Sengstaken Tube Removal under Direct Hemodynamic Monitoring after Post Transplantation Venous Occlusion.

The surgical procedure for orthotopic liver transplantation (OLT) is well standardized, and most groups use the retrohepatic caval preservation or piggyback technique to improve hemodynamic tolerance. However, when a discrepancy between the site in the right upper quadrant of the liver recipient and a small graft is present, this technique can provoke a rotation on the axis of the vena cava and cause an occlusion of the suprahepatic vein drainage. This problem can be detected intraoperatively, and several methods have been described to resolve it by placing different devices to correct the position. Early withdrawal may cause the development of clinical hepatic congestion with ascites unresponsive to medical treatment. We present three cases of OLT who developed obstruction of the venous drainage solved intraoperatively with the placement of a Sengstaken-Blakemore tube. As a novelty, prior to the withdrawal of the device, a transjugular hemodynamic study was performed to ensure the correct position of the liver with adequate venous drainage.

Pigmented mammary Paget's disease in a man

Mammary Paget's disease is one clinical expression of an underlying breast carcinoma. It manifests as persistent erythema, oozing and scaling of the nipple, areola or both. The occurrence of this disease in men is uncommon. This is a report of a pigmented lesion of Paget's disease occurring on the breast of a man. This presentation is unusual and may be confused with melanoma. Its early recognition is important so that adequate therapy may be instituted when the disease has a favorable prognosis

N-(3-(aminomethyl)benzyl)acetamidine, an inducible nitric oxide synthase inhibitor, decreases colonic inflammation induced by trinitrobenzene sulphonic acid in rats.

Gastrointestinal inflammation has been associated with an increased generation of nitric oxide (NO) and the expression of the inducible NO synthase (iNOS). Using an experimental model of colitis induced by trinitrobenzene sulphonic acid (TNBS), we sought to determine whether the administration of N-(3-(Aminomethyl)benzyl)acetamidine (1400W), a specific inhibitor of iNOS, has a beneficial action on the colonic injury. 1400W (0.4 and 2 mg/kg/day) was administered intraperitoneally from day 5 to 10 after intrarectal instillation of TNBS. TNBS led to colonic ulceration and inflammation, an increase of colonic myeloperoxidase activity and the expression of the calcium-independent NOS from days 1 to 15. 1400W reduced the macroscopic damage and the histological changes induced by TNBS as well as the calcium-independent NOS activity and myeloperoxidase activity determined over 30 min after sacrifice. These findings indicate that the expression of iNOS accounts for most of the damage caused by TNBS and that the administration of 1400W after the onset of colitis has a beneficial action on the colonic injury.

Implication of TNF-alpha convertase (TACE/ADAM17) in inducible nitric oxide synthase expression and inflammation in an experimental model of colitis.

Tumour necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine which is shed in its soluble form by a disintegrin and metalloproteinase (ADAM) called TNF-alpha convertase (TACE; ADAM17). TNF-alpha plays a role in inflammatory bowel disease (IBD) and is involved in the expression of inducible nitric oxide synthase (iNOS) which has also been implicated in IBD. The study was designed to investigate whether colitis induced by trinitrobenzene sulphonic acid (TNBS) in rats produces an increase in TACE activity and/or expression and whether its pharmacological inhibition reduces TNF-alpha levels, iNOS expression and colonic damage in this model. TNBS (30 mg in 0.4 ml of 50% ethanol) was instilled into the colon of female Wistar rats. Saline or TACE inhibitor BB1101 (10 mg/kg/day) was administered intraperitoneally 5 days after TNBS instillation. On day 10, colons were removed and assessed for pathological score, myeloperoxidase (MPO), NO synthase (NOS), TACE enzymatic activity and protein levels, colonic TNF-alpha and NOx- levels. Instillation of TNBS caused an increase in TACE activity and expression and the release of TNF-alpha. TNBS also resulted in iNOS expression and colonic damage. BB1101 blocked TNBS-induced increase in TACE activity, TNF-alpha release and iNOS expression. Concomitantly, BB1101 ameliorated TNBS-induced colonic damage and inflammation. TNBS causes TNF-alpha release by an increase in TACE activity and expression and this results in the expression of iNOS and subsequent inflammation, suggesting that TACE inhibition may prove useful as a therapeutic means in IBD.