Calcium metabolism and hyperparathyroidism after renal transplantation

Plasma calcium and albumin levels were measured serially in 100 patients for two years following successful renal transplantation. Mean plasma calcium increased during the first six months after grafting, in large part attributable to an increase in plasma albumin. The variance around the mean plasma calcium did not increase suggesting that mechanisms responsible for hypercalcaemia were common to the majority of patients. 36 per cent of patients developed hypercalcaemia within two years of grafting but the incidence fell to 11 per cent when more rigorous criteria for hypercalcaemia were used. The mechanisms maintaining plasma calcium were studied in 29 of the patients, nine of whom were hypercalcaemic and 20 of whom were normocalcaemic. Before transplantation, mean plasma calcium and phosphate levels were higher, the prevalence of subperiosteal erosions and extraskeletal calcification radiographically was greater, and the duration of haemodialysis treatment was longer in the hypercalcaemic patients than in the normocalcaemic recipients. At assessment after transplantation, hypercalcaemic patients had lower levels of plasma phosphate, higher plasma levels of alkaline phosphatase and parathyroid hormone, and higher hydroxyproline excretion. Renal function and 47Ca absorption were similar in the two groups. The major cause for apparent hypercalcaemia in transplanted patients appeared to be an increase in plasma albumin. In patients with true hypercalcaemia the major cause was pre-existing hyperparathyroidism where hypercalcaemia was mediated by increased renal tubular reabsorption of calcium.     

Quantitative MRI and loss of free ambulation in Duchenne muscular dystrophy

The purpose of this ethics approved trial was to correlate quantitative MRI with functional abilities in both ambulant and non-ambulant Duchenne muscular dystrophy (DMD). Twenty patients with genetically confirmed DMD were recruited. Physical assessment was performed using the motor function measurement (MFM) scale. Axial 3T MRI scans of the thighs were acquired using T1-weighted in- and opposed-phase images (TR = 20 ms, TE₁ = 2.45 ms, TE₂ = 3.68 ms, flip angle = 15°) to calculate the relative fat fraction according to the two-point Dixon method in the knee extensors, flexors, and adductor muscles. The average MFM was 65.3 % and correlated negatively to age (r ² = 0.60). Overall mean fat fraction correlated positively to age (r ² = 0.51–0.64). An average of 5 % increase in mean fat fraction per year was calculated. Mean fat fraction of the quadriceps showed a high negative correlation (r ² = 0.93) to the D1 (standing position and transfers) component of the MFM. A cutoff for mean fat fraction of 50 % predicted loss of ambulation with a sensitivity of 100 % and a specificity of 91 %. Therefore, quantitative muscle MRI seems to be a promising endpoint for short clinical trials evaluating the effect of newer treatments on the time of loss of ambulation in DMD.     

Developing a nurse-led education program to enhance self-care agency in leg ulcer patients

Patients with leg ulceration face changing self-care demands associated with the consequences of the disease and treatment. Often patients can manage their self-care for some time, but new therapeutic self-care demands may emerge that require more complex self-care actions. The purpose of this article is to describe the development of a nurse-led education program in North-Rhine Westphalia, Germany, that aims to help patients with leg ulcers to meet their therapeutic self-care demands. Orem's self-care deficit nursing theory is used as a framework to provide the conceptual context for this supportive-educative nursing system that is being tested in a multi-site clinical trial.     

Requirement of interleukin 17 receptor signaling for lung CXC chemokine and granulocyte colony-stimulating factor expression, neutrophil recruitment, and host defense

Bacterial pneumonia is an increasing complication of HIV infection and inversely correlates with the CD4(+) lymphocyte count. Interleukin (IL)-17 is a cytokine produced principally by CD4(+) T cells, which induces granulopoiesis via granulocyte colony-stimulating factor (G-CSF) production and induces CXC chemokines. We hypothesized that IL-17 receptor (IL-17R) signaling is critical for G-CSF and CXC chemokine production and lung host defenses. To test this, we used a model of Klebsiella pneumoniae lung infection in mice genetically deficient in IL-17R or in mice overexpressing a soluble IL-17R. IL-17R-deficient mice were exquisitely sensitive to intranasal K. pneumoniae with 100% mortality after 48 h compared with only 40% mortality in controls. IL-17R knockout (KO) mice displayed a significant delay in neutrophil recruitment into the alveolar space, and had greater dissemination of K. pneumoniae compared with control mice. This defect was associated with a significant reduction in steady-state levels of G-CSF and macrophage inflammatory protein (MIP)-2 mRNA and protein in the lung in response to the K. pneumoniae challenge in IL-17R KO mice. Thus, IL-17R signaling is critical for optimal production of G-CSF and MIP-2 and local control of pulmonary K. pneumoniae infection. These data support impaired IL-17R signaling as a potential mechanism by which deficiency of CD4 lymphocytes predisposes to bacterial pneumonia.     

Long-term survival of patients with glioblastoma multiforme (GBM)

Long-term survival is an often used, yet poorly defined, concept in the study of glioblastoma multiforme (GBM). This study suggests a method to define a time-point for long-term survival in patients with GBM. Data for this study were obtained from the Surveillance, Epidemiology and End-Results database, which was limited to the most recent data using the period approach. Relative survival measures were used and modelled using piecewise constant hazards to describe the survival profile of long-term survivors of GBM. For patients with GBM, the first quarter of the second year (5th quarter) post-diagnosis is considered to be the peak incidence of mortality with an excess hazard ratio of 7.58 (95% confidence interval = 6.54, 8.78) and the risk of death due to GBM decreases to half of its rate at 2.5 years post-diagnosis. The 2.5-year cumulative relative survival (CRS) for all patients is approximately 8%, with a CRS of approximately 2% at 10 years. Using the definition of long-term survival suggested here, the results indicate that long-term survivors are patients who survive at least 2.5 years post-diagnosis. The most likely time period for patients with GBM to die is the 5th quarter post-diagnosis.