Epidermal growth factor and gastrin in scleroderma/CREST syndrome.

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.

[The role of insulin-like growth factor in polycystic ovary syndrome]. / Participación del factor de crecimiento insulinoide (IGF), en el síndrome de ovario poliquístico (SOP).

The partnership the insulin-like growth factor (IGF) in women with polycystic ovary syndrome (PCOS) is characterized by mechanisms underlying alterations in the GH/IGF-1, axis. In the pathogenesis exist a synergism markedly enhanced between IGF-1 and insulin, and IGF-1 with LH to increase androgen production, causing a reduced IGFBPs and SHBG production, the resulting hyperandrogenism, within and outside the ovary, may inhibitor follicular maturation and the biosynthesis of estrogen. At the present, the data suggests up to date paracrine, autocrine as well as endocrine actions in the ovary in normal conditions and the lost of this homeostasis can be followed by neuro-endocrine.