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Journal club is an interactive forum, where medical and health professionals can discuss online.The main feature of the forum included summary of an article selected from the recent medical literature and comments from the Author/Specialist. This would set the ball rolling and provides readers to comment.The feedback from the readers is appended to the article summaries.

 
1).Yoga for epilepsy

Ramaratnam S, Sridharan K.

Summary

BACKGROUND: Stress is considered an important precipitating factor for seizures.Yoga is believed to induce relaxation and stress reduction. The effect of yogaon the EEG and the autonomic nervous system have been reported. Yoga would be anattractive therapeutic option for epilepsy (if proved effective), in view of itsnonpharmacological nature, minimal side effects and international acceptance.
OBJECTIVES: To assess the efficacy of yoga in the treatment of patients withepilepsy.
SEARCH STRATEGY: We searched the Cochrane Epilepsy Group trialregister, the Cochrane Controlled Trials Register (The Cochrane Library Issue 4,1998), MEDLINE for articles published up to the middle of 1998, and alsoregistries of the research council for complimentary medicine were searched. Inaddition, we searched the references of all the identified studies. Finally, wecontacted the members of the Neurological Society of India, severalneurophysiology institutions and yoga institutes to seek any ongoing studies orstudies published in nonindexed journals or unpublished studies.
SELECTIONCRITERIA: Randomized control trials and controlled clinical trials of treatmentof epilepsy with yoga.
DATA COLLECTION AND ANALYSIS: The data were extractedindependently by both reviewers and any discrepancies were resolved bydiscussion. The main outcomes assessed were percentage of patients renderedseizure free, number of patients with more than 50% reduction in seizurefrequency or seizure duration and the overall reduction in seizure frequency.Analyses were on an intention to treat basis.
MAIN RESULTS: Only one study metthe selection criteria, and recruited a total of 32 patients, 10 to sahaja yogaand 22 to control treatments. Antiepileptic drugs were continued in all.Randomization was by roll of a dice. The results of this study are as follows:(i) Four patients treated with yoga were seizure free for six months compared tonone in the control groups. The Odds Ratio (OR) (95% Confidence Interval (CI))for yoga versus sham yoga group was 14.5 (0.7, 316.7) and for yoga versus notreatment group 17.3 (0.8, 373.5). (ii) Nine patients in the yoga group had morethan 50% reduction in seizure frequency compared to only one among the controls.The OR (95% CI) for yoga versus sham yoga group was 81 (4.4, 1504.5) and for theyoga versus no treatment group was 158.3 (5.8, 4335.9). (iii) There was adecline in the average number of attacks per month compared to the baselinefrequency among the patients treated with yoga. The weighted mean difference (95% CI) between yoga versus sham yoga group was -2.1 (-3.1, -1.0) and for theyoga versus no treatment group -1.1 (-1.8, -0.4). (iv) More than 50% reductionin seizure duration was found in seven of the 10 patients treated with yoga,compared to none among the 22 controls. The OR (95%CI) for yoga versus sham yogagroup was 45 (2.0, 1006.8) and for yoga versus no treatment group 53.57 (2.4,1187.3).
REVIEWER'S CONCLUSIONS: No reliable conclusions can be drawn regardingthe efficacy of yoga as a treatment for epilepsy. Further studies are necessary to evaluate the efficacy of yoga in the treatment of epilepsy.

        

 


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2). Vitamin E supplementation and cardiovascular events in high risk patients 

Authors The Heart Outcomes Prevention Evaluation (HOPE) study investigators.
Source New England Journal of Medicine 342:154-60. January 20, 2000. 
Institutions Multi-institutional and international.
Support Medical Research Council of Canada, Natural Source Vitamin E Association, Negma, Hoechst- Marion Roussel, AstraZeneca, King Pharmaceuticals,  and the Heart and Stroke Foundation of Ontario.

Background

Experimental and observational studies have indicated a role for the antioxidant vitamin E in the prevention of atherosclerosis and cardiovascular events.  However, the few randomized trials conducted so far have not been unequivocally positive and have suffered from a number of limitations.  This study examined the effect of vitamin E supplementation on cardiovascular events in high risk patients.  It was conducted as part of the HOPE trial, which also looked at the benefit of an ACE inhibitor in patients at risk for cardiovascular events.

MethodsPatients

Eligible:  Patients at least 55 years old with a history of: any of the following:

  • coronary disease
  • stroke
  • peripheral vascular disease
  • diabetes plus another cardiovascular risk factor (hypertension, elevated cholesterol, low HDL, cigarette smoking or microalbuminuria)

Exclusion criteria:  

  • congestive heart failure or a documented ejection fraction less than 40%
  • patients taking an ACEI or vitamin E
  • MI or stroke within the previous 4 weeks
  • uncontrolled hypertension
  • overt nephropathy

Intervention

Patients were randomized to either 400 IU of vitamin E from natural sources or to placebo (in addition to being randomized to ramipril or placebo, as the other part of the HOPE study).

Follow-up

Follow-up visits occurred at one month, 6 months and every 6 months thereafter, with follow-up planned for 5 years.

Analysis

The primary outcome was a composite of cardiovascular death, MI or stroke; each of these outcomes was also analyzed separately.  Secondary outcomes were all-cause mortality, hospitalization for CHF or unstable angina, revascularization and the occurrence of diabetic complications.  A number of other cardiovascular complications were also recorded.

ResultsPatients

Of 10,576 patients who enrolled in the study and participated in the run-in phase for the ACEI part of the study, 1,035 were excluded because of withdrawal of consent, noncompliance, electrolyte abnormalities or side-effects.  Of the 9,541 remaining patients, 4,761 were assigned to receive vitamin E and 4,780 were assigned to placebo.

Baseline characteristics included (my approximate average of both groups):

  • Male sex: 73%; age: 66 years
  • BP: 139/79; BMI: 28
  • History of coronary disease: 80% (prior MI 53%; CABG 26%; history of angina 56%)
  • History of stroke or TIA: 11%
  • Peripheral vascular disease: 43%
  • Hypertension: 47%; diabetes: 38%; hypercholesterolemia: 66%; current smokers: 14%
  • Currently on beta-blockers: 39%; aspirin: 76%; lipid agents: 29%; calcium blockers: 47%

Subsequent chart review of randomized patients revealed that 54% had had their LV function determined; it was less than 40% (an exclusion criterion) in about 8% of patients.

Length of treatment and compliance

Patients were recruited between December, 1993 and June, 1995.  Length of treatment and follow-up was to be 5 years, but the trial was halted approximately one year early (April, 1999) because of interim analyses showing clear efficacy for the ACE inhibitor.  The mean length of follow-up was 4.5 years.

At the end of the study, 89.2% of patients assigned to vitamin E were taking it, and 3.4% of patients assigned to placebo were taking vitamin E.

Main outcomes

There was no significant difference in the primary endpoints between patients receiving vitamin E or placebo.

  Vitamin E Placebo Relative risk p-value
Death from cardiovascular causes 7.2% 6.9% 1.05 NS (0.54)
Death from non-cardiovascular causes 4.0% 4.4%    
Death from any cause 11.2% 11.2% 1.0 NS (0.99)
Myocardial infarction 11.2% 11.0% 1.02 NS (0.74)
Stroke 4.4% 3.8% 1.17 NS (0.13)
Composite endpoint: MI, stroke or cardiovascular death 16.2% 15.5% 1.05 NS (0.33)

These results were not different in patients receiving or not receiving the ACE inhibitor.

The incidence of the secondary endpoints also did not differ between patients receiving vitamin E and placebo.

Subgroup analyses and adverse effects

These results were not heterogeneous across various subgroups, including age, sex, cardiovascular disease, medications, diabetes or smoking status.

There was no difference between the groups in the incidence of adverse effects or drug discontinuation (data not given).

Author's discussion

According to the authors, this study did not demonstrate any significant reduction in the incidence of cardiovascular events by the administration of 400 units of vitamin E for four to six years.

They describe and comment on the results of four randomized clinical trials of vitamin E:

  • A chinese trial that randomized patients to a combination of vitamin E, beta carotene and selenium or placebo.  This trial showed a 9 percent decrease in all-cause mortality, but no decrease in cardiovascular events.  The effect of vitamin E could not be separated out, and the nutritional status of the population is different from that in the population studied here.
  • The ABC trial (Alpha- Tocopherol, Beta Carotene Cancer Prevention) studied over 29,000 male smokers between the ages of 50 and 70. Fifty mg of vitamin E daily showed no significant beneficial effect on cardiovascular events.
  • The Cambridge Heart Antioxidant Study assigned patients with coronary disease to vitamin E (400 IU or 800 IU) or placebo.  There was a significant decrease in the number of nonfatal MI's, but not in cardiovascular mortality.  The numbers were small, the effects were seen too quickly to be easily attributable to the antioxidant properties of vitamin E and there were imbalances in the study groups.
  • An Italian study randomized 11,000 post-MI patients to 300 IU vitamin E or placebo; there was no statistically significant effect on cardiovascular events.

The authors note that their results could be due to inadequate length of follow-up, but observational studies suggest that effects should be apparent within 2 years.  Furthermore, in a nested substudy of this trial they are now examining a surrogate marker for atherosclerosis which would be expected to show earlier results: the carotid artery intima-media thickness.

Another possible explanation for the negative results could be a need for vitamin E to be combined with other antioxidants; other trials looking at this hypothesis are in progress. 

Comment

This randomized trial of 400 IU of vitamin E vs. placebo failed to show any decrease in cardiovascular events after 4.5 years of follow-up.  This, despite the fact that multiple observational trials had suggested a beneficial effect.  One of the areas where observational trials are most likely to be influenced by bias is when analyzing data that reflect "healthy" behaviors.  Since healthy diets and vitamin supplementation are strongly associated with other beneficial lifestyle aspects, it is extremely difficult to avoid the intruduction of bias.

The trial was halted early because of a significant benefit in the ACE inhibitor portion of the study.  This could have led to an inadequate length of follow-up to detect a beneficial effect of vitamin E.  But, as the authors point out, a beneficial effect of vitamin E would have been expected before the 4.5 years of follow-up that were available here, so the early termination is unlikely to have played a major role in the negative result.

This study does not disprove the role of vitamin E in cancer prevention (still being followed in some of the patients enrolled in this trial), does not necessarily disprove a potential role when combined with other antioxidants, and certainly doesn't negate the potential beneficial role of a diet that is naturally high in vitamin E.  It does, however, call into question the role of vitamin E supplements alone for the prevention of cardiovascular events.

 July 4, 2000


ReferencesReferences related to this article from the NLM's PubMed database. 
 


Reader Comments

July 5, 2000
From: Samim Chalabi Çelebi [samim.celebi@fornet.net.tr]

Dear Dr Jacobson,

Thank you for always interesting cases. It is important to stress that a single cause for vascular disease and events does not apply or else it would have been sorted out earlier.

First, we need to look at the stress factor involved in these patients and this might be difficult.

Second, we need to know in younger generations that are at high risk whether vit e is preventive before disease starts, like 20 - 30 years of age, as probably prevention is much more effective than treatment in those patients.

Third, we hope that genetics will give us insight on who wil benefit and who willl not.

thank you, samim

Factors like stress and genetics, although important in the pathogenesis of vascular disease, were presumably evenly distributed between the patients assigned to vitamin E and placebo, and thus should not invalidate the results presented here.

Since the study was limited to just a few years, you are right that we can not be sure that earlier and longer treatment would not be effective.  The authors partially address this question in the article.

In general, I agree with you that once there is better understanding of a disease process, it is easier to target smaller groups who are much more likely to benefit from an intervention on that process.  -- mj


July 5, 2000
From: Enrique S. Corvalan, MD [
corvalan@U.Arizona.EDU]

This study deals entirely with "secondary prevention" of CV events in a fairly sick population. I would be interested to know same outcomes for a "primary prevention" point of view. Example: patients without CV proven disease but with hyperlipidemia, HTN, Diabetes, etc.

Enrique S. Corvalán, MD, ABFP, FAAFP
Assistant Professor Clinical 
Family & Community Medicine

It is true that these results apply to a very specific population, those at highest risk.  However, this is precisely the population in which prevention should be the easiest to demonstrate.  If it can't be shown in this population, then it's unlikely to be demonstrable in a population at lower risk.

Unless, of course, you postulate that these patients are at such high risk that a  beneficial intervention such as vitamin E is powerless to help them, or that lower-risk patients are somehow susceptible to vitamin E's effects in a way that high-risk patients aren't.  Not impossible, but unlikely, in my opinion.  --mj

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Literature Alert

This is a current awareness service built from one or two selected type of literature viz. highly cited paper, clinical alerts from NLM, reviews on a selected topic, reviews of the month and trend papers .


FDA Approves Surgically Implanted Stomach Band to Treat Obesity

Reviewed by Dr. Dominique S. Walton

On June 5, 2001, The FDA approved a device made by California firm BioEnterics System, which uses an adjustable band that is surgically fitted around the stomach to help severely obese people to lose weight. Here is more information about the newly approved product:

Name: Lap-Band Adjustable Gastric Banding System

How It Works: According to the FDA, the band is placed through a small surgical incision and around the upper portion of the stomach. Then it is inflated with saline and can be adjusted for tightness. It makes the stomach pouch smaller, so users eat less and feel full sooner.

Who Can Use It: The FDA says this device is intended for use only in people who are severely obese who have not been able to lose weight through exercise, dieting, and other programs. These people typically are at least 100 lb over their ideal body weight.

Basis of Approval: Nearly 300 patients participated in a clinical trial involving eight medical centers. In addition to getting the band, they also had to exercise at least 30 minutes a day and follow a strict diet. As the study went on for three years, most patients steadily lost weight, losing an average of 36% of their excess weight. Two percent of the patients gained weight and 5% remained the same.

For more details about the weight loss the participants experienced, read a release from the FDA.

Cautions: This device could offer a less-invasive option to the appropriate patients, because traditionally, surgical procedures for obesity require a big surgical incision and cutting, stapling, or rerouting the stomach. But using this band has its own set of side effects that patients should consider. Nearly 90% of patients experienced at least some side effects, which included nausea and vomiting, heartburn, abdominal pain, and band slippage. The band was tested in about 300 patients, and roughly a quarter of them had to have the band removed because of side effects or because they still were not losing weight.


Consumer Information on: LAP-Band® Adjustable Gastric Banding (LAGB®) System - P000008

 



The following is the list of articles authored by Doctors from Apollo Group of Hospitals. For your comments or if you find any omissions, please let us know at vml@medvarsity.com

Alphabetical List of Authors

Author Name      No.of
                    
Articles
Author Name     No.of
                   
Articles
Author Name            No.of
                         
 Articles
Author Name         No.of
                       
Articles
1.Agrawal R)          (1) 15.Kodali VR           (1) 29.Poonacha P          (1) 43.Shankar V          (1)    
2.Baraskar VJ         (1) 16.Kumar KP           (1) 30.Prabhakar KS        (1) 44.Shanmugam RP   (1)
3.Bhaskaran S.       (1) 17.Kumar SR           (1) 31.Prakash KC           (1) 45.Shrivastava MP   (1)
4.Bharat V           (1) 18.Makroo RN          (2) 32.Prakash T          (1) 46.Sibal A            (1)
5.Bose SK              (1) 19.Mani MK             (6) 33.Rajasekar MR        (1) 47.Singh RB            (1)
6.Chakraborty R      (1) 20.Manjari R            (1) 34.Ramaratnam S       (4) 48.Soin AS             (2)
7.Chandra KS.        (1) 21.Mathavan A        (1) 35.Ramachandran.P    (1) 49.Sridhar K            (1)
8.Ganesh Y            (2) 22.Mehta SS           (1) 36.Rao BH                 (2) 50.Sridharan R         (11)
9.Girinath MR          (1) 23.Mishra D             (1) 37.Rao SS                 (1) 51.Srivastava R        (1)
10.Gurudev KC        (2) 24.Misra KP             (1) 38.Rath PC                (8) 52.Srivastava RN      (3)
11.Halbe S             (1) 25.Oomman A          (1) 39.Reddy DR              (2) 53.Stumpf J             (1)
12.Janardhan G       (1) 26.Pancholia AK       (1) 40.Sathyamurthy I      (1) 54.Vatsal DK           (1)
13.Javid M              (1) 27.Pandiyan N         (1) 41.Shah D                 (3) 55.Vidhya MR          (2)
14.Kanwar MS         (1) 28.Parthiban A        (1) 42.Shah DC               (8) 56.Vijaykumar M      (1)
15.Kaul S               (1)

 

1: J Assoc Physicians India 2000 Jul;48(7):715-8

Author Index



2:
J Assoc Physicians India 1998 Mar;46(3):263-7


 

3: J Indian Med Assoc 2000 Nov;98(11):715-8


4: J Assoc Physicians India 1996 Feb;44(2):147


5: J Invasive Cardiol 1997 Apr;9(3):197-199


6: J Invasive Cardiol 1998 Nov;10(9):558-560


7: J Invasive Cardiol 1999 Sep;11(9):559-562


8: J Invasive Cardiol 1999 Feb;11(2):83-86


9: Cathet Cardiovasc Diagn 1998 Jan;43(1):43-7

Author Index



10:
J Assoc Physicians India 1998 Apr;46(4):341-4


11: J Assoc Physicians India 2000 Feb;48(2):216-20

Author Index



12:
J Assoc Physicians India 1998 Jun;46(6):533-7

Author Index



13:
Transplant Proc 2001 Feb-Mar;33(1-2):1997-8


14: Transplant Proc 2000 Nov;32(7):1585

Author Index


15: Indian Pediatr 2001 Mar;38(3):309-10


16: Indian J Pediatr 1999 Mar-Apr;66(2):199-205


17: Indian Pediatr 2000 Feb;37(2):173-8

Author Index



18:
Indian Pediatr 2001 Mar;38(3):287-91

Author Index



19:
J Assoc Physicians India 1997;Suppl 2:60-1

Author Index



20:
J Assoc Physicians India 1997;Suppl 2:12-3

Author Index



21:
J Assoc Physicians India 1998;Suppl 1:30-40

Author Index



22:
Seizure 2001 Jan;10(1):3-6


23: Cochrane Database Syst Rev 2000;(2):CD001524


24: Cochrane Database Syst Rev 2000;(3):CD001909


25: Cochrane Database Syst Rev 2000;(3):CD001524

Author Index



26:
Neurol India 2000 Dec;48(4):396-8

Author Index



27:
Indian J Pediatr 1999;66(1 Suppl):S56-62

Author Index



28:
Indian J Pediatr 1999;66(1 Suppl):S120-3

Author Index



29:
Transplant Proc 2000 Nov;32(7):1581

Author Index



30:
Indian Heart J 2000 Mar-Apr;52(2):205-6


31: Indian Heart J 1996 Mar-Apr;48(2):161-2

Author Index



32:
Indian Heart J 2000 Mar-Apr;52(2):201-2

Author Index



33:
J Invasive Cardiol 1996 Nov;8(9):443-446

Author Index



34:
J Assoc Physicians India 1999 Oct;47(10):998-1002

Author Index



35:
Trop Gastroenterol 1999 Oct-Dec;20(4):191-2

Author Index



36:
Indian Heart J 1999 Sep-Oct;51(5):545-7

Author Index



37:
Indian J Med Res 1999 Oct;110:123-5


38: Indian J Pathol Microbiol 1996 Apr;39(2):139-4

Author Index



39:
>J Indian Med Assoc 1999 Jul;97(7):278-81

Author Index



40:
J Indian Med Assoc 1999 Jul;97(7):271-5

Author Index



41:
Indian Heart J 1999 Jul-Aug;51(4):429-31

Author Index



42:
Indian J Chest Dis Allied Sci 1999 Jul-Sep;41(3):145-51

Author Index



43:
Perit Dial Int 1999 May-Jun;19(3):277-80

Author Index



44:
Indian J Gastroenterol 1999 Jul-Sep;18(3):122

Author Index



45:
Perit Dial Int 1999;19 Suppl 2:S283-

Author Index


46: Current Science Vol 82, No 6, 25th March 2002, page 664 - 670.


47: Epilepsia 1999 May;40(5):631-6


47: Neuroepidemiology 1992;11(1):24-30


48. Neurology India 36, 183, 1988.


49. Neurology India 36, 238, 1988.


50. Neurology India 36, 252, 1988.