Effect of multipolar electrocoagulation on EUS findings in Barrett's esophagus.
The patients had a mean age of 49.6 ± 13.4 years, a median posttransplantation time of 7.6 years, and a mean estimated glomerular filtration rate (eGFR) of 51.9 ± 18.46 mL/min. The prevalence of hyperuricemia was 42.1% (n = 127). Hyperuricemic patients were predominately male (P = .004), older (P = .038), and with lower eGFR (P < .001). They also had a higher prevalence of hypertension (P = .001), dyslipidemia (P = .004) and proteinuria (P = .001). Multivariate adjusted regression model showed as significant predictors of hyperuricemia: male gender (odds ratio [OR], 2.46; P = .002); impaired renal function (OR 1.33 for every 10 mL/min reduction in eGFR; P < .001), higher body weight (OR 1.09 for every 1 kg/m(2) increase of body mass index; P = .044), prednisolone use (OR 2.12; P = .035), and cyclosporine versus tacrolimus use (OR 2.44; P = .039).
This was a prospective, single center, open-label study. Included patients were ≥ 18 years old and receiving a stable dose of tacrolimus for at least 6 months. Patients receiving stable treatment of twice daily tacrolimus were switched to a once-daily dose of modified release tacrolimus, on a milligram-to-milligram basis, with the modified release formulation administered for at least 4 weeks. Blood levels of tacrolimus were obtained before and 1 month after treatment was switched to the modified release formulation.
Anidulafungin is a new echinocandin antifungal agent which inhibits beta-1,3-D-glucan synthase and disrupts fungal cell-wall synthesis. It has marked antifungal activity against Candida spp. and Aspergillus spp., including amphotericin B and triazole resistant strains. Due to the limited oral availability, anidulafungin in clinical use is available for parenteral administration only. Elimination of anidulafungin takes place via slow non-enzymatic degradation to inactive metabolites. Less than 10% and 1% of the initially administered drug is excreted unchanged into feces and urine, respectively. It does not require dosage adjustment in subjects with hepatic or renal impairment established. Anidulafungin is generally well tolerated. Adverse events appear not to be dose or infusion related. The most common treatment related adverse events are phlebitis, headache, nausea, vomiting and pyrexia. The lack of interactions with tacrolimus, cyclosporine and corticosteroids and its limited toxicity profile places anidulafungin as an attractive new option for the treatment of invasive fungal infections especially in transplant patients.
Crohn's disease can be complicated by the development of fistulas, 54% of which involve the perianal region. The presence of perianal fistulas predicts a disabling course of Crohn's disease. The treatment of complex perianal disease is difficult and the chance of complete fistula healing is no more than 50%. The best management of this condition is a combining medical and surgical therapy. Studies which evaluated the efficacy of medical treatments in this setting are small, open label and considered the efficacy on perianal disease as a second outcome or as the result of a subgroup analysis. In the few available trials the efficacy outcomes were evaluated by the Fistula Drainage Assessment but recently it was observed that inflamed fistula tracks often persist, despite the apparent closure of external orifices. Up to now the most strongly evaluated medical treatments for perianal Crohn's disease are the anti-TNFα antibodies. In presence of complex fistulas they are considered the first choice of medical treatment, in combination with surgical therapy. Antibiotics and immunomodulators have not been demonstrated to result in sustained closure of fistulas in Crohn's disease. Their use is recommended as a second line medical treatment. The use of tacrolimus and thalidomide is limited by its side effects. A few evidences support the use of methotrexate and cyclosporine but they are insufficient.
De novo lupus nephritis (LN) is a rare complication in renal transplantation recipients. We present the clinical manifestations of de novo LN in a 12-year-old boy who received a cadaveric renal transplant. The cause of end-stage renal disease was prune belly syndrome with renal dysplasia. His immunosuppressive drugs included tacrolimus, mycophenolate sodium, and prednisolone. After 3 years of treatment, he developed nephrotic syndrome (NS) without other symptoms of systemic lupus erythematosus (SLE). The renal pathology of the transplanted kidney showed suspicious acute cellular rejection and LN World Health Organization class IV-G (A/C). Antinuclear antibody was positive, but anti-dsDNA and anti-Smith were negative. The serum complements were initially normal. Pulse methylprednisolone was given and the dosages of all immunosuppressive drugs increased; notwithstanding, his edema and hypoalbuminemia worsened. Repeated biopsy of the transplanted kidney was done. A full-house pattern was documented under immunofluorescent examination which confirmed LN WHO class IV-G (A/C) without evidence of rejection. He then developed macrophage-associated hemophagocytic syndrome and cytomegalovirus pneumonia. He ultimately developed pulmonary hemorrhage and died owing to severe pneumonia. De novo LN should be considered in renal transplant recipients with new onset of NS despite there not being any other clinical manifestations of SLE.