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769 results on '"Pruthi, Rajiv K"'

201. Clinical characteristics and platelet phenotype in a family with RUNX1 mutated thrombocytopenia.

Author

Perez Botero, Juliana, Chen, Dong, Cousin, Margot A., Majerus, Julie A., Coon, Lea M., Kruisselbrink, Teresa M., Klee, Eric W., Lazaridis, Konstantinos N., Pruthi, Rajiv K., and Patnaik, Mrinal M.

Subjects
THROMBOCYTOPENIA, FLOW cytometry, TRANSMISSION electron microscopes, GENETIC mutation, PHENOTYPES
Abstract

The article presents a case study of a 29-year-old female with chronic thrombocytopenia. Topics discussed include flow cytometry and platelet transmission electron microscopy (PTEM) performed using clinically validated laboratory tests, germline heterozygous RUNX1 mutations causing autosomal dominant, and the clinical phenotype of patients with germline RUNX1 mutations found to be heterogeneous.

Published
2017
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202. Diagnostic Testing Approaches for Activated Protein C Resistance and Factor V Leiden: A Comparison of Institutional and National Provider Practices.

Author

Botero, Juliana Perez, Majerus, Julie A., Strege, Ann K., Johnson, Ryan D., Dong Chen, and Pruthi, Rajiv K.

Subjects
FACTOR V Leiden, COST effectiveness, HYPERCOAGULATION disorders
Abstract

Objectives: To analyze the economic impact of testing for activated protein C resistance (APC-R) due to factor V Leiden (FVL) mutation with APC-R with reflexive FVL genotyping (algorithmic approach) or genotyping alone. Methods: OptumLabs Data Warehouse (OLDW) data were used to assess testing approaches. Insurance claims for APC-R and FVL in 2013 were compared with the Mayo Clinic database. Centers for Medicare & Medicaid Services diagnostic fee schedules were used to assign costs. Results: Of 19.3 million OLDW-covered individuals, 74,242 (0.385%) received 75,608 tests: APC-R, 2,265 (2.9%); FVL genotyping, 70,619 (90.1%); and both APC-R and FVL, 2,724 (7.0%). In total, 1,317 tests were performed at Mayo Clinic: APC-R with reflex FVL (1,256; 95.4%) and FVL alone (61; 4.6%). Costs per evaluated individual and per total population (person/ year) in OLDW and algorithmic approach were $83.77 vs $36.38 and $0.32 vs $0.14, respectively. Conclusions: The cost-optimized algorithmic approach reduces health care costs. [ABSTRACT FROM AUTHOR]

Published
2017
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204. Clinical and laboratory characteristics in congenital ANKRD26 mutation-associated thrombocytopenia: A detailed phenotypic study of a family.

Author

Perez Botero, Juliana, Chen, Dong, He, Rong, Viswanatha, David S., Majerus, Julie A., Coon, Lea M., Nguyen, Phuong L., Reichard, Karen K., Oliveira, Jennifer L., Tefferi, Ayalew, Gangat, Naseema, Pruthi, Rajiv K., and Patnaik, Mrinal M.

Subjects
THROMBOCYTOPENIA, GENETIC mutation, PHENOTYPES, MOLECULAR genetics, THROMBOSIS, HEMOSTASIS
Abstract

The clinical and laboratory characteristics of patients with non-syndromic, autosomal dominant thrombocytopenia secondary to germ lineANKRD26mutations appear to be heterogeneous. Except for a targeted molecular genotyping approach, there is no distinct clinical or laboratory phenotype that has been specifically associated with this particular gene mutation. Such heterogeneity could be due to variations in mutation and genetic background in different families. To understand the phenotypic heterogeneity, we thoroughly studied one affected family using the International Society for Thrombosis and Haemostasis bleeding assessment tool and both clinically validated standard and esoteric platelet testing (electron microscopy (EM) and flow cytometry). We found that decreased platelet aggregation with arachidonic acid and epinephrine agonists was common in affected family members. EM studies demonstrated persistent borderline low mean dense granules per platelet, decreased alpha granules and an increased canalicular network pattern in all affected members. Since these characteristics are subtle or non-pathognomonic, molecular testing forANKRD26mutation remains the most reliable test to render a diagnosis and should be considered when evaluating a patient or family with congenital thrombocytopenia, particularly if there is a history of myeloid neoplasms. [ABSTRACT FROM PUBLISHER]

Published
2016
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205. Self-reported reproductive health experiences in women with von Willebrand disease: a qualitative interview-based study.

Author

Marshall, Ariela L., Dasari, Harika, Warner, Nathaniel D., Grill, Diane E., Nichols, William L., and Pruthi, Rajiv K.

Subjects
REPRODUCTIVE health, VON Willebrand disease, WOMEN'S health
Abstract

The article offers information on a study related to the reproductive health experiences in women with von Willebrand disease (VWD). It notes that the women with VWD experienced heavy menstrual bleeding also known as menorrhagia. It notes that the options for the treatment of menorrhagia include combined oral contraceptives, intrauterine devices and endometrial ablation.

Published
2019
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208. Intravenous Bevacizumab for Refractory Hereditary Hemorrhagic Telangiectasia–Related Epistaxis and Gastrointestinal Bleeding

Author

Iyer, Vivek N., Apala, Dinesh R., Pannu, Bibek S., Kotecha, Aditya, Brinjikji, Waleed, Leise, Michael D., Kamath, Patrick S., Misra, Sanjay, Begna, Kebede H., Cartin-Ceba, Rodrigo, DuBrock, Hilary M., Krowka, Michael J., O'Brien, Erin K., Pruthi, Rajiv K., Schroeder, Darrell R., and Swanson, Karen L.

Abstract

To present a multiyear clinical experience with intravenous bevacizumab for the management of severe gastrointestinal bleeding and/or epistaxis in patients with hereditary hemorrhagic telangiectasia (HHT).

Published
2018
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210. Autologous Stem Cell Transplantation In Immunoglobulin Light Chain Amyloidosis With Factor X Deficien

Author

Cordes, Stefan F, primary, Gertz, Morie A, additional, Buadi, Francis K, additional, Lin, Yi, additional, Lacy, Martha Q, additional, Kapoor, Prashant, additional, Kumar, Shaji K, additional, McCurdy, Arleigh, additional, Dispenzieri, Angela, additional, Dingli, David, additional, Hayman, Suzanne R, additional, Hogan, William J., additional, and Pruthi, Rajiv K, additional

Published
2013
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213. Management Of PICC-Associated Thrombosis In Patients Receiving Chemotherapy For Hematologic Malignancies

Author

Sridharan, Meera, primary, Al-Kali, Aref, additional, Ashrani, Aneel A., additional, Begna, Kebede, additional, Elliott, Michelle, additional, Hogan, William J., additional, Hook, Carl C., additional, Kaufmann, Scott H., additional, Letendre, Louis, additional, Litzow, Mark R., additional, Patnaik, Mrinal M., additional, Pardanani, Animesh D., additional, Tefferi, Ayalew, additional, Wolanskyj, Alexandra, additional, and Pruthi, Rajiv K., additional

Published
2013
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222. Acquired factor V deficiency in myeloproliferative neoplasms: a Mayo Clinic series of 33 patients.

Author

Ashrani, Aneel A., Tefferi, Ayalew, Pruthi, Rajiv K., and Pardanani, Animesh

Subjects
VON Willebrand disease, MYELOPROLIFERATIVE neoplasms, AUTOIMMUNE diseases, BLOOD coagulation factor VIII, CANCER patients
Abstract

The article focuses on a research related to acquired von Willebrand syndrome in patients with myeloproliferative neoplasms (MPN). Topics discussed include risks of acquired factor V (FV) deficiency in patients with autoimmune diseases and malignancy, high incidence of acquired FVIII inhibitors in MPN, and high incidence of bleeding complications.

Published
2015
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223. Comparison of complication rates of Hickman®catheters versus peripherally inserted central catheters in patients with acute myeloid leukemia undergoing induction chemotherapy

Author

Lim, Ming Y., primary, Al-Kali, Aref, additional, Ashrani, Aneel A., additional, Begna, Kebede H., additional, Elliott, Michelle A., additional, Hogan, William J., additional, Hook, C. Christopher, additional, Kaufmann, Scott H., additional, Letendre, Louis, additional, Litzow, Mark R., additional, Patnaik, Mrinal S., additional, Pardanani, Animesh, additional, Tefferi, Ayalew, additional, Wolanskyj, Alexandra P., additional, Grill, Diane E., additional, and Pruthi, Rajiv K., additional

Published
2012
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224. Von Willebrand Factor Multimer Analysis and Classification: A Comprehensive Review and Updates.

Author

Saadalla, Abdulrahman, Seheult, Jansen, Pruthi, Rajiv K., and Chen, Dong

Subjects
*VON Willebrand factor, *VON Willebrand disease, *FACTOR analysis, *BLOOD coagulation factor VIII
Abstract

Von Willebrand factor (VWF) is a multimeric glycoprotein with essential roles in primary hemostasis. Patients with von Willebrand disease (VWD), due to quantitative and/or qualitative defects of VWF usually experience mucocutaneous bleeding. Based on the laboratory results of VWF antigen, various VWF activities, factor VIII activity, and VWF multimer patterns, VWD can be categorized as type 1, 2, and 3 VWD. VWF multimer analysis by either manual or semi-automated electrophoresis and immunoblotting is a critical part of the laboratory testing to differentiate type 1, type 2 VWD, and subtypes of type 1 or 2 VWD. The multimer distribution patterns can also help to understand the underlying molecular mechanism of VWF synthesis, multimerization, and clearance defects in VWD. This review will cover VWF synthesis, multimerization, secretion, VWF multimer analysis, and VWF multimer interpretation of various types and subtypes of VWD. [ABSTRACT FROM AUTHOR]

Published
2023
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226. The value of the chromogenic activity assay in diagnosis and therapeutic monitoring of hemophilia.

Author

Adcock, Dorothy M., Tiefenbacher, Stefan, and Pruthi, Rajiv K.

Subjects
BLOOD coagulation factors, BLOOD coagulation tests, CALIBRATION, CHROMOGENIC compounds, DRUG monitoring, GENETIC mutation, HEMOPHILIA, RECOMBINANT proteins, CONTINUING education units, SEVERITY of illness index, DIAGNOSIS
Abstract

The article discusses pathogenicity, diagnosis, and treatment options for hemophilia. Topics explored include the clinical characteristics and severity of hemophilia A and B, the need for functional factor VIII (FVIII) and factor IX (FIX) assessment to be accurate to ensure effective coagulation factor replacement monitoring, and the patient outcomes associated with the administration of modified recombinant factor replacement products.

Published
2017

227. Therapy-related acute promyelocytic leukemia: observations relating to APL pathogenesis and therapy*

Author

Elliott, Michelle A., primary, Letendre, Louis, additional, Tefferi, Ayalew, additional, Hogan, William J., additional, Hook, Christopher, additional, Kaufmann, Scott H., additional, Pruthi, Rajiv K., additional, Pardanani, Animesh, additional, Begna, Kebede H., additional, Ashrani, Aneel A., additional, Wolanskyj, Alexandra P., additional, Al-Kali, Aref, additional, and Litzow, Mark R., additional

Published
2011
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240. From Vitamin K Antagonists to Liver International Normalized Ratio: A Historical Journey and Critical Perspective.

Author

Gatt, Alexander, Dong Chen, Pruthi, Rajiv K., Kamath, Patrick S., Leise, Michael D., Ashrani, Aneel A., Nichols, William L., and Rong He

Subjects
TREATMENT of chronic kidney failure, INTERNATIONAL normalized ratio, ANTICOAGULANTS, VITAMIN K, KIDNEY failure, VITAMIN therapy, THERAPEUTICS
Abstract

Adoption of international normalized ratio (INR) to harmonize prothrombin time has greatly improved the safety and effectiveness of vitamin K antagonists (VKA) oral anticoagulant therapy. INR is also a major laboratory variable in calculating the widely used Model for End-Stage Liver Disease (MELD) score for liver transplant organ prioritization. However, since the conventional INR (INRVKA) is calibrated specifically for VKA patients, its interlaboratory variation has a significant impact on the accuracy of MELD score. Though still requiring further clinical validation in large numbers of waitlisted patients, the alternative liver INR calibrated by using plasma from liver disease patients instead of VKA patients may harmonize the differences and thus more suitable for MELD score calculation. The objective of this article is to review the history of INR, MELD score, and liver INR, and discuss the challenges and solutions of liver INR implementation. [ABSTRACT FROM AUTHOR]

Published
2014
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244. Natural history of thromboembolism in AL amyloidosis

Author

Halligan, Christine S., primary, Lacy, Martha Q., additional, Vincent Rajkumar, S., additional, Dispenzieri, Angela, additional, Witzig, Thomas E., additional, Lust, John A., additional, Fonseca, Rafael, additional, Gertz, Morie A., additional, Kyle, Robert A., additional, and Pruthi, Rajiv K., additional

Published
2006
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247. Thromboembolism in Adults with Acute Lymphoblastic Leukemia During Induction with L-Asparaginase-containing Multi-agent Regimens: Incidence, Risk Factors, and Possible Role of Antithrombin

Author

Elliott, Michelle A, primary, Wolf, Robert C, additional, Hook, Christopher C, additional, Pruthi, Rajiv K, additional, Heit, John A, additional, Letendre, Louis L, additional, Tefferi, Ayalew, additional, Kaufmann, Scott H, additional, Mesa, Ruben A, additional, and Litzow, Mark R, additional

Published
2004
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250. Coagulation Disorders.

Author

Bagg, Adam, Caliendo, Angela M., Kaul, Karen L., Van Deerlin, Vivianna M., Leonard, Debra G. B., Pruthi, Rajiv K., and Heit, John A.

Abstract

Reduced to its simplest form, the vascular system is a series of interconnected biologic conduits filled with fluid moving under pressure. This system is subject to injury and must repair itself in order to avoid exsanguination. This latter function is provided by the hemostatic system. Thus, normal hemostasis is a reparative process and consists of three major mechanisms: (1) vasospasm, which is the main mechanism for controlling bleeding after transection/avulsion injuries of large arteries, arterioles, and veins; (2) platelet plug formation; and (3) the procoagulant system. The procoagulant system consists of the mechanisms by which fluid blood is converted into an insoluble hemostatic thrombus. While inherited or acquired disorders of all three mechanisms can cause clinically abnormal bleeding, this chapter reviews the molecular basis of inherited disorders of the procoagulant system (e. g., hemophilia A and B, von Willebrand disease). Inherited vascular and platelet disorders associated with abnormal bleeding are not discussed here. [ABSTRACT FROM AUTHOR]

Published
2007
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