Background Osteoporosis remains underrecognized and undertreated in both men and women, but men who sustain fragility fractures experience greater morbidity and mortality. While men exhibit advanced comorbidity at the time of hip fracture presentation, there are distinct sex-and gender-specific factors related to the pathophysiology and treatment of osteoporosis that further influence morbidity and mortality. Questions/purposes With a selective review of the literature, we evaluated sex-and gender-based differences contributing to increased morbidity and mortality in men with osteoporosis.
Long-term alendronate treatment did not appear to cause thickened femoral cortices within the detection limits of our method. This finding contrasts with the notion that long-term alendronate treatment leads to generalized cortical thickening.
Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.
Background Men with hip fractures are more likely to experience postoperative complications than women. The Medical Orthopaedic Trauma Service program at New York Presbyterian Hospital utilizes a multidisciplinary team approach to care for patients with hip fractures. The service is comanaged by an attending hospitalist and orthopaedic surgeon, with daily walking rounds attended by the hospitalist, orthopaedic resident, physical therapist, social worker, and a dedicated Medical Orthopaedic Trauma Service physician assistant. Questions/purposes We asked whether a multidisciplinary service for patients with hip fracture decreases (1) the incidence of inpatient complications in men, (2) the length of hospitalization, and (3) 90-day and 1-year mortality. Patients and Methods We retrospectively reviewed the charts of 74 men who had surgery for a nonperiprosthetic femoral neck, intertrochanteric, or subtrochanteric fracture for two 7-month periods before and after implementation of the Medical Orthopaedic Trauma Service. Age, ethnicity, comorbidity status, time to surgery, and postoperative complication data were collected. Regression modeling was used to evaluate the likelihood of postoperative complications, length of hospitalization, and 90-day and 1-year mortality while controlling for age, Charlson Comorbidity Index score, fracture type, and time from admission to surgery. Results We observed a decrease in the likelihood of experiencing at least one inpatient complication in male patients after implementation of the Medical Orthopaedic Trauma Service (odds ratio = 0.264). There was no difference in length of hospitalization, 90-day mortality, or 1-year mortality. Conclusions Multidisciplinary collaboration for patients with hip fractures can decrease the likelihood of experiencing inpatient complications in male patients.Each author certifies that he or she has no commercial associations (eg, consultancies, stock ownership, equity interest, patent/licensing arrangements, etc) that might pose a conflict of interest in connection with the submitted article. Each author certifies that his or her institution approved the human protocol for this investigation and that all investigations were conducted in conformity with ethical principles of research.
Pheochromocytomas are neuroendocrine tumors that commonly lead to excess catecholamine secretion, resulting in elevated blood pressure. In addition to potentiating vasoconstriction, catecholamines promote endothelial dysfunction, as evidenced by elevated markers of endothelial dysfunction, ADMA and sVCAM-1, in patients with pheochromcytoma. Importantly, catecholamine-induced endothelial dysfunction and hypertension may not only be due to catecholamine production by neuroendocrine tumors, as vascular endothelial cells have now been demonstrated to synthesize and secrete catecholamines. This local vascular catecholamine release appears to be triggered by hypoxia. In fact, chronic intermittent hypoxia both in vitro and in vivo leads to stabilization of hypoxic-inducible factors that increase gene expression of catecholamine-synthesizing enzymes. In an effort to target catecholamines as a means of treating hypertension, novel therapeutic options are being explored, including the generation of pharmacophores that mimic the suppressive effects of catestatin on catecholamine release as well as the use of renalase enhancers to increase catecholamine metabolism.
Background Fracture leads to local and systemic catabolic physiologic changes. As teriparatide is an agent used to treat osteoporosis in patients with fragility fractures, it is unclear whether teriparatide treatment alters bone mineral density (BMD) and bone markers when given to patients with fractures. Questions/purposes We asked whether BMD and bone marker responses would be blunted in patients with fractures placed on teriparatide after fracture compared with patients without fractures on teriparatide. Patients and MethodsWe retrospectively collected data from 141 patients treated with teriparatide for osteoporosis. Seventy-seven patients received teriparatide after fractures (fracture group), whereas 64 were treated for other indications (nonfracture group). We determined BMD at the lumbar spine and at the proximal femur before and 12 and 24 months posttreatment. Bone markers (urine N-telopeptide [urine NTX], bone-specific alkaline phosphatase [BALP]) were measured at baseline and 3, 12, and 24 months posttreatment. Results Mean lumbar spine and hip BMDs at last followup increased from baseline with no differences between groups to approximately 9% and 4% at 24 months, respectively. Both bone markers increased from baseline in the nonfracture group, peaking at 12 months. For the fracture group, only urine NTX increased at 3 and 12 months posttreatment. Although the peak levels of both bone markers in the nonfracture group were greater, there was no difference between the two groups. Conclusions Fracture does not have a negative effect on the BMD and bone marker responses to teriparatide treatment. Clinicians should anticipate comparable BMD responses when treating patients with teriparatide for osteoporotic fractures and for other indications. Level of Evidence Level III, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.
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