Few reports are available on bone turnover in type 2 diabetes. Impaired bone turnover in type 2 diabetes appears to result from decreased bone formation. Studies also suggest that poor glycaemic control in type 2 diabetes may contribute to osteopaenia. The aim of this study was to investigate biochemical markers of bone turnover in males with poorly controlled type 2 diabetes and look for correlations with glycaemic control and gonadal and hypophyseal hormonal axis. Consecutive male patients with poorly controlled type 2 diabetes and attending the internal medicine department during a period of 6 months were enrolled. The patients were receiving oral hypoglycaemic agents (metformin or sulphonylureas or both). None of the patients had any evidence of macroangiopathy, nephropathy or neuropathy. Only two patients had proliferative retinopathy. Serum osteocalcin, crosslaps (C-telopeptide, CTx), parathyroid hormone (PTH), testosterone, oestrogen, prolactin, follicle-stimulating hormone (FSH) and luteinising hormone (LH) were measured in 35 patients and 35 controls. The mean age of the study population was 53.7 (10.3) years (range: 50.2-57.3) and the mean disease duration was 8.6 (6.0) years (range: 6.5-10.7). No differences between patients and controls were observed in serum calcium, phosphorus, creatinine, albumin, PTH, CTx, oestrogen, testosterone, LH, FSH, prolactin and urinary calcium. Patients had lower serum levels of osteocalcin than controls with a significant statistical difference [15.3 (4.1) vs 18.3 (5.3), p=0.012]. There was a negative significant statistical correlation between CTx levels and HbA1c (r=-0.41, p< 0.05). Our study suggested that bone formation is altered in type 2 diabetes and that bone turnover is affected by glycaemic control status.

BackgroundHypovitaminosis D is associated to accentuated bone loss. However, association between osteoporotic vertebral fractures (VFs) and vitamin D status has not been clearly established.ObjectiveTo determine serum vitamin D status and to assess the association of vitamin D status with bone mineral density (BMD) and asymptomatic VFs prevalence using vertebral fracture assessment (VFA) in a cohort of Moroccan menopausal women.Methodsfrom June to September 2010, 178 menopausal women 50 years old and over were enrolled in this cross-sectional study. The mean ± SD (range) age, weight, height and BMI were 58.8 ± 8.2 (50 to 79) years, 73.2 ± 13.8 (35 to 119) Kgs, 1.56 ± 0.06 (1.43 – 1.79) m and 29.8 ± 5.9 (17.5 – 49.8) kg/m2, respectively. VFA images and scans of the lumbar spine and proximal femur were obtained using a GE Healthcare Lunar Prodigy densitometer. VFs were defined using a combination of Genant semiquantitative approach and morphometry. Serum levels of 25-hydroxyvitamin D (25(OH)D) were measured.ResultsAmong the 178 women, 45 (25.2%) had densitometric osteoporosis, and on VFA, VFs (grade 2 or 3) were detected in 20.2% while grade 1 were identified in 33.1%. The mean values of serum levels of 25(OH)D were 15.8 ± 11.6 ng/ml (range: 3.0 – 49.1) with 152 patients (85.3%) having levels <30 ng/ml (insufficiency) and 92 (51.6%) <10 ng/ml (deficiency). Stepwise regression analysis showed that presence of VFs was independently related to age, 25(OH)D and densitometric osteoporosis.Conclusionour study shows that advanced age, hypovitaminosis D and osteoporosis are independent risk factors for asymptomatic VFs in Moroccan postmenopausal women.

The objective of this study was to determine bone mineral density (BMD) distribution in ankylosing spondylitis (AS) using quantitative computed tomography (QCT), to study bone turnover and anterior pituitary and gonadal hormonal axis in AS, and to look for correlations between BMD, bone remodeling markers and gonadal and anterior pituitary hormones. Forty-three male consecutive patients with AS were enrolled prospectively [mean (SD) age of 36.4 (11.3) years (range: 17-67) and mean disease duration of 6.8 (5.2) years (range: 0.4-19)]. Spine BMD was measured in all patients by QCT, and the results were compared to 29 male patients undergoing lumbar CT scan for sciatica. Bone turnover and anterior pituitary and gonadal axis were assessed in 29 patients, and the results were compared to 30 male healthy blood donors. The mean (SD) BMD was 127.7 mg/cm(3) (48.9) (range: 8.8-265.7) and 152.1 (25.3) (range: 34.2-190.4) in patients and controls, respectively (p = 0.018). Patients had lower serum levels of osteocalcin and higher levels of serum testosterone, luteinizing hormone (LH), and prolactin than controls with a significant statistical difference. There was a positive significant statistical correlation between BMD and chest expansion, Schober's test, C7-wall distance, and negative significant statistical correlation with age, disease duration, Bath Ankylosing Spondylitis Metrology Index (BASMI), Bath Ankylosing Spondylitis Radiology Index (BASRI), and serum prolactin. No correlation was observed between bone turnover parameters and AS symptomatic and structural severity indexes. BMD is lower with increasing age and late and severe disease. Decreased bone formation with normal resorption and increased levels of serum prolactin may be involved in its pathophysiology.

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The aim of this study was to describe biological features and aetiology of monoclonal gammopathy diagnosed during a 10-year period in the biochemistry department of the Moroccan Military Hospital Mohamed V in Rabat. The study was performed from 1 January 2000 to 31 December 2009. The records of 261 patients living in the Rabat area in which either serum protein electrophoresis and serum and/or urine immunofixation were performed at the biochemistry department of Military Instruction Hospital in Rabat were analysed. A cohort of 182 (70%) men and 79 (30%) women, the mean ± SD (range) ages were 60.21 ± 12.56 years. All patients were Caucasian. Electrophoresis found that 211 (80.84%) of the patients had a monoclonal gammopathy. Immunofixation confirmed that 251 (96.17%) patients had a monoclonal band in serum. In our cohort, MM was the most frequent diagnosis, our patients were late diagnosed.

Aims The main objective of this work was to evaluate the influence of end-stage renal disease (ESRD) on concentrations of five tumor markers (TMs): carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 19-9 (CA19-9), CA15-3, CA125, and prostate specific antigen (PSA) in a group of chronic hemodialysis patients (CHPs); and to study the influence of hemodialysis (HD) sessions on concentrations of the same TMs. Methods We compared TMs levels in CHP before HD sessions to a control group of 50 healthy volunteers, the dosages were determined before and immediately after the HD session Comparisons were made before and after correction for dialysis-induced hemoconcentrations. Results We enrolled 74 CHPs, all TM concentrations were higher in this group compared to control group, but this increase was significant for CEA (4.25 ± 2.89 vs 2.41 ± 1.81ng/ml; p<0.0001), CA125 (27.84 ± 92.27 vs 13.30 ± 9.85 ng/ml; p = 0.048) and CA19-9 (19.65 ± 25.02 vs 10.23 ± 11.00 U/ml; p = 0.011). Post-dialysis levels were significantly higher than those in pre-dialysis. CEA (3.35 [2,46-5.51] vs 4,06 [2.60-6.78] ng/ml; p<0.0001), CA125 (13.24 [9.66-18.63] vs 16.01 [11.33-22.53] ng/ml; p<0.0001), CA19-9 (12.29 [5.59-21.97] vs 16.29 [7.18-24.7] U/ml; p<0.0001), CA15-3 (13.06 [10.05-17.48] vs 14.58 [11.72-19.35] ng/ml; p<0.0001 and PSA (0.83 [0.5-1.24] vs 1.06 [0.62-1.43] ng/ml; p<0.0001). Conclusions Our work confirms that HD increases concentrations of the five TMs evaluated and suggests that the use of CA15-3 and PSA remains valid in CHPs since their concentrations were not altered by ESRD, unlike CEA, CA125, and CA19-9.

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