The role of proximal pulleys in preventing tendon bowstringing: pulley rupture and tendon bowstringing.

PURPOSE: The aim of this study was to investigate factors that contribute to tendon bowstringing at the proximal phalanx. We hypothesised that: (1) a partial rupture of the A2 pulley leads to significant bowstringing, (2) the location of the A2 rupture, starting proximally or distally, influences bowstringing, (3) an additional A3 pulley rupture causes a significant increase in bowstringing following a complete A2 pulley rupture and (4) the skin and tendon sheath may prevent bowstringing in A2 and A3 pulley ruptures. METHODS: Index, middle and ring fingers of eight freshly frozen cadaver arms were used. A loading device pulled with 100 N force was attached to the flexor digitorum profundus (FDP). The flexor digitorum superficialis (FDS) was preloaded with 5 N. Bowstringing was measured and quantified by the size of the area between the FDP tendon and the proximal phalanx over a distance of 5 mm with ultrasonography (US). RESULTS: US images showed that already a 30% excision of the A2 pulley resulted in significant bowstringing. In addition, a partial distal incision of the A2 pulley showed significantly more bowstringing compared to a partial proximal incision. Additional A3 pulley incision and excision of the proximal tendon sheath did not increase bowstringing. Subsequently, removing the skin did increase the bowstringing significantly. CONCLUSION: A partial A2 pulley rupture causes a significant bowstringing. A partial rupture of the A2 pulley at the distal rim of the A2 pulley resulted in more bowstringing than a partial rupture at the proximal rim.

Systematic review and meta-analysis of the association between diabetes mellitus and incidence and mortality in breast and colorectal cancer.

BACKGROUND: Increasing evidence suggests that diabetes mellitus (DM) is associated with increased cancer incidence and mortality. Several mechanisms involved in diabetes, such as promotion of cell proliferation and decreased apoptosis, may foster carcinogenesis. This study investigated the association between DM and cancer incidence and cancer-specific mortality in patients with breast and colorectal carcinoma. METHODS: A meta-analysis of controlled trials, prospective cohort studies and pooled cohort studies published after 2007 was conducted. Embase, PubMed and the Cochrane Library were searched. Summary hazard ratios (HRs) were calculated using a random-effects model. Sensitivity and subgroup analyses were performed to adjust for confounders, mode of DM assessment and follow-up time. RESULTS: Twenty studies were included to investigate the association between DM and breast and colorectal cancer incidence and cancer-specific mortality. The studies predominantly comprised patients with type II DM. The overall HR for breast cancer incidence was 1·23 (95 per cent confidence interval 1·12 to 1·34) and that for colorectal cancer was 1·26 (1·14 to 1·40) in patients with DM compared with those without diabetes. The overall HR was 1·38 (1·20 to 1·58) for breast cancer- and 1·30 (1·15 to 1·47) for colorectal cancer-specific mortality in patients with DM compared with those without diabetes. CONCLUSION: This meta-analysis indicated that DM is a risk factor for breast and colorectal cancer, and for cancer-specific mortality.