PubMed · 12976956
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W T MCCOLLUM. 1952. Mesenteric thrombosis.. https://doi.org/10.7326/0003-4819-37-3-579
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INTRODUCTION: Compression of the median nerve at the wrist by a persistent median artery is one of the uncommon reasons for carpal tunnel syndrome. Most of the studies in the literature deal with thrombosed persistent median artery. MATERIALS AND METHOD: In this study, we present surgical treatment of four carpal tunnel syndromes, which had persistent median arteries. The mean age of the patients was 51 years. All four median arteries were patent and only transverse carpal ligament releases were performed using a standard anterior open approach for decompression of the carpal tunnel. Neither ligation nor transposition of the arteries was done. RESULTS: All patients became symptom free after a few weeks. Only one patient had a slight recurrence 13 months postoperatively. Splint use and modification of her activities reduced her disturbance, and no further treatment was applied. CONCLUSION: If the patient has no additional anomaly, our clinical experiences lead us not to advise resection or transposition because simple release of the transverse carpal ligament can relieve symptoms.
Nitric oxide (NO) serves many vasoprotective roles, but the massive release of NO causes arterial wall degeneration. We investigated whether enhanced nitric oxide synthase (iNOS) expression in peripheral blood leukocytes and circulating endothelial cells mirrors the progression of coronary arterial lesions in 55 children with acute Kawasaki disease (KD), including 24 with and 31 without coronary artery lesions (CAL). Patients were treated with i.v. gamma-globulin at the time of diagnosis and blood samples were collected before and after treatment. The cellular origin of NO synthesis was determined by flow cytometric analysis of iNOS expression in peripheral blood, and by immunohistochemical analysis of circulating endothelial cells and coronary arteries. iNOS expression in neutrophils peaked at the time of diagnosis, but did not peak in monocytes until 2 wk post onset of disease. Levels were significantly higher in both cell types in patients with CAL (p = 0.001 and p = 0.035, respectively). In addition, the number of circulating endothelial cells and levels of iNOS expression were higher in patients with CAL (p = 0.011 and p = 0.012, respectively). Immunohistochemical analysis of the coronary arteries from three patients with acute KD revealed iNOS immunoreactivity in endothelial cells, as well as infiltrating monocytes/macrophages in the aneurysms. We conclude that the expression of iNOS in peripheral blood leukocytes, as well as circulating endothelial cells, correlates with the severity of coronary arterial wall injury and the progression of CAL in patients with acute KD.
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