PubMed · 15197968
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Misako Suzuki, Yasuo Ikeda. 2004. [TTP/HUS].. https://pubmed.ncbi.nlm.nih.gov/15197968/
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Thrombotic thrombocytopenic purpura (TTP) is a syndrome characterized by microangiopathic hemolytic anemia and thrombocytopenia with varying degrees of renal dysfunction, neurologic signs and symptoms, and fever. Evidence has supported that a large proportion of cases of acquired TTP are due to the accumulation of ultralarge von Willebrand factor (vWF) multimers due to an acquired deficiency in the vWF cleaving protease, ADAMTS-13. TTP is rare in the post-surgical setting but is best described after cardiothoracic and vascular surgeries. We present a case of postoperative TTP first presenting with microangiopathic hemolytic anemia and thrombocytopenia 9 days after emergent appendectomy for a ruptured appendix. ADAMTS-13 and factor H levels returned normal and an ADAMTS-13 inhibitor was not identified. To our knowledge, this is the first case report of postoperative TTP after an appendectomy and the first report with correlative ADAMTS-13 data. Plasma exchange with fresh frozen plasma followed by cryopoor plasma, along with steroids resulted in eventual remission of TTP in our patient. Early postoperative diagnosis and aggressive management with consideration of initiation of plasma exchange is imperative to decrease the morbidity and morality associated with TTP.
BACKGROUND: ADAMTS1 and ADAMTS8 are proteases involved in extracellular matrix proteolysis and antiangiogenesis, but little is known about their expression and function in cerebral ischemia. We investigated the changes in ADAMTS1 and ADAMTS8 in a rat model of permanent middle cerebral artery occlusion (pMCAO). The expressions of glyseraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin, cyclophilin, and RPL13A were examined in order to validate the appropriate housekeeping genes for a long duration after inducing cerebral ischemia. METHODS: Male Sprague-Dawley rats were subjected to pMCAO, and ischemic penumbra was collected at 2, 24 h, 3, 7, and 21 days after inducing ischemia, ADAMTS1, ADAMTS8, and the four housekeeping genes were quantified using real-time polymerase chain reaction (PCR). RESULTS: The expression of beta-actin increased up to 21 days, and that of GAPDH decreased at 24 h after pMCAO, with no statistically significant changes in RPL13A and cyclophilin being detected. ADAMTS1 mRNA increased at 2 h after pMCAO, peaked at 24 h, and remained at a high level until 21 days. The expression of ADAMTS8 mRNA decreased at 2 and 24 h after pMCAO, followed by a slight increase at 3 days, and then decreased again at 7 days. CONCLUSION: The results suggest that RPL13A and cyclophilin are two appropriate housekeeping genes for the rat pMCAO model up to 21 days. ADAMTS1 mRNA levels increased, but ADAMTS8 decreased after pMCAO. Our data provide new insight into the mechanism of brain ischemia and self-repair after injury.