PRESIDENT’S MESSAGE

Dear All

At the outset let me thank Dr Banwari Sharma and his team for doing a great job with E-newsletter of IRA. Now the baton has been passed on to Dr Sapan Pandya and I am sure that he will take it new heights.

As is true with anything change brings a new thought and E-newsletter will also have a new look now, It will serve as a vehicle to disseminate information about IRA to its members including activities done in the preceding 3 months and what is planned for future. Other new additions are Patients perspectives and a fellow corner. There is lot more to it I hope you like the changes that have been made.

Feedback by the members goes a long way in improving any activity. Please send information about any activity that you have done for Rheumatology so that we can include that in E-newsletter as well as put up on our website. You will be happy to know that soon a new version of IRA website is going to be launched and E news letter will also be available on our website.

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EDITORIAL IRA

Dear All

Monsoon greetings. Let it rain rheumatology this season !

Science, especially written, has always been accused of monotony. And that’s why I guess, newsletters came into existence. By their very nature, newsletters ought to be informal, reflective, accommodative and a pleasure to read. While you would prefer reading an indexed journal in the tranquility and solitude of a library, newsletters can be brushed through in the TV room of your hospital where you get together for coffee and discuss sports and politics. And that is exactly we, from the editorial team, have tried and made this one. Our job was tough having taken over from the hard taskmaster Dr Banwari Sharma. His are shoes impossible to fill in ( both literally and otherwise !). We’ve tried our best and hope you go through the issue without putting it down, in one go and remember a thing or two from it, in permanence. The issue, which is going to be quarterly from now on, will have scientific material (Quarterly highlights) in which we will try to cover abstracts of, what we deciphered, has been path breaking or most relevant in the last quarter of the year - both clinical and basic.

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QUARTERLY HIGHLIGHTS

Dr C Balakrishnan, Consultant Rheumatologist, Hinduja hospital, Mumbai

Factors Associated With Sustained Remission in Rheumatoid Arthritis in Patients Treated With Anti–Tumor Necrosis Factor, Arthritis Care and Research (pages 783–793), Arthritis Care Res (Hoboken). 2017 Jun;69(6):783-793. doi: 10.1002/acr.23016. Epub 2017 May 8.

Anti–tumor necrosis factor (anti-TNF) antibody has dramatically improved the treatment of rheumatoid arthritis (RA), however to predict which patients are most likely to attain a sustained response remains a challenge. Thus an in-depth analysis to answer this question was undertaken and 6 studies were identified. Concomitant methotrexate use was associated with an increased likelihood of achieving sustained remission. Greater baseline disease activity, tender joint count, age, disease duration, baseline functional impairment, and female sex were associated with reduced likelihood of achieving sustained remission.

This evidence supports current recommendations for methotrexate co-prescription and highlights the negative impact of particular clinical and demographic features on the likelihood of achieving optimal response to anti-TNF treatment.

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FELLOWS’ CORNER

Dr Shefali Sharma, Rheumatology, PGIMER, Chandigarh

Hamman's crunch in Amyopathic Dermatomyositis

DrAdarsh M B, DrPreksha Dwivedi, DrVarun Dhir, DrShefali K Sharma,

Dr A Sharma, Prof Sanjay Jain

Department of internal medicine, PGIMER, Chandigarh

23 year old male with symmetrical inflammatory polyarthritis and fever for last 2 years, presented with progressive breathlessness for last 3 months and acute worsening since last 5 days. On examination he had periorbital lilac rash and gottronssign(Fig 1,2). He had no muscle weakness. On auscultation Hamman’s crunch was audible and had subcutaneous emphysema in neck. HRCT of thorax showed pneumomediastinum, subcutaneous emphysema and organizing pneumonia in lower lobe(Fig 3,4). His Creatine kinase and LDH levels were normal and EMG was unremarkable. ANA was negative by IIF. Anti JO1, PM-Scl and U1RNP were not deteced by ELISA.

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MY LIFE, MY TIMES

Interviewer : Dr Banwari Sharma, Interviewee : Dr V R Joshi

Que 1 : What made you to develop interest in rheumatology? Who was the source of inspiration?

I,though fascinated, had not planned rheumatology spcialisation. It wasunplanned, unexpected. I had given up neurology.So, following the death of Dr. M. M. Desai,Itook charge of rheumatology at Nair Hospital.

Que 2 :Tell us how you & your few colleagues builtthe foundation of rheumatology in our country when most people are still unaware about this specialty including most doctors.

I had no formal training in rheumatology. Therefore,I learnt clinical rheumatology at RNHRD, Bath, laboratory techniques at Hammersmith hospital, London,and trained our biochemist at Dr. Malaviya’s laboratory in relevant rheumatology laboratory techniques. Establishing the tests was not easy. e.g. we collected rat livers from pharmacology department, microsectioned the livers in anatomy department, performed IF staining, and walked ½ km to a municipal hospital that had the microscope to report the slides. Wemanaged to establishthe relevant tests.

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CLINICAL PEARLS

CRP in lupus

Lupus vs Infection: A physician’s Fright; CRP: A physician’s delight!

Most common causes of mortality in the first decade in lupus are infections [1]. Etiology and foci may vary but bacteria are most commonly implicated as the cause. Effect of disease and immunosuppression predisposes them to increased risk of infections. Ascertaining the cause of fever in a patient of lupus poses a great challenge. One of the dictum says lupus here, lupus there and lupus everywhere does help but infection can be a great mimicker and may co-exist and hence underscoring the importance of a good biomarker.

CRP, member of pentraxin family,recognises phosphorylcholine and carbohydrate moiety on micro-organisms and is bound by Fc receptors (FcRs) forIgG found on most phagocytes. CRP level rises significantly in lupus patients with infection [2].It rises within 6 hours and peaks by 48 hours and has a half-life of 19 hours. [3].Conventional methods can detect CRP levels above 3-10mg/l but newer methods can detect as low as 0.2 mg/l (hsCRP).

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Disclaimer
The views expressed in this newsletter do not necessarily reflect those of the sponsor. The sponsor does not assume any responsibility for copyright infringement, if any. Please consult full prescribing information before prescribing any of the products mentioned in the newsletter. The information provided in this newsletter is for scientific dissemination to medical professionals only and does not necessarily reflect the opinions of IPCA Labs. Dosages, indications, method of use of products and all other related information by the authors may reflect their own clinical experience.