الفهرس 
DIABETES MELLITUSOnly 14 pages are availabe for public view
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Abstract
Background:
Type 1 diabetes mellitus (T1DM) increases fragility fractures due to low bone mas, micro architectural alterations and decreased bone formation scterostin is expressed by osteocytes and inhibits osteoblatic bone formation.
Aim of the work:
To measure the plasma sclerostin in patients with type1 diabetes mellitus and to correlate its levels with serum markers of bone disease and metabolic control.
Subject and Methods:
The current study was a case control cross sectional study. Included 40 type 1 diabetic patients; 11 males represent (27.50%) and 29 females represent (72.50%) compared to 40 age- and sex-matched healthy subjects served as controls. The control group consisted of 9 males represent (22.50%) and 31females represent (77.50%). The mean age of patients was 13.02±3.31 years (range: 7-20 years) while that of controls was 11.7±2.93 years (range: 6-17 years). In the patients the mean of age of onset of diabetes 5.67±2.4 years (range: 1 – 10) and the mean of Disease duration 7.41±2.88 (range: 5-17). Bone mineral denisity was measueied by Dual-Energy X-Ray Absorptiometry, bone marker (calcium, phosphorus and Alkaline Phosphatase) and sererostin were assessed.
Results:
Upon comparison of serum sclerostin, total body DEXA and lumbar spine DEXA between all patients and control subjects, it was found that type 1 diabetic patients had higher significant serum sclerostin, lower total body DEXA and lower lumbar spine DEXA than control groups. There was no statistical significance difference between female cases (-0.72±1.15) when compared to male cases (-0.55 ± 1.38) as regards bone mineral density (p>0.05).Also there was no statistical difference between diabetic patients and control group as regards serum calcium, serum phosphorus and serum alkaline phosphatase (p>0.05). Correlation studies revealed significant positive correlations between sclerostin, disease duration, frequency of hospital admission due to DKA, Random blood glucose, HA1C and Urinary albumin excretion (P<0.01) and as regard total body DEXA showed a negative correlation with disease duration, Random blood glucose, HA1C and Urinary albumin excretion (P<0.01). Moreover there was a negative correlation between serum sclerostin and total body DEXA. Comparison between non-complicated and complicated type 1 diabetic patients and control group as regards glycated hemoglobin concentration, urinary albumin excretion and insulin dose, diabetic complicated patient had higher hemoglobin concentration, urinary albumin excretion and insulin dose (p<0.05). With respect to microvascular complications of diabetes we found that diabetic complicated patients showed more frequency of neuropathy when compared to diabetic non complicated patients (p<0.001) and there was no statistical significant difference between diabetic complicated patients and diabetic non complicated patients as regards retinopathy (P>0.05).
Conclusion: There was impairment of bone mineral density during childhood and adolescence diabetic patients in this study. It can be detected early by performing regular DEXA scan for diabetic cases. Females are being more prone to have lower BMD. High serum sclerostin also have deleterious effects on bone in diabetic patients of all ages