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Table 1 Changes in serum sclerostin levels in various physiologic and pathological conditions

From: Role of sclerostin in the pathogenesis of chronic kidney disease-mineral bone disorder

Condition Directional change Comments
Physiologic states   
 Age: adults and elderly Increase with age Serum sclerostin levels increase with age, but bone marrow sclerostin mRNA is not increased in older patients.
 Gender Higher in men Likely due to higher bone mass (osteocyte number); lower in premenopausal women because of estrogen effect.
 Menopause Higher after menopause Lack of inhibitory effect of estrogen or decreased bone formation leading to low osteocyte number.
 Malnutrition Blunts sclerostin changes In patients with anorexia nervosa, sclerostin does not decrease with estrogen therapy.
Hormones   
 Parathyroid hormone Decrease Direct effect on osteoblast, osteocyte number, and on Wnt signaling.
 Vitamin D Increase Limited data; one study each in normal and dialysis patients; confounding by PTH is likely.
 Estrogen Decrease Direct effect of estrogen and possibly SERMs on osteoblast/osteocyte number and function.
 Androgen Data unclear Increased in prostate cancer patients and during androgen deprivation therapy.
 Leptin Increased Sclerostin levels were higher in obese patient and correlated with leptin and PTH levels.
 Growth hormone/IGF Data unclear IGF is obligatory to the anabolic action of PTH; may be for osteocyte function and sclerostin as well.
Pathologic conditions   
 Bone and mineral disorders   
  Hyperparathyroidism (Primary) Decrease Lower levels compared with controls in untreated patients and normalize after parathyroidectomy.
  Paget’s disease of bone Increased Sclerostin did not correlate with P1NP or CTX.
  Glucocorticoid-induced osteoporosis Early increase/later decline Varies with timing of the study with reference to steroid use.
  Cushing’s disease Decreased Increased after treatment, suggesting suppressive effects on osteocyte and osteoblast function.
 Osteoporosis treatment effects   
  Bisphosphonates and denosumab Increase Results may vary due to timing of data collection after denosumab or zolendronic acid administration.
  Teriparatide and strontium ranelate Decreased Compensatory increase in Dkk1 levels may limit continued anabolic action.
  Estrogen and raloxifene Decreased Suggesting estrogen and estrogen effect of raloxifene may modulate osteocyte and osteoblast function.
 Systemic disorders   
  Diabetes mellitus type 1 Slight increase Age-related increase maintained, but sclerostin response to PTH is blunted.
  Diabetes mellitus type 2 Increased Age-related increase is absent, sclerostin response to PTH is impaired, and pioglitazone therapy increases sclerostin levels by 11 %.
  Chronic kidney disease Increased Sclerostin excretion increases with declining renal function with negative correlation with GFR.
  Kidney disease Increased Sclerostin levels increase despite increased PTH and increased excretion of sclerostin in renal failure.