Single-Dose Prevention or Short-Term Treatment with Fibroblast Growth Factor-20 (CG53135-05) Reduces the Severity and Duration of Oral Mucositis

AbstractFibroblast growth factor-21 (FGF21) is elevated in patients with the metabolic syndrome. Although the exact underlying mechanisms remain ill-defined, chronic low-grade inflammation with increased Interleukin-(IL)-1β expression may be responsible. The aim of this study was to investigate effects of two different anti-inflammatory treatments (IL-1 antagonism or high-dose corticosteroids) on FGF21 in patients with the metabolic syndrome. This is a secondary analysis of two interventional studies in patients with obesity and features of the metabolic syndrome. Trial A was an interventional trial (n = 73) investigating short-term effects of the IL-1 antagonist anakinra and of dexamethasone. Trial B was a randomized, placebo-controlled, double-blinded trial (n = 67) investigating longer-term effects of IL-1 antagonism. In total, 140 patients were included in both trials. Median age was 55 years (IQR 44–66), 26% were female and median BMI was 37 kg/m2 (IQR 34–39). Almost half of the patients were diabetic (45%) and had increased c-reactive protein levels of 3.4 mg/L. FGF21 levels correlated with fasting glucose levels, HOMA-index, C-peptide levels, HbA1c and BMI. Short-term treatment with anakinra led to a reduction of FGF21 levels by − 200 pg/mL (95%CI − 334 to − 66; p = 0.004). No effect was detectable after longer-term treatment (between-group difference: − 8.8 pg/mL (95%CI − 130.9 to 113.3; p = 0.89). Acute treatment with dexamethasone was associated with reductions of FGF21 by -175 pg/mL (95%CI − 236 to − 113; p < 0.001). Anti-inflammatory treatment with both, IL-1 antagonism and corticosteroids reduced FGF21 levels at short-term in individuals with the metabolic syndrome.Trial registration: ClinicalTrials.gov Identifiers NCT02672592 and NCT00757276.

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Fibroblast growth factor 20 (FGF20) gene polymorphism and risk of Parkinson’s disease: a meta-analysis

Neurological Sciences ◽

10.1007/s10072-014-1853-y ◽

2014 ◽

Vol 35 (12) ◽

pp. 1889-1894 ◽

Cited By ~ 11

Author(s):

Ruixia Zhu ◽

Ying Zhu ◽

Xu Liu ◽

Zhiyi He

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Growth Factor ◽

Gene Polymorphism ◽

Fibroblast Growth Factor ◽

Meta Analysis ◽

Fibroblast Growth ◽

Factor 20

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An Engineered Human Fibroblast Growth Factor-1 Derivative, TTHX1114, Ameliorates Short-term Corneal Nitrogen Mustard Injury in Rabbit Organ Cultures

Investigative Opthalmology & Visual Science ◽

10.1167/iovs.18-24568 ◽

2018 ◽

Vol 59 (11) ◽

pp. 4720 ◽

Cited By ~ 3

Author(s):

David D. Eveleth ◽

Jennifer J. Eveleth ◽

Amuthakannan Subramaniam ◽

Rita Hahn ◽

Peihong Zhou ◽

...

Keyword(s):

Growth Factor ◽

Fibroblast Growth Factor ◽

Human Fibroblast ◽

Nitrogen Mustard ◽

Fibroblast Growth ◽

Organ Cultures ◽

Short Term

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Short-term effects of sevelamer-carbonate on fibroblast growth factor 23 and pulse wave velocity in patients with normophosphataemic chronic kidney disease Stage 3

Clinical Kidney Journal ◽

10.1093/ckj/sfz027 ◽

2019 ◽

Vol 12 (5) ◽

pp. 678-685 ◽

Cited By ~ 5

Author(s):

Annet Bouma-de Krijger ◽

Frans J van Ittersum ◽

Tiny Hoekstra ◽

Pieter M ter Wee ◽

Marc G Vervloet

Keyword(s):

Chronic Kidney Disease ◽

Growth Factor ◽

Kidney Disease ◽

Pulse Wave Velocity ◽

Fibroblast Growth Factor ◽

Pulse Wave ◽

Fibroblast Growth Factor 23 ◽

Fibroblast Growth ◽

Short Term ◽

Sevelamer Carbonate

Abstract Background High concentrations of both phosphate and fibroblast growth factor 23 (FGF23) observed in chronic kidney disease (CKD) are associated with an increased risk of cardiovascular morbidity and mortality. Pulse wave velocity (PWV) is a surrogate marker for cardiovascular events and all-cause mortality. It is not known whether a reduction of FGF23 or phosphate alters cardiovascular risk. Sevelamer has shown to have the ability to reduce both phosphate and FGF23 concentrations. Furthermore, reduction of PWV is reported with sevelamer use as well, but it is unclear if this is mediated by decline of phosphate or FGF23. We investigated if sevelamer induced a decline in PWV and if this was associated with a reduction in FGF23. Methods In all, 24 normophosphataemic CKD Stage 3 patients started treatment with a fixed dose of sevelamer-carbonate (Renvela®) 2.4 g twice daily, with their usual diet for 8 weeks in a single-arm study. PWV was measured and blood samples were obtained before, during and after washout of treatment with sevelamer. Vascular calcification was quantified using the Kauppila Index (KI). The primary outcome was the change of PWV from baseline to 8 weeks of treatment and the secondary endpoint was the difference of FGF23 following treatment with sevelamer. One of the linear mixed models was used to analyse the association between treatment and outcome. Mediation analysis was performed as a sensitivity analysis. The study was registered in the Dutch trial register (http://www.trialregister.nl: NTR2383). Results A total of 18 patients completed 8 weeks of treatment with sevelamer and were analysed. Overall, treatment with sevelamer did not induce a significant reduction of PWV (β = −0.36, P = 0.12). However, in patients with less vascular calcification (lower KI score), there was a statistically significant reduction of PWV, adjusted for mean arterial pressure, after treatment (β = 0.63, P = 0.02). Addition of FGF23 to the model did not alter this association. Mediation analysis yielded similar results. FGF23 did not decrease during treatment with sevelamer. Conclusion In this short-term pilot study in normophosphataemic CKD patients, treatment with sevelamer did not improve PWV. In subgroup analysis, however, PWV improved in patients with no or limited abdominal aorta calcifications. This was not associated with a decline of FGF23.

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Effect of Basic Fibroblast Growth Factor on Perforated Chinchilla Tympanic Membranes

Ear Nose & Throat Journal ◽

10.1177/014556139707600812 ◽

1997 ◽

Vol 76 (8) ◽

pp. 559-564 ◽

Cited By ~ 11

Author(s):

Norman R. Friedman ◽

Charles G. Wright ◽

Karen S. Pawlowski ◽

William L. Meyerhoff

Keyword(s):

Growth Factor ◽

Connective Tissue ◽

Tympanic Membrane ◽

Fibroblast Growth Factor ◽

Basic Fibroblast Growth Factor ◽

Healing Process ◽

Fibroblast Growth ◽

Short Term ◽

Tympanic Membrane Perforations ◽

Perforated Tympanic Membrane

Basic fibroblast growth factor (bFGF) is a polypeptide mitogen which stimulates proliferation of epidermal and connective tissue cells. When applied to tympanic membrane perforations it has been reported to enhance healing and produce connective tissue hyperplasia. Previous work with animal models has shown that hyperplastic alterations of the tympanic membrane play an essential role in cholesteatoma development. This study was designed to further investigate the hyperplastic effects of bFGF and to determine if it might induce cholesteatoma formation during the healing process. Ten chinchillas received bilateral tympanic membrane perforations. In each animal, three doses of bFGF (400 nanograms per dose) were applied to the perforated tympanic membrane on one side; the opposite (control) ear received saline alone. The animals were terminated at either two or four weeks and studied histologically. Although the dosage and administration schedule used were consistent with previous studies utilizing other rodent species, there was little evidence that bFGF affected tympanic membrane healing in chinchillas. In both control and bFGF-treated ears, dense connective tissue occupied the lamina propria of the tympanic membrane, providing an effective barrier against ingrowth of skin toward the middle ear. No cholesteatomas developed in any animals included in the study. The results of this work indicate that the risk of cholesteatoma formation following administration of bFGF is minimal when it is applied short-term to acute perforations.

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