Serotonin has recently been identified as a major regulator of bone formation. Gut-derived serotonin inhibits bone formation, and early animal studies have shown that inhibition of gut-derived serotonin has anabolic effects on bone in ovariectomised rodents. This pathway has potential to be developed as a new anabolic treatment for osteoporosis in humans. Carcinoid neuro-endocrine tumours produce very high levels of serotonin, and so it might be expected that patients with carcinoid disease would have reduced bone formation, low bone mass and fractures. However, this has not been apparent in clinical practice. There may be a discrepancy between rodent models and human disease. This study aims to identify whether patients with carcinoid disease have reduced bone mass, reduced bone formation or high fracture rates. The investigators will conduct a cross-sectional observational case-control study of patients with carcinoid disease in the Sheffield neuro-endocrine tumour clinic and gender-, age- and body mass index (BMI)-matched controls.
Study Type
OBSERVATIONAL
Enrollment
52
Academic Unit of Bone Metabolism (Sheffield)
Sheffield, South Yorks, United Kingdom
Lumbar spine and total hip Bone Mineral Density BMD) measured by Dual-emission X-ray absorptiometry (DXA)
Self-reported fracture history
Vertebral fracture assessment
Radius and tibia geometry and microarchitecture by HR-pQCT
Serum osteocalcin
Blood serotonin and 5HIAA
24h urine 5HIAA
Time frame: 24 hours
Serum type 1 procollagen (N-terminal)(PINP)
Bone Alkaline Phosphatase (BAP)
Carboxy-terminal collagen crosslinks (CTX)
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