Osteoporotic fractures are well-known complications of organ transplantation. Fracture rates up to 35% have been previously reported following heart and lung transplantations. Our institutional pretransplant protocols include DXA scans, vitamin D screening, and appropriate antiresorptive therapy. We aimed to assess the incidence of fragility fractures following cardiac or lung transplantation. In a retrospective study 210 electronic medical records of patients who underwent LT (110 men, 100 women) and 105 HT (88 men, 17 women) between 2005 and 2010 were analyzed. Both clinical and radiographic fractures were recorded. DXA scans were obtained immediately after transplant. 17 out of 210 LT patients (8.0%) had fractures after transplantation and 9 out of 105 HT patients (8.6%) had fractures. The median time to the first fracture was 12 months and the mean time was 18 months for both LT and HT. In the HT recipients, the median femoral neck T score was statistically lower in the fracture group versus the nonfracture group. Similar results were seen in the LT patients. Conclusion. Our findings demonstrate a much lower incidence of fractures in heart and lung transplant recipients in comparison with earlier reports. Comprehensive bone care and early initiation of antiresorptive therapy are possible contributors to these improved outcomes.

Severe methanol poisoning requires treatment with prolonged and intensive hemodialytic therapy. Such treatment can engender either the de novo development of hypophosphatemia or the worsening of pre-existing hypophosphatemia. Phosphorus-enriched hemodialysis therapy can prevent the occurrence of this complication. We report three patients with severe methanol poisoning who were treated with phosphorus-enriched hemodialysis. Prevention or treatment of hypophosphatemia was successfully achieved with this dialytic technique.

ADT is considered an effective first-line treatment for men with both advanced and non-metastatic prostate cancer. Despite the importance of ADT in prostate cancer treatment, ADT is associated with potential side effects, including BMD reduction, resulting in increased risk of osteoporosis and fractures. 1,2 The pathophysiologic reason is that when testosterone is reduced the usual balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption is disrupted, with bone resorption outstripping formation. Osteoclast activity is at least in part mediated by parathyroid hormone (PTH). Studies have shown that testosterone increases bone density by inhibiting PTHmediated osteoclast activity. 3-5 Testosterone also exerts a bone-protective effect via conversion to estrogen. In men who have low testosterone concentration due to ADT (or any cause), osteoclast activity is not appropriately inhibited, leading to increased bone resorption and therefore bone loss or osteoporosis. 6 It has been shown that during the first year of exposure to ADT, there is a five-to 10-fold increase in the rate of bone loss as well as fracture risk. This risk increases as the duration of ADT therapy increases. 7,8 In men with non-metastatic prostate cancer receiving ADT, BMD can be maintained or increased significantly by treatment with bisphosphonates, zoledronic acid, alendronate, or pamidronate. [9][10][11][12][13] At Loyola University Medical Center, 5222 men were diagnosed with prostate cancer between January 2006 and January 2014. Of 513 men who were treated with a gonadotropin-releasing-hormone (GnRH) agonist, 105 (20%) had a DXA scan. Of 487 men who were treated with antiandrogen therapy, 103 (21%) had a DXA. Out of 278 men who received both GnRH agonist and anti-androgen therapy, 64 (23%) received a DXA.These findings suggest that the deleterious effects of ADT on bone are not well recognized and that efforts should be made to raise the level of awareness of this important risk factor. Conflict of interestNone declared.