Naturopathic Medical Research Dragon's Medical Bulletin July Aug 2010

September 2010 Newsletter

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TARGETED RESEARCH

Coagulation-and Thrombosis-Related Research

Impact of thrombophilia on risk of arterial ischemic stroke or cerebral sinovenous thrombosis in neonates and children: a systematic review and meta-analysis of observational studies.

Background: The aim of this study was to estimate the impact of thrombophilia on risk of first childhood stroke through a meta-analysis of published observational studies.

Methods and Results: A systematic search of electronic databases (Medline via PubMed, EMBASE, OVID, Web of Science, The Cochrane Library) for studies published from 1970 to 2009 was conducted. Data on year of publication, study design, country of origin, number of patients/control subjects, ethnicity, stroke type (arterial ischemic stroke [AIS], cerebral venous sinus thrombosis [CSVT]) were abstracted. Publication bias indicator and heterogeneity across studies were evaluated, and summary odds ratios (ORs) and 95% confidence intervals (CIs) were calculated with fixed-effects or random-effects models.

Twenty-two of 185 references met inclusion criteria. Thus, 1764 patients (arterial ischemic stroke [AIS], 1526; cerebral sinus venous thrombosis [CSVT], 238) and 2799 control subjects (neonate to 18 years of age) were enrolled. No significant heterogeneity was discerned across studies, and no publication bias was detected. A statistically significant association with first stroke was demonstrated for each thrombophilia trait evaluated, with no difference found between AIS and CSVT. Summary ORs (fixed-effects model) were as follows: antithrombin deficiency, 7.06 (95% CI, 2.44 to 22.42); protein C deficiency, 8.76 (95% CI, 4.53 to 16.96); protein S deficiency, 3.20 (95% CI, 1.22 to 8.40), factor V G1691A, 3.26 (95% CI, 2.59 to 4.10); factor II G20210A, 2.43 (95% CI, 1.67 to 3.51); MTHFR C677T (AIS), 1.58 (95% CI, 1.20 to 2.08); antiphospholipid antibodies (AIS), 6.95 (95% CI, 3.67 to 13.14); elevated lipoprotein(a), 6.27 (95% CI, 4.52 to 8.69), and combined thrombophilias, 11.86 (95% CI, 5.93 to 23.73). In the 6 exclusively perinatal AIS studies, summary ORs were as follows: factor V, 3.56 (95% CI, 2.29 to 5.53); and factor II, 2.02 (95% CI, 1.02 to 3.99).

Conclusions: The present meta-analysis indicates that thrombophilias serve as risk factors for incident stroke. However, the impact of thrombophilias on outcome and recurrence risk needs to be further investigated.

Kenet G, et al. Circulation. 2010 Apr 27;121(16):1838-47. Epub 2010 Apr 12.

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Lack of prophylaxis before the onset of acute venous thromboembolism among hospitalized cancer patients: the SWIss Venous ThromboEmbolism Registry (SWIVTER).

Background: Venous thromboembolism (VTE) prophylaxis remains underutilized, particularly in cancer patients. We explored clinical predictors of prophylaxis in hospitalized cancer patients before the onset of acute VTE.

Methods: In the SWiss Venous ThromboEmbolism Registry, 257 cancer patients (61 ± 15 years) with acute VTE and prior hospitalization for acute medical illness or surgery within 30 days (91% were at high risk with Geneva VTE risk score ≥3) were enrolled.

Results: Overall, 153 (60%) patients received prophylaxis (49% pharmacological and 21% mechanical) before the onset of acute VTE. Outpatient status at the time of VTE diagnosis [odds ratio (OR) 0.31, 95% confidence interval (CI) 0.18–0.53], ongoing chemotherapy (OR 0.51, 95% CI 0.31–0.85), and recent chemotherapy (OR 0.53, 95% CI 0.32–0.88) were univariately associated with the absence of VTE prophylaxis. In multivariate analysis, intensive care unit admission within 30 days (OR 7.02, 95% CI 2.38–20.64), prior deep vein thrombosis (OR 3.48, 95% CI 2.14–5.64), surgery within 30 days (OR 2.43, 95% CI 1.19–4.99), bed rest >3 days (OR 2.02, 95% CI 1.08–3.78), and outpatient status (OR 0.38, 95% CI 0.19–0.76) remained the only independent predictors of thromboprophylaxis.

Conclusions: Although most hospitalized cancer patients were at high risk, 40% did not receive any prophylaxis before the onset of acute VTE. There is a need to improve thromboprophylaxis in cancer patients, particularly in the presence of recent or ongoing chemotherapy.

Kucher N, et al. Ann Oncol. 2010:21 (5): 931-935.

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BOLUOKE® Q & A

Q: Is it necessary to take Boluoke® and probiotics at different times? Also what type of enzymes are you referring to in the FAQ, where it said to take Boluoke® and enzymes at least two hours apart? Are digestive enzymes included? I have been diagnosed with Lyme disease and have just started taking Boluke this week. Any other helpful info you can pass on to me would be very helpful!

Thanks. R.A. Graybill

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A: Boluoke® can be taken at the same time as probiotics. Yes, we do recommend taking Boluoke® separately from other proteolytic enzymes (e.g. digestive enzymes, bromelain, etc…) Boluoke® can be taken 1/2 an hour before meals, then take your digestive enzymes right before meals. Or you can take Boluoke® two hours after meals. With Lyme disease, some patients may exhibit Herxheimer reactions when starting Boluoke®, so some doctors start with a lower dosage, then work up gradually. However, other doctors actually start immediately with a high dosage. So you should consult your doctor. In general, Lyme patients are VERY hypercoagulable, so you would probably need to be on a higher dosage soon or later.

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Q: I feel nauseated when I take Bolouke® on an empty stomach. Can I take it with food? What is the reason for taking it away from enzymes? Does it destroy the enzymes? Would it cause me to feel more bloated when I eat? I would like to understand what it does, so I know why to do something. Thanks for your help with this.

R.A.Graybill

A: We suggest taking Boluoke® alone and not with other enzymes because they might interfere with the effectiveness of Boluoke®; though this is only theoretical. Some doctors have dosed Boluoke® with other enzymes and had no problem. Boluoke® is enteric-coated, so if you cannot take it on an empty stomach, then take it after meals. The other option is to drink ginger tea (a few cups a day) or take ginger capsules which prevents nausea, and then you might be able to take Boluoke® on an empty stomach. If you have bloating or nausea issues with Boluoke®, it makes me suspect that your digestive system may need more support.

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Q: Am I correct to assume that a patient with low platelet count would not be adversely affected by Boluoke® because it does not impact platelet count (though it does focus on stopping the aggregation)?

Thanks, D. Schoen, California

Boluoke® reduces platelet aggregating function, making them less "sticky." As long as the patient has no bleeding/bruising issues and the platelets are above 100 giga/L (norm is 150-400), it should be fine.

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