How 'preventable' are lower extremity amputations? A qualitative study of patient perceptions of precipitating factors.

PURPOSE: Clinicians commonly believe that lower extremity amputations are potentially preventable with coordinated care and motivated patient self-management. We used in-depth interviews with recent amputees to assess how patients viewed their initial amputation risk and causes. METHOD: We interviewed 22 patients at a rehabilitation hospital 2-6 weeks after an incident amputation. We focused on patients' representations of amputation cause and methods of coping with prior foot and leg symptoms. RESULTS: Patients reported unexpected onset and rapid progression of ulceration, infection, progressive vascular disease, foot trauma and complications of comorbid illness as precipitating events. Fateful delays of care were common. Many had long histories of painful prior treatments. A fatalistic approach to self-management, difficulties with access and communication with providers and poor understanding of medical conditions were common themes. Few patients seemed aware of the role of smoking as an amputation risk factor. CONCLUSIONS: Most patients felt out of control and had a poor understanding of the events leading to their initial amputations. Prevention of subsequent amputations will require rehabilitation programs to address low health literacy and psychosocial obstacles to self-management.

Abdominal aortic aneurysm as a complex multifactorial disease: interactions of polymorphisms of inflammatory genes, features of autoimmunity, and current status of MMPs.

The role of matrix metalloproteinases (MMPs) in the pathogenesis of abdominal aortic aneurysm (AAA) has focused on the degradation of the extracellular matrix (ECM). The new frontier of MMP biology involves the role of MMPs in releasing cryptic fragments and neoepitopes from the ECM and the impact of MMPs on the regulation of the inflammatory response. The ECM is a complex structure, much more important than an inert scaffold. Both MMP-2 and MMP-9 expose a cryptic epitope that controls angiogenesis. MMPs inhibit angiogenesis through the release of endostatin, endorepellin, arresten, canstatin, and tumstatin. Other breakdown products of the ECM include fragments of fragmin and elastin degradation products (EDPs). In addition, the ECM contains embedded vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta). Inflammation is a complex, highly regulated system that involves the identification of injury or infection, response to the injury or infection, repair and healing, and return to normal homeostasis. In some instances, the inflammatory process leads to a pathologic process that is damaging to the host. MMPs play an important role in the control of the inflammatory response through the modification of proinflammatory cytokines, chemokines, and shedding of membrane receptors. Genetic association studies have been performed to help determine the genetic risk associated with certain single nucleotide polymorphisms (SNPs) However, because of the variability in the patient populations and the size of the population, it is difficult to draw any conclusions from these studies. While the etiology of AAA remains unknown, understanding of the inflammatory process and its regulatory points will develop new strategies for the treatment of AAA. Perhaps one difficulty with understanding the pathogenesis of AAA is the lack of precise definition of the phenotype.