Mortality after osteoporotic hip fracture: incidence, trends, and associated factors.

BACKGROUND: It is known that mortality after hip fracture increases compared to the general population; the trend in mortality is a controversial issue. The objective of this study is to examine incidence, trends, and factors associated with mortality in patients with osteoporotic hip fractures. METHODS: This is a retrospective cohort study that uses the Registry for Hospital Discharges of the National Health System of our hospital. Patients older than 45 having an osteoporotic hip fracture between 1999 and 2015 were identified. Demographic data and comorbidities were obtained. A survival analysis was performed (Cox regression and Kaplan-Meier). Incidence rate, standardized death rate (SDR), trend (Poisson regression), and risk (hazard ratio) were calculated. RESULTS: During 1999-2015, in our hospital, there were a total of 3992 patients admitted due to osteoporotic hip fracture. Out of these 3992 patients, 3109 patients (77.9%) were women with an average age of 84.47 years (SD 8.45) and 803 (22.1%) were men with an average age of 81.64 years (SD 10.08). The cumulative incidence of mortality was 69.38%. The cumulative mortality rate for 12 months was 33%. The annual mortality was 144.9/1000 patients/year. The 1-year mortality rate increased significantly by 2% per year (IRR 1.020, CI95% 1.008-1.033). The median overall survival was 886 days (CI95% 836-951). The probability of mortality density for a period of 10 years following a hip fracture was 16% for women and 25% for men (first 90 days). The SDR was 8.3 (CI95% 7.98-8.59). Variables that showed statistically significant association with mortality were aged over 75, masculine, institutionalization, mild to severe liver disease, chronic kidney disease, COPD, dementia, heart failure, diabetes, the Charlson Index > 2 , presence of vision disorders and hearing impairment, incontinence, and Downton scale. CONCLUSIONS: For the last 17 years, an increase of mortality for patients with hip fracture and a higher mortality rate in men than in women were observed. Institutionalization combined with comorbidities is associated with a higher mortality.

Subcellular localization of NAPE-PLD and DAGL-α in the ventromedial nucleus of the hypothalamus by a preembedding immunogold method.

The hypothalamus and the endocannabinoid system are important players in the regulation of energy homeostasis. In a previous study, we described the ultrastructural distribution of CB1 receptors in GABAergic and glutamatergic synaptic terminals of the dorsomedial region of the ventromedial nucleus of the hypothalamus (VMH). However, the specific localization of the enzymes responsible for the synthesis of the two main endocannabinoids in the hypothalamus is not known. The objective of this study was to investigate the precise subcellular distribution of N-arachidonoylphospatidylethanolamine phospholipase D (NAPE-PLD) and diacylglycerol lipase α (DAGL-α) in the dorsomedial VMH of wild-type mice by a high resolution immunogold electron microscopy technique. Knock-out mice for each enzyme were used to validate the specificity of the antibodies. NAPE-PLD was localized presynaptically and postsynaptically but showed a preferential distribution in dendrites. DAGL-α was mostly postsynaptic in dendrites and dendritic spines. These anatomical results contribute to a better understanding of the endocannabinoid modulation in the VMH nucleus. Furthermore, they support the idea that the dorsomedial VMH displays the necessary machinery for the endocannabinoid-mediated modulation of synaptic transmission of brain circuitries that regulate important hypothalamic functions such as feeding behaviors.

An artificial neural network approach for predicting functional outcome in fibromyalgia syndrome after multidisciplinary pain program.

OBJECTIVE: The objective of this study was to evaluate the ability of artificial neural networks (ANNs) to predict, on the basis of clinical variables, the response of persons with fibromyalgia syndrome (FMS) to a standard, 4-week interdisciplinary pain program. DESIGN: The design of this study is retrospective longitudinal. SETTING: Fibromyalgia outpatient clinic in a tertiary-care general hospital. SUBJECTS: The subjects of this study include outpatients with FMS. INTERVENTION: Multidisciplinary pain program including pain pharmacotherapy, cognitive-behavioral therapy, physical therapy, and occupational therapy. OUTCOME MEASURES: Reliable change (RC) of scores on the Stanford Health Assessment Questionnaire (HAQ), and accuracy of ANNs in predicting RC at discharge or at 6-month follow-up as compared to Logistic Regression. RESULTS: ANN-based models using the sensory-discriminative and affective-motivational subscales of the McGill Pain Questionnaire, the HAQ disability index, and the anxiety subscale of Hospital Anxiety and Depression Scale at baseline as input variables correctly classified 81.81% of responders at discharge and 83.33% of responders at 6-month follow-up, as well as 100% of nonresponders at either evaluation time-point. Logistic regression analysis, which was used for comparison, could predict treatment outcome with accuracies of 86.11% and 61.11% at discharge and follow-up, respectively, based on baseline scores on the HAQ and the mental summary component of the Medical Outcomes Study-Short Form 36. CONCLUSIONS: Properly trained ANNs can be a useful tool for optimal treatment selection at an early stage after diagnosis, thus contributing to minimize the lag until symptom amelioration and improving tertiary prevention in patients with FMS.

Transient, 5-HT2B receptor-mediated facilitation in neuropathic pain: Up-regulation of PKCγ and engagement of the NMDA receptor in dorsal horn neurons.

Spinal nociception can be facilitated by 5-HT2 receptors in neuropathic pain. We investigated the involvement of glutamate receptors in dorsal neuron hyperexcitation that is promoted by 5-HT2B receptor (5-HT2BR) after spinal nerve ligation (SNL) in the rat. Augmentation of C-fiber-evoked potentials by spinal superfusion with 5-HT2BR agonist BW 723C86 in nerve-ligated rats was impeded by co-administration of NMDA receptor (NMDAR) antagonist D-AP5, but not by mGluR1/5 antagonist AIDA or mGluR2/3 antagonist LY 341495. Evoked potentials were increased by cis-ACPD in nerve-injured rats, irrespective of simultaneous 5-HT2BR blockade by SB204741. In uninjured rats, NMDAR agonist cis-ACPD enhanced evoked potentials in the presence of BW 723C86 but not if administered alone or during exposure to protein kinase C γ (PKCγ) inhibitor peptide. Triple immunofluorescence labelings revealed co-localization of NMDAR and 5-HT2BR in PKCγ-expressing perikarya in lamina II neurons. As a result of SNL, PKCγ was transiently and bilaterally up-regulated in synaptic fraction from dorsal horn homogenates, peaking at day 2 and returning to basal levels by day 9. Chronic blockade of 5-HT2BR with selective antagonist SB 204741 after SNL bilaterally decreased the following: (i) PKCγ up-regulation in synaptic fraction, (ii) phosphorylation of NMDAR subunit NR1 (serine 889) in synaptic fraction, and (iii) co-localization of both PKCγ and phosphorylated NR1 with postsynaptic marker PSD-95. Chronic delivery of SB 204741 bilaterally attenuated thermal and mechanical allodynia occurring after SNL, particularly at day 2 post injury. These findings suggest that transient activation of the PKCγ/NMDAR pathway is critically involved in 5-HT2BR-mediated facilitation in the SNL model of neuropathic pain.