Search

Abstract Background Nonunion of femoral shaft fractures in children is rare, and there is no clear treatment protocol. In this case report, a pediatric femoral shaft fracture that developed in nonunion due to vitamin deficiency after osteosynthesis, which was successfully treated with vitamin augmentation and replacement with a rigid antegrade intramedullary nail, is described. Case presentation The patient is an 11-year-old Japanese girl. She injured her right femoral shaft fracture when she hit a wall after kickboarding down a hill and underwent osteosynthesis with a titanium elastic nail. Six months postoperatively, she developed nonunion, was found to be deficient in vitamins D and K, and was started on vitamin supplementation. She underwent replacement with a rigid antegrade intramedullary nail at 7 months postoperatively, and bone union was achieved 3 months after reoperation. Conclusion When delayed union of a fracture is observed postoperatively, even in children without underlying disease, the cause of the problem must be investigated and treated promptly.

Objectives: Chronic kidney disease (CKD) complicated by secondary hyperparathyroidism (SHPT) is associated with an increased risk of fragility fractures. Etelcalcetide (EC) is a treatment for SHPT that reduces serum parathyroid hormone (PTH) levels. However, the effects of combined treatment with osteoporosis drugs such as teriparatide (TPTD) remain unclear. This study investigates the combined effects of EC and TPTD on bone in CKD model rats. Methods: The CKD model was established in 8-week-old male Wistar rats by feeding them a 0.75% adenine diet for 4 weeks. At 20 weeks of age, the rats were divided into 4 groups (N = 9–10 in each group): CKD group (vehicle administration), TPTD group (30 μg/kg, 3 times/week), EC group (0.6 mg/kg, daily), and Comb group (TPTD and EC combined). EC was injected for 12 weeks starting at 20 weeks of age, and TPTD was injected for 8 weeks starting at 24 weeks of age. After treatment, the followings were evaluated: bone mineral density, bone strength, biochemical tests, bone and fat histomorphometry, and micro-computed tomography. Results: In CKD model rats, the combination of EC and TPTD was more effective in increasing cortical bone thickness and bone strength and inhibiting porosity. In addition, the combined treatment decreased bone marrow adiposity and fibrosis, and it increased bone mass and improved bone microstructure in trabecular bone. Conclusions: With the observed benefits such as improved bone mass, bone strength, structural properties, and bone marrow adiposity, combination therapy may be a potential way to improve bone fragility in CKD.

This study evaluated changes over time in skeletal muscle atrophy, expressions of skeletal muscle anabolic and catabolic genes, and mitochondrial activity by skeletal muscle type in an adenine-induced chronic kidney disease (CKD) model. A CKD model was successfully established by feeding male Wistar rats a 0.75% adenine diet for 4 weeks starting at 8 weeks of age. Control and CKD groups were sacrificed at 12 and 20 weeks of age. The back muscles were analyzed histologically, and succinate dehydrogenase (SDH) staining was performed to evaluate mitochondrial activity. Gene expressions of myogenic determination gene number 1 and myogenin as indicators of muscle anabolism, atrogin-1 and muscle RING-finger protein-1 (MuRF1) as indicators of muscle catabolism, and peroxisome proliferator-activated receptor-γ coactivator-1-α as a marker of mitochondrial biogenesis were assessed. Type I and type II muscle cross-sectional areas (CSAs) were decreased at 12 weeks, but type I muscle CSA was recovered at 20 weeks. SDH staining was lower in CKD than in control rats at 12 weeks, but no significant difference was observed at 20 weeks. Increased expressions of myogenin, atrogin-1, and MuRF-1 were observed only at 12 weeks, but no differences were observed at 20 weeks. The adenine-induced CKD rat model appears to show changes in muscle atrophy over time.

Abstract Background Owing to the aging population, fragility fractures of the pelvis are occurring more frequently. Fixation of the fracture and stabilization of the pelvic ring usually provide good clinical results. A case of distal sacral nerve roots severed by a fragility fracture of the sacrum is presented. Case presentation A 62-year-old Japanese woman with schizophrenia with low back pain, gait disorder, dysuria, and fecal incontinence presented to an emergency department, and plain X-rays showed no findings. She also complained of dysuria, and neurogenic bladder and cystitis were diagnosed. One month later, she was admitted to a psychiatric hospital for exacerbation of schizophrenia. In hospital, she had a urethral catheter inserted and spent 3 months in bed. She was referred to our orthopedic department because a gait disorder was discovered after her mental condition improved and she was permitted to walk. On examination, she could not walk and had decreased sensation from the buttocks to both posterior thighs and around the anus and perineum. Manual muscle testing of her lower limbs showed mild weakness of about 4 in bilateral flexor hallucis longus and gastrocnemius, and bilateral Achilles tendon reflexes were lost. Her anal sphincter did not contract, and urinary retention continued after urethral catheter removal. Imaging examinations showed an H-shaped sacral fracture consisting of a transverse fracture with displacement of the third sacral vertebra and vertical fractures of the bilateral sacral wings, with severe stenosis of the spinal canal at the site of the transverse fracture. The patient was diagnosed as having bladder and rectal dysfunction due to a displaced, unstable sacral fracture. First to third sacral laminectomy and alar–iliac fixation using percutaneous pedicle screws and sacral alar–iliac screws were then performed. The bilateral distal sacral nerve roots (S3, S4, S5) were completely severed at the second to third sacral levels, but bilateral second sacral nerve roots were not compressed from the bifurcation to the sacral foramen. Postoperatively, bladder and rectal dysfunction remained, but the low back pain was alleviated. Two weeks postoperatively, she could walk with a walker and was discharged. Three months after the operation, bone fusion of the fracture was observed. Conclusions In cases of bladder–rectal dysfunction with low back pain, the possibility of sacral fracture should be considered, and computed tomography, magnetic resonance imaging, and X-ray examinations should be performed. Even sacral fractures without displacement require attention because they can cause serious injury in the event of a nerve root being severed if not diagnosed early and given appropriate treatment.

Background: Antipsychotics are used in treatment of schizophrenia. Although antipsychotic monotherapy is recommended in most guidelines, the prescription rate of antipsychotic polypharmacy is still high, and the rates of antipsychotics and other concomitant psychotropics are different among each institution. Although the detailed causes for these differences are not well known, one of the reasons of psychotropics polypharmacy, including antipsychotics polypharmacy, may be associated with severity of schizophrenia including treatment resistant schizophrenia (TRS). With regard to TRS, institutions with a low TRS examination rate was associated with a low clozapine prescription rate. Thus, the differences of institutions, which is available to clozapine prescriptions or not, may be affected the treatment characteristics of overall schizophrenia in each institution. Aims & Objectives: We examined the characteristics of psychotropic prescriptions, including antipsychotics, at the time of discharge depending on whether the institutions were available to clozapine prescriptions or not. Methods: We assessed 8155 schizophrenia patients nationwide from 207 institutions from 2017 to 2020 in Japan. We divided patients into clozapine-available institutions (CAI) group and clozapine-unavailable institutions (CUI) group. We analyzed and compared the psychotropic prescription data at discharge between two groups. We defined "antipsychotic monotherapy" as the prescription of a single antipsychotic regardless of concomitant use of other psychotropics, and we defined "complete antipsychotic monotherapy" as the prescription of a single antipsychotic without concomitant use of other psychotropics. Furthermore, to investigate that the diagnosis of subgroups about TRS or not may influence the treatment, we analyzed the description of subgroups about TRS (DSTRS) or no description of subgroups about TRS (NDSTRS), and we divided the patients into four groups such as CAI with DSTRS, CAI with NDSTRS, CUI with DSTRS, and CUI with NDSTRS, and compared between four groups using the same method. We defined p <1.9 × 10-3 (0.05/27) as significant by post hoc analyses for multiple comparisons of categories. Results: The number of patients was 6793 in the CAI group and 1362 in the CUI group. The rate of antipsychotic monotherapy in the CAI group was significantly higher than that in the CUI group (58.3% vs 50.7%), and the rate of complete antipsychotic monotherapy in the CAI group was significantly higher than that in the CUI group (20.4% vs 15.6%). The rate of DSTRS was significantly lower in the CAI group than the CUI group (43.6% vs 49.4%). The rate of antipsychotic monotherapy (56.0%) and complete antipsychotic monotherapy (20.0%) in the CAI group except patients prescribed clozapine were also significantly higher than that in the CUI group. The rate of antipsychotic monotherapy in the CAI with DSTRS group (63.3%) and the rate of complete antipsychotic monotherapy in the CAI with DSTRS group (22.6%) were significantly higher than that in the other three groups. Discussion & Conclusion: Both establishment of clozapine prescription and the precise diagnosis of subgroups about TRS or not at discharge in each institution would lead clinicians to the treatment which may contribute to the higher psychotropic monotherapy rate for overall schizophrenia treatment. [ABSTRACT FROM AUTHOR]

Background/Aim: This study aimed to evaluate the effects of doxorubicin (Dox) on bone microstructure and metabolism in a mouse model of soft tissue sarcoma. Materials and Methods: CCRF S-180? cells (2-4×105 cells/0.2 ml) were injected subcutaneously into the back of mice. The mice were divided into four groups according to tumor and treatment status and were reared and sacrificed after 2 or 4 weeks. Micro-computed tomography (CT) was performed to calculate the architecture of the femoral bone. The proximal tibia was double stained with tartrate-resistant acid phosphatase (TRACP) and alkaline phosphatase (ALP), and bone morphometry was performed. Results: Trabecular bone mass was significantly reduced in the Sarcoma and Sarcoma+Dox groups. Cortical bone thickness was reduced in the DOX group, with a stronger effect observed in the Sarcoma+Dox group. In bone morphometry, osteoclast number at the bone surface (Oc.N/BS) was significantly lower in the Dox, Sarcoma, and Sarcoma+Dox groups than in the Control group at 2 weeks. The osteoblast surface at the bone surface (Ob.S/BS) was significantly lower in the Dox and Sarcoma groups than in the Control group at 2 weeks. At 4 weeks, the differences were smaller for both Oc.N/BS and Ob.S/BS. Conclusion: The use of doxorubicin alone worsened the cortical bone structure; however, the presence of both soft-tissue sarcoma and doxorubicin use worsened both cortical and trabecular bone structures from an early stage. [ABSTRACT FROM AUTHOR]