Administration Of Nonsteroidal Anti-inflammatory Drugs Research Articles

Equine Laminitis: A retrospective study of 55 cases (2000-2004)

Laminitis is a common equine disease. In order to have a good prognosis, prompt therapy is essential. Fifty-five cases of equine laminitis, that were treated in the Clinic of Surgery, School of Veterinary Medicine, were included in this study. More specifically, the clinical presentation and the diagnostic approach are described and the therapeutic protocol is evaluated. At the same time, the literature is reviewed as far as the epidemiology, the pathogenesis, the clinical signs, the diagnosis and the treatment is concerned. It is worth mentioning that several therapeutic protocols have been put forward for the treatment of laminitis, perhaps due to the fact that its pathogenesis is still under dispute. Prolonged rest, frog support, cols hosing of the feet, severe diet, administration of antibiotics and non-steroidal anti-inflammatory drug were the key points of the protocol of this study that led to extremely good results for the majority of the cases.

Non-steroidal anti-inflammatory drugs attenuate agonist-evoked activation of transient receptor potential channels

Transient receptor potential (TRP) cation channels are the largest group of sensory detector proteins expressed in the nerve terminals of many receptors including nociceptors, and are activated by temperature and chemicals that elicit hot or cold sensations. Antagonists of these channels are likely promising targets for new analgesic drugs at the peripheral and central levels. Because some non-steroidal anti-inflammatory drugs (NSAIDs) are structural analogs of prostaglandins and NSAIDs attenuate heat nociception and mechanical allodynia in models of inflammatory and neuropathic pain, we investigated whether three widely used NSAIDs (diclofenac, ketorolac, and xefocam) affect thermal and mechanical hyperalgesia following the activation of TRPA1 and TRPV1 channels. We measured nociceptive thermal paw withdrawal latencies and mechanical thresholds bilaterally at various time points following intraplantar injection of the TRPA1 agonists, cinnamaldehyde (CA) and allyl isothiocyanate (AITC) or the TRPV1 agonist capsaicin, or vehicle. When pretreated with vehicle, intraplantar injection of CA, AITC and capsaicin each resulted in significant decreases in thermal withdrawal latency and mechanical threshold in the ipsilateral hindpaw that did not return to baseline for more than 2h. To test effects of NSAIDS either diclofenac, ketorolac or xefocam was pre-injected in the same hindpaw 35min prior to CA, AITC or capsaicin. Pretreatment with each of the three NSAIDs produced strong antinociceptive and antihyperalgesic effects lasting approximately 60min. Thus, we show for the first time that local administration of NSAIDs reduces thermal and mechanical hyperalgesia following TRPA1 or TRPV1 activation.

Perioperative use of nonsteroidal anti-inflammatory drugs and the risk of anastomotic failure in emergency general surgery.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used analgesic and anti-inflammatory adjuncts. Nonsteroidal anti-inflammatory drug administration may potentially increase the risk of postoperative gastrointestinal anastomotic failure (AF). We aim to determine if perioperative NSAID utilization influences gastrointestinal AF in emergency general surgery (EGS) patients undergoing gastrointestinal resection and anastomosis. Post hoc analysis of a multi-institutional prospectively collected database was performed. Anastomotic failure was defined as the occurrence of a dehiscence/leak, fistula, or abscess. Patients using NSAIDs were compared with those without. Summary, univariate, and multivariable analyses were performed. Five hundred thirty-three patients met inclusion criteria with a mean (±SD) age of 60 ± 17.5 years, 53% men. Forty-six percent (n = 244) of the patients were using perioperative NSAIDs. Gastrointestinal AF rate between NSAID and no NSAID was 13.9% versus 10.7% (p = 0.26). No differences existed between groups with respect to perioperative steroid use (16.8% vs. 13.8%; p = 0.34) or mortality (7.39% vs. 6.92%, p = 0.84). Multivariable analysis demonstrated that perioperative corticosteroid (odds ratio, 2.28; 95% confidence interval, 1.04-4.81) use and the presence of a colocolonic or colorectal anastomoses were independently associated with AF. A subset analysis of the NSAIDs cohort demonstrated an increased AF rate in colocolonic or colorectal anastomosis compared with enteroenteric or enterocolonic anastomoses (30.0% vs. 13.0%; p = 0.03). Perioperative NSAID utilization appears to be safe in EGS patients undergoing small-bowel resection and anastomosis. Nonsteroidal anti-inflammatory drug administration should be used cautiously in EGS patients with colon or rectal anastomoses. Future randomized trials should validate the effects of perioperative NSAIDs use on AF. Therapeutic study, level III.

The risk factors associated with postoperative hemorrhage after tooth extraction: a multi-center retrospective study of patients receiving oral antithrombotic therapy.

The purpose of this study was to retrospectively investigate the multivariate relationships between specific risk factors and postoperative hemorrhage after tooth extraction in patients who were prescribed oral antithrombotic therapy. Risk factors for postoperative hemorrhage after tooth extraction were evaluated using univariate and multivariate analyses. Patient characteristics such as age and gender; the presence or absence of known comorbidities such as diabetes mellitus, hypertension, cerebral infarction, and alcohol consumption; and perioperative diarrhea were assessed. The drug used for antithrombotic therapy, preoperative blood test results, the presence or absence of preoperative antibiotics or nonsteroidal anti-inflammatory drug (NSAID) administration, the total number of extracted teeth, and the type of surgical procedures were also evaluated. We found that the preoperative administration of antibiotics (odds ratio (OR)=2.52), an increased prothrombin time international normalized ratio (PT-INR) value (OR=1.94), and the extraction of multiple teeth (OR=2.10) were significantly associated with postoperative hemorrhage. There was no significant association between postoperative hemorrhage and any other demographic factors or comorbidities, including concomitant alcohol use. We demonstrated the multivariate relationship between the risk factors and postoperative hemorrhage after tooth extraction in patients receiving oral antithrombotic therapy. Surgeons should be aware of these risks and monitor the PT-INR of anticoagulated patients.

A Multicenter, Prospective, Randomized Controlled Trial Evaluating the Efficacy of Rectal Diclofenac and Sublingual Nitrate as a Combined Prophylactic Treatment for Post-ERCP Pancreatitis.

Acute pancreatitis is the major complication of endoscopic retrograde cholangiopancreatography(ERCP). A preliminary research suggested that the administration of nonsteroidal anti-inflammatory drugs (NSAIDs) with nitrate might reduce the incidence of post-ERCP pancreatitis (PEP) more effectively than NSAIDs alone. We conduct a two-arm, multicenter, prospective, randomized, superiority trial to evaluate the additional effect of nitrate for prevention of PEP. A total of 900 patients randomly receive 50 mg diclofenac suppository either alone or with 5 mg isosorbide dinitrate sublingual tablet. The primary endpoint is the occurrence of PEP. This study will clarify whether NSAIDs plus nitrate can prevent PEP.

024 Timing and frequency of antibiotic and nonsteroidal anti-inflammatory drug administration does not affect wound healing in recently weaned beef calves after band castration

024 Timing and frequency of antibiotic and nonsteroidal anti-inflammatory drug administration does not affect wound healing in recently weaned beef calves after band castration

Rectal nonsteroidal anti-inflammatory drugs administration is effective for the prevention of post-ERCP pancreatitis: An updated meta-analysis of randomized controlled trials

BackgroundAcute pancreatitis is one of the most common complications of endoscopic retrograde cholangiopancreatography (ERCP). Whether the prophylactic administration of rectal non-steroidal anti-inflammatory drugs (NSAIDs) peri-ERCP is effective in preventing post-ERCP pancreatitis (PEP) remains controversial. The aim of this study was to assess the effect of rectal NSAIDs on PEP. MethodsA systematic search of literature databases (Cochrane Library, PubMed, EMBASE, and Web of Science) was performed to identify eligible randomized controlled trials (RCTs). The Jadad score for assessing risk of bias was used to evaluate the quality of included studies. The primary endpoint of the study was efficacy for PEP prevention. Sub-analyses were performed to determine the risk reduction for different NSAID types, for general vs. high-risk patients, by timing of administration and for moderate to severe PEP. ResultsTwelve RCTs, including a total of 3989 patients, were identified and included in the analysis. The risk of PEP was lower in the NSAIDs group than in the placebo group (RR 0.52; 95% CI 0.43–0.64; P < 0.01). The risk of moderate to severe PEP was also lower in the NSAIDs group. (RR 0.44; 95% CI 0.28–0.69; P < 0.01). There was no difference in efficacy between rectal indomethacin and diclofenac, nor between pre-ERCP and post-ERCP administration timing of rectal NSAIDs. ConclusionsA single rectal dose of NSAIDs is effective in preventing PEP both in high-risk and in unselected patients, regardless of timing of administration (pre- or post-ERCP) and NSAID type (indomethacin or diclofenac).

Subclinical Kidney Injury in Children Receiving Nonsteroidal Anti-Inflammatory Drugs After Cardiac Surgery

To investigate the association of nonsteroidal anti-inflammatory drug (NSAID) administration with urinary neutrophil gelatinase-associated lipocalin (NGAL) levels in children following cardiopulmonary bypass (CPB) who did not develop acute kidney injury (AKI). In this prospective observational study, urinary NGAL levels were investigated in 210 children who underwent cardiothoracic surgery requiring CPB. Children with clinical AKI (defined as an increase in serum creatinine ≥50% from baseline within 72 hours of CPB) were excluded from the analysis. NSAIDs were administered no sooner than 24 hours after CPB. NGAL levels were compared between children who received NSAIDs (n = 146) and those who did not receive NSAIDs (n = 64). The median age was 3.2 years in the children who received NSAIDs and 2.5 years in those who did not receive NSAIDs (P = .05). Before NSAID administration at 24 hours following CPB, the median NGAL level was 15 ng/mL in both groups (P = .92). Following NSAID administration, the median urinary NGAL level increased to 83 ng/mL (IQR, 45-95 ng/mL) at 72 hours after CPB in those receiving NSAIDs (P < .001). In contrast, the median NGAL level decreased to 10 ng/mL (IQR, 5.4-15.9 ng/mL) at 72 hours after CPB in those who did not receive NSAIDs (P = .01). In multivariable analysis, children receiving NSAIDs demonstrated a 5-fold elevation of urinary NGAL levels at 60-72 hours following CPB compared with those who did not receive NSAIDs (P < .001). NSAID administration was associated with a significant increase in urinary NGAL in children who did not develop clinical AKI following CPB. This indicates that NGAL can detect NSAID-induced subclinical kidney injury in this population.

Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis

Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.

Preoperative intravenous ibuprofen does not influence postoperative narcotic use in patients undergoing elective hernia repair: a randomized, double-blind, placebo controlled prospective trial

IntroductionInguinal and umbilical hernia repairs are among the most common surgical procedures performed in the US. Optimal perioperative pain control regimens remain challenging and opioid analgesics are commonly used. Preoperative nonsteroidal anti-inflammatory drug (NSAID) administration has been shown to reduce postoperative narcotic requirements. This study sought to evaluate the efficacy of perioperative intravenous (IV) ibuprofen on postoperative pain level and narcotic use in patients undergoing open or laparoscopic inguinal and/or umbilical hernia repair.MethodsA single center, randomized, double-blind placebo-controlled trial involving patients ≥18 years undergoing inguinal and/or umbilical hernia repair was performed. Patients were randomized to receive 800 mg of IV ibuprofen or placebo preoperatively. Outcomes assessed included postoperative pain medication required and visual analog scale (VAS) pain scores.ResultsForty-eight adult male patients underwent inguinal and/or umbilical hernia repair. Patients receiving IV ibuprofen used more oxycodone/acetaminophen (32% vs 13%) and IV hydromorphone (12% vs 8.7%), and fewer combinations of pain medications (44% vs 65.2%) in the first two postoperative hours compared to placebo (p=0.556). The IV ibuprofen group had more patients pain free (28% vs 8.7%, p=0.087) and lower VAS scores (3.08±2.14 vs 3.95±1.54, p=0.134) at 2 hours postoperatively, compared to the placebo group, however, this was not statistically significant. Similar pain levels at 1, 3, and 7 days, postoperative and similar use of rescue medications in both groups were observed.ConclusionPreoperative administration of IV ibuprofen did not significantly reduce postoperative pain among patients undergoing elective hernia repair. Considerable variability in postoperative narcotic analgesic requirement was noted, and larger scale studies are needed to better understand the narcotic analgesic requirements associated with IV ibuprofen in inguinal/umbilical hernia repair patients.

Multilevel Thoracic Paravertebral Block Using Ropivacaine With/Without Dexmedetomidine in Video-Assisted Thoracoscopic Surgery

Thoracic paravertebral block (TPVB) is reported to have advantages in postoperative pain management in unilateral thoracic surgeries. Previous studies have demonstrated that dexmedetomidine could be used as an adjuvant to local anesthetics, with the aim of prolonging the duration of neural blockade. However, little is known about whether such a combination could improve the quality of postoperative analgesia compared with local anesthetic only when TPVB is used for patients undergoing video-assisted thoracoscopic surgery (VATS). A prospective, randomized, controlled study. Single-center university hospital. The study included 60 patients undergoing VATS under general anesthesia. The patients were allocated randomly into the following 2 groups: 0.375% ropivacaine, 20 mL only (group R, n = 30), and 0.375% ropivacaine, 20 mL plus 1 μg/kg of dexmedetomidine (group RD, n = 30). At the end of surgery, TPVB guided using ultrasound was performed at 4 points-T4-5, T5-6, T6-7, and T7-8-of the surgical side; 5 mL of solution were injected at each point. Postoperatively, the intravenous nonsteroidal anti-inflammatory drug flurbiprofen was used as part of multimodal analgesia. Pain scores at rest and during coughing were evaluated by a blinded observer in the postanesthesia care unit postoperatively at 1, 2, 4, 8, 12, 24, 36, and 48 hours, and the dermatomal levels of sensory blockade, postoperative requirements for rescue analgesia, adverse events, and patient satisfaction also were recorded. There was a significant reduction in postoperative pain scores at rest starting from the postoperative 8th hour until the 48th hour and during coughing starting at the postoperative 4th hour until the 48th hour in the group RD compared with those in group R (p = 0.043). The dermatomal levels of sensory blockade were comparable in the 2 groups. Patient satisfaction after surgery was significantly higher in the group RD than in group R (p < 0.001). Total consumption of the intravenous rescue analgesic morphine and adverse events were not significantly different between the 2 groups. Compared with ropivacaine only, the addition of dexmedetomidine, 1 μg/kg, to local anesthetic for multilevel TPVB in patients undergoing VATS prolonged the duration of postoperative analgesia and improved patient satisfaction without serious side effects when combined with postoperative intravenous nonsteroidal anti-inflammatory drug administration.

Prostaglandin E2 is essential for efficacious skeletal muscle stem-cell function, augmenting regeneration and strength

Skeletal muscles harbor quiescent muscle-specific stem cells (MuSCs) capable of tissue regeneration throughout life. Muscle injury precipitates a complex inflammatory response in which a multiplicity of cell types, cytokines, and growth factors participate. Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets MuSCs via the EP4 receptor, leading to MuSC expansion. An acute treatment with PGE2 suffices to robustly augment muscle regeneration by either endogenous or transplanted MuSCs. Loss of PGE2 signaling by specific genetic ablation of the EP4 receptor in MuSCs impairs regeneration, leading to decreased muscle force. Inhibition of PGE2 production through nonsteroidal anti-inflammatory drug (NSAID) administration just after injury similarly hinders regeneration and compromises muscle strength. Mechanistically, the PGE2 EP4 interaction causes MuSC expansion by triggering a cAMP/phosphoCREB pathway that activates the proliferation-inducing transcription factor, Nurr1 Our findings reveal that loss of PGE2 signaling to MuSCs during recovery from injury impedes muscle repair and strength. Through such gain- or loss-of-function experiments, we found that PGE2 signaling acts as a rheostat for muscle stem-cell function. Decreased PGE2 signaling due to NSAIDs or increased PGE2 due to exogenous delivery dictates MuSC function, which determines the outcome of regeneration. The markedly enhanced and accelerated repair of damaged muscles following intramuscular delivery of PGE2 suggests a previously unrecognized indication for this therapeutic agent.

The efficacy of non-narcotic analgesics on post-operative endodontic pain: A systematic review and meta-analysis: The efficacy of non-steroidal anti-inflammatory drugs and/or paracetamol on post-operative endodontic pain.

The objective of this review was to evaluate the efficacy of non-narcotic analgesics including non-steroidal anti-inflammatory drugs (NSAIDs) and/or paracetamol in the treatment of post-operative endodontic pain. Additionally, we aimed to examine the possible association of study covariates on the pain scores using meta-regression analysis. An electronic search was performed in 2016. After data extraction and quality assessment of the included studies (n=27, representing 2188 patients), meta-analysis was performed using a random-effect inverse variance method. Meta-regression analysis was conducted to examine the associations between effect sizes and study-level covariates (P<0·05). The results showed that administration of non-narcotic analgesic was more effective than placebo in the management of post-operative pain, resulting in a lower pain scores with a standardised mean difference of -0·50 (95% CI= -0·70, -0·30), -0·76 (95%CI= -0·95, -0·56), -1·15 (95% CI= -1·52, -0·78), -0·65 (95% CI= -1·05, -0·26) for immediately after the procedure, 6-, 12- and 24h post-operative follow-ups (test for statistical heterogeneity: P=0·000, P=0·000, P=0·000 and P=0·001), respectively. Our meta-regression analysis provided the evidence for association between some study covariates with treatment effect, each at different follow-ups. We concluded that the clinicians can manage post-operative endodontic pain by administration of NSAIDs and/or paracetamol. However, analgesic regimens should be considered as important determinants when prescribing a pharmacological adjuvant.

Food Effect on Oral Bioavailability: Old and New Questions.

Food Effect on Oral Bioavailability: Old and New Questions.

Effect of NSAIDs on Recovery From Acute Skeletal Muscle Injury: A Systematic Review and Meta-analysis

Background: There is debate as to whether the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is beneficial after acute skeletal muscle injury. Some studies have suggested that NSAID use may be detrimental to injured muscle. Purpose: To determine whether NSAID use affects recovery from skeletal muscle injury as assessed by strength loss, soreness, and/or blood creatine kinase level. Study Design: Systematic review and meta-analysis. Methods: An extensive systematic review was completed searching 16 databases (eg, PubMed, Cochrane Library, EMBASE). Inclusion criteria were (1) acute injury to skeletal muscle, (2) use of a control condition, (3) certainty of the NSAID dose administered, and (4) use of 1 or more of the 3 desired outcome measures. A total of 5343 study reports were screened, of which 41 studies were deemed suitable for inclusion. The standardized mean difference was used as the effect size (ES) and was calculated such that a positive ES indicated NSAID efficacy. Meta-analyses were run using a random-effects model. Results: For all studies, time points after injury, and injury markers combined, NSAID use was found to elicit a small to medium, significant decrease in the markers of injury (overall ES = +0.34; P = .0001). Because heterogeneity in study ES was apparent (ie, Q−df = 52.4, P = .000005; I2 = 57%), subgroup meta-analyses and meta-regressions were run in an attempt to explain the heterogeneity. In human studies, study ESs were higher when lower body muscles were injured (P = .045). In animal studies, study ESs were lower with longer NSAID administration durations (P = .023) and at longer follow-up times after injury (P = .010). Conclusion: Overall, our analysis supports NSAID use for reducing strength loss, soreness, and blood creatine kinase level after an acute muscle injury, at least for humans and in the short term. Additional research is required to determine why NSAID use appears to be more effective when lower-body muscles in humans are injured. It would also be important to determine why NSAID use appears detrimental at later times after injury in animals but not humans.

Natural evolution in patients with nonsteroidal anti-inflammatory drug-induced urticaria/angioedema.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent triggers of drug hypersensitivity with NSAIDs-induced urticaria/angioedema (NIUA) the most common phenotype. Loss of hypersensitivity has been reported for IgE-mediated reactions; however, it has not been assessed in nonimmunological reactions such as NIUA. We evaluated NSAID-hypersensitivity over time in NIUA patients. Patients confirmed as NIUA by positive drug provocation test (DPT) with acetylsalicylic acid (ASA) during 2005-2012 (V1) were included (n=38). Subjects were prospectively re-evaluated by DPT with ASA/other NSAIDs at two time points between 2013 and 2015 (V2 and V3). Atopy was assessed by skin prick test (SPT) using inhalant and food allergens. Patients were evaluated at V1 and re-evaluated after 60 months (V2; IR:48-81) and a further 18 months (V3; IR:14-24). At V2, the majority (24; 63.15%) tolerated ASA and other NSAIDs (Group A) while 14 (36.84%) still reacted (Group B). At V3, all Group A patients remained tolerant; all Group B patients remained hypersensitive. The number of previous episodes reported at V1 and the percentage of reactions induced by ASA/ibuprofen were significantly lower in Group A (P=.005 and P=.006, respectively). Group A patients developed tolerance 72 months (IR:45-87) after their last evaluated reaction (V1); this interval was shorter in nonatopics (P=.003), patients who experienced reactions over 1 hour after NSAIDs administration (P=.001), and those who experienced isolated urticaria after NSAID intake (P=.024). NIUA patients may develop tolerance to NSAIDs over time, a process that seems to be influenced by atopy and type of clinical reaction.

Immunosuppressive agents are associated with peptic ulcer bleeding.

Peptic ulcer bleeding can be fatal. Non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids and immunosuppressive agents are administered for long-term usage. The present study assessed the association between peptic ulcer bleeding and administration of NSAIDs, corticosteroids and immunosuppressive agents. Furthermore, the efficacy of lowering the risk of peptic ulcer bleeding with proton pump inhibitors (PPI) and histamine 2 receptor antagonists (H2RA) was evaluated. Medical records were retrospectively analyzed for patients subjected to an upper gastrointestinal (GI) endoscopy performed at the National Hospital Organization Shimoshizu Hospital (Yotsukaido, Japan) from October 2014 to September 2015. During this period, a total of 1,023 patients underwent an upper GI endoscopy. A total of 1,023 patients, including 431 males (age, 68.1±12.9 years) and 592 females (age, 66.4±12.3 years), who had been administered NSAIDs, corticosteroids, immunosuppressive agents, PPIs and H2RAs, were respectively enrolled. Endoscopic findings of the patients were reviewed and their data were statistically analyzed. Logistic regression analysis was used to determine the odds ratio of peptic ulcer bleeding for each medication; immunosuppressive agents had an odds ratio of 5.83, which was larger than that for NSAIDs (4.77). The Wald test was applied to confirm the correlation between immunosuppressive agents and peptic ulcer bleeding. Furthermore, χ2 tests were applied to the correlation between peptic ulcer bleeding and administration of PPIs or H2RAs. Immunosuppressive agents had the largest χ2, and the P-value was 0.03. Administration of PPIs was significantly correlated with non-peptic ulcer bleeding (P=0.02); furthermore, a tendency toward non-peptic ulcer bleeding with administration of H2RA was indicated, but it was not statistically significant (P=0.12). In conclusion, immunosuppressive agents were correlated with peptic ulcer bleeding and PPIs were effective at lowering the risk of peptic ulcer bleeding.

The treatment of desmoid tumors associated with familial adenomatous polyposis: the results of a Japanese multicenter observational study.

Familial adenomatous polyposis (FAP)-associated desmoid tumor (DT) is sometimes life threatening. However, the optimal treatment for DTs has not been established. The aim of this study was to analyze the outcomes of surgical and pharmacological treatments for DT in Japanese FAP patients. We retrospectively reviewed the data of 303 patients who underwent colectomy for FAP between 2000 and 2012. We analyzed 41 patients with DTs in which the location was apparent. The selection of treatment for intra-abdominal DTs was also evaluated according to Church's classification. Surgery was frequently used to treat extra-abdominal DTs. Multimodal treatments, including surgery, and the administration of non-steroidal anti-inflammatory drugs, hormonal therapy, and chemotherapy were widely used for intra-abdominal DTs. The most effective pharmacological treatment was cytotoxic chemotherapy, which was associated with a response rate of 45.5% and a disease control rate of 72.7%. After a median follow-up period of 53.0 months, the 5-year DT-specific survival rate in patients with stage IV disease was 71.4%; in contrast, the rate in patients with other stages was 100%. Four-stage IV patients died of DT due to uncontrollable rapid progression. No cytotoxic chemotherapy was administered; however, incomplete resection was performed in three cases. Our findings will provide clues that may help physicians in selecting the optimal strategy for this rare disease.

Incidence of heterotopic ossification in minimally invasive short-stem THA using the modified anterolateral approach.

Heterotopic ossification (HO) is known to be a common complication after total hip arthroplasty (THA). The minimal invasive (MIS) modified anterolateral approach has become popular in combination with a short stem. We analysed the incidence of HO following short-stem THA using this approach in combination with a postoperative administration of nonsteroidal anti-inflammatory drugs (NSAIDs). 216 short stems were implanted in 162 patients. NSAIDs were administered for 2 weeks after surgery in 154 patients (95.1%). Standardised pre- and postoperative radiographic imaging was done at 2-year follow-up. HO was analysed according to the Brooker classification. Influence of age, gender, body mass index (BMI), and blood transfusion were analysed. Harris Hip Score (HHS) and visual analogue scale (VAS) of satisfaction were assessed. Operation time and blood-transfusion rate was documented. Short-term gastrointestinal side effects were recorded. The overall incidence of HO was 7.8% (16 cases). HO Brooker type 3 and 4 occurred in only 1 case (0.5%). No correlation with age, gender or BMI was revealed. HHS improved largely from 45.8 (SD 15.9) before surgery to 98.1 (SD 4.7) after a minimum of 2 years. At that point VAS satisfaction was 9.7 (SD 0.9). Mean operative time was 45.8 minutes (SD 18.7). 12 patients (7.4%) received at least 1 blood-transfusion. Gastrointestinal side effects occurred in 13 of 154 patients (8.4%). The combination of short-stem THA, the MIS modified anterolateral approach and a postoperative application of NSAIDs resulted in the effective prevention of HO and excellent clinical results.

Effects of delayed NSAID administration after experimental eccentric contraction injury - A cellular and proteomics study.

BackgroundAcute muscle injuries are exceedingly common and non-steroidal anti-inflammatory drugs (NSAIDs) are widely consumed to reduce the associated inflammation, swelling and pain that peak 1–2 days post-injury. While prophylactic use or early administration of NSAIDs has been shown to delay muscle regeneration and contribute to loss of muscle strength after healing, little is known about the effects of delayed NSAID use. Further, NSAID use following non-penetrating injury has been associated with increased risk and severity of infection, including that due to group A streptococcus, though the mechanisms remain to be elucidated. The present study investigated the effects of delayed NSAID administration on muscle repair and sought mechanisms supporting an injury/NSAID/infection axis.MethodsA murine model of eccentric contraction (EC)-induced injury of the tibialis anterior muscle was used to profile the cellular and molecular changes induced by ketorolac tromethamine administered 47 hr post injury.ResultsNSAID administration inhibited several important muscle regeneration processes and down-regulated multiple cytoprotective proteins known to inhibit the intrinsic pathway of programmed cell death. These activities were associated with increased caspase activity in injured muscles but were independent of any NSAID effect on macrophage influx or phenotype switching.ConclusionsThese findings provide new molecular evidence supporting the notion that NSAIDs have a direct negative influence on muscle repair after acute strain injury in mice and thus add to renewed concern about the safety and benefits of NSAIDS in both children and adults, in those with progressive loss of muscle mass such as the elderly or patients with cancer or AIDS, and those at risk of secondary infection after trauma or surgery.