Pub Date : 2020-08-10DOI: 10.1515/9783110610185-003
E. Hanson
High-dose methotrexate–induced nephrotoxicity is a medical emergency. Renal methotrexate excretion, which typically accounts for 90% of the drug’s elimination, is delayed, resulting in prolonged exposure to high methotrexate concentrations. The duration of exposure is the primary determinant of the drug’s toxic effects, and early recognition and prompt efforts to lower methotrexate concentrations are critical to preventing severe systemic toxicity. High-dose methotrexate–induced renal dysfunction is heralded by an increasing serum creatinine concentration during or shortly after the methotrexate infusion. Urine output is usually maintained despite a rapid decline in glomerular filtration. Daily monitoring of serum creatinine and methotrexate concentrations is essential to early detection of this complication. Leucovorin provides a source of the tetrahydrofolates that are depleted by methotrexate’s inhibition of dihydrofolate reductase, but methotrexate competes with leucovorin for cell uptake. Therefore, leucovorin rescue is less effective at methotrexate concentrations that exceed 10 mol/L for 48 h. The leucovorin dose must be increased in proportion to the serum methotrexate concentration when methotrexate clearance is delayed (e.g., 1000 mg/m every 6 h for a methotrexate concentration 10 mol/L at 48 h). High leucovorin doses (250 mg/m every 6 h) should also be continued for 48 h after glucarpidase administration because the enzyme hydrolyzes leucovorin and its active circulating metabolite, 5-methyltetrahydrofolate, to inactive forms. Glucarpidase rapidly and efficiently lowers the serum methotrexate concentration by providing an alternative route of elimination and, when administered as soon as possible after the recognition of nephrotoxicity, can effectively prevent methotrexate toxicity. Patients who receive inadequate leucovorin rescue or receive glucarpidase 96 h after the start of the methotrexate infusion are at greater risk for developing lifethreatening methotrexate toxicity (1 ). As illustrated by the case study, commercial methotrexate assays will underestimate the impact of glucarpidase on serum methotrexate concentrations because of the interference by the inactive byproduct, DAMPA. DAMPA is subsequently metabolized by hydroxylation and glucuronide conjugation and is cleared more rapidly than residual methotrexate.
{"title":"Commentary","authors":"E. Hanson","doi":"10.1515/9783110610185-003","DOIUrl":"https://doi.org/10.1515/9783110610185-003","url":null,"abstract":"High-dose methotrexate–induced nephrotoxicity is a medical emergency. Renal methotrexate excretion, which typically accounts for 90% of the drug’s elimination, is delayed, resulting in prolonged exposure to high methotrexate concentrations. The duration of exposure is the primary determinant of the drug’s toxic effects, and early recognition and prompt efforts to lower methotrexate concentrations are critical to preventing severe systemic toxicity. High-dose methotrexate–induced renal dysfunction is heralded by an increasing serum creatinine concentration during or shortly after the methotrexate infusion. Urine output is usually maintained despite a rapid decline in glomerular filtration. Daily monitoring of serum creatinine and methotrexate concentrations is essential to early detection of this complication. Leucovorin provides a source of the tetrahydrofolates that are depleted by methotrexate’s inhibition of dihydrofolate reductase, but methotrexate competes with leucovorin for cell uptake. Therefore, leucovorin rescue is less effective at methotrexate concentrations that exceed 10 mol/L for 48 h. The leucovorin dose must be increased in proportion to the serum methotrexate concentration when methotrexate clearance is delayed (e.g., 1000 mg/m every 6 h for a methotrexate concentration 10 mol/L at 48 h). High leucovorin doses (250 mg/m every 6 h) should also be continued for 48 h after glucarpidase administration because the enzyme hydrolyzes leucovorin and its active circulating metabolite, 5-methyltetrahydrofolate, to inactive forms. Glucarpidase rapidly and efficiently lowers the serum methotrexate concentration by providing an alternative route of elimination and, when administered as soon as possible after the recognition of nephrotoxicity, can effectively prevent methotrexate toxicity. Patients who receive inadequate leucovorin rescue or receive glucarpidase 96 h after the start of the methotrexate infusion are at greater risk for developing lifethreatening methotrexate toxicity (1 ). As illustrated by the case study, commercial methotrexate assays will underestimate the impact of glucarpidase on serum methotrexate concentrations because of the interference by the inactive byproduct, DAMPA. DAMPA is subsequently metabolized by hydroxylation and glucuronide conjugation and is cleared more rapidly than residual methotrexate.","PeriodicalId":51937,"journal":{"name":"NEW ZEALAND JOURNAL OF HISTORY","volume":"13 1","pages":"40 - 42"},"PeriodicalIF":0.2,"publicationDate":"2020-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/9783110610185-003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43247924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"历史学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Approximately 23 species of thrips were recorded from flowers of 26 species of Australian subtropical rainforest trees, shrubs and vines (in 17 families) in the Manning Valley, coastal northern New South Wales. Pollination by thrips (thripophily) appears more widespread in rainforest communities than has been previously recognized. The pollination ecology of Wilkiea huegeliana (Monimiaceae) was studied in detail. Wilkiea huegeliana is a small, unisexual, annually flowering tree or shrub of rainforest and associated ecotones in eastern Australia, and is a larval food plant for the Regent Skipper butterfly Euschemon rafflesia rafflesia (Hesperiidae). At this latitude W. huegeliana is pollinated solely by a species of thrips, Thrips setipennis, but T. setipennis is not restricted to W. huegeliana and was recorded from flowers of 13 rainforest plant species. It appears to be the obligate pollinator also for Rapanea howittiana and R. variabilis (Myrsinaceae). Pollinator exclusion experiments were inconclusive but W. huegeliana may be facultatively agamospermous. The recruitment pathway to unrewarding female W. huegeliana flowers is uncertain but attraction may function by automimicry. Both male and female flowers serve as brood sites for T. setipennis larvae. Although the pollination ecology of W. huegeliana is specialized, the family Monimiaceae exhibits a broad diversity of pollination strategies. A number of these are discussed. The apparent obligate and restricted pollinator requirements of W. huegeliana may make it, and any associated phytophagous fauna, vulnerable to the impacts of habitat fragmentation.
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Pub Date : 1971-07-01DOI: 10.1080/00076797100000020
W. Cheong
{"title":"The Beginnings of Credit Finance on the China Coast: The Canton Financial Crisis of 1812–1815","authors":"W. Cheong","doi":"10.1080/00076797100000020","DOIUrl":"https://doi.org/10.1080/00076797100000020","url":null,"abstract":"","PeriodicalId":51937,"journal":{"name":"NEW ZEALAND JOURNAL OF HISTORY","volume":"5 1","pages":"70 - 92"},"PeriodicalIF":0.2,"publicationDate":"1971-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00076797100000020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58758560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"历史学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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