Friday, May 29, 2015

(LML) Alternative MDT drugs and treatment duration

Leprosy Mailing List – May 29,  2015

Ref.:    (LML) Alternative MDT drugs and treatment duration

From:  Tarun Narang, Chandigarh, India


 

Dear Dr. Schreuder,

 

May I ask Dr. Warren (LML, May 29, 2015) a few questions regarding the patient she brought to our attention:

-       How long is this patient on treatment;

-       What is the status of the skin and nerves?

 

If the patient has received 1-2 years of MDT and his BI has decreased from 5 to 2 then he has responded well to treatment and we should stop treatment and observe him. That is normally done in our setup of fixed duration treatment.

 

Or if we want to give MDT till smear negativity the once monthly dose of Rifampicin, minocycline and Moxifloxacin (ROM) for 1-2 years can be tried. Another option is the use of immunotherapy in the form of Mycobacterium indicus pranii or BCG once in 3-4 months as adjunct to MDT in highly smear positive patients and in patients who have a high BI after 1-2 years of MDT.

 

Best regards,

 

Tarun Narang M.D


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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(LML) Alternative MDT drugs and treatment duration

Leprosy Mailing List – May 29,  2015

Ref.:    (LML) Alternative MDT drugs and treatment duration

From:  Paul Saunderson, Älesund, Norway


 

Dear Pieter,

The problem raised by Grace Warren(LML, May 29, 2015) is interesting and it is one that some of us have been discussing recently: a person who has had adequate MDT (according to WHO guidelines) but still appears to have active disease.

From the description given by Grace Warren, it appears that this patient has had about 2 years of treatment with a multi-drug regimen containing rifampicin and clofazimine; it is thought that he has taken the treatment properly because of his skin discoloration and the BI has declined as expected.  The problem is that "......so far, his progress is slow."  It would be interesting to have a fuller description of this lack of progress: for example, is it slow resolution of the old skin lesions, or new skin lesions, or is it the development of reactions and/or nerve damage?

My view, and I think it is shared by several others, is that 24 months and even 12 months of a rifampicin containing multi-drug regimen has proved to be adequate treatment for multibacillary leprosy whatever the BI (from what we hear about the U-MDT trials, 6 months may also be adequate).  A small number of patients relapse after these courses of treatment, but relapses are late (generally occurring more than 7 to 10 years after completing treatment), and seem to be due to persisters or to re-infection, neither of which can be prevented by longer courses of MDT.

There are, however, quite a number of cases like the one described by Grace Warren, in whom the skin lesions remain active and inflamed in the early years after completion of adequate chemotherapy.  I do not think the answer is simply a matter of more chemotherapy, or different antibiotics.  In discussion with Diana Lockwood and others this week, we concluded that there is ongoing inflammation in many patients, due to residual antigen in the tissues, but not related to a leprosy reaction, nor to ongoing infection with live bacilli. 

This phenomenon leads many people to give more antibiotics, but a more nuanced approach would be to look more directly at reducing the inflammation.  Clearly one would not advocate steroids if there is no recent nerve damage, but perhaps NSAIDs may be of benefit?

Paul

 

Paul Saunderson

Medical Director American Leprosy Missions

Greenville, USA


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com

 




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(LML) Alternative MDT drugs and treatment duration

Leprosy Mailing List – May 29, 2015

Ref.:   (LML) Alternative MDT drugs and treatment duration

From:  Grace Warren, Sidney, Australia


Dear Pieter,

I have just been thrown a problem patient to deal with.- by correspondence.

It concerns a person from Indonesia who came to Australia about 5 years ago. He says he had anaesthetic patches on his knees when he  came but no one bothered and it was only 2 years ago that a student of mine did slit skin smear and got 5+  !!!!   We gather that he was BBish initially. We assume he had downgraded for by the time she saw him he had nodules and was BL\\LLish!

He was put onto Rifampicin, Clarithromycin and Clofazamine (he has dapsone allergy!!  So we cannot give that – and was already anaemic on arrival!) ). He does not like the pigmentation of the Clofazamine!  We think he has been taking it because of the skin colour but he does not want to take any more!   New smears just done are still 2-3+ and the  Medical Department boss agrees that we do not stick to the WHO  limit on drug duration  so I was wondering what your LML readers would recommend in drugs. I feel that if we give the Clofazamine he will not take it regularly; we cannot give dapsone; Rifampicin and Clarithromycin should be ok but so far his progress is slow. Have you any other recommendations and are any other drugs available? I am not in a situation now where I always hear the latest and in fact am confined to hop myself with a fractured ankle.  Thanks Pieter I am always interested in notes, in LML, from round the world and as you know send notes sometimes when I think I can contribute.

With thanks,  

Grace Warren

Previously consultant with the Leprosy Mission.


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com

 




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Thursday, May 28, 2015

(LML) Treatment and prevention of reversal reaction (T1R) and nerve damage in leprosy

 

Leprosy Mailing List – May 28,  2015

Ref.:  (LML)  Treatment and prevention of reversal reaction (T1R) and nerve damage in leprosy

From:  Ben Naafs, Munnekesburen, the Netherlands


 

Dear Editor,

 

Challenged by dr Muherman Harun from Jakarta, I would like to write my thoughts about treatment and possible prevention of Reactions and nerve damage in leprosy.

I will start with the Reversal or Type 1 leprosy reaction.

 

Treatment and prevention of reversal reaction (T1R) and nerve damage in leprosy

 

Introduction

Although most of the nerve damage in leprosy takes place during episodes of exacerbation of the disease called “reactions”, there is damage that occurs before,  even during and after reactions that cannot be accounted for by the reaction. In this paper we deal with treatment and prevention of nerve damage, keeping the theoretical pathophysiologic mechanisms in mind.

 

Contact and complement mediated demyelination

The nerve damage start most likely by M.leprae making contact with the nerve and its entrance into the Schwann cell with demyelination as consequence.

This contact mediated demyelination can be prevented by anti-leprosy treatment (MDT).

At the same time complement activation occurs which leads to Schwann cell death and in this way to demyelination too. For the complement activation probably lipoarabinomannan (LAM), a cell wall component of M.leprae, is responsible. LAM is degraded only slowly after the bacillus is dead. Treatment, killing M.leprae, is therefore only effective in the long run when the LAM is degraded. Thus the damage may occur over a long time.

High dose steroids may diminish complement activation in general. A lower dose may stop only the T-cell mediated complement activation. A new drug eculizamab may stop the action of Complement factor 5 (C5), and thus the formation of the final Membrane Attack Complex (MAC), responsible for the dead of the Schwann cell.  This has, as far as I know, not been tried. Action of heparin, antimalarials, promethazine and chlorpromazine against complement activation has been proposed but not researched in this condition.

 

Damage due to Cell Mediated Immunity

Most of the damage is due to a T cell mediated action ( this seems to be against antigenic epitopes of M.leprae either on remnants of bacteria or on/in host own cells as an autoimmunity), the T1R, which can be stopped, in my experience, with relative low dose (30- 40 mg) prednisolone in BB-LLs  and usually higher dose (40- 60) mg in BT. The difference in starting dose is determined by the strength of the CMI and thus the place in the spectrum. These dosages can be tapered off to 0,25 mg/kg (15-20 mg) within 2-3 months, stay at that level 2-10 months and stopped when no further improvement occurs within 1-2 months. The progresses of improvement and deterioration of the nerve function should be monitored, at least monthly, in the initial period preferably twice a month. This can be done by VMT, ST, electro-neurophysiology or imaging by echo-Doppler duplex. When these parameters deteriorate due to tapering down the anti-reaction treatment, the treatment has to be increased to the previous dose till a next trial of renewed tapering off. Be aware that a T1R may last months!

 

Mechanical compression of the axon

The inflammatory oedema within the osteo-fibrous passages and within epi- and particular endoneurium may lead to compression and thus demyelination and axonal dead. If the axon does not die directly from the demyelination the compression compromises the flow in the axon too, the peripheral part of the axon does not receive nutrients anymore from the cell body and dies. Even when the immunological inflammation weans, a venostatic oedema, due to a compression of the draining veins within the perineurium, may remain and thus the compression within the endoneurium continues. This compression will contribute to further damage. The fact that the blood flow is diminished by the compression of the veins will contribute to a bad nutrient supply of the endoneurium , depriving the remaining Schwann cells and axons from oxygen and nutrients.

 

Bolus dose of steroids

As we just theorized, some of the early damage in a T1R may be due to inflammatory oedema in the nerve. A bolus dose of 100-150 mg hydrocortisone IV can be considered for 1-3 days where after the usual prednisolone dose can be given. Some authors advocate to take away the compression be surgery. For T1R reactions I have only experience with a higher dose of oral steroids not with a IV bolus and not with initial surgery. I would not advice surgical intervention at start but may be very useful later on.

 

Alternative treatments for T1R

After an initial treatment with steroids of about 1 week (important against the compressing oedema in the nerve), cyclosporine can be given instead of the steroids to diminish the CMI.

I have only little experience with azathioprine, but I think it is not very effective. Some use it for enabling them to lower the steroid dosage.

From the biologicals TNF-alpha inhibiters may be of help. I used it once with effect. But it should be given during the whole T1R which lasts between 4 and 18 months. All biologicals and biosimilars are very expensive and not yet investigated in T1R.

It has been noticed that dapsone prevents the development of a T1R in “active” patients and it even can be used in some patients for treatment but due to the high dosage needed, side effects (haemolyse) are common often independent of the G6PD status.

When with medical treatment in one or two nerves no improvement occurs when other nerves improve in one to two month time, a nerve release operation should be considered, the inflammatory oedema has than changed to a venostatic one. In my experience this is very effective.

In my hands clofazimine does not improve T1R, neither does thalidomide.

It is clear that all types of nerve damage will benefit from decreased antigen and bacterial load.  For the present time MDT seems most appropriate.

 

In summary

Present anti-reactional treatment restores nerve function and prevents further deterioration of nerve function.  It is effective in the majority of the patients, but it does not lead to full recovery in an estimated quarter of the victims. It is therefore essential that the search for alternative treatments continues.

But for all nerve damage it is adamant to diminish the antigens. For the present MDT seems most appropriate, but its duration is disputable.

The mechanism behind chronic neuritis and pain with or without continued deterioration of nerve function (after release from treatment, with no signs of reaction or relapse) is not known and stays an enigma and again deserves investigation.

These treatments can be given to outpatients. Only for severe reactions and bolus treatment patients have to be attended to in the clinic and for surgery they have to be admitted too.

 

Acknowledgment:

I thank Salvatore and Pieter for their careful reading and comments.


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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Friday, May 15, 2015

(LML) WHO Goodwill Ambassador's Newsletter No.73, April 2015 Issue

Leprosy Mailing List – May 15,  2015

Ref.:   (LML)  WHO Goodwill Ambassador's Newsletter No.73, April 2015 Issue 

 

From:  Hiroe Soyagimi, Tokyo, Japan


 

 

Dear Dr Schreuder and Friends,

 

 

Warm greetings from Sasakawa Memorial Health Foundation in Tokyo. We have uploaded our latest edition of "WHO Goodwill Ambassador's Newsletter No.73, April 2015 Issue" to our website. 

 

Please visit http://www.smhf.or.jp/e/ambassador/index.html to obtain electronic version of this issue. 

 

In this issue we feature articles about ...

 

Message : MESSAGE: Our Work Is Gandhi’s Vision

 

Report: Shared Passions -International gathering forges bonds during three-day retreat in Japan.

 

Voices: Restoring Family Ties - What it means to find out who you really are and where you came from.

 

Column: Breaking Boundaries - ILEP adopts new strategy and decides to learn from and share with other diseases.

 

Ambassador's Journal: Geneva and New Delhi - A flying visit to Geneva to meet with members of the Human Rights Council Advisory Committee and a journey to New Delhi for the annual conference of state leprosy officers, followed by a national stakeholders’ meeting.

 

News: Act Now, India’s Law Panel Urges - Calls on government to fulfill obligations to eliminate leprosy discrimination.

 

From the Editors: Last Resting Place

 

 

We hope you enjoy our latest Newsletter!

 

 

Hiroe Soyagimi

Sasakawa Memorial Health Foundation

 


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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(LML) In Memoriam David Sacket, Founding Chair Cochrane

Leprosy Mailing List – May 15,  2015

Ref.:  (LML) In Memoriam David Sacket, Founding Chair Cochrane 

From:  Linda Lehman, Belo Horizonte, Brazil


 

Pieter

Your readers may find this of interest.

Linda


Dear colleagues,

Dave Sacket, the founding chair of Cochrane, has died. For many of us, Dave was an inspiration sparking our interest in evidence-based medicine and he will sorely missed. He was a giant in the field.

A memorial service in planned in the coming weeks in Hamilton, Canada.

We will be setting up an online memory book. If you reply to this message, we will ensure your comments are included.

A more formal memorial will follow in the coming days.

Jeremy Grimshaw

Cochrane Canada Director

 

In memoriam:

Dr David Sackett, Founding Chair of The Cochrane Collaboration. (1934-2015)

It is with great sadness that Cochrane announces the death of its founding chair and medical pioneer, Dr. David Sackett. He was 80 years old.

Our thoughts and condolences are with Dave’s family, friends, and colleagues across the world.

Born in Chicago, Illinois, Dave Sackett was an originator of clinical epidemiology and evidence-based medicine and the first chair of the Cochrane Collaboration Steering Group in 1993. He founded the first department of Clinical Epidemiology and Biostatistics in the world, at McMaster University in Hamilton, Ontario, in 1967 and founded the Oxford Centre for Evidence-Based Medicine in the UK in 1994.

Dave contributed extensively to the development of research methods through his books and published articles, as well as through education and lectures at McMaster and around the world. Notably he turned clinical research into a scientifically sound and practical multidisciplinary “team sport,” and has changed for the better the quality of healthcare research and clinical practice.

After obtaining his medical degree at the University of Illinois, Dave went on to train in nephrology and internal medicine, and earn a Master of Science in Epidemiology from Harvard University.  He was a former Physician-in-Chief at Chedoke-McMaster Hospitals, and Head of the Division of General Internal Medicine for the Hamilton, Ontario region.  In 2000, he was inducted into the Canadian Medical Hall of Fame, and a year later was made an Officer of the Order of Canada.  Dave was the recipient of the 2009 Gairdner Foundation Wightman Award.

He retired from clinical practice in 1999 at the age of 65, and returned to Canada to establish the Trout Research & Education Centre, where he researched, wrote, and taught about randomized clinical trials.  He has published 10 books, chapters for 50 others, and over 300 papers in medical and scientific journals.

Dave’s contributions to Cochrane’s work date from the earliest days of the organization have made a substantial impact on its development and reputation over the past two decades.

Dave’s colleagues at McMaster and Cochrane plan to commemorate his contribution to evidence-based medicine in various ways, including The Dave Sackett Research Symposia and during the 23rd Cochrane Colloquium in Vienna in October 2015.

A memory book will be available online on the Cochrane Community site for friends and contributors to express condolences, recount memories, and share photographs. Donations can be made to the David L Sackett Scholarship fund via McMaster University Giving (http://www.mcmaster.ca/impact/).

 

Cochrane Central Executive

Cochrane, St Albans House, 57-59 Haymarket, London SW1Y 4QX United Kingdom

www.cochrane.org

Trusted evidence. Informed decisions. Better health.


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com

 




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Thursday, May 14, 2015

(LML) Symposium on Leprosy and Human Rights

Leprosy Mailing List – May 14,  2015
Ref.:   (LML) Symposium on Leprosy and Human Rights
From:  Katsuhiro Motoyama, the Nippon Foundation, Japan 


Dear Friends,

Greetings from the Nippon Foundation!

Though medical advances have made leprosy no longer a public health threat in many parts of the world, political, legal, economic or social discrimination associated with this ancient disease continue to exist today.  The issue of leprosy is not only a matter of medicine, but also one of discrimination which can give rise to a clear violation of human rights,

On Thursday, June 18, 2015, the Nippon Foundation, along with the Graduate Institute in Geneva, will hold an international symposium on leprosy and human rights at the Graduate Institute the Ivan Pictet Auditorium, starting at 9am. Please find attached the tentative programme of the symposium

This is the last and the final symposium of the Five-Region Symposium Series that the Nippon Foundation has organized since 2012. The Five Region Symposium Series aim to enhance dissemination and implementation of the Principles and Guidelines for the elimination of discrimination against persons affected by leprosy and their family members. This was noted with appreciation in the resolutions Japan submitted and which was adopted unanimously at the United Nations Human Rights Council and the General Assembly in 2010,

The Nippon Foundation has tackled the issue of leprosy over four decades and has successfully organized the Five-Region Symposium Series as follows:
(1) For the Americas, on 31 January and 1 February 2012 in Rio de Janeiro, Brazil, 
(2) For Asia, on 3-4 October 2012 in New Delhi, India,
(3) For Africa, on 17-18 September 2013 in Addis Ababa, Ethiopia,
(4) For the Middle East, on 27-28 October 2014 in Rabat, Morocco.

We have learned from the government of Japan that they plan to submit a resolution at the 29th session of the UN Human Rights Council (to be held in Geneva from 15 June to 3 July, 2015).  We understand that the new resolution targets to achieve effective implementation of the Principles and Guidelines, and we have therefore decided to organize our final symposium also in Geneva, during the 29th session of the Human Rights Council. 

Your participation to our fifth and the last symposium would be most welcome. 
If you will be able to attend the symposium, please let us know your information<name, title, organization and email address> by sending your email to Sagal@raittorr.co.uk by 31 May.

We look forward to seeing you.

Sincerely,

Katsuhiro Motoyama 
Manager, International Network Team
The Nippon Foundation



LML - S Deepak, B Naafs, S Noto and P Schreuder
Contact: Dr Pieter Schreuder << editorlml@gmail.com



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(LML) Parenteral treatment of leprosy reactions

Leprosy Mailing List – May 14,  2015

Ref.:   (LML) Parenteral treatment of leprosy reactions

From:  Ben Naafs, Munnekesburen, the Netherlands


Dear Pieter,

Thanks for the reactions, comments and questions from Dr. Harun, Dr. Jingquan, Dr Van Brakel, Dr Kar and Dr. Theuvenet.

Concerning Wim van Brakel’s comment on the paper of Walker at all (LML 5 May 2015):   

- This paper investigates the effects after only 16 weeks prednisolone treatment, which is shorter than I advise. The short treatment influences the outcome more than the initial treatment.

- Concerning his second comment: I think he cannot talk about not-ethical since the mentioned trial does not show any additive effect. And moreover this trial he referred to was not using parameters sensitive enough to detect an additive effect on the nerve.

Garbino et all (Arq. Neuropsiquiatr. 66 (2008) 861-866) showed that high dose prednisone at start has more effect than lower doses. However after long time follow-up with continuing treatment this difference disappears, at least with the evaluation methods used. High dose has thus an initial effect. Thus is worth as a short bolus dose to be investigated.

Dr Kar points to supposed evidence based studies that point to a 1mg/kg prednisone start dose for both the leprosy reactions with a gradual tapering and with a minimal maintenance dose for a certain period of time. He is right that this is done for T1R and shows clear results. However, not for T2R which is a definitive other type of reaction than T1R.

His remark about the anti-adrenal effect of a short high bolus dose is refuted by the actual effect observed in the treatment of many other diseases. The chronic long time maintenance dose may be more dangerous than the bolus dose.

This is also shown in the “fatal case from China”. I am glad that this patient is presented. His history shows clearly what can go wrong. Nevertheless, it may not be concluded that this is due to the initial bolus therapy.

I can fully agree with the summary of Dr. Harun. The bolus (125 mg methylprednisolone i.v.) for type 1 reaction will take care of an initial anti-edematous effect in nerves (Garbino et al). It may take some of the compression away. The initial extra effect in this way may diminish the nerve damage already at start of an anti-reaction treatment. Whether in the long run it will contribute to the total improvement after long term of anti-T1R reaction treatment should be studied in a double blind trial with sensitive parameters. I do not see any ethical constrains regarding this.

Concerning the T2R, a bolus steroïds is an excellent idea. It will work quickly on the intra-neural edema which leads to a conduction block in the nerves and moreover it may help to stop the T2R immunologically too.

Since a T2R is episodic and lasts in the majority of the patients only 1-4 weeks it may shorten the treatment and diminish the side effects of the usually practiced ENL treatment. Also here a trial is warranted.

I thank Dr. Harun for initiating this discussion.

dr Ben Naafs


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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Friday, May 8, 2015

(LML) Parenteral treatment of leprosy reactions

Leprosy Mailing List – May 8,  2015

Ref.:   (LML) Parenteral treatment of leprosy reactions

From:  Wim van Brakel, Amsterdam, the Netherlands


Dear Pieter,

My response to the suggestion by Dr. Harun (LML, May 8, 2015) is that this would not ethical, since a randomised controlled trial has shown no additional benefit of parenteral high-dose treatment of leprosy reactions. I am particularly concerned with Dr Harun’s statement: “it is only to find out, whether by  parenteral  addition of corticosteroids, we can much sooner relieve the severe pain and agony caused by the leprosy reactions.”

If the trial done in Nepal were to be repeated – assuming it would pass ethical approval, which I doubt – it can only be done as a randomised controlled trial, otherwise Dr Harun’s question will remain unanswered. Signs and symptoms will be relieved through parenteral treatment. Evidence to date suggests that the improvement is not better or faster than with oral prednisolone. Perhaps Dr Harun intends to carry out a trial, but this is not clear from his statement.

 

With best wishes,

 

Wim van Brakel


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com

 




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(LML) Parenteral treatment of leprosy reactions

Leprosy Mailing List – May 8,  2015

Ref.:   (LML) Parenteral treatment of leprosy reactions

From:  Herman Harun, Jakarta, Indonesia


Dear Pieter,

 

May I summarize the initial parenteral treatment for leprosy reactions, as follows:

In Type 1 reaction, we can give 125 mg methylprednisolone (the equivalent of approximately 150 mg of prednisone) in one bolus. We may use less, but since each ampoule already contains 125 mg prednisolone (and there is actually ‘no’ maximum dose of corticosteroids in emergency cases), I would suggest not to dispose of excessive prednisolone). After that, proceed with oral prednisone as prescribed.

In type 2 reaction, we can give up to three days, each day a bolus of 125 mg prednisolone parenteral. Then proceed with oral prednisone as prescribed.

If gastric complaints are present or suspected,  I would give 20 mg omeprazole before breakfast. The injections can also be given intramuscularly, same dose.

Let it be clear, I am not introducing a new method of treating leprosy reactions, it is only to find out, whether by  parenteral  addition of corticosteroids, we can much sooner relieve the severe pain and agony caused by the leprosy reactions.

 With sincere thanks to Dr Ben Naafs for his instructive advice on this subject,

 

Muherman Harun


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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(LML) Parenteral treatment of leprosy reactions

Leprosy Mailing List – May 8, 2015

Ref.:    (LML) Parenteral treatment of leprosy reactions    

From:  Hermanta Kumar Kar, New Delhi, India


 

 

Dear Pieter,

 

 

Referring to the recent discussions by Dr. Harun and Dr Jingquan in LML  regarding “Parenteral treatment of leprosy reactions” I want to add the following:

 

The evidence based research studies in the past, guide all of us to follow a standard guideline/protocol for management of leprosy reactions (T1R and T2R). Standard dose of prednisolone:1mg /kg body weight to start with gradual tapering of the dose to a minimal maintenance  dose for certain period of time(depending on several other factors) to prevent recurrence  is the key for management of reactions. High bullous dose of steroid is not desirable keeping in mind the possibility of occurrence adrenal crisis in many cases with chronic/recurrent ENL, one of the causes of death in leprosy. 

 

 

Regards,

 

 

Dr. Hemanta Kumar Kar
Professor in Dermatology, NDMC Medical College Delhi -110007
Former Director, Dean, Med. Superintendent and Professor(HOD) Dermatology
P.G.I.M.E.R. and Dr Ram Manohar Lohia Hospital
Baba Kharag Singh Marg
New Delhi-110001


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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Tuesday, May 5, 2015

(LML) Parenteral treatment of leprosy reactions

Leprosy Mailing List – May 5,  2015

Ref.: (LML) Parenteral treatment of leprosy reactions    

From:  Wim van Brakel, Amsterdam, the Netherlands


 

Dear Pieter,


I would like to draw the attention of Dr. Harun (LML, April 28, 2015) and that of the LML readers to a trial of high-dose intravenous methylprednisolone carried out by Walker and colleagues at Anandaban Leprosy Hospital in Nepal. This trial was published in PLoS NTD in 2011 (DOI: 10.1371/journal.pntd.0001041).

To our disappointment, the intravenous prednisolone did not have any dramatic beneficial effects, as seen in other conditions. In fact, the study highlighted the need for a longer steroid regimen in the treatment of leprosy reactions. This is currently being trialled in the so-called TENLEP trials; a large multi-country study led by Dr Erik Post, Royal Tropical Institute, Amsterdam.

 

With best wishes,

 

Wim van Brakel

 

Wim van Brakel, MD MSc PhD

Head Technical Department

Netherlands Leprosy Relief (NLR)

Email: w.v.brakel@leprastichting.nl

URL: www.leprosyrelief.org

 


LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << editorlml@gmail.com




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