1.Influence of long-term biologic therapy on metabolic biochemical parameters in moderate to severe plaque psoriasis.
Xiangxian LIU ; Yi LIN ; Jinzhu GUO
Journal of Peking University(Health Sciences) 2025;57(5):934-940
OBJECTIVE:
To assess the impact of long-term biologic therapy on metabolic biochemical parameters in moderate to severe plaque psoriasis patients.
METHODS:
The study included patients over 18 years old who had been treated by biological agents for at least 24 weeks for moderate to severe plaque psoriasis from Novermber 2015 to January 2024. According to the biological agents the patients used, they were divided into three groups: interleukin-17 (IL-17) inhibitor group, IL-23 and IL-12/23 inhibitor group and tumor necrosis factor-α (TNF-α) inhibitor group. The metabolic biochemical parameters of each group were evaluated and compared before and after the administration of the biologic therapies.
RESULTS:
A total of 174 patients with moderate to severe plaque psoriasis were included in the long-term treatment with biologics, including 127 males (73.00%), 47 females (27.00%), with a median age of 38.00 (31.50, 49.00) years and a median duration of psoriasis of 12.00 (10.00, 20.00) years. The median duration of biologic treatment was 61.00 (49.00, 96.25) weeks, ranging from 26 to 301 weeks. There were 101 patients in the IL-17 inhibitor group, 38 patients in the IL-23 and IL-12/23 inhibitor group, and 35 patients in the TNF-α inhibitor group. After long-term treatment with IL-17 inhibitors, no statistically significant changes were observed in body weight, body mass index (BMI), alanine aminotransferase (ALT), aspartate aminotransferase (AST), fasting glucose (GLU), total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C) compared with baseline measurements (P>0.05). However, low-density lipoprotein cholesterol (LDL-C) levels were significantly reduced [(2.90±0.75) mmol/L vs. (3.05±0.79) mmol/L, t=-2.100, P=0.038], while uric acid (UA) levels showed a significant increase [(401.13±99.13) μmol/L vs. (364.94±91.11) μmol/L, t=5.215, P < 0.001]. The group with normal UA levels before treatment showed a significant increase after long-term application of biological agents compared with before treatment [(370.69± 89.59) μmol/L vs. (324.66±64.50) μmol/L, t=5.856, P < 0.001]. Following long-term application of IL-23 and IL-12/23 inhibitors, no statistically significant differences were observed in body weight, BMI, ALT, AST, GLU, TC, TG, HDL-C and UA levels when compared with baseline measurements (P> 0.05). However, LDL-C levels exhibited a significant reduction from baseline [(2.85±0.74) mmol/L vs. (3.12±0.68) mmol/L, t=-2.082, P=0.045]. After long-term treatment with TNF-α inhibitor, there were no significant differences in body weight, BMI, ALT, AST, GLU, TC, TG, HDL-C, LDL-C and UA compared with baseline measurements (P>0.05).
CONCLUSION
Long-term application of IL-17 inhibitors in moderate to severe plaque psoriasis patients may result in elevated uric acid levels, particularly in patients with normal uric acid levels before treatment. The long-term use of IL-17 inhibitors, IL-23 inhibitors or IL-12/23 inhibitors might reduce LDL-C levels.
Humans
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Psoriasis/blood*
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Male
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Female
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Adult
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Middle Aged
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Interleukin-17/antagonists & inhibitors*
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Interleukin-23/antagonists & inhibitors*
;
Tumor Necrosis Factor-alpha/antagonists & inhibitors*
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Interleukin-12/antagonists & inhibitors*
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Biological Therapy
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Biological Products/therapeutic use*
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Triglycerides/blood*
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Cholesterol, LDL/blood*
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Cholesterol, HDL/blood*
2.The immune-stimulating peptide WKYMVm has therapeutic effects against ulcerative colitis.
Sang Doo KIM ; Soonil KWON ; Sung Kyun LEE ; Minsoo KOOK ; Ha Young LEE ; Ki Duk SONG ; Hak Kyo LEE ; Suk Hwan BAEK ; Chan Bae PARK ; Yoe Sik BAE
Experimental & Molecular Medicine 2013;45(9):e40-
In this study, we examined the therapeutic effects of an immune-stimulating peptide, WKYMVm, in ulcerative colitis. The administration of WKYMVm to dextran sodium sulfate (DSS)-treated mice reversed decreases in body weight, bleeding score and stool score in addition to reversing DSS-induced mucosa destruction and shortened colon. The WKYMVm-induced therapeutic effect against ulcerative colitis was strongly inhibited by a formyl peptide receptor (FPR) 2 antagonist, WRWWWW, indicating the crucial role of FPR2 in this effect. Mechanistically, WKYMVm effectively decreases intestinal permeability by stimulating colon epithelial cell proliferation. WKYMVm also strongly decreases interleukin-23 and transforming growth factor-beta production in the colon of DSS-treated mice. We suggest that the potent immune-modulating peptide WKYMVm and its receptor FPR2 may be useful in the development of efficient therapeutic agents against chronic intestinal inflammatory diseases.
Adjuvants, Immunologic/pharmacology/*therapeutic use
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Animals
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Caco-2 Cells
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Cell Proliferation
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Colitis, Ulcerative/*drug therapy/metabolism
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Colon/pathology
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Humans
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Interleukin-23/genetics/metabolism
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Intestinal Mucosa/drug effects/metabolism/pathology
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Mice
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Mice, Inbred C57BL
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Oligopeptides/pharmacology/*therapeutic use
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Permeability
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Receptors, Formyl Peptide/antagonists & inhibitors
;
Transforming Growth Factor beta/genetics/metabolism
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