Spreadsheet: 139498d1328276114-excel-2007-copy-data-from-cells-in-one-workbook-to-another-based-on-the-cell-headings-jama-eletters-data
Sheet: 305 13 1336

305 9 923 | Response ID | Status | Title, Author | Responder | [NAME] | Response
 | jama_el;787 | P | Re:Taking care of 61 year old female with unprovoked venous thromboembolism Beverley P Edwards, July 5, 2011 | Beverley P Edwards,  MD  Indiana University | [EMAIL] | This woman should be checked for a congenital coagulopathy and if present receive a permanent IVC filter. The question of continued long- term anti-coagulation should be an in-depth doctor-patient discussion.   Conflict of Interest: None declared
 | jama_el;725 | NR | [NAME] deficiency [NAME], March 8, 2011 | [NAME],  M.D.  Robarts Research Institute, University of Western Ontario | [EMAIL] | A cause of venous thrombosis that is frequently missed is elevated plasma total homocysteine, due to metabolic B12 deficiency. A normal level of serum B12 (~ 160-600 pmol/L) does not exclude metabolic B12 deficiency; the serum B12 needs to be above 400 pmol/L to be 90% confident that metabolic B12 deficiency is excluded1. In a vascular prevention practice, metabolic B12 deficiency exists in 12% of patients age <50, 13% age 50- 71, and 30% age 71 or [NAME]. In folate-replete subjects (virtually all North Americans, now that we have folate fortification of the grain supply), a plasma total homocysteine substitutes for methylmalonic acid3. For this patient I would investigate metabolic B12 deficiency by measuring serum B12 and plasma total homocysteine; if the homocysteine is elevated and the serum B12 is below 400 pmol/L, I would treat her with vitamin B12. If her serum B12 is very low, she might need a series of B12 injections to restore her intestinal villi4 so that she could absorb oral B12 supplements.   Reference List   (1) [NAME], Oulhaj A, Smith AD et al. Determinants of plasma methylmalonic acid in a large population: implications for assessment of vitamin B12 status. Clin Chem 2009;55:2198-2206.   (2) Spence JD. Nutrition and stroke prevention. Stroke 2006;37:2430- 2435.   (3) Robertson J, Iemolo F, Stabler SP, [NAME], [NAME]. [NAME], homocysteine and carotid plaque in the era of folic acid fortification of enriched cereal grain products. CMAJ 2005;172:1569-1573.   (4) Arvanitakis C. Functional and morphological abnormalities of the small intestinal mucosa in pernicious anemia--a prospective study. [NAME] (Stuttg) 1978;25:313-318.   Conflict of Interest: I have received a grant from Pan American Laboratories to support our study of vitamin therapy for homocysteine in patients with diabetic nephropathy, published in JAMA in 2010.
 | jama_el;732 | H | Taking care of 61 year old female with unprovoked venous thromboembolism [NAME], March 20, 2011 | [NAME],  MD  MD Anderson Cancer Center | [EMAIL] | Patients who have had unprovoked VTE have worse prognosis than VTE due to transient underlying risk factors such as recent surgery, immobilization etc. While several factors influence the prognosis of a patient with VTE, modified Pulmonary Embolism Severity Index (PESI) states these following as the most important. They are age, male sex, heart rate, cancer, Congestive heart failure, preexisting lung conditions, high systolic blood pressure and oxygen saturation <90. It has been reported that VTE causing pulmonary embolism causing around 300,000 deaths annually in United states. Several studies have reported 5 year cumulative incidence of recurrent VTE as 21.5% for unprovoked cases. Investigation for thrombophilia is appropriate in conditions such as recurrent VTEs, young patients etc. However routine investigation for thrombophilia isn't recommended as finding one does not alter the treatment or course of disease in adults and it is costly and time consuming.   In hemodynamically stable patients with normal Right heart function prevention of further clot formation with anticoagulants is enough. It is done by either intravenous heparin or subcutaneous low molecular heparin. During the second day of hospitalization [NAME] is added to heparin. Once the patient is adequately anticoagulated heparin is discontinued and oral [NAME] is continued. In cases of PE with persistent hypotension thrombolysis is indicated in acute management. If there is any contraindication to thrombolytic therapy or if it is ineffective, surgical embolectomy is done for acute management. If the cause of VTE is non recurrent, 3 months of treatment is considered enough. In patients with proximal DVT without PE 3 to 6 months of [NAME] treatment is indicated. In patients with inherited thrombophilias and recurrent VTEs lifelong [NAME] therapy with careful INR monitoring is considered.   The chance of having a recurrent Thromboembolism is high for Ms W because her VTE is unprovoked and not due to a temporary risk factor. Mortality for such recurrence is about 50 %( vs. 10% without RV dysfunction) as she has right ventricle hypokinesis. Hence it is strongly recommended that she is on lifelong anticoagulation preferably with [NAME], as its effect is easy to monitor with regular INR studies. But unfortunately when she was restarted on Coumadin three days after appendectomy she had severe abdominal bleeding. [NAME] is on levothyroxine which is known to increase the action of Coumadin. And it can be assumed that patient was on antibiotics after surgery. Macrolides and Quinolones are known to cause drug interactions with [NAME]. These factors might have caused here bleeding. With tight control of her Coumadin dosage keeping other drug interactions in view and with regular INR monitoring she can be safely maintained on [NAME]. Her chance of having a recurrent PE clearly outweighs her risk of bleeding. Patient is concerned about lifelong commitment to [NAME] and regular blood monitoring. She can be considered for the placement of [NAME] filter which isn't as effective as anticoagulation. Another alternative is to use direct thrombin inhibitors such as Ximelgatran, an oral preparation with no need of regular anticoagulant monitoring and predictable action.   1. [NAME] T, Luddington R, [NAME], [NAME] of recurrent venous Thromboembolism in relation to clinical and thrombophilic risk factors: prospective cohort study. Lancet, 2003 Aug 16;362(9383): 523-6.   2. Ulrike Nowak-Gottl, [NAME], [NAME], [NAME], [NAME], [NAME], [NAME] and Silke Ehrenforth. Risk of recurrent venous thrombosis in children with combined prothrombotic risk factors. Blood, 15 February 2001, [NAME]. 97, No.4, pp 858-862.   3. [NAME], MB, MRCPI, FRCPC, PhD. Natural History of Venous Thromboembolism. Circulation 2003; 107: 122-130.   4. Kearon C, [NAME], [NAME], et al. Antithrombotic therapy for venous thromboembolic diseases: American College of Chest Physicians Evidence Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:454S.   5. Won-Ho Choi, [NAME], [NAME], [NAME], [NAME], [NAME], [NAME], June Namgung, [NAME] and [NAME]. The Pulmonary Embolism Severity Index in Predicting the Prognosis of Patients with Pulmonary Embolism. Korean J intern Med. 2009 June; 24(2): 123-127   6. Fiessinger JN, Huisman MV, [NAME], Bournameauz H, [NAME], Eriksson H, Lundstrom T, Berkowitz SD, Nystrom P, Thorsen M, Ginsberg JS, THRIVE Treatment study investigators. Ximelgatran vs low molecular weight heparin and Warfarin for the treatment of deep vein thrombosis: a randomized trial. [NAME] Feb 9; 293(6): 681-9   Conflict of Interest: None declared