Effectiveness of infliximab biosimilars in the treatment of moderate to severe chronic plaque psoriasis: experience of real-world data from the register of the program "Treatment of moderate and severe forms of plaque psoriasis (B.47)" of the National Health Fund in Poland.

Introduction: Infliximab (IFX) is a monoclonal antibody that binds to and neutralizes TNF-α. IFX (Remicade) was approved by the U.S. Food and Drug Administration in 2006 for the treatment of severe plaque psoriasis. In 2013 two infliximab biosimilars: Remsima and Inflectra were also registered. The introduction of biosimilar drugs is associated with a significant reduction in treatment costs. Aim: To evaluate the efficacy of treatment with biosimilar IFX with non-medical switch option in patients with plaque psoriasis under the drug program "Treatment of moderate and severe plaque psoriasis" of the Ministry of Health in Poland. Material and methods: The group of 91 adult patients with moderate to severe plaque psoriasis, unresponsive or with contraindications to the standard treatment were qualified to the drug program (in 2016-2018). Efficacy of treatment with biosimilar IFX was evaluated using the Psoriasis Area and Severity Index, body surface area and Dermatology Life Quality Index scoring performed at week 0, 14, 46 and 94. Results: The mean change in PASI, DLQI, and BSA scores at week 14 was 89.92%, 93.75% and 90.91%, respectively. By week 14, 83.52% of patients achieved PASI75, 49.45% PASI ≥ 90 and 26.37% PASI100. At week 46, 84.62% of patients achieved PASI75, 54.95% PASI ≥ 90, and 21.98% PASI100. At week 94 of therapy, 80.22% of patients achieved PASI75, 48.35% PASI ≥ 90, and 18.68% PASI100. At week 94 of therapy, PASI100 was maintained by 37.5% of patients who achieved PASI100 at week 14. Conclusions: 94-week therapy with biosimilar infliximab results in high and sustained clinical efficacy in patients with moderate to severe psoriasis.

Comparative effectiveness of adalimumab versus ustekinumab in the treatment of severe chronic plaque psoriasis: The results based on data from the program "treatment of moderate and severe forms of plaque psoriasis (B.47)" of the National Health Fund in Poland.

Biological agents: TNF-α inhibitors, IL-12, and IL-23 blockers, IL-17 inhibitors are used in the treatment of plaque psoriasis. Adalimumab (ADA) is an antibody that binds to TNF-α. Ustekinumab (UST) blocks IL-12 and IL-23. The data obtained from medical records is of exceptional value. The aim of the study was to evaluate the efficacy of ADA and UST during a single 40-week period of biological treatment of patients under the drug program "Treatment of moderate and severe form of plaque psoriasis." The group of 620 adult patients with moderate to severe form of plaque psoriasis, who were unresponsive or had contraindications to the standard treatment were qualified to the drug program. In the evaluated group, 50.64% patients were treated with UST, 49.36% with ADA. The efficacy of treatment was assessed during weeks 0, 4, 16, 28, and 40. At week 16th, PASI75 reached 80.72% patients in ADA treated group, PASI ≥90 54.88%, PASI100 19.6% of patients. In the UST group (week 16th) PASI75 reached 70.38%, PASI90 44.26%, PASI100 15.6% of patients. At week 28th PASI90 and PASI100 were more pronounced in the ADA group than in UST. In addition, the total percentage of PASI improvement was significantly higher in the ADA group (p = 0.0006). The percentage of PASI improvement in week 40 was statistically higher in ADA group compared to UST (p = 0.015). Compared to UST, ADA was clinically more effective during a 40-week observation. Patients receiving ADA achieved PASI75, PASI90, and PASI100 more frequently and faster than those treated with UST. Additionally, ADA improved the quality of life of psoriatic patients more substantially compared to UST.

Pulmonary blastoma in a pregnant woman: a case report and brief review of the literature.

BACKGROUND: Pulmonary blastoma (PB) comprises a rare heterogeneous group of lung tumours typically containing immature epithelial and mesenchymal structures that imitate the embryonic lung tissue and extremely rarely occurs during pregnancy. Although cough and haemoptysis are the most common PB symptoms, they usually indicate other serious pregnancy-related complications. CASE PRESENTATION: The article presents the unusual case of a 22-year-old pregnant woman diagnosed with PB during pregnancy. CONCLUSIONS: PB is characterized by poor prognosis and patients' outcome relies on a rapid diagnosis. Surgery remains the most common and effective treatment. Due to the extreme rarity, the literature contains only single mentions of PB in pregnancy, thus its impact on the course of pregnancy and the developing fetus remains unknown.

Human leptin stimulates systemic nitric oxide production in the rat.

OBJECTIVE: Apart from having an effect on energy balance, leptin is also involved in cardiovascular regulation and in the pathogenesis of obesity-associated hypertension. We investigated the effect of leptin on nitric oxide (NO) production. RESEARCH METHODS AND PROCEDURES: Wistar rats were placed in metabolic cages, and urine was collected in 2-hour periods. After the control period, leptin (1 mg/kg intraperitoneal) was administered, and urine collection was continued for up to 6 hours. Blood was obtained 0.5, 1, 2, 4, and 6 hours after hormone injection. RESULTS: Leptin increased plasma concentrations of NO metabolites (nitrates + nitrites, NO(x)) by 32.5%, 58.0%, and 29.7% at 1, 2, and 4 hours, respectively. Urinary NO(x) excretion increased by 28.8% in the first and by 20.1% in the second 2-hour period after injection. The plasma concentration of the NO second messenger, cyclic guanosine 3',5'-monophosphate (cGMP), increased by 83% and 50.6% at 2 and 4 hours after leptin administration, respectively. Urinary excretion of cyclic GMP increased by 36.1% in the first and by 43.1% in the second 2-hour period. Leptin had no effect on the plasma concentration of atrial natriuretic peptide (ANP). The effect of leptin on plasma and urinary NO(x) was abolished by the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) (30 mg/kg intraperitoneal) administered 15 minutes before leptin injection. L-NAME alone caused a 32.2% increase in systolic blood pressure, but this increase was not observed in rats receiving L-NAME and leptin. DISCUSSION: The results indicate that leptin stimulates systemic NO production; leptin prevents blood pressure elevation induced by acute NO blockade, suggesting that leptin also triggers additional hypotensive mechanisms; and ANP is not involved in renal and vascular effects of leptin.