|Year : 1983 | Volume
| Issue : 2 | Page : 89-95
Picrorrhiza kurroa in bronchial asthma.
VB Doshi, VM Shetye, AA Mahashur, SR Kamat
V B Doshi
|How to cite this article:|
Doshi V B, Shetye V M, Mahashur A A, Kamat S R. Picrorrhiza kurroa in bronchial asthma. J Postgrad Med 1983;29:89-95
|How to cite this URL:|
Doshi V B, Shetye V M, Mahashur A A, Kamat S R. Picrorrhiza kurroa in bronchial asthma. J Postgrad Med [serial online] 1983 [cited 2020 Jan 25 ];29:89-95
Available from: http://www.jpgmonline.com/text.asp?1983/29/2/89/5544
Several drugs are useful for relieving an attack of bronchospasm or 'asthma'. However, none of the oral drugs have a proven prophylactic role. We earlier reported a pilot experience using, whole root powder of Picrorrhiza kurroa for such purpose. As some patients did show improvement it was decided to do a full scale trial, to assess its beneficial role.
MATERIAL AND METHODS
From the outpatients clinic, patients with characteristics of chronic obstructive pulmonary disease (bronchial asthma) were considered for the trial. For the actual study, patients were selected according to the following criteria:, 
(i) Clinically stable status.
(ii) At least twice weekly paroxysmal attacks.
(iii) 20% reversibility in FEV1 after a bronchodilator aerosol.
(iv) Co-operation for a follow-up.
Patients having chronic severe episodes needing regular doses of steroid and/or antibiotics and those with chronic productive cough were excluded from the trial.
With a random double blind design, 72 patients selected over 20 months were followed for 14 weeks. All received placebo tablets thrice daily for the first two weeks (weeks 1 and 2). Then the tablets of picrorrhiza kurroa root 300 mg thrice daily were given in three schedules randomly allocated as follows: (i) Group A: Long duration of 12 weeks: Active drugs from weeks 3 to week 14. (ii) Group B: Short duration of weeks: Active drug from week 3 to week 6 only with placebo during other weeks (week 7 to week 14). (iii) Group C: Intermittent duration of 8 weeks: Active drug was given from week 3 to week 6 and from week 9 to week 12 and placebo in other weeks. All patients were assessed weekly for their clinical status and lung function (FVC, FEV1, PEF, MEFR). Patients were asked to keep a diary to record their daily symptoms, clinical paroxysmal attacks and additional treatment. For this, they were allowed to take tablets of orciprenaline/aminophylline or injectable theophylline for the control of exacerbations. The records were evaluated as in the earlier studies.,  Briefly, the clinical response was graded as worse (1-), same (0) and improved (1+ or 2+) in relation to their pre-trial status. Similarly, the lung function was marked as improved if it increased by at least 10% over the basal values. Routine investigations were done and side effects were noted in all cases.
A total of 72 patients were included in this trial. Out of these, 24, 26 and 22 patients were put in schedules A, B and C respectively [Table 1] Thirty-eight patients were males and 34 were females. Forty-eight patients were below 30 years of age whereas 24 belonged to 31-60 year age group. There were no significant differences for age, sex and initial lung function status among the three schedules. Clinical severity was initially graded as severe in 14, moderate in 11 and mild in 47 cases. Those having severe status had more frequent and intense attacks of bronchospasm which needed frequent injections and/or additional drugs and this resulted in frequent absentees at work/school. Those having mild clinical status had occasional attacks needing additional oral drugs but no interference at work/school. Moderate degree of clinical status meant an intermediate disability.
[Table 1] also gives details on clinical and functional changes seen at the end of study. Out of 72 cases, in 24, we did not have any post-drug evaluation. It was seen that 50% subjects showed clinical improvement and 48%, improved by lung function. Among the various schedules, `schedule C' seemed worse (p < 0.05). There was no evidence that longer administration of active drug produced a significantly greater improvement though there was a trend toward lesser proportions showing deterioration with a prolonged course. Also in a large proportion there was no improvement seen with the drug, as seen with changes in clinical attacks
[Table 1] and need for additional treatment.
[Table 2] gives serial changes with mean lung function tests in various drug schedules. There is some reduction in all lung functions while on placebo as compared to pretrial period. But while there is slight improvement with drug ingestion for FVC and PEF, particularly in schedule A, none of the changes are significant. Similar results were seen with midexpiratory flow rates at various intervals.
As there was no clear improvement seen with drug periods in any of the schedules and as there were no differences among 3 schedules to detect any drug effect, further analyses were done with all schedules together [Table 3]
[Table 3] (B) shows that 50 patients were lost to assessment at various periods of study. Of these, 21 were given placebo and 29 active drug. In 20 patients, there was clear evidence of clinical deterioration before default. These were slightly oftener while on drug. As these proportions of defaults are larger than in our earlier studies,,  our longterm assessment has naturally been compromised. As there are sufficient number of patients available at least till 8 weeks of trial and there was no evidence of benefit with longer drug administration, these analyses seemed worthwhile. The defaults were distributed equally in all 3 schedules and with drug or placebo. In one case only, default under nonco-operation is attributed to side effects but in many others under this category also lack of clinical improvement, may have a role.
These were seen in 10 (out of 52; 20%) patients in whom active drug was administered; 4 had vomiting, 1 cutaneous rash, 3 anorexia, 2 diarrhoea, 2 itching and 1 giddiness. Only in one case, vomiting was severe enough to discontinue trial, while in another 5 toxicity was significant. The trial could be continued.
[Table 3] (C&D) lists the patterns of clinical and functional changes in relation to pre-trial status. It is seen that in the placebo period (1-2 weeks), 20 patients defaulted. Of these, 6 defaulted due to deterioration but 13 (21%) were clinically worse. Though further 7 patients defaulted while on drug (3-6 weeks), most were due to deterioration. Though a slightly larger proportion showed clinical improvement on drug (38% as against 19% on placebo), the difference is not significant. If one pools all periods there is a trend where clinical improvement is seen oftener with drug (49%) as opposed to placebo (30%) (p < 0.01). However, this seemed not to be associated with significant improvements in lung functions. Thus, though there is some evidence of the drug giving subjective improvement in a few cases, there is no evidence of improvement in others. Despite a large number defaulting over the full trial period, there is no greater evidence of sustained improvement with the active drug.
In our pilot study, administration of the root powder of Picrorrhiza kurroa had shown some evidence of improvement. We had observed a proportion of patients also getting significant side effects. In the present study, a large number of patients with bronchial asthma were on Picrorrhiza kurroa on a large dose of 900 mg daily over several weeks. The drug produced a large proportion of defaults but a small evidence of subjective clinical improvement. On other counts or on lung function changes, there was no evidence of benefit attributable to the active drug either in pooled analyses or over several trial periods or among different schedules. A prolonged administration did not seem to make much difference. Despite other workers' claim of benefits and a reduced need for additional medicines with Picrorrhiza, our data does not corroborate such encouraging concepts, particularly for the prophylaxis. While there is some evidence of clinical benefit seen in a small proportion of patients, this is inferior to that seen with routine bronchodi lator,  or prophylactic preparations.
Therefore we do not feel justified in claiming that the root of Picrorrhiza kurroa in its present form has a useful role in prevention or treatment of bronchial asthma.
The authors thank Dr. C. K. Deshpande, Dean, K.E.M. Hospital and Seth G.S. Medical College, for permission to carry out this work. The consistent guidance given by Dr. D. Rajaram and Prof. U. K. Sheth (retired Professor of Pharmacology) is gratefully acknowledged. The drug supply and tablet preparations were made available through Dr. A. V. Mody of Unichem Laboratories.
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