Archives of medical research · 1998
Epidermal growth factor and gastrin in scleroderma/CREST syndrome.
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Jiménez-Balderas F, Zonana-Nacach A, Fonseca-Yerena M E, Ruíz-Chaparro A, Pascoe-Lira D
Аннотация
BACKGROUND: The objective of this study was to determine levels of epidermal growth factor (EGF) and gastrin (GA) in saliva, serum, and urine in scleroderma (Scl) and CREST syndrome.
METHODS: EGF and GA levels were measured by radioimmunoassay in saliva, serum and urine in 10 patients (51 years, median; range, 35-66 years); 9 females and 1 male with Scl, 3 females with CREST syndrome, and 18 age- and sex-matched controls, 17 females and 1 male free of any systemic inflammatory disease.
RESULTS: In serum, the EGF was lower in Scl/CREST than controls (p = 0.02), while GA serum concentrations were higher in Scl/CREST (p = 0.02). In urine, EGF in Scl/CREST was slightly lower than controls (p = NS) and GA concentrations were higher than controls (p = 0.03). In saliva, the EGF levels in Scl/CREST were also slightly lower than controls (p = NS), while GA concentrations in both Scl/CREST and controls were not different (p = NS).
CONCLUSIONS: Low concentrations of EGF in serum probably play a role in the pathogenesis of Scl/CREST. GA concentration can be increased as a consequence of the low levels of EGF because of the structural homology of this peptide with urogastrone, a GA inhibitor factor.
METHODS: EGF and GA levels were measured by radioimmunoassay in saliva, serum and urine in 10 patients (51 years, median; range, 35-66 years); 9 females and 1 male with Scl, 3 females with CREST syndrome, and 18 age- and sex-matched controls, 17 females and 1 male free of any systemic inflammatory disease.
RESULTS: In serum, the EGF was lower in Scl/CREST than controls (p = 0.02), while GA serum concentrations were higher in Scl/CREST (p = 0.02). In urine, EGF in Scl/CREST was slightly lower than controls (p = NS) and GA concentrations were higher than controls (p = 0.03). In saliva, the EGF levels in Scl/CREST were also slightly lower than controls (p = NS), while GA concentrations in both Scl/CREST and controls were not different (p = NS).
CONCLUSIONS: Low concentrations of EGF in serum probably play a role in the pathogenesis of Scl/CREST. GA concentration can be increased as a consequence of the low levels of EGF because of the structural homology of this peptide with urogastrone, a GA inhibitor factor.