Preliminary Evaluation of a Cycling Cleat Designed for Diabetic Foot Ulcers.

BACKGROUND: Offloading devices for diabetic foot ulcers (DFU) generally restrict exercise. In addition to traditional health benefits, exercise could benefit DFU by increasing blood flow and acting as thermotherapy. This study functionally evaluated a cycling cleat designed for forefoot DFU. METHODS: Fifteen individuals at risk of developing a DFU used a recumbent stationary bicycle to complete one 5-minute cycling bout with the DFU cleat on their study foot and one 5-minute bout without it. Foot stress was evaluated by plantar pressure insoles during cycling. Laser Doppler perfusion monitored blood flow to the hallux. Infrared photographs measured foot temperature before and after each cycling bout. RESULTS: The specialized cleat significantly reduced forefoot plantar pressure (9.9 kPa versus 62.6 kPa, P < .05) and pressure time integral (15.4 versus 76.4 kPa*sec, P < .05). Irrespective of footwear condition, perfusion to the hallux increased (3.97 ± 1.2 versus 6.9 ± 1.4 tissue perfusion units, P < .05) after exercise. Infrared images revealed no changes in foot temperature. CONCLUSIONS: The specialized cleat allowed participants to exercise with minimal forefoot stress. The observed increase in perfusion suggests that healing might improve if patients with active DFU were to use the cleat. Potential thermotherapy for DFU was not supported by this study. Evaluation of the device among individuals with active DFU is now warranted.

Clinical improvement in psoriasis with treatment of associated hyperlipidemia.

Psoriasis is associated with an increased risk of cardiovascular disease, a principal cause of which is atherosclerosis caused by hyperlipidemia. However, it is not known whether treatment of hyperlipidemia in patients with psoriasis lead to clinical improvement in psoriasis condition. In this study, the authors summarize the existing literature relevant to this inquiry. They also describe the potential pathways believed to link psoriasis with atherosclerosis and the role of hyperlipidemia therapy in this setting. A few studies indicated clinical improvement in psoriasis with treatment of associated hyperlipidemia. Some studies showed that a low-fat diet improved psoriasis. Others indicated a decreased risk of psoriasis associated with intake of cholesterol-lowering drugs such as "statins." Treatment with statins increased lactate dehydrogenase level and diminished Psoriasis Area and Severity Index score, ie, reduced cutaneous lesion in psoriasis. Beneficial effects of statin therapy on psoriasis included downregulation of lymphocyte function-associated antigen-1, inhibition of leukocyte endothelial adhesion, extravasation and natural killer cell activity, inhibition of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin 1 and 6, lowering of C-reactive protein, promotion of a T(H)1 to T(H)2 cells and inhibition of T(H)1 cytokine receptors on T cells, leading to inhibition of activation of lymphocytes and infiltration into the inflammation sites. Taken together, current literature indicates clinical improvement in psoriasis condition with treatment of associated hyperlipidemia, particularly with statins of which the mechanisms could be attributed to immunomodulatory and anti-inflammatory effects.

Pathogenic mechanisms shared between psoriasis and cardiovascular disease.

Psoriasis is associated with an increased risk of cardiovascular disease, a hallmark of which is atherosclerosis. The objective of this study was to review the pertinent literature and highlight pathogenic mechanisms shared between psoriasis and atherosclerosis in an effort to advocate early therapeutic or preventive measures. We conducted a review of the current literature available from several biomedical search databases focusing on the developmental processes common between psoriasis and atherosclerosis. Our results revealed that the pathogenic mechanisms shared between the two diseases converged onto "inflammation" phenomenon. Within the lymph nodes, antigen-presenting cells activate naive T-cells to increase expression of LFA-1 following which activated T-cells migrate to blood vessel and adhere to endothelium. Extravasation occurs mediated by LFA-1 and ICAM-1 (or CD2 and LFA-3) and activated T-cells interact with dendritic cells (and macrophages and keratinocytes in psoriasis or smooth muscle cells in atherosclerosis). These cells further secrete chemokines and cytokines that contribute to the inflammatory environment, resulting in the formation of psoriatic plaque or atherosclerotic plaque. Additionally, some studies indicated clinical improvement in psoriasis condition with treatment of associated hyperlipidemia. In conclusion, therapeutic or preventive strategies that both reduce hyperlipidemia and suppress inflammation provide potentially useful approaches in the management of both diseases.