispol'zovanii minisekvenirovaniya. CHastota vstrechaemosti nulevoj mutacii filaggrina 2282delACTG okazalas' na urovne 5,3%, R501X — na urovne 0,5%, R2447X — na urovne 1%. Nulevaya mutaciya S3247X gena FLG v vyborke pacientov ne obnaruzhena. Sravnenie rezul'tatov s rossijskimi i evropejskimi vyborkami vyyavilo sopostavimyj uroven' analiziruemyh mutacij gena filaggrina u vzroslyh pacientov s AtD iz razlichnyh regionov Rossijskoj Federacii.

Objective. The development of a method for identifying frequent genetic determinants of Mycobacterium leprae clinical isolates resistance to three groups of antimicrobial drugs: dapsone, rifampicin and fluoroquinolones using SNaPshot technique. Materials and Methods. The study included M. leprae clinical isolates obtained from skin biopsies of patients undergoing leprosy treatment at the Sergiev Posad branch of the State Research Center of Dermatovenereology and Cosmetology of the Ministry of Health of Russia. One of the patients has the diagnosis ‘Leprosy, lepromatous type’, the second one has the diagnosis ‘Leprosy. Multibacterial leprosy, borderline’. The selection of oligonucleotide sequences and hybridization probes for M. leprae drug resistance-determining genomic regions PCR was carried out according to information from the BLAST, the synthesis was performed by ‘Synthol’ LLC (Russia). The first PCR was carried out using the QIAGEN Multiplex PCR kit (Germany), and subsequent SNP analysis using the “SNaPshot” kit at the ABI 3130 Genetic Analyzer. The data obtained were depicted using Peak Scanner Software. Results. A method of six most frequent genetic determinants of antimicrobial resistance of M. leprae identification in patient skin biopsies was developed. Drug resistance of the disease is caused by the M. leprae genome mutations located in drug resistance-determining regions in the genomic loci: folP1 for dapsone, rpoB for rifampicin and gyrA for fluoroquinolones resistance. The SNP polymorphisms stipulated drug resistance as a result of changes in the amino acid sequence of the transcribed protein, are determined in following M. leprae genome regions: rpoB: D441, H451, S456; gyrA: A91; folp1: T53, T55. The technique is SNaPshot determination of nine SNP performed on DNA isolated from the patient’s biological material. The control reaction confirming the presence of M. leprae DNA in the sample is PCR using primers to the non-coding repeat element of the leprosy genome RLEP. The pilot application of the technique developed to the samples of clinical material from patients showed the absence of M. leprae resistance determinants to antimicrobial drugs most often used to treat leprosy. Conclusions. The use of a system for rapid identification of leprosy clinical isolates resistance to antimicrobial therapy will personalize the provision of medical care and provide the opportunity to select the optimal chemotherapy regimen, which will lead to increased efficiency of treatment of the disease.

Atopic dermatitis (AD) is a widespread multifactorial genetically determined inflammatory skin disease caused by, among other causes, impaired functions of the epidermal barrier. Loss-of-function mutations of the filaggrin gene (important component of the natural moisturizing factor system) that arrest production of the full-fledged precursor protein are associated with AD. This work investigated the frequency of the 2282delACTG (rs558269137), R501X (rs61816761), S3247X (rs150597413), R2447X (rs138726443) loss-of-function mutations of the filaggrin gene in adult European patients with moderate to severe AD. The study involved 99 adult patients of both sexes aged 18-68 years. The mutations were identified with the help of the purpose-developed method of multiplex analysis of four single nucleotide polymorphisms that relies on the SNaPshot technique (minisequencing). The incidence of loss-of-function mutation of filaggrin 2282delACTG was 5.3%, that of R501X - 0.5%, R2447X - 1%. No S3247X mutation was detected in the sample. Collation of the results with Russian and European samples revealed a comparable level of the analyzed filaggrin gene mutations in adult patients with AD from different regions of the Russian Federation.

Background — Psoriasis is an immune-mediated genetic skin disease with a deregulated immune response governed by a proinflammatory cytokine network. Apremilast has demonstrated high safety and tolerability both in clinical trials and in clinical practice. The effectiveness of the apremilast use in clinical practice may differ from major clinical trials. Our study assessed changes in the levels of immune gene expression in patients suffering from severe psoriasis in the course of apremilast treatment in order to investigate the predictors of its effectiveness. Methods — We assessed the expression levels of IFNγ, IRF3, GLIS1, HR, STAT1, STAT3, VEGFA, ICAM1, TNF, IL1α, IL1β, IL4, IL6, IL10, IL11, IL12B, IL17A, IL17F, IL18, IL20, IL21, IL22, IL23A, IL25, IL31, IL33 genes in both lesional and nonlesional skin before the treatment, as well the expression at lesional skin after the treatment. RNA expression was assessed in skin biopsy samples by RT-PCR using TaqMan probes with StepOne5 equipment and normalized with endogenous control. The study included 16 patients diagnosed with a moderate-to-severe or severe psoriasis using clinical examination by a dermatologist. The clinical outcome after 26 weeks of apremilast treatment was assessed with delta PASI, resulting in a patient group with high effectiveness of treatment (delta PASI>75%) and a group including all other patients. Results — We confirmed elevated levels of expression in STAT1, IFNγ, IL1β, IL12B, IL17A, IL17F, IL20, IL21, IL22, and IL23A genes in lesional vs. nonlesional psoriatic skin samples, while GLIS1 gene expression was reduced. The expression levels of cytokine genes after apremilast treatment decreased considerably in cytokines IFNγ, IL1β, IL20, IL21, and IL22; and to a lesser extent in STAT1, IL6, IL17F, IL22 and IL31. In the group of those who effectively responded to treatment with apremilast, a five-to-eleven-fold reduction in the expression level of the IL1B, IL6, and IL17F genes was observed, as compared with other patients. Conclusion — The increased expression of cytokine genes in lesional vs. nonlesional skin was reduced after apremilast treatment of psoriasis. We established that fold changes in the expression of the IL1β, IL6 and IL17F genes during treatment with apremilast were different in groups of patients with different therapy outcomes. Hence, we propose that they are the predictors of the effectiveness of apremilast treatment for severe psoriasis.

The goal of the study was molecular typing of current Neisseria gonorrhoeae clinical isolates in Russia for the identification of epidemiologically significant NG-MAST and MLST sequence types carrying a “mosaic” penA gene allele with reduced sensitivity to third-generation cephalosporins, which are recommended as first-line antimicrobials for gonococcal infection therapy. The study included 326 N. gonorrhoeae clinical isolates collected in Russia in 2018–2020. NG-MAST typing was based on sequencing of variable regions of porB and tbpB genes. MLST typing was performed on the basis of the nucleotide sequences of seven housekeeping genes: abcZ, adk, aroE, fumC, gdh, pdhC, and pgm. The penA gene structure was analyzed according to the Sanger protocol. Molecular typing assigned the examined N. gonorrhoeae clinical isolates to 110 NG-MAST and 41 MLST different sequence types. The penA gene sequencing revealed a “mosaic”-type XXXIV allele encoding penicillin-binding protein 2 with reduced affinity to cephalosporins in 7 (2.1

Background. Psoriatic arthritis is a chronic inflammatory disease of the joints, spine and entheses that can occur in patients with psoriasis. The prevalence of psoriatic arthritis is 19.7%. In 70% of cases, psoriasis precedes the development of arthritis. It has been proven that a delay in the diagnosis of psoriatic arthritis even by 6 months is associated with a deterioration in long-term radiological and functional results, leading to disability. The problem of early diagnosis of joint damage can be solved by identifying predictors of the risk of developing psoriatic arthritis in patients with psoriasis. Aims. To determine possible predictors for the development of psoriatic arthritis in patients with psoriasis. Methods. The open, uncontrolled, prospective study enrolled 250 patients. The main group consisted of 190 patients diagnosed with plaque psoriasis. The control group consisted of 60 patients with psoriatic arthritis. In order to identify associations of clinical and genetic (HLA-B27 carriage) parameters with the development of psoriatic arthritis, we compared the frequency of occurrence of these parameters in patients with psoriatic arthritis and without. Results. Among 190 patients with plaque psoriasis 128 (67.4%) men, 62 (32.6%) women, aged 18 to 84 years (40.30 ± 15.56), the average duration of psoriasis was 10.09 ± 11.08 years (0–57). Among 60 patients with psoriatic arthritis 39 (65%) men, 21 (35%) women aged 18 to 86 years (44.43 ± 14.15), the average duration of psoriasis was 20.47 ± 13.22 years (2–57), the average duration of psoriatic arthritis was 7.97 ± 9.95 years (0–47). Сlinical predictors for the development of psoriatic arthritis in patients with psoriasis: nail psoriasis (OR = 2.244 [95% CI: 1.245–4.045]); severe psoriasis (PASI ≥ 20) (OR = 2.148 [95% CI: 1.161–3.975]); arterial hypertension (OR = 1.982 [95% CI: 1.031–3.812]); duration of psoriasis over 25 years (OR = 3.365 [95% CI: 1.676–6.756]), р 0,05. Conclusions. The joint consideration of informative predictors will allow us to develop an original multi-parameter mathematical model for calculating the risk of developing psoriatic arthritis in patients with psoriasis.

Background. The initial stages of androgenetic alopecia in men are characterized by a variety of clinical manifestation in the parietal or occipital scalp regions. However, the differences in the pathogenesis of hair loss patterns are not well understood, selective treatment has not been developed. Aims. Trichological characteristics of patients with initial stages of androgenetic alopecia with identification of genetic and non-genetic factors that determine the hair loss in the different scalp regions, and their response to conservative therapy. Materials and methods: Trichograms were photodocumented using an AramoSG microcamera (Republic of Korea). The genetic factor was analyzed by mini-sequencing of single nucleotide polymorphisms rs929626, rs5919324, rs1998076, rs12565727, rs756853. The non-genetic factors study included hormonal status (total and free testosterone, dihydrotestosterone, 17OH-progesterone, dehydroepiandrostenone, SHBG) and blood content of trace elements (Mg, Ca, Zn, Cu, Se, Fe) and vitamins (B12, D, E, folic acid). Conservative treatment was topical application of a minoxidil 5% (twice-a-day, 4 months) and a micronutrient deficiencies personalized correction. Results. The study included 47 man with initial stages of androgenetic alopecia. Their trichological examination showed two patterns, consisting a predominant decrease in the hair density and diameter in the parietal and occipital scalp regions, which were subgroups formation criteria. An intergroup comparison revealed similar genetic risk, while hormonal parameters (increased dihydrotestosterone levels, a decrease in free testosterone) characterized the subgroup with parietal hair loss pattern. Also, a multiple deficiency of Zn, Cu, Se and vitamins B12, D, folic acid was detected in all patients. Subsequent conservative treatment had a positive effect in patients with parietal hair loss pattern, while in patients with occipital pattern no significant response was observed. Conclusions. The study develops ideas about differences between androgen-dependent parietal and androgen-independent occipital hair loss patterns in the initial stages of androgenetic alopecia, which requires different approaches to their conservative therapy.

Uncovering the molecular mechanisms of the rosacea pathogenesis and treatment are still of great importance. The review encompasses the modern knowledge of rosacea classification, characterization of the severity of the course of the subtypes, and pathogenesis features. Recent methods of rosacea treatment are presented, including the use of botulinum neuroprotein for the correction of the erythematous-telangiectatic subtype of the dermatosis. The relevance of this problem is due to the chronic course of the disease and the peculiarity of the localization of rosacea manifestations that leads to a traumatic effect and often causes social exclusion of patients. The rise of the rosacea incidences, along with other reasons like characteristics of the course of dermatosis, accompanied by frequent long-term relapses, is due to the resistance to generally accepted methods of drug therapy, often resulting in shortened clinical remission. All the factors lead to decreasing of patients life quality that require the search for effective therapy approaches. Among modern rosacea therapy, the application of botulinum neuroprotein is widely used; however, the clinical studies confirming the effectiveness of this technique are not presented enough.

Background. Basal cell carcinoma is the most widespread malignant skin neoplasm. Angiogenesis is critical for the growth and metastasis of malignant tumors. Aims. To study the levels of representation of transcripts in the foci of basal cell skin cancer before and after the therapy of genes for angiogenesis proteins and their receptors: angiopoietin 2 ANGPT2, calcitonin-related polypeptide alpha CALCA, epidermal growth factor receptor EGRF, fibroblast growth factor FGF2, intracellular adhesion molecule ICAM1, vascular endothelial growth factor VEGFA and its type 2 receptor VEGFR2, matrix metalloproteinase MMP9, homologue protein of phosphatase and tensin PTEN, tachykinin receptor TAC1, and tumor necrosis factor protein genes TNF. Methods. The study included 31 patients with histologically confirmed basal cell skin cancer who received treatment at the consultative and diagnostic center of the State Research Center of Dermatovenereology and Cosmetology of Russian Ministry of Health, Moscow in the period from 2020 to 2021, using a pulsed dye laser (wavelength — 585 nm) and long-pulsed neodymium laser (wavelength — 1064 nm). The patients provided skin punch biopsies from BCC lesions and after therapy from the same localization. The gene expression was analyzed with real-time reverse transcription PCR using endogeneous control, and the gene expression ration changes during the therapy were calculated according to Livak’s double delta formulae. Results. An increased expression of the matrix metalloproteinase MMP9 and the tachykinin precursor TAC1 genes were revealed in skin biopsy samples of the superficial form of basal cell skin cancer during laser pulsed therapy. The expression of tumor necrosis factor TNF, epidermal growth factor receptor EGFR, fibroblast growth factor FGF2 genes increases to a lesser extent. The increasing expression of MMP9 and TAC1 genes also established in skin biopsy samples of the nodular form of basal cell skin cancer. It was shown that the expression of the calcitonin-related polypeptide alpha CALCA gene in the skin of patients is at basal level, which makes it possible to exclude the influence of the neuropeptide on the basal cell skin cancer pathogenesis. Despite the bidirectional changes in expression due to individuality of patients, the average values allow to conclude the expression of all the studied genes is increased after pulse laser destruction therapy. This means neoangiogenesis is continued at the skin even after the destruction of basal cell skin cancer lesions. This could be due to the presence of the basal cell carcinoma microenvironment, likely mast cells, at the affected skin area. Conclusions. Among the factors of neoangiogenesis potentially influencing the development of basal cell skin cancer, the leading role of expression of the MMP9 matrix metalloproteinase and TAC1 precursor protein of tachykinin has been shown. Simultaneous changes in the level of these proteins may be due to neuroimmune interactions in the epidermis, which is probably realized by mast cells as the microenvironment of the basal cell carcinoma. In the process of laser destruction, there is also a slightly pronounced increased expression of additional factors of neoangiogenesis.

Introduction. The role of the cytokine environment and immune deregulation in the pathogenesis of mycosis fungoides is unquestionable. Despite the fact that one of the methods of therapy for the early stages of mycosis fungoides is phototherapy (PUVA, UVB-311 nm), the effect of ultraviolet radiation on the lymphoproliferative substrate and pathogenetic links in mycosis fungoides has not been fully studied. Aim: to evaluate the effect of NB-UVB and PUVA therapy on the dynamics of cytokine mRNA expression in the affected skin of patients with mycosis fungoides. Material and Methods. A comparative non-randomized study of the cytokine mRNA expression dynamics in the affected skin and of the effectiveness of phototherapy was carried out in 28 patients with early stage of mycosis fungoides. The IL4, IL17A, IL17F, and IL22 mRNA expression was determined relative to the endogenous control GAPDH using the real-time reverse transcription PCR (RT-PCR). Evaluation of the effectiveness of NB-UVB and PUVA therapy was carried out using a BSA score (skin lesion area) and a modified severity-weighted assessment tool (mSWAT) score. Results. The study included 28 patients with early stages (IA–IIA) of mycosis fungoides; 9 patients received NB-UVB and 19 received PUVA therapy. 3.71-fold decrease in mSWAT (p < 0.008), and 3-fold decrease in BSA scores (p < 0.013) were observed in the NB-UVB-treated group. In the PUVA-treated group 3.47- and 2.19-fold lower scores of mSWAT (p < 0.001) and BSA (p < 0.001) were found. There were no significant differences in the expression of the studied cytokines in the NB-UVB-treated group; however, a significant 19 and 72 % increase in IL17F (p = 0.003) and IL22 (p = 0.021) was revealed afterPUVA therapy. Correlation analysis has shown a weak correlation between IL4 and IL17A (r = 0.43, p < 0.027), and IL17F (r = 0.43, p < 0.028) before the treatment. Under the influence of phototherapy, the formation of a cytokine network in the affected skin was observed: there were positive associations between IL4 and IL17A (r = 0.73, p < 0.001), IL17F (r = 0.7, p < 0.001) and IL22 (r = 0.43, p < 0.024); IL17A and IL17F (r = 0.78, p < 0.001); IL22 and IL17A (r = 0.63, p < 0.001) and IL17F (r = 0.66, p < 0.001). In the PUVA-treated group a high negative correlation between IL17A and mSWAT (r = -0.79415, p =0.010586), BSA (r = -0.75432, p = 0.018849) were found. Conclusion: The positive correlations between IL4, IL17A, IL17F and IL22 in the affected skin of patients with mycosis fungoides may underlie the positive effect of phototherapy.

Two patients with lepromatous leprosy relapse cases were analyzed. Despite WHO combined drug therapy treatment after the period of remission the disease comes back, with deterioration in the condition of patients. PCR analysis revealed Mycobacterium leprae DNA in skin biopsies of the patients both before and after therapy. The taxonomic identification confirmed Mycobacterium leprae by 16S rRNA sequencing. The study of drug resistance determining region at folp1, rpoB, gyrA genes was carried out before and after the therapy, resulting the absence of mutations leading to the development of drug resistance in Mycobacterium leprae. To select the strategy of leprosy alternative chemotherapy a number of approaches used in cases of relapsing course of the disease are considered. Key words: leprosy, Mycobacterium leprae, relapse cases, genetic determinants, antimicrobial resistance, non effective chemotherapy

Diffuse cutaneous leishmaniasis is a rare form of cutaneous leishmaniasis characterized by an inadequate immune response of the host cells to parasitic invasion (weak T-helper (Th)1 response or Th2 response with the production of interleukin IL-4 and IL-10). The characteristic features of the disease include diffuse nodular eruption, masquerading as leprosy and a frequent association with immunosuppression (HIV co-infection, for example). The Russian Federation is a non-endemic country for leishmaniasis, but this disease can be brought into the country by tourists, immigrants, refugees and military personnel. A clinical case of diffuse cutaneous leishmaniasis and HIV co-infection is presented. The patient was a citizen of Uzbekistan, a country endemic for leishmaniasis. The authors were unable to find domestic scientific publications describing cases of diffuse cutaneous leishmaniasis detected in the Russian Federation. The presented clinical case of diffuse cutaneous leishmaniasis in a patient with HIV is the first in the Russian literature.

We analyzed the sequence of the gene encoding 16S ribosomal RNA in 2 samples containing a mixture of human DNA and Mycobacterium leprae DNA obtained from two patients from the Russian Federation. We found that our sequence matched the sequence of the reference strain deposited at the National Center for Biotechnology Information (NCBI, USA). The analysis was performed using Sanger sequencing with a mixture of microbial and human DNA isolated from skin biopsy specimens. We assume that the difficulties associated with sequencing of the full-size rrs gene can be addressed by using a speciesspecific sequence of the rrs promoter region to identify M. leprae. Key words: leprosy, Mycobacterium leprae, rrs, 16S rRNA

BACKGROUND:Mycosis fungoides (MF) is the most common subtype of cutaneous T-cell lymphoma. The aim of the present study was to produce up-to-date information on different phototherapy approaches on skin cytokines in patients with MF.METHODS:A total of 27 patients with mycosis fungoides were treated with phototherapy: NB-UVB (narrow-band ultraviolet B therapy) (10 patients) and PUVA (long-wavelength ultraviolet radiation of spectrum A with the use of skin-photosensitizing furocoumarins) therapy (17 patients). Evaluation of the effectiveness of treatment was carried out using BSA (body surface area) and the modified assessment of the severity of the skin lesions scale (mSWAT) used to quantify tumor mass in cutaneous T-cell lymphomas. Average numbers of procedures were 30.2 and 27.8 in the NB-UVB and PUVA groups, respectively. The median total dose of NB-UVB irradiation was 19.9 J/cm2 and PUVA therapy was 104.0 J/cm2. The overall response to therapy including complete and partial remission was 74.9% in the total group; 70% in the NB-UVB group, and 77.7% in the PUVA therapy group. In the obtained biopsies from lesions, surrounding tissue before treatment and skin samples of four healthy volunteers, the concentration of the IL-1β, IL-4, IL-6, IL-10, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, IFN-γ, sCD40L, and TNF-α cytokines was studied. An increase in IL-4 and TNF-α levels was shown in the lesional skin of patients compared to the skin of healthy controls. After the treatment, positive correlations of mSWAT with the levels of IL22, IL33, and TNF-α in the tumor tissue were found. The levels of IL10 and IFN-γ after PUVA treatment were increased in comparison to baseline. There was no difference in cytokine levels before/after NB-UVB therapy.

Psoriatic arthritis often develops in patients with psoriasis and can lead to joint deformity, stiffness, dysfunction, and disability. Psoriatic arthritis is a polygenic disease. and the issue of personalizing the prognosis of its development can only be resolved taking into account the variability of plenty genomic loci associated with the development of the disease. The personification of the prognosis of the disease can be solved taking into account the variability of the set of genomic loci with which its development is associated. The review examines genomic polymorphisms associated with the development of psoriatic arthritis not psoriasis, except of HLA polymorphisms. Genome regions containing polymorphisms, allelic variants of which are associated both with the development of psoriatic arthritis and reducing the likelihood of its occurrence, are described. It has been reported that the predisposition to the development of psoriatic arthritis in patients with psoriasis is determined by genes encoding proteins involved in inflammation and bone metabolism.

The review is devoted to the appearance of resistance of a slowly developing disease leprosy to antimicrobial therapy (AMP), primarily recommended by the World Health Organization. The main danger of drug resistant leprosy is in the difficulty of identifying, since the causative agent of the disease is not cultivated on artificial media, and the methods for diagnosing drug resistance that are currently used take a long time. The drug resistance of the Mycobacterium leprae strain even to individual components of combination drug therapy result to the development of symptoms of the disease despite undergo anti-leprosy therapy, which in turn can cause the patient to become disabled. Currently, in the Russian Federation, there is no approved test for detecting Mycobacterium leprae DNA, and the determination of genetic determinants of resistance is carried out by sequencing genome regions determined by WHO recommendations: small gyrA, folP and rpoB genes loci. At the same time, modern studies in endemic regions reveal an increased level of Mycobacterium leprae strains resistant to individual components of combined drug therapy. The use of next generation sequencing (NGS) has made it possible to identify additional genetic determinants of leprosy resistance to the components of combination drug therapy. The current situation is relevant to antimicrobal drug resistance surveillance by using of quick identification systems for most frequent genetic resistance determinants of Mycobacterium leprae. The literature search was carried out using keywords in the Scopus, PubMed and RSCI databases.

In patients with moderate-to-severe and severe psoriasis and high efficacy of therapy (PASI≥75) with signaling pathway inhibitors (apremilast, tofacitinib), cytokine spectra in the skin and blood plasma were studied using xMAP technology at baseline and on weeks 14 and 26 of treatment. Comparison of cytokine levels in psoriatic lesional skin and plasma samples of patients treated with apremilast or tofacitinib revealed statistical difference only for IFNγ level (р<0.05) at week 26.

One of the target drugs for plaque psoriasis treatment is apremilast, which is a selective phosphodiesterase 4 (PDE4) inhibitor. In this study, 34 moderate-to-severe and severe plaque psoriasis patients from Russia were treated with apremilast for 26 weeks. This allowed us to observe the effectiveness of splitting patient cohorts based on clinical outcomes, which were assessed using the Psoriasis Area Severity Index (PASI). In total, 14 patients (41%) indicated having an advanced outcome with delta PASI 75 after treatment; 20 patients indicated having moderate or no effects. Genome variability was investigated using the Illumina Infinium Global Screening Array. Genome-wide analysis revealed apremilast therapy clinical outcome associations at three compact genome regions with undefined functions situated on chromosomes 2, 4, and 5, as well as on a single single-nucleotide polymorphism (SNP) on chromosome 23. Pre-selected SNP sets were associated with psoriasis vulgaris analysis, which was used to identify four SNP-associated targeted therapy efficiencies: IL1β (rs1143633), IL4 (IL13) (rs20541), IL23R (rs2201841), and TNFα (rs1800629) genes. Moreover, we showed that the use of the global polygenic risk score allowed for the prediction of onset psoriasis in Russians. Therefore, these results can serve as a starting point for creating a predictive model of apremilast therapy response in the targeted therapy of patients with psoriasis vulgaris.