Difference in clinical outcome between total shoulder arthroplasty and reverse shoulder arthroplasty used in hemiarthroplasty revision surgery.

INTRODUCTION: The increase of shoulder replacements will lead to a higher revision rate of shoulder arthroplasties. The aim of this study is to evaluate the clinical results of revision surgery performed in our hospital, distinguish the differences in clinical outcome according to revision indication and differences between total shoulder arthroplasty (TSA) and reverse shoulder arthroplasty (RSA) in hemiarthroplasty (HA) revision surgery. MATERIALS AND METHODS: All patients with an indication for revision of HA were retrospectively included. Clinical evaluation consisted of pre- and post-operative constant scores, disability of arm-shoulder-hand-score (DASH), Dutch translation of the simple shoulder test ((D)SST), Oxford shoulder score test (OSS), short form (SF-36) and the complication rate. RESULTS: From July 1994 to July 2008, 39 patients (40 shoulders) underwent revision arthroplasty. Of 19 patients (19 shoulders) we obtained a complete follow-up. The mean age at revision surgery 69 ± 10 years (range: 46-83) and the mean follow-up 41 ± 31 months (range: 10-113). In 7 cases TSA was used for revision when the cuff was intact, 12 times RSA was performed. The indications for the revision were glenoid erosion (n = 4), humeral component malposition (n = 2), cuff-pathology (n = 12) and infection (n = 1). Postoperative constant score 51.7 ± 11.4 for TSA and 31.1 ± 18.7 for RSA (P = 0.008). The DASH was 48.3 ± 25.1 and 68.7 ± 17.5, respectively (P = 0.09). DSST showed 6 ± 4 and 4 ± 4 (P = 0.414). OSS 41.3 ± 10.1 and 28.1 ± 10.3 (P = 0.017). SF-36 43.3 ± 22.1 and 24.5 ± 12.8 (P = 0.072). Four shoulders (21%) presented four complications. CONCLUSIONS: In this study, revision surgery showed poor to reasonable postoperative results and better clinical outcome for TSA. When a revision after HA was needed, and the soft-tissue component of the shoulder was intact, a TSA proved to be a preferable solution.

CD44 deficiency increases tubular damage but reduces renal fibrosis in obstructive nephropathy.

CD44 is a glycoprotein involved in inflammation and cell-cell/cell-matrix interactions. CD44 is upregulated in the kidney upon injury; however, its role in the pathogenesis of renal damage and fibrosis remains largely unknown. The authors show that mice lacking CD44 developed more tubular damage, associated with decreased proliferation and increased apoptosis of tubular epithelial cells, but less renal fibrosis after unilateral ureteral obstruction. In addition, impaired influx of macrophages and decreased accumulation of myofibroblasts was observed in the obstructed kidney of CD44(-/-) mice compared with CD44(+/+) mice. Hepatocyte growth factor (HGF) and transforming growth factor-beta1 (TGF-beta1) exert reciprocal functions in the progression of renal diseases and interact with CD44 in vitro. For the first time, the authors establish diminished HGF-signaling, via its high affinity receptor c-Met, in the absence of CD44 in vivo. In parallel, the signaling of TGF-beta1 reflected by the relative phosphorylation and nuclear translocation of Smad-2 and Smad-3 was reduced in the obstructed kidney of CD44(-/-) mice. In conclusion, CD44 exerts protective effects on tubuli but contributes to renal fibrogenesis at least in part through enhancement of HGF and TGF-beta1 signaling pathway in obstructive nephropathy.

Cholestatic interleukin-6-deficient mice succumb to endotoxin-induced liver injury and pulmonary inflammation.

Circulating and hepatic interleukin (IL)-6 levels are strongly increased during clinical and experimental cholestasis. Cholestatic liver injury is associated with increased susceptibility to endotoxin-induced toxicity. To determine the role of IL-6 herein, extrahepatic cholestasis was induced by bile duct ligation (BDL) in IL-6-gene deficient (IL-6(-/-)) and normal (IL-6(+/+)) mice. BDL elicited increased levels of hepatic IL-6 mRNA and protein in normal mice. Hepatocellular injury 2 weeks after BDL was similar in IL-6(-/-) and IL-6(+/+) mice as demonstrated by clinical chemistry and histopathology. Administration of endotoxin to cholestatic mice 2 weeks after BDL was associated with enhanced cytokine release, severe liver damage, and death when compared with sham-operated mice. Effects of endotoxin were largely similar in sham-operated IL-6(-/-) and IL-6(+/+) mice, but cholestatic IL-6(-/-) mice were more susceptible to the toxic effects of endotoxin, as reflected by increased cytokine release, more profound liver injury and lung inflammation, and higher mortality. Although endogenous IL-6 is not important in the development of liver injury after experimentally induced obstructive jaundice, this cytokine plays an important role in decreasing hypersensitivity to endotoxin in cholestatic mice.

Interleukin-18 facilitates the early antimicrobial host response to Escherichia coli peritonitis.

To determine the role of endogenous interleukin-18 (IL-18) during peritonitis, IL-18 gene-deficient (IL-18 KO) mice and wild-type mice were intraperitoneally (i.p.) infected with Escherichia coli, the most common causative agent found in septic peritonitis. Peritonitis was associated with a bacterial dose-dependent increase in IL-18 concentrations in peritoneal fluid and plasma. After infection, IL-18 KO mice had significantly more bacteria in the peritoneal lavage fluid and were more susceptible for progression to systemic infection at 6 and 20 h postinoculation than wild-type mice. The relative inability of IL-18 KO mice to clear E. coli from the abdominal cavity was not due to an intrinsic defect in the phagocytosing capacity of their peritoneal macrophages or neutrophils. IL-18 KO mice displayed an increased neutrophil influx into the peritoneal cavity, but these migratory neutrophils were less activate, as reflected by a reduced CD11b surface expression. These data suggest that endogenous IL-18 plays an important role in the early antibacterial host response during E. coli-induced peritonitis.

Endogenous interferon gamma protects against cholestatic liver injury in mice.

Cholestatic patients suffer from high perioperative morbidity and mortality, but the pathophysiology is still unknown. Interferon gamma (IFN-gamma) may play a role during cholestasis. Therefore, bile duct ligation (BDL) was induced in IFN-gamma alpha-chain receptor-deficient (IFN-gammaR(1)-/-) and wild-type (IFN-gammaR(1)+/+) mice. BDL elicited increased IFN-gamma messenger RNA and protein levels in the liver. One week after BDL, IFN-gammaR(1)+/+ mice showed less severe jaundice and liver injury than IFN-gammaR(1)-/- mice, as reflected by lower bilirubin and liver enzyme levels. In accordance, livers of IFN-gammaR(1)+/+ mice displayed smaller areas of necrosis by two-thirds than IFN-gammaR(1)-/- mice on histopathologic examination (P <.05), whereas mitotic activity and proliferating cell nuclear antigen (PCNA) labeling index was more than twice as high in IFN-gammaR(1)+/+ mice (P <.05). Livers of IFN-gammaR(1)+/+ mice displayed higher rates of apoptosis as indicated by DNA fragmentation rate, the number of apoptotic bodies, and poly ADP-ribose polymerase (PARP) immunostaining. BDL was not associated with lethality in IFN-gammaR(1)+/+ mice; IFN-gammaR(1)-/- mice, however, died from 10 days onward and survival after 2 weeks was 62% (10 of 16). In conclusion, these data suggest that IFN-gamma protects against liver injury during extrahepatic cholestasis by stimulation of apoptosis and subsequent proliferation of hepatocytes, leading to elegant removal of damaged hepatocytes, thus preventing necrosis and concomitant inflammatory responses.

A meta-analysis on the efficacy of preoperative biliary drainage for tumors causing obstructive jaundice.

OBJECTIVE: To review the effectiveness of preoperative biliary drainage (PBD) in patients with obstructive jaundice resulting from tumors. SUMMARY BACKGROUND DATA: This was a systematic review, including a meta-analysis, of randomized controlled trials and comparative cohort studies conducted worldwide and published between 1966 and September 2001, classified on methodologic strength and subdivided into level 1 (randomized controlled trials) and level 2 (comparative cohort studies). METHODS: Comparison was made of PBD versus no PBD in jaundiced patients undergoing resection of a tumor. Outcome measures were in-hospital death rate, overall complications resulting from the treatment modality (drainage- and surgery-related complications), and hospital stay. Effect sizes were calculated and combined in meta-analyses. Relative differences (%) were calculated to compare effects on outcome measures. RESULTS: Five randomized controlled studies comprising 302 patients met the inclusion criteria for level 1 studies, and 18 cohort studies comprising 2,853 patients met the criteria for level 2 studies. Meta-analysis of level 1 studies showed no difference in the overall death rate between patients who had PBD and those who had surgery without PBD. The overall complication rate, however, was significantly adversely affected by PBD compared with surgery without PBD. At level 2, there was no difference in the death rate between the two treatment modalities. The overall complication rate, however, was significantly adversely affected by PBD compared with surgery without PBD. If PBD had been without complications, then complications would be in favor of drainage based on level 1 studies, and no difference based on level 2 studies. Further, PBD was not able to reduce the length of postoperative hospital stay compared with surgery without PBD; instead, it prolonged the stay. CONCLUSIONS: This meta-analysis shows that PBD with current standards for patients with obstructive jaundice resulting from tumors carries no benefit and should not be performed routinely. The potential benefit of PBD in terms of postoperative rates of death and complications does not outweigh the disadvantage of the drainage procedure. Only if PBD-related complications could be reduced by 27% and consequently diminish hospital stay could PBD be beneficial. Further randomized controlled trials with improved PBD techniques are necessary.

Interleukin-1 receptor type I gene-deficient bile duct-ligated mice are partially protected against endotoxin.

Cholestatic liver injury is associated with an increased susceptibility toward endotoxin-induced toxicity. To determine the role of interleukin 1 (IL-1) herein, extrahepatic cholestasis was induced by bile duct ligation (bdl) in IL-1 receptor type I gene-deficient (IL-1R(-/-)) mice, which are unresponsive to IL-1alpha and IL-1beta, and normal IL-1R(+/+) mice. Bdl elicited increases in hepatic IL-1alpha and IL-1beta messenger RNA (mRNA) and protein. Hepatocellular injury at 2 weeks after bdl was similar in IL-1R(-/-) and IL-1R(+/+) mice as shown by clinical chemistry and histopathology. Administration of endotoxin to cholestatic mice at 2 weeks after bdl was associated with enhanced cytokine release, more severe liver damage, and occurrence of death when compared with sham-operated mice. Endotoxin effects in sham-operated IL-1R(-/-) and IL-1R(+/+) mice were largely similar, but cholestatic IL-1R(-/-) mice were better protected against toxic effects of endotoxin, as reflected by lowered cytokine release, less profound liver injury, and reduced mortality. These data indicate that IL-1alpha and IL-1beta are produced in the liver after bdl, but that these cytokines do not play a significant role in cholestatic liver damage; however, endogenous IL-1 activity is an important denominator of enhanced endotoxin sensitivity that is observed during cholestasis induced by bdl.