Urinary hypoxanthine and xanthine levels in acute coronary syndromes

Ischemia leads to impaired ATP metabolism, with increased production of purine degradation products, such as hypoxanthine and xanthine, which are useful markers of tissue hypoxia. These extracellular markers of ischemia have been studied extensively in many clinical conditions of oxidative stress, including perinatal asphyxia, acute respiratory distress syndrome, cerebral ischemia, and preeclampsia. The aim of this study was to explore the usefulness of urinary hypoxanthine and xanthine as ischemia markers in acute coronary syndromes. Urinary excretion of hypoxanthine and xanthine was assessed by high-performance liquid chromatography in 30 patients with acute coronary syndromes and in 30 age- and sex-matched controls. Serum and urine uric acid, creatinine, and urea concentrations were also determined. Hypoxanthine excretion was significantly elevated in patients compared with healthy controls (84.37+/-8.63 and 42.70+/-3.97 nmol/mg creatinine, mean+/-SEM, P<0.0001). Urinary xanthine levels were also increased in patients with acute coronary syndromes (100.13+/-12.14 and 34.74+/-4.07 nmol/mg creatinine patients and controls, respectively; P<0.0001). Hypoxanthine and xanthine excretion showed a strong positive correlation in both groups. Significant negative correlations between urinary hypoxanthine and uric acid and xanthine and uric acid were observed in the patients, but not in controls. In conclusion, increased levels of ATP degradation products hypoxanthine and xanthine are observed in various hypoxic clinical conditions. This study suggests that these parameters may be useful markers of ischemia in patients with acute coronary syndromes.     

Phenobarbital-induced Alterations in the Metabolism of [3H]Vitamin D3 by the Perfused Rachitic Rat Liver In Vitro

Anticonvulsant therapy of seizure disorders in man is associated with the development of complications involving bone and mineral metabolism including hypocalcemia, elevated serum immunoreactive parathyroid hormone levels, and increased amounts of unmineralized bone or osteoid. The latter has been attributed to a reduction in serum-25-hydroxycholecalciferol levels resulting from increased hepatic metabolism of vitamin D. Using an in vitro recycling hepatic perfusion system, we have demonstrated that 5 d of phenobarbital treatment increases the hepatic production of [(3)H]25-hydroxyvitamin D(3) (4.3+/-0.3 vs. 3.3+/-0.2%/h, P <0.025) without affecting the biliary excretion of radioactivity. Furthermore, rachitic livers perfused with blood obtained from animals treated with phenobarbital for 5 d also manifested an increase in [(3)H]25-hydroxyvitamin D(3) production (4.6+/-0.5 vs. 3.3+/-0.2%/h, P < 0.02). Addition of phenobarbital or its major metabolite, p-hydroxyphenobarbital, directly to the perfusion apparatus had no effect on [(3)H]25-hydroxyvitamin D(3) production. Phenobarbital treatment was also attended by a decrease in the intrahepatic content of [(3)H]vitamin D(3) (11.7+/-0.4 vs. 17.5+/-0.7 dpm/mg liver protein, P < 0.001) without alterations in the content of [(3)H]25-hydroxyvitamin D(3). The data collectively suggest that the increased hepatic conversion of [(3)H]vitamin D(3) to [(3)H]25-hydroxyvitamin D(3) attending phenobarbital treatment is secondary to stimulation of the hepatic 25-hydroxylation system(s) by a metabolite of phenobarbital other than p-hydroxyphenobarbital and/or by metabolic alterations resulting from phenobarbital therapy.     

Os efeitos condrotóxicos e apoptóticos de levobupivacaína e bupivacaína na articulação do joelho de coelhos

Background

A single dose injection or continuous infusion of local anesthetics into the joint space is considered to be a well‐defined analgesia technique. The aim of this study was to investigate the chondrotoxic and apoptotic effects of single‐dose intra‐articular injection of levobupivacaine and bupivacaine on rabbit knee joint tissues.

Chlorine-induced extensive tracheobronchial necrosis concomitantly benzene-induced pancytopenia presented with severe pneumonia

We report a case of 25-year-old woman with severe tracheobronchial necrosis caused by chlorine released from a mixture household cleaning agents. She subsequently exposed benzene while she was fixing the seats with benzene containing gum. The case was found interesting with its history, delayed diagnosis, bronchoscopic features, and fatal outcome. We presented its bronchoscopic and pathological images which has not been shown in the literature up to date.     

Allogeneic Haematopoietic Stem Cell Transplantation as Therapy for Chronic Granulomatous Disease��Single Centre Experience

Chronic granulomatous disease (CGD) is phagocytic cell metabolic disorder resulting in recurrent infections and granuloma formation. This paper reports the favourable outcome of allogeneic transplantation in six high-risk CGD patients. The following donors were used: HLA-matched, related (two) and unrelated (three), and HLA-mismatched, unrelated (one). One patient was transplanted twice using the same sibling donor because of graft rejection at 6 months after reduced-intensity conditioning transplant (fludarabine and melphalan). Myeloablative conditioning regimen consisted of busulphan and cyclophosphamide. Stem cell source was unmanipulated bone marrow containing: 5.2 (2.6-6.5) × 10(8) nucleated cells, 3.8 (2.0-8.0) × 10(6) CD34+ cells and 45 (27-64) × 10(6) CD3+ cells per kilogramme. Graft-versus-host disease prophylaxis consisted of cyclosporine A and, for unrelated donors, short course of methotrexate and anti-T-lymphocyte globulin. Mean neutrophile and platelet engraftments were observed at day 22 (20-23) and day 20 (16-29), respectively. Pre-existing infections and inflammatory granulomas resolved. With the follow-up of 4-35 months (mean, 20 months), all patients are alive and well with full donor chimerism and normalized superoxide production.     

Organ Donation: A Portrait of Family Refusal in Québec

Many studies from around the world have reported different reasons why families refuse organ donation. In Quebec, however, there are no known data on the subject. To enable us to better communicate with families, a research project was conducted from January to December 2007 in hospital centers with personnel who specialize in supporting families. Our objective was to identify the reasons why Quebecers refuse a request for organ donation. The findings demonstrate that knowing the express wishes of the deceased person about organ donation and end-of-life treatment influences the family. When these wishes are not known, the partners of older donors refuse in greater numbers, primarily for familial or circumstantial reasons. Refusal based on religion or ethnicity is rare. Some families approached before neurologic death is diagnosed do not wish to wait until all the criteria for neurologic death are met.     

Induction Therapy in Cardiac Transplantation: When and Why?

Induction therapy has continued to be a subject of controversy in heart transplantation for more than 20 years. It is an example of a therapy that is logical, and ought to be better than "doing without." However, a careful review of the evidence suggests otherwise. Except for patients where the benefits clearly outweigh the short and long-term risks, the use of induction therapy should be avoided. In immunosuppression, as in life, there is no "free lunch." Clinicians need to be certain they fully understand what they are ordering when asking for induction therapy to be administered to their patients.