No abstract

Risk factors for increased mortality in hip fracture patients include older age, male sex, fracture type, bone mineral density, and pre-existing co-morbidities. The role of biochemical and other anthropometric parameters on hip fracture mortality remains unclear. The aim of this study was to identify the risk factors for one-year mortality in patients with hip fractures. A total of 236 consecutive patients (59 males) with hip fractures were followed over a one-year period. Patient age, gender, type of fracture, type of treatment, time from admission to surgery, type of anesthesia, body mass index, and electrocardiograms were recorded. Complete blood counts, serum electrolytes, urea, creatinine, d-dimers, calcium, phosphate, osteocalcin, and beta-isomerised C-terminal telopeptide of collagen type I (β-CTX) were measured at admission and estimated glomerular filtration rate (eGFR) was calculated. Multivariate Cox regression models were used to analyze the association of these parameters with survival. One-year mortality rate was 28.4%. Age was independently associated with mortality (HR 1.117, 95% CI 1.062-1.174, P < 0.001). In a multivariable model, mortality was increased in patients with higher β-CTX (HR 4.63 95% CI 1.87-11.45, P = 0.001) and lower eGFR (HR 0.972, 95% CI 0.956-0.987, P < 0.001). Patients younger than 84 years, with eGFR < 55.4 ml/min had ten times higher mortality rates (3.2 vs. 24.5%, HR 9.73, 95% CI 2.06-45.93) as well as those with β-CTX > 0.276 g/L (3.5 vs. 25.7%, HR 9.5, 95% CI 2.11-42.76). Advanced age, high β-CTX levels, and impaired renal function are independent risk factors of mortality in patients with hip fractures.

Alteration in vitamin D metabolism has a central role in the pathogenesis of secondary hyperparathyroidism (SHPT) and is also associated with increased cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). For more than sixty years, vitamin D, nutritional vitamin D (ergocalciferol, cholecalciferol or calcifediol) and nonselective vitamin D receptor (VDR) activators (calcitriol, alfacalcidol) have been used in the prevention and treatment of SHPT. In the last twenty years, selective VDR activators (paricalcitol, maxacalcitol) have been used to target SHPT. However, there are many open questions regarding use of nutritional vitamin D or VDR activators. The K/DOQI and KDIGO guidelines recommended testing for vitamin D insufficiency and deficiency in patients with CKD, but there is no consensus on the definition of vitamin D insufficiency in CKD. There are a many open questions, for example, regarding the optimal nutritional vitamin D type and the dose and co-administration of nutritional vitamin and VDR activators. Therapy with VDRAs is required in the majority of patients with CKD, particularly in dialysis patients. However, when to start with VDRAs is not so apparent. Is PTH level the only indication of when to start therapy? Although VDRAs are very effective in lowering PTH levels and bone metabolism the effect of patients mortality is not so straightforward. Despite many unanswered questions, there is a large body of experimental and clinical data to support vitamin D use in patients with CKD. To obtain answers to the open questions, we need more randomized controlled trials.

Male patients with high adiponectin, leptin, and β-CTX levels have a 5-fold increase in all-cause one-year mortality after hip fracture.

SUMMARY -In this article, we document a conclusive case of nebivolol-induced hyperkalemia for the fi rst time in the known medical literature. Hyperkalemia is associated with serious conditions such as cardiac arrhythmias and sudden cardiac death. Nebivolol was not known to cause hyperkalemia, and this event is not listed in its summary of product characteristics (SmPC). For older beta blockers, hyperkalemia is recognized as a rare adverse event linked to cytochrome P450 2D6 (CYP2D6) polymorphism and poor drug degradation. Our patient, a 47-year-old woman taking nebivolol for hypertension developed persistent hyperkalemia, with serum potassium levels up to 6.4 mmol/L. After extensive diagnostic evaluation and exclusion of other known conditions leading to hyperkalemia, its cause remained occult. Since hyperkalemia coincided with increased doses of nebivolol, dose reduction and discontinuation were attempted, resulting in normalized serum potassium. Poor drug metabolism could not explain this adverse eff ect, since pharmacogenetic testing showed no relevant aberrations. In conclusion, hyperkalemia is a harmful adverse event with possible lethal outcome, and it may be caused by nebivolol. Th erefore, medical professionals have to be aware of this side eff ect and hyperkalemia should be listed as an adverse event in nebivolol SmPC.