Purpose: To evaluate and compare the acute effect of electromagnetic and electrohydraulic extracorporeal shockwave lithotripsy (SWL) on the urothelial layers of kidney and ureter. Materials and Methods: Fifty patients, 29 males (58%) and 21 females (42%), with an average age of 51.68 years (range: 37-70) who underwent SWL application in two different centers were included. Twenty-eight patients (56%) were treated with electrohydraulic and 22 (44%) were treated with electromagnetic lithotripsy. Urinary cytologic examinations were done immediately before and after SWL therapy and 10 days later. The average numbers of epithelial cells, red blood cells (RBC), and myocytes were counted under 40 · magnification. Results: There were significant differences in the number of epithelial cells and RBC before and after immediate application of SWL: 1.66 and 14.9 cells/field, ( p = 0.001), 5.44 and 113.45 cells/field, respectively ( p = 0.001). The number of RBC was significantly higher in patients treated with electromagnetic lithotripsy than those treated with electrohydraulic: 141.9 and 93.4 cells/field, respectively ( p = 0.02). No myocyte or basement membrane elements were detected in any of the cytologic examinations. Cytologic examinations done after 10 days of SWL therapy revealed recovery of all abnormal cytologic findings. Conclusions: The acute increments in the number of epithelial cells and RBC after SWL were statistically significant but it was not permanent. SWL-induced urinary urothelial lesion is limited to the mucosal layer and there was no evidence of damage to the basal membrane or muscle layer. Electromagnetic lithotripsy caused high numbers of RBC than the electrohydraulic device on the postimmediate urine cytologic examination.
Upshaw-Schulman syndrome is a rare inherited form of thrombotic thrombocytopenic purpura disease caused by deficiency of ADAMTS13 and reversible by fresh frozen plasma infusions. Unlike the more common acquired thrombotic thrombocytopenic purpura, patient with Upshaw-Schulman syndrome generally presents early life with a repeated episodes of microangiopathic haemolytic anaemia, usually triggered by acute illness. There are few reported cases about congenital thrombotic thrombocytopenic purpura and long term prognosis. We describe a 16 months old Palestinian male patient with history of severe neonatal jaundice, microangiopathic haemolytic anaemia and thrombocytopenia triggered by febrile illness associated with facial palsy as neurological manifestation favoured congenital thrombotic thrombocytopenic purpura. Low ADAMTS13 level and improvement in platelet counts after fresh frozen plasma infusion with novel mutation of Leu209Pro in exon 6 of the ADAMTS13 gene confirmed the diagnosis of congenital thrombotic thrombocytopenic purpura in our patient who later on developed coarctation of aorta suggested thrombotic complication of ADAMTS13/VWF missing axis dysfunction.
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