SFE2003 Poster Presentations Cytokines (6 abstracts)
1Rheumatology, Ysbyty Gwynedd, Bangor, Gwynedd; 2Clinical Chemistry, Ysbyty Gwynedd, Bangor, Gwynedd; 3Endocrinology, Ysbyty Gwynedd, Bangor, Gwynedd; 4School of Sports, Health and Exercise Sciences, University of Wales, Bangor, Gwynedd.
Background: We have previously shown that systemic levels of the growth hormone (GH) dependent proteins IGF-I and IGFBP-3 are significantly lower in rheumatoid arthritis (RA) patients than in age and sex matched healthy controls.
Aim: To investigate whether low levels of systemic IGF-I and IGFBP-3 levels in RA patients are due to GH deficiency or GH insensitivity.
Methods: Eight RA patients (6 females, mean plus/minus SD, age 52.5 plus/minus 8.4 years) known to have severe IGF-I and/or IGFBP-3 deficiency (serum levels less than 2 SD of mean of controls) were evaluated for GH reserve by insulin tolerance test. In a further group of 30 unselected RA patients (22 females, mean age 52 years) and 30 age and sex matched healthy controls, serum concentration of growth hormone binding protein (GHBP), a peripheral marker of GH receptor number, was measured. All patients were stable on disease-modifying antirheumatic drugs and/or low dose prednisolone.
Results: In all 8 ITT patients plasma glucose fell below 2 mili moles per litre within the first 30 minutes coincidental with development of clinical hypoglycaemia. The mean plus/minus SD serum GH peak response was 19.95 plus/minus 9.10 mili units per litre and in 5 patients the peak was less than 20 mili units per litre. In the larger group of RA patients, circulating GHBP was 35% lower than in healthy controls (mean plus/minus SD: 1035 plus/minus 627 versus 1585 plus/minus 807 pico moles per litre; P<0.01).
Conclusion: These results suggest that low systemic levels of IGF-I and IGFBP-3 in RA reflect combined partial GH deficiency and target tissue insensitivity probably secondary to decreased GH receptor numbers.