The evolution of laparoscopic antireflux surgery and its influence on postoperative stay.

Laparoscopic fundoplication is an established treatment for refractory gastro-oesophageal reflux disease. This study aims to compare the outcome of two laparoscopic antireflux techniques in a regional specialist unit. A sequential audit was carried out on patients undergoing laparoscopic Nissen (LN: performed May 1994 to November 2000) or laparoscopic anterior (LA: performed March 2001 to December 2004) fundoplication. Patient satisfaction was assessed by postal questionnaire. The cohorts undergoing each operation were also divided into two chronological groups of 51 patients, to study the effect of possible learning curve progression on the number of nights spent in the hospital postoperatively. In all, 142/204 (70%) questionnaires were returned from patients with follow-up ranging from 5 to 40 months postoperation. Overall, 102/142 (72%) reported a good or excellent outcome. Patients who underwent LA had a higher rate of antacid medication use (LN 17.4% versus LA 34.2%, P = 0.036) but there was a higher score for inability to belch following LN (LN 2.03 versus LA 1.53, P = 0.034). When comparing the chronologically divided cohorts, LN was associated with a significantly longer hospital stay than LA (P < 0.001, Mann-Whitney U test). There was a significant decrease in hospital stay from the first to second group of 51 LNs (P < 0.001, Mann-Whitney U test) and a further significant reduction in hospital stay from the first 51 to second 51 LAs (P < 0.001, Mann-Whitney U test). In conclusion, both procedures provide good symptom control. Increased requirement for acid suppression following LA and inability to belch following LN, may suggest more long-term durability of the LN wrap. The decrease in the number of nights spent in hospital may be related to the procedure performed but seems more likely to be an effect of increasing volume of surgical experience.

Mechanical responses and integrin associated protein expression by human ankle chondrocytes.

Metabolic, biochemical and biomechanical differences between ankle and knee joint cartilage and chondrocytes including resistance to the effects of catabolic cytokines and fibronectin fragments may be relevant to differences in prevalence of OA in these joints. Although there is increasing information available on how chondrocytes from knee and hip joint cartilage recognise and respond to mechanical stimuli, knowledge of mechanotransduction in ankle joint chondrocytes is limited. This study was undertaken to (i) establish whether the response of normal ankle joint derived chondrocytes to mechanical stimulation in vitro was similar to that of normal and osteoarthritic knee joint derived chondrocytes and (ii) to investigate whether these chondrocytes showed differences in expression of integrin associated regulatory and signalling molecules. Unlike normal knee joint chondrocytes, ankle joint chondrocytes did not show an increase in relative levels of aggrecan mRNA when mechanically stimulated. No obvious change in protein tyrosine phosphorylation was seen in ankle chondrocytes subsequent to mechanical stimulation but these cells expressed elevated levels of tyrosine phosphorylated proteins at rest when compared to normal knee joint chondrocytes. Ankle joint chondrocytes showed an increase in protein kinase B phosphorylation following 1 min 0.33 Hz stimulation which was inhibited by the presence of antibodies to alpha5beta1 integrin. Ankle joint chondrocytes appeared to show significant differences in levels of the integrin-associated proteins CD98, CD147 and galectin 3, PKCgamma and differences in responses to glutamate were seen. Chondrocytes from ankle and knee joint cartilage respond differently to 0.33 Hz mechanical stimulation. This may be related to modified integrin-dependent mechanotransduction as a result of changes in expression of integrin regulatory molecules such as CD98 or differential expression and function of downstream components of the mechanotransduction pathway such as PKC or NMDA receptors.