Fatal disseminated Anncaliia algerae myositis mimicking polymyositis in an immunocompromised patient.

We report the first New Zealand case of Anncaliia algerae myositis in a 55-year-old man with a history of psoriatic arthritis, treated with long-term immunosuppressive therapy. He resided in the city of Rotorua, which is famous for geothermal hot springs. A vastus lateralis muscle biopsy was performed to investigate the cause of an unexplained myositis. Light microscopy demonstrated a necrotizing myositis with scattered clusters of ovoid spores within the myocyte cytoplasm resembling microsporidia. DNA analysis by PCR and electron microscopy confirmed microsporidial myositis with features characteristic of A. algerae. Immunosuppressive drugs were stopped and the patient was treated with cholestyramine wash and albendazole. The patient deteriorated with involvement of bulbar and respiratory muscles requiring intensive care and ventilation. He died 3 weeks after diagnosis. Post-mortem examination of skeletal muscle from tongue and intercostal muscles also revealed numerous organisms confirming disseminated disease.

Dizygotic twin pregnancy with a normal fetus and a nodular embryo associated with a partial hydatidiform mole.

Although twin pregnancies complicated by a coexisting complete hydatidiform mole are uncommon, those with partial hydatidiform mole (PHM) are exceedingly rare; there are only several well-documented cases diagnosed antenatally. Here we present the first case of a twin placenta containing a nodular embryo associated with PHM diagnosed on routine placental examination. This dizygotic twin pregnancy featured viable embryos at 8 weeks' gestation, death of 1 embryo at 12 weeks, and delivery of a healthy infant by caesarean section at 28 weeks because of worsening maternal reflux nephropathy. Macroscopic and microscopic placental examination and fluorescence in situ hybridization showed one part of the placenta to be diploid and the other to contain a vanishing triploid embryo and a PHM, which had eluded antenatal ultrasound diagnosis. Careful pathologic examination of vanishing twins and their placentas may disclose an unexpected PHM, which can be associated, albeit infrequently, with persistent gestational trophoblastic disease or a trophoblastic tumor.

Epithelial-to-mesenchymal transition of human proximal tubular epithelial cells: effects of rapamycin, mycophenolate, cyclosporin, azathioprine, and methylprednisolone.

Epithelial-to-mesenchymal transition (EMT) of renal proximal tubular epithelial cells (PTEC) into myofibroblasts is an important step in the pathogenesis of chronic allograft nephropathy. The effects of commonly used immunosuppressives in renal transplantation on EMT are not known. PTEC were cultured in transforming growth factor-beta to induce EMT. The effects of the immunosuppressives on cell morphology and alpha-smooth muscle actin were studied by phase contrast microscopy, immunocytochemistry, and western blotting. The effects on versican were studied by [S] labeling and polyacrylamide gel electrophoresis. Rapamycin and mycophenolate mofetil (MMF) prevented EMT and moreover returned myofibroblasts to PTEC morphology. These immunosuppressives also reduced versican production by both PTEC and myofibroblasts. Cyclosporine A, azathioprine, and methylprednisolone were less effective than rapamycin and MMF. Moreover, these immunosuppressives did not decrease versican. Rapamycin and MMF have a greater inhibitory effect on EMT in vitro than older immunosuppressives and may result in less fibrosis and a better long-term allograft survival.