Systematic review with network meta-analysis: comparative efficacy and tolerability of different intravenous iron formulations for the treatment of iron deficiency anaemia in patients with inflammatory bowel disease.

BACKGROUND: Iron deficiency anaemia (IDA) is a common complication of inflammatory bowel disease (IBD) associated with reduced quality of life and increased hospitalisation rates. While the best way of treating IDA in IBD patients is not clearly established, current European guidelines recommend intravenous iron therapy in IBD patients with severe anaemia or intolerance to oral iron compounds. AIM: To compare the efficacy and tolerability of different intravenous iron formulations used to treat IDA in IBD patients in a systematic review and Bayesian network meta-analysis (NMA), PROSPERO registration number: 42016046565. METHODS: In June 2016, we systematically searched for studies analysing efficacy and safety of intravenous iron for IDA therapy in IBD. Primary outcome was therapy response, defined as Hb normalisation or increase ≥2 g/dL. RESULTS: Five randomised, controlled trials (n = 1143 patients) were included in a network meta-analysis. Only ferric carboxymaltose was significantly more effective than oral iron [OR=1.9, 95% CrI: (1.1;3.2)]. Rank probabilities showed ferric carboxymaltose to be most effective, followed by iron sucrose, iron isomaltose and oral iron. Pooled data from the systematic review (n = 1746 patients) revealed adverse event rates of 12.0%, 15.3%, 12.0%, 17.0% for ferric carboxymaltose, iron sucrose, iron dextran and iron isomaltose respectively. One drug-related serious adverse event (SAE) each was reported for ferric carboxymaltose and iron isomaltoside, and one possibly drug-related SAE for iron sucrose. CONCLUSIONS: Ferric carboxymaltose was the most effective intravenous iron formulation, followed by iron sucrose. In addition, ferric carboxymaltose tended to be better tolerated. Thus, nanocolloidal IV iron products exhibit differing therapeutic and safety characteristics and are not interchangeable.

Thermal modification of connective tissues: basic science considerations and clinical implications.

Wound healing is a natural and well-orchestrated biologic event. Indeed, the ability of wounds to heal is the foundation on which the practice of surgery is predicated. The successful surgeon maintains a delicate alliance with nature, balancing the magnitude of the surgical insult against the capacity of the tissue for repair. Thermal injury is one of the most traumatic insults a tissue can sustain and the high degree of cell death and matrix alteration associated with thermal burns have been shown to result in a protracted healing time. Thus, the use of thermal energy as a stimulant for tissue shrinkage must be tempered with an appreciation of the biologic events that accompany this phenomenon. Furthermore, it must be realized that the initial degree of capsular shrinkage observed following the application of thermal energy may have little bearing on the long-term biologic and biomechanical status of the joint capsule. Therefore, the desire to see a redundant capsule shrink and become taut at surgery should be weighed very carefully against the level of damage imparted to the tissue to achieve this result. The simple initiation of the healing response may be sufficient to rehabilitate an incompetent structure via the creation of new cellular tissue. While the ultimate application(s) of thermal modification of connective tissues has yet to be completely defined, its ultimate role may be best suited to that of a low level stimulant for inducing a biologic repair response rather than a highly aggressive mechanism for primary tissue shrinkage.

Thermal modification of connective tissues: basic science considerations and clinical implications.

Thermal modification (shrinkage) of capsular connective tissue has gained increasing popularity as an adjunctive or even a primary procedure in the arthroscopic treatment of shoulder instability. Although the physical effects of heat on collagenous tissues are well known, the long-term biologic fate of these shrunken tissues is still a matter of debate. The temperatures required to alter the molecular bonding of collagen and thus cause tissue shrinkage (65 degrees C to 70 degrees C) are also known to destroy cellular viability. Therefore, thermally modified tissues are devitalized and must undergo a biologic remodeling process. During this remodeling, the mechanical properties of the treated tissues are altered (decreased stiffness) and can be at risk for elongation if the postoperative rehabilitation regimen is too aggressive. Although anecdotal reports suggest that thermal capsular shrinkage does have a beneficial effect, the exact mechanism responsible for this clinical improvement has yet to be fully defined. The reported improvement could be due to the maintenance of initial capsular shrinkage, secondary fibroplasia and resultant thickening of the joint capsule, a loss of afferent sensory stimulation due to the destruction of sensory receptors, or a combination of all three. The clinical role for thermal modification of connective tissues has not yet been defined, but it appears that it may prove most useful as a stimulant for inducing a biologic repair response.