Snodgrass Urethroplasty: Grafting the Incised Plate-10 Years Later.

J Urol. 2009 Aug 17; Ferro F, Vallasciani S, Borsellino A, Atzori P, Martini LPURPOSE: We report our retrospective, nonrandomized, single center experience with modified tubularized incised urethral plate repair, consisting of grafting the incised urethral plate before tubularization, as first introduced 10 years ago. Indications, technical points and results are described. MATERIALS AND METHODS: From 1997 to 2007 at our unit 1,095 cases of hypospadias were treated, including 75% primary and 25% repeat cases. Of primary cases 18 (8%) of those suitable for tubularized incised urethral plate were instead selected for a grafted tubularized incised urethral plate. All 18 patients were characterized anatomically by a small glans, a flat urethral groove and a long spongiosum defect. Of repeat cases 83 were suitable for a tubularized incised urethral plate, of which 44 (53%) were selected for the modified procedure. Grafted tubularized incised urethral plate surgery consisted of an extended longitudinal incision of the urethral plate distal beyond the neomeatal line associated with scar excision in repeat cases. The resulting urethral plate defect was then lined with a graft. RESULTS: Mean followup was 36 months (range 4 to 122). Complications were noted in 8 repeat cases (13% overall), representing 18% of this subgroup. CONCLUSIONS: Case selection is a crucial factor that influences the quality of tubularized incised urethral plate results. However, in most repeat cases scarring may lead to an increased complication rate after tubularized incised urethral plate surgery. The grafted modification has the advantage of extending indications for the tubularized incised urethral plate to cases in which another surgical procedure would be necessary. To our knowledge we present the first series of primary and repeat cases.

Increased Expression of Integrin-Linked Kinase Attenuates Left Ventricular Remodeling and Improves Cardiac Function After Myocardial Infarction.

Circulation. 2009 Aug 17; Ding L, Dong L, Chen X, Zhang L, Xu X, Ferro A, Xu BBACKGROUND: -Left ventricular (LV) remodeling is associated with the development of heart failure after myocardial infarction. Here we investigated whether integrin-linked kinase (ILK) may regulate LV remodeling and function after myocardial infarction. Methods and Results-Adenoviral vector expressing ILK (n=25) or empty adeno-null (n=25) was injected into rat peri-infarct myocardium after left anterior descending coronary artery ligation. ILK expression was confirmed by Western blotting and immunofluorescence. Echocardiographic and hemodynamic analyses demonstrated relatively preserved cardiac function in adeno-ILK animals. ILK treatment was associated with reduced infarct scar size, increased scar thinning ratio, and preserved LV diameter, wall thickness, cardiomyocyte size, and myofilament density. Enhanced angiogenesis and reduced fibrosis were observed in the adeno-ILK group, along with reduced apoptosis as demonstrated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis. Moreover, increased cardiomyocyte proliferation was found in adeno-ILK animals, as measured by proliferating cell nuclear antigen, Ki-67, and phosphohistone-H3 staining. At long-term follow-up, most indices of cardiac function and hemodynamics showed no difference between adeno-ILK and control animals by 9 weeks, although LV end-systolic diameter and infarct scar size were reduced in the adeno-ILK group at this time point. Additionally, ILK overexpression was found to exert a rescue effect on remodeling when administered in a delayed fashion 1 week after coronary artery ligation. Conclusions-ILK gene therapy improves cardiac remodeling and function in rats after myocardial infarction and is associated with increased angiogenesis, reduced apoptosis, and increased cardiomyocyte proliferation. This may represent a new approach to the treatment of postinfarct remodeling and subsequent heart failure.

Strong association between HLA-B*5801 and allopurinol-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a Thai population.

Pharmacogenet Genomics. 2009 Aug 18; Tassaneeyakul W, Jantararoungtong T, Chen P, Lin PY, Tiamkao S, Khunarkornsiri U, Chucherd P, Konyoung P, Vannaprasaht S, Choonhakarn C, Pisuttimarn P, Sangviroon A, Tassaneeyakul WOBJECTIVES: Allopurinol, a uric acid lowering drug commonly used for hyperuricemia and gouty arthritis, has been reported as a common cause of severe cutaneous adverse drug reactions (SCAR) including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). A strong association between allopurinol-induced SCAR and HLA-B*5801 was observed in a Han Chinese population with high frequency of this allele, whereas only a moderate association was observed in populations with low frequency (i.e. European and Japanese). This study investigated the relationship between SJS/TEN and HLA-B*5801 in a Thai population that has a high allelic frequency of this allele. METHODS: Twenty-seven allopurinol-induced SJS/TEN and 54 allopurinol-tolerant patients were enrolled in the study. The presence of HLA-B*5801 and HLA-B genotypes in these patients were analyzed using a PG5801 DNA detection kit and sequence-based typing, respectively. RESULTS: All of the 27 (100%) allopurinol-induced SJS/TEN patients who were examined carried HLA-B*5801 whereas only seven (12.96%) of the control patients had this allele. The risk of allopurinol-induced SJS/TEN was significantly greater in patients with HLA-B*5801 when compared with those who did not carry this allele, with an odds ratio of 348.3 (95% confidence interval=19.2-6336.9, P = 1.6x10). The sensitivity and specificity of the HLA-B*5801 allele for prediction of allopurinol-induced SJS/TEN were 100 and 87%, respectively. By assuming a 0.2% prevalence rate, the positive predictive value and the negative predictive value of the HLA-B*5801 allele was 1.52 and 100%, respectively. CONCLUSION: A strong association of allopurinol-induced SJS/TEN with the HLA-B*5801 allele was observed in a Thai population. The results suggest that HLA-B*5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.