Pub Date : 2011-01-01DOI: 10.17925/ohr.2011.07.2.91
Karen M Mustian, Katie Devine, Julie L Ryan, Michelle C Janelsins, Lisa K Sprod, Luke J Peppone, Grace D Candelario, Supriya G Mohile, Gary R Morrow
Nausea and vomiting are two of the most troubling side effects patients experience during chemotherapy. While newly available treatments have improved our ability to manage nausea and vomiting, anticipatory and delayed nausea and vomiting are still a major problem for patients receiving chemotherapy. Many cancer patients will delay or refuse future chemotherapy treatments and contemplate stopping chemotherapy altogether because of their fear of experiencing further nausea and vomiting. The purpose of this article is to provide an overview of the patho-psychophysiology of chemotherapy-induced nausea and vomiting and the recommended guidelines for treatment.
{"title":"Treatment of Nausea and Vomiting During Chemotherapy.","authors":"Karen M Mustian, Katie Devine, Julie L Ryan, Michelle C Janelsins, Lisa K Sprod, Luke J Peppone, Grace D Candelario, Supriya G Mohile, Gary R Morrow","doi":"10.17925/ohr.2011.07.2.91","DOIUrl":"10.17925/ohr.2011.07.2.91","url":null,"abstract":"<p><p>Nausea and vomiting are two of the most troubling side effects patients experience during chemotherapy. While newly available treatments have improved our ability to manage nausea and vomiting, anticipatory and delayed nausea and vomiting are still a major problem for patients receiving chemotherapy. Many cancer patients will delay or refuse future chemotherapy treatments and contemplate stopping chemotherapy altogether because of their fear of experiencing further nausea and vomiting. The purpose of this article is to provide an overview of the patho-psychophysiology of chemotherapy-induced nausea and vomiting and the recommended guidelines for treatment.</p>","PeriodicalId":89518,"journal":{"name":"US oncology & hematology","volume":"7 2","pages":"91-97"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898599/pdf/nihms544150.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32063647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-01-01DOI: 10.17925/ohr.2011.07.1.72
Majed A Refaai, Kelly F Henrichs, Sherry L Spinelli, Richard P Phipps, Edward Masel, Brian H Smith, Charles W Francis, Neil Blumberg
Since platelets possess A and B antigen, mismatched ABO platelets could, theoretically, become activated or hypofunctional by exposure to anti-A or anti-B antibodies found in transfused or recipient plasma. Following normal baseline platelet aggregation to adenosine diphosphate (ADP), platelets from normal donors of different blood types were incubated at 37°C for 10 minutes with 50μl of normal saline (NS), O plasma, or AB plasma. Aggregation was then induced with ADP. No significant changes from baseline were seen in platelet aggregation studies following incubation with NS. However, platelet aggregations of type A and type B platelets were significantly inhibited when incubated with O plasma (mean of 41 and 22%, respectively). Our findings indicate that mediators in group O plasma, very likely anti-A and anti-B antibodies, cause impaired platelet aggregation of ABO non-identical platelets.
{"title":"Platelet Activation Following Exposure to Anti-ABO Antibodies-An In Vitro Study.","authors":"Majed A Refaai, Kelly F Henrichs, Sherry L Spinelli, Richard P Phipps, Edward Masel, Brian H Smith, Charles W Francis, Neil Blumberg","doi":"10.17925/ohr.2011.07.1.72","DOIUrl":"https://doi.org/10.17925/ohr.2011.07.1.72","url":null,"abstract":"<p><p>Since platelets possess A and B antigen, mismatched ABO platelets could, theoretically, become activated or hypofunctional by exposure to anti-A or anti-B antibodies found in transfused or recipient plasma. Following normal baseline platelet aggregation to adenosine diphosphate (ADP), platelets from normal donors of different blood types were incubated at 37°C for 10 minutes with 50μl of normal saline (NS), O plasma, or AB plasma. Aggregation was then induced with ADP. No significant changes from baseline were seen in platelet aggregation studies following incubation with NS. However, platelet aggregations of type A and type B platelets were significantly inhibited when incubated with O plasma (mean of 41 and 22%, respectively). Our findings indicate that mediators in group O plasma, very likely anti-A and anti-B antibodies, cause impaired platelet aggregation of ABO non-identical platelets.</p>","PeriodicalId":89518,"journal":{"name":"US oncology & hematology","volume":"7 1","pages":"72-74"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3162317/pdf/nihms307396.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30104493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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