ABSTRACT
Restenosis remains a major problem after angioplasty in peripheral artery disease despite stenting. It occurs in 30 - 50% / year depending on lesion localization and characteristics. One main reason for restenosis is neointimal hyperplasia, which can be suppressed by the topical administration of antiproliferative drugs. In percutaneous coronary intervention the concept of "local drug delivery" has been used for almost a decade with great success. In recent years, drug-eluting stents and drug coated balloons have also been increasingly used in the treatment of peripheral arterial disease as a consequence of positive results of clinical trails. The following article is an overview of the currently available data of completed trials, ongoing and planned studies. Evidence suggests that "drug-coating technology" is reliable, safe and efficient in reducing the target lesion revascularization and binary restenosis rate significantly. With regard to limb salvage and mortality in critical limb ischemia, there is no benefit shown in current published studies.
Subject(s)
Angioplasty, Balloon/instrumentation , Cardiovascular Agents/administration & dosage , Catheters , Coated Materials, Biocompatible , Drug-Eluting Stents , Peripheral Arterial Disease/therapy , Angioplasty, Balloon/adverse effects , Angioplasty, Balloon/mortality , Equipment Design , Evidence-Based Medicine , Humans , Limb Salvage , Peripheral Arterial Disease/mortality , Prosthesis Design , Risk Assessment , Risk Factors , Secondary Prevention , Time Factors , Treatment OutcomeABSTRACT
BACKGROUND: A false-positive sweat test in patients with deficiency of glucose-6-phosphate-1-dehydrogenase (EC 1.1.1.49; G6PD) is repeatedly reported. METHODS: Sweat chloride or conductivity was measured in 11 patients with G6PD deficiency. RESULTS: Mean (SD) chloride level (n = 8, median age 9.2 years, range 1.9-48.5) was 18.8 (9.6 mmol/l) and, mean (SD) sodium level was 26.0 (10.0 mmol/l), respectively, and mean (SD) conductivity (n = 3, median age 6.6 years, range 1.9-40.5) was 34.3 (6.5 mmol/l). CONCLUSION: In sweat of 11 patients with G6PD deficiency we did not find any abnormality. The reason for alleged false-positive sweat test in patients with G6PD deficiency is not known and we were unable to identify any original reference. It appears that tables of putative false-positive sweat tests in several disease states have been directly "copied and pasted" from one paper or textbook to another without verifying the original literature, a phenomenon one can call "chain citation".