Preemptive Intravenous Human Immunoglobulin G Suppresses BK Polyomavirus Replication and Spread of Infection In Vitro.

BK polyomavirus (BKPyV) infection causes various diseases in immunocompromised patients. Cells from human lung and kidney were infected with BKPyV and treated with commercially available intravenous immunoglobulin G (IVIG). Its effects on BKPyV replication and spread of infection were investigated, focusing on administration timing. IVIG treatment 3 hours after infection suppressed BKPyV replication assessed by real-time PCR and expression of the viral capsid protein 1 and large T-antigen. IVIG effectively reduced the number of BKPyV-infected cells 2 weeks after infection in an antibody titer-dependent manner. Virus release in the culture supernatants was not influenced by IVIG treatment 6-80 hours and 3-9 days after infection. Collectively, IVIG did not affect viral release from infected cells but inhibited the spread of infection by neutralizing the released virus and blocking the new infected cell formation, indicating greater efficacy in early localized infection. BKPyV replication resumed in IVIG-treated cultures at 7 days after IVIG removal. Early prophylactic administration of IVIG is expected to reduce the growth and spread of BKPyV infection, resulting in the reduction of infected cell lesions and prevention of BKPyV-associated diseases.

Sex-distinct microglial activation and myeloid cell infiltration in the spinal cord after painful peripheral injury.

Chronic pain is a common and often debilitating problem that affects 100 million Americans. A better understanding of pain's molecular mechanisms is necessary for developing safe and effective therapeutics. Microglial activation has been implicated as a mediator of chronic pain in numerous preclinical studies; unfortunately, translational efforts using known glial modulators have largely failed, perhaps at least in part due to poor specificity of the compounds pursued, or an incomplete understanding of microglial reactivity. In order to achieve a more granular understanding of the role of microglia in chronic pain as a means of optimizing translational efforts, we utilized a clinically-informed mouse model of complex regional pain syndrome (CRPS), and monitored microglial activation throughout pain progression. We discovered that while both males and females exhibit spinal cord microglial activation as evidenced by increases in Iba1, activation is attenuated and delayed in females. We further evaluated the expression of the newly identified microglia-specific marker, TMEM119, and identified two distinct populations in the spinal cord parenchyma after peripheral injury: TMEM119+ microglia and TMEM119- infiltrating myeloid lineage cells, which are comprised of Ly6G + neutrophils and Ly6G- macrophages/monocytes. Neurons are sensitized by inflammatory mediators released in the CNS after injury; however, the cellular source of these cytokines remains somewhat unclear. Using multiplex in situ hybridization in combination with immunohistochemistry, we demonstrate that spinal cord TMEM119+ microglia are the cellular source of cytokines IL6 and IL1ß after peripheral injury. Taken together, these data have important implications for translational studies: 1) microglia remain a viable analgesic target for males and females, so long as duration after injury is considered; 2) the analgesic properties of microglial modulators are likely at least in part related to their suppression of microglial-released cytokines, and 3) a limited number of neutrophils and macrophages/monocytes infiltrate the spinal cord after peripheral injury but have unknown impact on pain persistence or resolution. Further studies to uncover glial-targeted therapeutic interventions will need to consider sex, timing after injury, and the exact target population of interest to have the specificity necessary for translation.

Everolimus reduces BK polyomavirus infection by suppressing its replication and spread of infection.

BK polyomavirus-associated nephropathy is one of serious complications in transplant recipients. Everolimus-a mammalian target of rapamycin inhibitor-has been shown to reduce the incidence of BK polyomavirus infection in transplant recipients. In this study, the effects of everolimus were examined on viral replication and the spread of infection in BK polyomavirus-infected cultures. BK polyomavirus replicated in renal and pulmonary cells, contrary to that in hepatocytes, and spread as diffusely scattered patterns of infected cells, unlike plaque formation through the cell-to-cell mode. BK polyomavirus is stable to heat up to 65 °C with a particle per infectivity ratio of 5000, and the replication cycle was for approximately 34 h. Everolimus administration remarkably reduced the viral replication to 20% in cells treated with 0.1-10 ng/mL, the concentration at which everolimus reached the serum of transplant recipients. In addition, it reduced the amount of viral capsid protein 1 at 5 ng/mL without reducing the ratio of viral capsid protein 1 versus ß-actin, and it also retained the pattern of viral capsid protein 1 localization in the nuclei. Everolimus suppressed the number of infected cells to 32.8% during a 14-day treatment, indicating the reduction of BK polyomavirus-infected cell mass to 18.8% of untreated cultures by modifying cellular functions. The reduction in the total number of BK polyomavirus infected cells by everolimus indicates that everolimus alleviates BK polyomavirus infection, including nephropathy in transplant recipients.

Involvement of spinal G-protein inwardly rectifying potassium (GIRK) channels in the enhanced antinociceptive effects of the activation of both µ-opioid and cannabinoid CB1 receptors.

Neuropathic pain is refractory to opioid analgesics. Since there are functional linkages between µ-opioid receptors (MOR) and cannabinoid receptors (CBR), the present study was designed to investigate the interactions between MOR and CB1R based on antinociceptive effects for neuropathic pain mediated through G protein-coupled inwardly-rectifying potassium channels (GIRKs). The antinociceptive effects against pseudonociceptive response or neuropathic pain of MOR and CBR agonists were assessed in mice with or without partial sciatic nerve ligation. To investigate the functional interaction between MOR and CB1R, electrophysiological recording through GIRK was performed using the two-electrode voltage-clamp method in oocytes along with Western blotting in the spinal cord of mice. Co-administration of the MOR agonist DAMGO and the CB1R agonist CP55,940 augmented inwardly rectifying K+ currents in Xenopus oocytes co-expressing MOR, CB1R and GIRK1/2. Further, combination of morphine and the CBR agonist WIN-55,212-2 produced prominent antinociceptive effects in an i.t. GIRK1 inhibitor-reversible manner. Furthermore, CB1R was upregulated under neuropathic pain in the spinal cord, and such upregulation and antinociceptive effects were not altered by repeated treatment with morphine plus WIN-55,212-2. Our findings suggest that co-administration of MOR and CBR agonists could enhance their antinociceptive effects through GIRK1 in the spinal cord of mice.

Surgical treatment of wrist joint dysfunction in rheumatoid arthritis: A report of two cases.

In rheumatoid arthritis (RA), it is important to actively treat wrist dysfunction to improve patient outcomes. Herein, we report two cases of wrist dysfunction in RA patients who required partial wrist fusion soon after drug initiation. Case 1: A 38-year-old woman was referred to our hospital because of left wrist joint pain. At the time of examination, swelling and tenderness of the left wrist joint were observed. After 6 months of medication, no improvement in symptoms was noted; therefore, partial wrist fusion was performed. Case 2: A 38-year-old woman was referred to our hospital because of right wrist joint pain. A plain X-ray image showed fusion of the carpal bones. Due to previous failure of drug treatment, the patient opted for arthrodesis. The postoperative course was good in both cases, and the pain improved. In these cases of monoarthritic RA, synovitis and bone destruction were observed, but blood tests showed no features of active disease, and drug treatment was ineffective. In such cases, early surgical treatment should be considered, rather than continuing conservative treatment, to ensure the best outcomes.

Limited Utility of Routine Tests Prior to Ophthalmologic Surgery: An Observational Study in a Japanese Hospital.

INTRODUCTION: Routine preoperative testing for low-risk surgeries without a clinical indication should be avoided; however, such tests are still frequently performed in Japan. This study was performed to assess the impact of routine preoperative tests in low-risk surgery in a Japanese medical setting. METHODS: We performed a retrospective chart review to examine the utility of routine tests with respect to anesthetic management and postoperative complications in all patients aged ≥ 18 years whom ophthalmologists consulted with anesthesiologists before ophthalmologic surgery under general anesthesia. RESULTS: During the 10-year study period, 1,234 anesthetic consultations and 1,211 routine preoperative tests (laboratory tests, chest X-rays, and electrocardiograms) were performed in Toyama University Hospital. In total, 59 patients (4.8% of the study population) canceled surgery after a battery of preoperative evaluation. Among them, 10 patients had incidental abnormalities that necessitated additional tests, and only three patients (0.2%) canceled surgery. In-hospital postoperative complications developed in nine patients (0.7%) whose routine test results made it difficult to predict development of these adverse events. No severe life-threatening events were noted in this survey. CONCLUSIONS: Routine tests prior to eye surgery for adults were of low value for perioperative management and prediction of development of in-hospital complications in this Japanese medical setting. Anesthesiologists and ophthalmologists should selectively order preoperative tests based on the medical interview and physical examination.

Temporal Contribution of Myeloid-Lineage TLR4 to the Transition to Chronic Pain: A Focus on Sex Differences.

Complex regional pain syndrome (CRPS) is a chronic pain disorder with a clear acute-to-chronic transition. Preclinical studies demonstrate that toll-like receptor 4 (TLR4), expressed by myeloid-lineage cells, astrocytes, and neurons, mediates a sex-dependent transition to chronic pain; however, evidence is lacking on which exact TLR4-expressing cells are responsible. We used complementary pharmacologic and transgenic approaches in mice to more specifically manipulate myeloid-lineage TLR4 and outline its contribution to the transition from acute-to-chronic CRPS based on three key variables: location (peripheral vs central), timing (prevention vs treatment), and sex (male vs female). We demonstrate that systemic TLR4 antagonism is more effective at improving chronic allodynia trajectory when administered at the time of injury (early) in the tibial fracture model of CRPS in both sexes. In order to clarify the contribution of myeloid-lineage cells peripherally (macrophages) or centrally (microglia), we rigorously characterize a novel spatiotemporal transgenic mouse line, Cx3CR1-CreERT2-eYFP;TLR4fl/fl (TLR4 cKO) to specifically knock out TLR4 only in microglia and no other myeloid-lineage cells. Using this transgenic mouse, we find that early TLR4 cKO results in profound improvement in chronic, but not acute, allodynia in males, with a significant but less robust effect in females. In contrast, late TLR4 cKO results in partial improvement in allodynia in both sexes, suggesting that downstream cellular or molecular TLR4-independent events may have already been triggered. Overall, we find that the contribution of TLR4 is time- and microglia-dependent in both sexes; however, females also rely on peripheral myeloid-lineage (or other TLR4 expressing) cells to trigger chronic pain.SIGNIFICANCE STATEMENT The contribution of myeloid cell TLR4 to sex-specific pain progression remains controversial. We used complementary pharmacologic and transgenic approaches to specifically manipulate TLR4 based on three key variables: location (peripheral vs central), timing (prevention vs treatment), and sex (male vs female). We discovered that microglial TLR4 contributes to early pain progression in males, and to a lesser extent in females. We further found that maintenance of chronic pain likely occurs through myeloid TLR4-independent mechanisms in both sexes. Together, we define a more nuanced contribution of this receptor to the acute-to-chronic pain transition in a mouse model of complex regional pain syndrome.

Further investigation of the rapid-onset and short-duration action of the G protein-biased µ-ligand oliceridine.

TRV130 (oliceridine), a G protein-biased ligand for µ-opioid receptor, has recently been synthesized. It is considered to have strong antinociceptive effects and only minor adverse effects. However, whether or not oliceridine actually exhibits an ideal pharmacological profile as an analgesic has not yet been fully clarified in animal studies. This study examined the pharmacological profile of oliceridine in cells and animals. Oliceridine (10 µM) did not produce any µ-opioid receptor internalization in cells even though it increased impedance, which reflects the activation of Gi protein using the CellKey™ system, and inhibited the formation of cAMP. In mice, oliceridine (0.3-10 mg/kg) produced a dose-dependent antinociceptive effect with a rapid-onset and short-duration action in the hot-plate test, as well as antihyperalgesia after sciatic nerve ligation without the development of antinociceptive tolerance using the thermal hyperalgesia test. On the other hand, oliceridine inhibited gastrointestinal transit. Furthermore, oliceridine produced rapid-onset hyperlocomotion at antinociceptive doses; sensitization developed in mice and an emetic effect was observed in ferrets. These results indicate that, although oliceridine may produce dopamine-related behaviors even through selective stimulation of the G-protein-biased µ-opioid receptor pathway, it still offers advantages for breakthrough pain without antinociceptive tolerance with adequate doses.

Analysis of the effects of a tricyclic antidepressant on secondary sleep disturbance induced by chronic pain in a preclinical model.

Chronic pain and sleep have a bidirectional relationship that promotes a vicious circle making chronic pain more difficult to treat. Therefore, pain and sleep should be treated simultaneously. In our previous study, we suggested that hyperactivation of ascending serotonergic neurons could cause secondary sleep disturbance in chronic pain. This study aimed to demonstrate the effects of a tricyclic antidepressant (amitriptyline) and a selective 5-hydroxy-tryptamine 2A (5-HT2A) antagonist (MDL 100907) that adjust serotonergic transmission, on secondary sleep disturbance induced in a preclinical chronic pain model. We produced a chronic neuropathic pain model by partial sciatic nerve ligation in mice, analyzed their electroencephalogram (EEG) and electromyogram (EMG) using the SleepSign software, and evaluated the sleep condition of the pain model mice after administration of amitriptyline or MDL 100907. Amitriptyline improved thermal hyperalgesia and the amount of sleep, especially non-REM sleep. Time change of normalized power density of δ wave in the nerve ligation group with amitriptyline administration showed a normal pattern that was similar to sham mice. In addition, MDL 100907 normalized sleep condition similar to amitriptyline, without improvement in pain threshold. In conclusion, amitriptyline could improve sleep quantity and quality impaired by chronic pain. 5-HT2A receptor antagonism could partially contribute to this sleep improvement, but is not associated with pain relief.

Treatment of spontaneous anterior interosseous nerve palsy.

OBJECTIVE: The purpose of this study was to clarify the clinical outcomes of spontaneous anterior interosseous nerve palsy (AINP) treated nonsurgically or surgically. METHODS: The authors retrospectively evaluated the clinical course of 27 patients affected with AINP, treated nonsurgically or surgically. Thirteen patients underwent surgical treatment (interfascicular neurolysis), and 14 patients underwent conservative nonsurgical treatment. The mean patient age at the onset of symptoms was 49 years (range 17-77 years). The mean follow-up duration from onset to the latest follow-up examination was 23 months (range 12-38 months). RRESULTS: In 12 of 14 patients receiving conservative treatment, signs of recovery from the palsy were obtained within 6 months. These patients showed a recovery of manual muscle test (MMT) grade ≥ 3. In contrast, 2 patients who took more than 12 months from symptom onset to initial recovery showed poor recovery (MMT grade ≤ 2). Surgical treatment was performed in 13 patients because of no sign of recovery from palsy. The mean period from symptom onset to the operation was 8.4 months (range 6-14 months). Ten of 13 patients who underwent surgical treatment within 8 months after symptom onset showed good recovery, with MMT grade ≥ 4. However, 3 patients who underwent surgical treatment more than 12 months after onset showed recovery with MMT grade ≤ 3. CONCLUSIONS: Conservative treatment for AINP may be continued when patients show signs of recovery within 6 months after symptom onset. In contrast, surgical treatment may be performed within 8 months from the onset of symptoms when the patients show no recovery signs for 6 months. ABBREVIATIONS: AIN = anterior interosseous nerve; AINP = anterior interosseous nerve palsy; FDP1 = flexor digitorum profundus of the index finger; FPL = flexor pollicis longus; MMT = manual muscle test; NSG = nonsurgical treatment group; SG = surgical treatment group.

Angiotensin receptor blockade mimics the effect of exercise on recovery after orthopaedic trauma by decreasing pain and improving muscle regeneration.

KEY POINTS: Our tibial fracture orthopaedic injury model in mice recapitulates the major manifestations of complex trauma, including nociceptive sensitization, bone fracture, muscle fibrosis and muscle fibre loss. Delayed exercise after complex orthopaedic trauma results in decreased muscle fibrosis and improved pain Losartan, an angiotensin-receptor blocker with anti-fibrotic abilities, recapitulates the effect of exercise on post-injury recovery and may provide an enhanced recovery option for those who are unable to exercise after injury ABSTRACT: Chronic pain and disability after limb injury are major public health problems. Early mobilization after injury improves functional outcomes for patients, although when and how to implement rehabilitation strategies remains a clinical challenge. Additionally, whether the beneficial effects of exercise can be reproduced using pharmacological tools remains unknown and may benefit patients who are unable to exercise as a result of immobilization. We developed a murine model of orthopaedic trauma combining tibia fracture and pin fixation with muscle damage. Behavioural measures included mechanical nociceptive thresholds and distances run on exercise wheels. Bone healing was quantified using microcomputed tomagraphic scanning, and muscle fibre size distribution and fibrosis were followed using immunohistochemistry. We found that the model provided robust mechanical allodynia, fibrosis and a shift to smaller average muscle fibre size lasting up to 5 weeks from injury. We also observed that allowing 'late' (weeks 1-2) rather than 'early' (weeks 0-1) exercise after injury resulted in greater overall running activity and greater reversal of allodynia. In parallel, the late running paradigm was associated with reduced muscle fibrosis, earlier increase in muscle fibre diameter and a short-term benefit in reducing callus volume. Providing the anti-fibrotic angiotensin receptor blocker losartan to mice in drinking water reduced both allodynia and muscle fibrosis. Combining losartan and late exercise provided no additional benefit. We conclude that early healing after orthopaedic trauma must be allowed prior to the initiation of exercise to achieve optimal pain, functional and physiological outcomes and that losartan is a viable candidate for translational studies.

Chronotherapeutic effect of orexin antagonists on glucose metabolism in diabetic mice.

Disrupted sleep is associated with increased risk of type 2 diabetes. Central actions of orexin, mediated by orexin-1 and orexin-2 receptors, play a crucial role in the maintenance of wakefulness; accordingly, excessive activation of the orexin system causes insomnia. Resting-phase administration of dual orexin receptor antagonist (DORA) has been shown to improve sleep abnormalities and glucose intolerance in type 2 diabetic db/db mice, although the mechanism remains unknown. In the present study, to investigate the presence of functional link between sleep and glucose metabolism, the influences of orexin antagonists with or without sleep-promoting effects were compared on glucose metabolism in diabetic mice. In db/db mice, 2-SORA-MK1064 (an orexin-2 receptor antagonist) and DORA-12 (a DORA) acutely improved non-rapid eye movement sleep, whereas 1-SORA-1 (an orexin-1 receptor antagonist) had no effect. Chronic resting-phase administration of these drugs improved glucose intolerance, without affecting body weight, food intake, locomotor activity, and energy expenditure calculated from O2 consumption and CO2 production. The expression levels of pro-inflammatory factors in the liver were reduced by 2-SORA-MK1064 and DORA-12, but not 1-SORA-1, whereas those in the white adipose tissue were reduced by 1-SORA-1 and DORA-12 more efficiently than 2-SORA-MK1064. When administered chronically at awake phase, these drugs caused no effect. In streptozotocin-induced type 1-like diabetic mice, neither abnormality in sleep-wake behavior nor improvement of glucose intolerance by these drugs were observed. These results suggest that both 1-SORA-type (sleep-independent) and 2-SORA-type (possibly sleep-dependent) mechanisms can provide chronotherapeutic effects against type 2 diabetes associated with sleep disturbances in db/db mice.

Everolimus delayed and suppressed cytomegalovirus DNA synthesis, spread of the infection, and alleviated cytomegalovirus infection.

Everolimus is an inhibitor of mammalian target of rapamycin (mTOR) and reduces the risk of cytomegalovirus (CMV) infection in transplant recipients. Everolimus inhibits mTOR complex 1, which regulates factors involved in several crucial cellular functions and is required for CMV replication. However, it is not clear how everolimus regulates CMV replication and prevents and alleviates CMV infection. Effects of everolimus on CMV infection, spread, and DNA synthesis and release from infected cells were assessed by plaque formation, infectious centre assay, real-time PCR of infected cells, and culture supernatant in CMV-infected cultures with and without everolimus. Everolimus enhanced plaque formation by 3.6 times, but the size of the plaques was reduced to 36.4% of untreated cultures in the absence of a pretreatment period. Everolimus reduced viral adsorption but enhanced the replication efficiency of inoculated virus, resulting in an increase in plaque number in the early phase of infection. Preinfection treatment of cells with everolimus efficiently exhibited its antiviral efficacy, and everolimus delayed and suppressed viral DNA synthesis and release from infected cells. Everolimus had suppressed the spread of infection and reduced the number of total infected cells to 40% of untreated cells on day 9, indicating reduction of the size of CMV lesions to one-sixth in 2-3 replication cycles. Preinfection treatment of the cells with everolimus augmented its suppressive effect on CMV infection and replication. Everolimus reduced the total number of infected cells and limited the CMV lesions, and this reduction in the spread of CMV infection would alleviate CMV infection in transplant recipients.

Physeal Bar Resection Under Guidance With a Navigation System and Endoscopy for Correction of Distal Radial Deformities After Partial Growth Plate Arrest.

Partial growth plate arrest caused by trauma may lead to severe deformity and dysfunction. The Langenskiöld method is a surgical technique that involves resection of the physeal bar causing partial growth plate arrest. However, it is a technically demanding procedure. We used the Langenskiöld method under guidance with a navigation system and endoscopy and obtained good results in 2 cases. We consider that use of these tools can be a helpful adjunct to the carrying out this procedure.

Increased risk of paclitaxel-induced peripheral neuropathy in patients using clopidogrel: a retrospective pilot study.

Paclitaxel-induced peripheral neuropathy (PIPN) is one of the serious adverse events associated with paclitaxel-based cancer treatments. A recent case study showed that the antiplatelet agent clopidogrel inhibits paclitaxel metabolism via cytochrome P450 (CYP) 2C8, resulting in severe PIPN. The aim of this study was to determine the impact of clopidogrel as a risk factor for the development of PIPN, using a retrospective cohort study. Data from paclitaxel-treated patients with or without clopidogrel and low-dose aspirin treatment were retrieved from medical charts. A total of 161 adult patients were included in this study: 135 were controls, 9 were clopidogrel-treated and 17 were aspirin-treated. The clopidogrel group had a greater proportion of males and a higher rate of comorbidities, such as diabetes mellitus and dyslipidemia, than the control group. However, patient characteristics were similar between the clopidogrel and aspirin groups. Severe PIPN was diagnosed in 3 (2.2%) and 2 (22.2%) patients in the control and clopidogrel groups, respectively (odds ratio: 12.0; p = 0.031). No patients in the aspirin group presented with severe neuropathy. These pilot data suggest that concomitant treatment with clopidogrel leads to a greater risk of PIPN. The avoidance of concomitant clopidogrel use may be effective in reducing clopidogrel-associated PIPN.

Joint Arthroplasty With Osteochondral Grafting From the Knee for Posttraumatic or Degenerative Hand Joint Disorders.

PURPOSE: To describe the operative procedure and report the clinical outcomes of articular surface reconstruction for various hand joint disorders using autologous osteochondral grafts from the knee. METHODS: Ten patients underwent articular surface reconstruction for hand joint disorders with autologous osteochondral grafts from the patellofemoral joint. Mean patient age was 35 years (range, 15-52 y). The patients were followed for an average of 48 months (range, 16-89 mo). Arthroplasty was performed on the metacarpophalangeal joint in 4 cases, and on the proximal interphalangeal joint in 6 cases. The patients' clinical outcomes were evaluated with joint range of motion, visual analog scale (0-10 points), and Disabilities of the Arm, Shoulder, and Hand (DASH) score. Histological examination was performed in 3 cases after surgery. RESULTS: Graft union was confirmed in all cases without radiographic evidence of resorption or necrosis. Follow-up radiographic examinations showed good graft incorporation without signs of osteoarthritis such as joint space narrowing. The finger flexion-extension arc improved significantly from an average of 21° to 61°. The mean visual analog scale also improved significantly from 7.0 to 1.5. The mean total active motion showed a significant improvement from 151° before surgery to 201° after surgery, and the mean DASH score improved significantly from 33 to 12. There were no significant differences for the arc of finger motion and DASH score between metacarpophalangeal and proximal interphalangeal joint disorders or between hemiarthroplasty and total joint arthroplasty. Histological examination revealed viable chondrocytes in the implanted cartilage. CONCLUSIONS: Autologous osteochondral grafting from the patellofemoral joint provided satisfactory outcomes and may be a useful option for joint surface reconstruction of traumatic or degenerative hand joint disorders. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

New option for surgical treatment of the trapeziometacarpal osteoarthritis: a case report.

We present the case of a 71-year-old, left-handed woman with left thumb carpometacarpal (CMC) joint arthritis. The patient had no pain and could use the hand actively in daily life with a new option of surgical treatment, a vascularized pedicled third CMC joint transfer to the thumb CMC joint.

Operative treatment of metacarpal and phalangeal fractures in athletes: early return to play.

BACKGROUND: Evaluating the outcomes of operative treatment for metacarpal and phalangeal fractures in athletes returning early to play and discussing the more effective methods that permit rapid early return to athletic activity. METHODS: We retrospectively identified a total of 105 metacarpal or phalangeal fractures in 105 athletes with conservative or operative treatment in our department. Of these, 20 athletes required an early return to sport because of a pending important game in their competition within 1 month after injury. Therefore, they underwent surgical treatment with open reduction and internal fixation of metacarpal or phalangeal fractures in an attempt to achieve an early return to their chosen sport at their usual competitive level. The patients included 6 rugby football players, 2 soccer goalkeepers, 3 American football players, 3 handball players, 2 baseball players and 4 who participated in other sports. The clinical records of preoperative and postoperative radiographs were available for all patients, and clinical outcome was evaluated by total active motion (TAM). RESULTS: The patients were followed up for a mean of 27 (24-43) months. At the latest follow-up examination, bone union was obtained in all cases. In cases with metacarpal and phalangeal fractures, the average TAM was 263° (range 240°-270°). CONCLUSION: We consider that an early comeback to training and competition can be permitted exclusively for patients with metacarpal and phalangeal fractures. It is important for the attending physician to administer such treatment after obtaining informed consent and develop a trusting relationship with the patient and other related individuals while paying attention to their hope of quick recovery.

Ultrasound-assisted closed reduction of distal radius fractures.

PURPOSE: To assess the accuracy and ability of ultrasound for monitoring closed reduction for distal radius fractures. METHODS: Consecutive patients undergoing ultrasound-guided closed reduction of acute, displaced distal radius fractures between January 2003 and December 2006 at our department were enrolled. The control group was extracted from patients who underwent a closed reduction for similar fractures under fluoroscopy or without any imaging assistance. To confirm the accuracy of the ultrasonography measurements, displacement distance values were compared with those on radiographic imaging before and after reduction. X-ray parameters for pre- and postreduction, reduction time, total cost, and success rate were compared between the ultrasound-guided and the control groups. RESULTS: The ultrasound-guided group consisted of 43 patients (mean age, 68 y) and the control group consisted of 57 patients, which included 35 patients (mean age, 74 y) with fluoroscopic reduction and of 22 patients (mean age, 72 y) with reduction unaided by imaging. There were no significant displacement differences between radiographic and ultrasound measurements. In x-ray parameters for pre- and postreduction, there were no significant differences between the 2 groups. Ultrasound-guided reduction took longer than the other 2 methods. The success rate of the ultrasound and the fluoroscopic groups were similar (95% and 94%, respectively). CONCLUSIONS: Our data suggest that ultrasound assistance can aid reduction of distal radius fractures as well as fluoroscopy. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic II.