Beta-thalassaemia major is associated with low bone mass and fractures. We conducted a 2 year randomized controlled trial of zoledronic acid 4 mg administered intravenously every 3 months or placebo in the treatment of beta-thalassaemia-associated osteopenla. We recruited 23 subjects from 2 university hospitals with a T score of less than -1.0 at either the lumbar spine or hip, and 23 subjects completed the study (17 M, 6 F). Treatment groups did not differ significantly with respect to bone mineral density (BMD), age, height, weight and body mass index (BMI) at baseline. BMD was assessed at baseline, 12 months and 24 months by dual-energy X-ray absorptiometry (DXA) at the lumbar spine, femoral reek, total hip and total body. After two years average lumbar spine BMD was 8.9% greater (95%CI 2.3-15.5%, P = 0.011), average femoral neck BMD was 9.1% greater (95%CI 5.5-12.7%, P < 0.0001), average total hip BMD was 9.6% greater (95%CI 6.5-12.6%, P < 0.0001) and average total body BMD was 4.7% greater (95%CI 2.7-6.8%, P < 0.0001) in the treated group compared to placebo. The absolute change in BMD from baseline to 2 years and the annualized rate of change of BMD was significantly greater in treated patients at all four sites. Age, gender, height, weight and BMI did not interact with the effect of treatment and so unadjusted data was used. The serum total ALP decreased 45% by 12 months (P = 0.004) and urinary deoxypyridinoline/creatinine ratio decreased 47% by 3 months (NS). We conclude that zoledronic acid (4 mg i.v. 3 monthly) suppresses bone turnover and increases BMD in beta-thalassaemia-associated osteopenia.

Background Endothelial dysfunction serves as an early marker for the risk of cardiovascular disease (CVD); therefore, it is a site of therapeutic interventions to reduce the risk of CVD. Aims To examine the effect of the Mediterranean diet (MedDiet), as an intervention, on structural and functional parameters of endothelial function, and how it may reduce the risk of CVD and associated mortality. Methods Medline database was searched for randomized controlled trials. Random-effects meta-analysis was conducted on 21 independent datasets. Meta-regression and subgroup analysis were performed to assess whether the effect of MedDiet was modified by health status (healthy subjects or with increased CVD risk), type of MedDiet intervention (alone or combined), type of parameter (functional or structural), study design (cross-over or parallel), BMI, age, and study duration. Our study used sample size, mean, and standard deviation of endothelial function measurements for both MedDiet intervention and control in the analyses. Results Inverse relationship between endothelial function and intake of MedDiet was observed (SMD: 0.34; 95% CI: 0.16, 0.52; P = 0.0001). Overall, MedDiet increased FMD by 1.39% (95% CI: 0.47, 2.19; P < 0.001). There was a significant improvement in endothelial function in both healthy patients and in those with an increased risk of CVD. No significant variation was observed in the effects of MedDiet on endothelial function, due to study design or type of intervention. Conclusions These findings support that MedDiet can reduce the risk of CVD by improving endothelial function.

As my manuscript is the letter to the editor therefor it has no abstract.

Calcineurin inhibitors (CNI) are the mainstay of immunosuppressant medications in both bone marrow transplants and solid organ transplants. Nephrotoxicity is a well-known adverse effect of this group. Type IV renal tubular acidosis is a potentially under-recognized complication. Here we report a case of Omenn syndrome in a patient who underwent a bone marrow transplant and developed type IV renal tubular acidosis while on treatment with cyclosporine.