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1. In Response

   • Mandeep S Dhami, MD

   Eastern Connecticut Hematology & Oncology

   HOPE 2 investigators have reported lack of clinical benefit in reducing the risk of recurrent venous thrombosis with Homocysteine- lowering therapy in patients with prior venous thromboembolism (VTE) and Hyperhomocystenemia. However, the mean homocysteine level of the patients in his trial was 12 micro-mole/L. Heijer et al showed that the odds ratio (OR) of venous thrombosis goes up as the level of Homocysteine increases. The OR is 2 when homocysteine level is over 18 micro-mole/l. However at a homocysteine level of 12 micro-mole/l, the OR of thrombosis is near baseline i.e around 1. This raises the possibility of having studied a population with only minimally increased risk of thrombosis and hence it would be difficult to show a benefit of lowering homocysteine in this particular group. Future trials are needed to study patients with baseline homocysteine level of over 18 micro-mole/l before abandoning vitamin supplementaton in these patients.

   Reference:

   Martin den Heijer, M.D. et al, NEJM: Volume 334, No.12: 759- 762,1996.

   Conflict of Interest:

   None declared

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   Published August 30, 2007
2. Question to Authors

   • Lynn A Bentson, MD

   FirstCare physicians

   This trial showed no effect of lowering homocysteine in a popualation with venous disease. Some of the patients had high homocysteine levels at baseline, some had low levels, and some had normal levels. They all got moderate doses of folate plus other B vitamins.

   If we gave every patient who was unable to jog a mile albuterol it would help those with asthma, or with "exertional athma" but not the others. Whether it showed a difference in the group analysis would depend on how many had asthma vs deconditioning or CAD or CHF or obesity or myopathy or a broken leg or some combination of these problems. It would tell me whether to give albuterol to the entire high school gym class, but not whether to give it to one patient with moderate wheezing.

   I would love to know if I am wasting my patients time and money looking for high homocysteine levels in what I consider to be "the right circumstance" . Should I look for this with an "unprovoked " DVT? If I find it, should I just tell the patient they have higher than average risk (do they?) or should I treat it? If I treat it , should I follow levels? I still don't know.

   I don't think anyone would argue homocysteine is as powerful as aspirin or statins or blood pressure control for prevention of arterial disease. There is no similar "800 pound gorilla" that muddies the waters when we look at venous disease. I am not surprised that when there are effective, well-tolerated (and profitable) medications to help patients with CAD and PVD that the probrbly much smaller effect of homocysteinemia is not well studied. I think we do have important poulation information that universal supplementation will not reduce arterial vascular disase very much, if at all. I am disappointed to have little immediately clinically helpful information from such a large study.

   Homocysteine levels were only measured in 60% at enrollment. A post hoc analysis of those with higher levels or who lived in places with universal fortification does not help me with decision making in individuals . As a clinician that is more important to me than the important public policy question of whether food should be supplemented. It is also more immediately relevant than the question of whether all patients with known DVT or recent MI or peripheral vascular disease should get folate and B vitamin supplements . I am disappointed to be left uninformed.

   Conflict of Interest:

   None declared

   Submit response
   Published June 7, 2007