Quit Smoking and Weight Gain

I have been interested in smoking and rheumatic diseases for quite a while. Some of my blog posts are only in German as I use these texts also for real life patient education and information. About 10 years ago we developed a leaflet for patient to promote smoking cessation. Some did und some had problems with weight gain. As weight gain is a constant problem in a setting, where steroids are used, I’m very concerned about this issue.

Today I stumbled upon a study by L. Biedermann and colleagues: “Smoking cessation induces profound changes in the composition of the intestinal microbiota in humans.” They observed “profound shifts in the microbial composition after smoking cessation” and “an increase in microbial diversity.” They concluded: “These results indicate that smoking is an environmental factor modulating the composition of human gut microbiota. The observed changes after smoking cessation revealed to be similar to the previously reported differences in obese compared to lean humans and mice respectively, suggesting a potential pathogenetic link between weight gain and smoking cessation.”

I think the paper is important not only as there is an explanation for the weight gain and a rehabilitation of people, who didn’t gain weight because of consuming more sweets, but it might also lead to therapies that actively change the composition of the intestinal microbiota. If this would help people, who quit smoking, maybe it could also help obese people.

Links:

Abstract on Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/23516617

Full article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597605/

http://rheumatologe.blogspot.de/2011/12/smoking-and-axial-spondyloarthritis.html

http://rheumatologe.blogspot.de/2011/11/fibromyalgia-and-smoking.html 

30.08.2013

Besides the above mentioned changes in the intestinal microbiota there are other mechanism involved as well, which will lead to weight gain. Nicotine suppresses appetite. Food might act as a replacement for smoking. Sweets and nicotine act on dopaminergic receptors in the brain, which make us feel good.

Link: http://quitsmoking.about.com/od/weightgain/a/weightgainquit.htm

Certolizumab in psoriatic arthritis effects of different imputation approaches - RAPID-PsA

What do they want to tell us?

D. van der Heijde and colleagues just published a paper on certolizumab in the treatment of psoriatic arthritis [results of the RAPID-PsA]: “Effect of different imputation approaches on the evaluation of radiographic progression in patients with psoriatic arthritis: results of the RAPID-PsA 24-week phase III double-blind randomised placebo-controlled study of certolizumab pegol”. In results we are told about an “overestimated radiographic progression (least squares mean placebo, 28.9; CZP, 18.3; p≥0.05).” Too bad that the abstract doesn’t tell any numbers about the results of the post hoc new imputation. We just get: “mTSS non-progression rate was higher in CZP than placebo groups in all analyses.” The authors concluded: “Inappropriate prespecified imputation methodology resulted in an unrealistic assessment of progression in all arms. Methodologies for imputing missing radiographic data can greatly affect assessment and reporting of mTSS progression.” Link: http://www.ncbi.nlm.nih.gov/pubmed/23942869

What do they really want to tell us? Maybe that they found a method in which certolizumab looks better on reducing radiographic progression?

Maybe I’m overreacting as I use certolizumab, but such abstracts just make me feel uneasy. Maybe someone can ease my scepticism.

Bubonic plague in Kyrgyzstan

Whistleblower (@MediterrNewsNet) had tweeted the link to an article of Al Jazeera “Kyrgyzstan boy dies of bubonic plague” (Link: http://www.aljazeera.com/news/asia/2013/08/201382744916818740.html).

Yersinia pestis is a bacterium, which cause bubonic plague. We might think of the plague during the Middle Ages, which swept across Europe killing a third of the population. Do we have to expect this in Kyrgyzstan? No, not at all. Yersinia pestis is endemic in rodents and other mammals in different parts of the world. Fleas might be a vector to transmit the disease to humans. The disease might be hard to treat, but one can treat it. According to Harrison’s Principle’s of Internal Medicine (the medical bible of internists, which I have always in the reach of my arms here at my computer) one treats the infection with gentamycin or streptomycin, tetracycline or chloramphenicol are other antibiotics, which could work. The earlier, antibiotics are started the better.

In the article of Al Jazeera we learn that contact persons are isolated and treated with antibiotics. If you have business in Kyrgyzstan, this news shouldn’t make you call off you travels. The situation is under control and there’s no reason to panic. But let’s not forget that a teenager has died and let our condolences be with the mourning relatives.

Link to article on Yersinia pestis on Wikipedia: http://en.wikipedia.org/wiki/Yersinia_pestis

28.08.2013
The Guardian: "A Russian public health official said cases of bubonic plague were registered in Kazakhstan every year, and the disease existed naturally in parts of Kyrgyzstan, Kazakhstan and Russia, Izvestiya reported." http://www.theguardian.com/world/2013/aug/27/bubonic-plague-outbreak-feared-central-asia 
The Independent: "Black death returns: ..." No, it doesn't! Please check above. The black death was possible only in pre antibiotic times, not nowadays! http://www.independent.co.uk/life-style/health-and-families/health-news/black-death-returns-herder-dies-of-bubonic-plague-in-kyrgyzstan-after-being-bitten-by-infected-flea-8785775.html 
There is no basic for panicmongering!

28.08.2013
AFP published on Yahoo more details: three people, who had direct contact with the dead teenager showed symptoms. 800 people in the small town of Bishkek have been screened. 
The Mail has a picture of a blood smear, where you can see Yersinia pestis, in the middle of the picture you see two small bacteria in a shape resembling an eight, near one of larger red blood cells. The bacteria look darker.
Link: http://news.yahoo.com/three-more-sick-kyrgyzstan-battles-bubonic-plague-135609415.html  http://www.dailymail.co.uk/news/article-2403099/Kyrgyzstan-lock-boy-15-dies-bubonic-plague.html

02.09.2013
The quarantine has been lifted.

11.12.2013
Now, there's another outbreak in another part of the world: Madagascar! "Bubonic plague kills 20 in Madagascar village": "Twenty people have died following a deadly outbreak of the bubonic plague, medical experts on the island of Madagascar have confirmed." ... "According to the ICRC, an average of 500 cases have been recorded on the island every year since 2009. Africa is now believed to account for more than nine out of ten bubonic plague cases worldwide." Read the article of THE INDEPENDENT here:
http://www.independent.co.uk/news/world/africa/bubonic-plague-kills-20-in-madagascar-village-8997280.html


12.12.2013

There’s a good article on Medscape on “Epidemiologic Features of Four Successive Annual Outbreaks of Bubonic Plague in Mahajanga, Madagascar”, published in 2002, but as we see still of interest. http://www.medscape.com/viewarticle/432069_1 

Let's hope that the outbreak is going to be under control like in Kyrgyzstan earlier this year.

Rituximab a look at off-label use

I only just now chanced to look at a study from the German registry RABBIT on rituximab (RTX). A. Richter and colleagues looked at [FRI0212]: “Is there a downside in off-label use of rituximab? - 2-year data from the German biologics register RABBIT.” We look at 709 patients in all groups, but we don’t know anything on the distribution on groups like RTX + MTX, RTX + LEF , and RTX mono; the authors also calculated for RF pos. and RF neg. The authors concluded: “Off-label uses of RTX in combination with LEF or of RTX in monotherapy are not inferior to RTX+MTX therapy regarding safety, effectiveness and therapy adherence. RTX+LEF or RTX monotherapy are useful alternatives for patients being intolerant to MTX, with the particular feature that RTX monotherapy should be restricted to rheumatoid factor positive patients to ensure therapy adherence.“ The last conclusion is due to “rheumatoid factor negative patients had a two-fold increased hazard to drop-out if treated in RTX monotherapy (2.15, p≤0.01).”

Somehow I think this is good news as we have to work under conditions, where RTX + LEF is considered off-label and RTX won’t be reimbursed. Some rheumatologists here in Germany prescribe a very, very low dose MTX co medication not to risk being off-label. So any study proving that monotherapy is effective, is welcome. We would also like to reduce the prednisolone and maybe twice 500 mg RTX are as effective as twice 1000 mg. Lots of questions and I hope, we’ll see the answers soon.

28.08.2013

I’ve just looked at an article, which is of interest. M. Bredemeier and colleagues looked at: “Low- versus high-dose rituximab for rheumatoid arthritis: A systematic review and meta-analysis.” The authors concluded: “Low-dose RTX has similar effectiveness and met non-inferiority criteria for most primary outcomes. Considering the lower cost, it should be the standard RTX regimen for rheumatoid arthritis.”

The study looked at 2x500 mg against 2x1000 mg rituximab. It didn’t look at intervals. Spacing the interval might not look like a straight forward infringement of an off-label prohibition. But I’m already happy about this study as it points in the right direction, leading to cost reduction without loosing effectiveness. Link: http://onlinelibrary.wiley.com/doi/10.1002/acr.22116/abstract?systemMessage=Wiley+Online+Library+will+be+disrupted+on+31+August+from+10%3A00-12%3A00+BST+%2805%3A00-07%3A00+EDT%29+for+essential+maintenance

Shiatsu in the Management of Fibromyalgia

There has been an article in the “Journal of Manipulative and Physiological Therapeutics” on the “Effects of shiatsu in the management of fibromyalgia symptoms: a controlled pilot study” (link: http://www.ncbi.nlm.nih.gov/pubmed/23830713). Mark the word manipulative!

Maybe you don’t know what shiatsu is. If you look up Wikipedia (link: http://en.wikipedia.org/wiki/Shiatsu) you find: “There is no scientific evidence for any medical efficacy of shiatsu.” Bearing this in mind we’ll have a look at the study.

The authors concluded: “This pilot study showed the potential of Shiatsu in the improvement of pain intensity, pressure pain threshold, sleep quality, and symptoms impact on health of patients with fibromyalgia.” Wow! Great! You might want to shout out loud. But you’d better restrain yourself. The shiatsu group “received full-body Shiatsu twice a week for 8 weeks” - and the control group? The control group “received an educational booklet.” This isn’t science, this is manipulation. It simply isn’t a control group. You would have to do a sham shiatsu treatment for the same amount of time. 

Massage has a strong negative recommendation and reiki has a negative recommendation according to the German guideline for fibromyalgia.

I don't recomment shiatsu for the treatment of fibromyalgia. 

Carpe Diem Haiku Tan Renga „Cricket Silence“

cricket silence

between scraping sounds

autumn begins                                   (Jane Reichhold)

coloured foliage falling

each bearing written wishes

a light rain leaves damp the leaves

night will start with wafts of mists

harvest fires are burning

reminiscing idle times

http://chevrefeuillescarpediem.blogspot.de/

Carpe Diem Haiku Japanese Spring

Sweet kittens 

With spring’s arrival 

They’re hunting 

Warm spring's evening 

Silvery moon and hunger 

Smell of BBQ 

Blossoms and temple 

Bell sounds and flower fragrance 

Japanese spring 

Hototogisu 

The sky wears pastel colours 

Spring’s grace reigns again

Spring in the mountains 

Clouds are going on and on 

Guests enter the ryokan

http://chevrefeuillescarpediem.blogspot.de/

Apremilast in Ankylosing Spondylitis

I had been interested in apremilast in psoriatic and rheumatoid athritis. Now, there’s a new development: apremilast is tested for treatment of ankylosing spondylitis. Apremilast is an oral phosphodiesterase 4 inhibitor (PDE-4), which modulates inflammatory mediators.

E. Pathan and colleagues “just” published a study with the title: “Efficacy and safety of apremilast, an oral phosphodiesterase 4 inhibitor, in ankylosing spondylitis”. They concluded: “Although a small pilot study, these results suggest that apremilast may be effective and well tolerated in AS and modulates biomarkers of bone biology. These data support further research of apremilast in axial inflammation.” But if you look at the result part, you get disenchanted: “Although the primary end-point (change in BASDAI at week 12) was not met, apremilast was associated with numerically greater improvement from baseline for all clinical assessments compared with placebo with mean change in BASDAI (-1.59±1.48 vs -0.77±1.47), BASFI (-1.74±1.91 vs -0.28±1.61) and BASMI (-0.51±1.02 vs -0.21±0.67); however, differences did not achieve statistical significance.” CRP didn’t change, no difference between verum and placebo groups. The data might also suggest stopping further testing.

The authors argue to conduct a suitably powered study, because of the “current lack of effective oral DMARDs in AS”.

I’m happy that I don’t have to decide as I’m sceptical about apremilast in treating ankylosing spondylitis. Maybe apremilast will be useful against psoriatic arthritis, so it won’t be the last we hear on apremilast, but that’s another story.

Links:

Psoriatic Arthritis: http://rheumatologe.blogspot.de/2012/12/psoriatic-arthritis-at-acr-2012-in.html

Rheumatoid Arthritis and others: http://rheumatologe.blogspot.de/2012/01/efficacy-and-safety-of-apremilast-oral.html

Ankylosing Spondylitis: http://www.ncbi.nlm.nih.gov/pubmed/22984171  

H7N7 – a new strain of avian flu virus found in China (H7N7病毒)

According to the Epoch Times (link see below) there’s a new strain of pneumonia virus (H7N7), which might be more dangerous than the H7N9 strain, which caused 135 infections and 40 deaths earlier this year (研究：中国市场发现H7N7病毒. 更易感染给人).

The new strain can kill birds and ferrets alike, which means that it can also spread to humans. The new strain has been found while checking  poultry for H7N9. Prof. Guan Yi of Hongkong University and his team found the new strain H7N7 in Wenzhou City of Zhejiang Province.  

Sohu Health quotes Bitish media, that “new studies confirm H7N9 avian flu virus originated from chickens” (新研究确认H7N9禽流感病毒源自家鸡).

There’s also an article in the Guardian (luckily this laptop hadn’t been smashed to pieces): “New H7N7 bird flu strain discovered that could pose threat to humans”.

Right now there hasn’t been a report on humans being infected. Let’s hope it stays this way.

Links:

Epoch Times / Chinese article (22.08.2013):

http://www.epochtimes.com/gb/13/8/22/n3947075.htm%E7%A0%94%E7%A9%B6-%E4%B8%AD%E5%9B%BD%E5%B8%82%E5%9C%BA%E5%8F%91%E7%8E%B0H7N7%E7%97%85%E6%AF%92-%E6%9B%B4%E6%98%93%E6%84%9F%E6%9F%93%E7%BB%99%E4%BA%BA.html

Blog post on H7N9: http://rheumatologe.blogspot.de/2013/04/new-strain-of-bird-flu-h7n9.html

Guardian 21.08.2013: http://www.theguardian.com/world/2013/aug/21/new-h7n7-bird-flu-strain-discovered-china


26.08.2013
Nothing new, one Chinese source translated a German text of Spiegel-Online into Chinese: http://de.hujiang.com/new/p526967/.
No news on this subject mean good news.

03.09.2013
You might be wondering about the recent discovery of H7N7 virus in poultry in Northern Italy. The virus has been found on two poultry farms. This virus has no connection to the one found in China. There's good information on all aspects, even on the genome, very interesting reading:
http://ec.europa.eu/food/animal/diseases/controlmeasures/avian/docs/20130827-105434_hpai_h7n7_italy.pdf 

Tabalumab in Rheumatoid Arthritis – new developments?

Today I received the September issue of the Annals of the Rheumatic Diseases. I was quite surprised looking at two articles on tabalumab in rheumatoid arthritis.

Mark C Genovese and colleagues: “Extended report: A phase 2 dose-ranging study of subcutaneous tabalumab for the treatment of patients with active rheumatoid arthritis and an inadequate response to methotrexate” (Ann Rheum Dis 2013;72:9 1453-1460 Published Online First: 18 April 2013 doi:10.1136/annrheumdis-2012-202864).

Mark C Genovese and colleagues: “Extended report: Tabalumab, an anti-BAFF monoclonal antibody, in patients with active rheumatoid arthritis with an inadequate response to TNF inhibitors” (Ann Rheum Dis 2013;72:9 1461-1468 Published Online First: 25 December 2012 doi:10.1136/annrheumdis-2012-202775).

The first study showed “significantly higher ACR50 and ACR20 response rates versus placebo (p smaller than 0.05)” in the 120 mg dose group. After the completion of this study phase 3 were undertaken, but recently discontinued, because the expected efficacy wasn’t met. Link: http://newsroom.lilly.com/releasedetail.cfm?ReleaseID=738769.

In the second study we look at the following conclusion: “At week 16, the primary end point was not achieved, but an indication of efficacy was observed at earlier time points.” As this study already had been accepted in December 2012, Lilly’s discontinuation of the Phase 3 rheumatoid arthritis (RA) program for tabalumab could not be included.

So, all in all the published data rounds up the picture I already had (Link: http://rheumatologe.blogspot.de/2013/06/tabalumab-at-eular-2013-meeting.html - maybe I should have consulted Lilly’s announcement earlier!). Tabalumab isn’t a drug, which could be used for the benefit of patient with rheumatoid arthritis. Let’s wish tabalumab all the best concerning Lupus.

Carpe Diem Haiku A Journey to India

Rice and curry

Chapatis, dhal and raitas

Forget the burgers

Morning in glory

Walking the marble on bare feet

So cool, yet so warm

Guard's eyes

Lie on the houses below

As the falcon sails

Offerings all over

People chanting Hare Krsna

Vibrating nature

Lotus posture

Opening the third eye

Which looks into yourself

http://chevrefeuillescarpediem.blogspot.de/

Rheumatoid Arthritis and future treatments by MABs

I’ve read an abstract recently on “Monoclonal antibody treatments for rheumatoid arthritis” by L. Bossaller and A. Rothe (Link: http://www.ncbi.nlm.nih.gov/pubmed/23789825).
As we already have quite a number of agents and more will be added, let’s have a look at targets already being uses successfully and possible targets.

TNF-alpha: TNF stands for tumor necrosis factor. We already have five TNF-alpha-Inhibitors.

IL-6: IL stands for interleukin. Interleukins for a large group of cytokines, which have the task to communicate between white blood cells (leukocytes), hence the word interleukins. IL-6 is a multitask cytokine, which induces acute phase proteins, plays a role in B cell differentiation and hepatocytes as well as others. We already use one IL-6 inhibitor – tocilizumab. Another IL-6 inhibitor is near to be launched: Sarilimumab (Link: http://rheumatologe.blogspot.de/2013/07/sarilumab-at-eular-2013-meeting.html). An we have an anti-IL-6 receptor nanobody® (ALX-0061), which would be different to the the MABs, but also interfering with the IL-6 signal.

IL-1: we already have anakinra, an interleukin-1 receptor antagonist, which isn’t as successful as TNF alpha inhibitors, when it comes to rheumatoid arthritis. Anakinsa is successful in some familial periodic fever syndromes. Maybe to treat RA it’s the wrong approach.

IL-17: some IL-17 inhibitors are studied in rheumatoid arthritis: secukinumab, ixekizumab and brodalumab (Link: http://rheumatologe.blogspot.de/2013/06/targeting-interleukin-17-in-patients.html). I’m not too optimistic we’ll hear much more about IL-17 inhibition as a treatment of rheumatoid arthritis.

VEGF: Vascular endothelial growth factor is a signal protein that stimulates vasculo-/angiogenesis. TNF alpha stimulates the release of VEGF in rheumatoid arthritis, so that more capillaries are formed and permeability of vessels is increased, which would result in more swelling. “VEGF – appears to be a promising avenue for the future treatment of RA.” Were the concluding remarks of Ewa M Paleolog in 2002 (Link: http://www.biomedcentral.com/content/pdf/ar575.pdf). As we haven’t heard more by now, it doesn’t seem to be the broad road to a successful therapy.

RANKL: it’s the receptor activator of nuclear factor kappa-B ligand, which is important for otheoclast formation and differentiation. Osteoclasts break down bone tissue. As this is what happens in erosions, RANKL is interesting in the treatment of rheumatoid arthritis. We already have denosumab, a RANKL inhibitor (MAB), which has been developed against osteoporosis, and is effective against erosions, but it isn’t effective against articular signs and symptoms of rheumatoid arthritis (Link: http://www.hopkinsarthritis.org/arthritis-news/denosumab-suppresses-erosions-but-has-no-effect-on-articular-signs-and-symptoms-in-rheumatoid-arthritis/).


B-cell function (CD20 [rituximab], CD38 [only of use in leukaemia?], B-cell activating factor [doubtful in RA], transmembrane activator and calcium-modulating and cyclophilin interactor) T-cell function (CD3 [CIA study in 2010], CD4 [no big breakthrough during the past 3 years], CD28 [?]) will be added later.

CD 20: We have rituximab. Other MABs are being studied: ocaratuzumab, which failed to show new data at the EULAR 2013 (Link to more information: http://rheumatologe.blogspot.de/2012/12/ocaratuzumab-at-acr-2012-in-washington.html), or ocrelizumab, which also failed to show new data at the EULAR 2013 (Link: http://rheumatologe.blogspot.de/2012/06/anti-cd-20-monoclonal-antibody.html). But there’s also ofatumumab, on which there had been news prior to the EULAR meeting (Link: http://rheumatologe.blogspot.de/2013/06/ofatumumab-just-before-eular-2013.html). All in all there is activity to get a new anti-CD 20 MAB, but it isn’t a new principle. So it’s only someone else reaching for the pie.

CD 38: There’s bortezomib being tested in multiple myeloma. A. Chillemi and colleagues don’t mention rheumatoid arthritis in a recent overview article (Link: http://molmed.org/files/1047).

BAFF: Tabalumab is an anti-BAFF Monoclonal Antibody, which has been disappointing at the EULAR 2013 (Link: http://rheumatologe.blogspot.de/2013/06/tabalumab-at-eular-2013-meeting.html), but there are two articles on tabalumab in the fresh from the press issue of the Annals of the Rheumatic Diseases (September 2013), so that I might have to revise my former statement on tabalumab. I’ll deal with this new information in a blog post of its’ own.

TACI: TACI is short for transmembrane activator and calcium modulator and cyclophilin ligand interactor, which also interacts with BAFF. There’s atacicept, but it isn’t working in RA (Link: http://rheumatologe.blogspot.de/2012/06/atacicept.html).

CD 3: There has been a CIA study in 2010, but I haven’t found anything new since then.

CD 4: The lack 0f CD 4 cell depletion in rituximab patients is associated with no response (Link: http://www.ncbi.nlm.nih.gov/pubmed/23918413). There had been a study in mice, which Rawarrior commented on 3 years ago (Link: http://rawarrior.com/will-cd4-lead-to-a-rheumatoid-arthritis-cure/). Since then nothing new.

CD 28: Do you remember TGN1412? Here’s the Wikipedia link: http://en.wikipedia.org/wiki/TGN1412. Maybe we do better not trying the luck of people again.   

To treat rheumatoid arthritis, we might get another IL-6 inhibitor (sarilimumab), another anti-CD 20 agent, and maybe tabalumab will prove to be effective (I’m still sceptical, but I’ll tell you more about the recent studies on tabalumab in another blog post).

Carpe Diem Haiku Silent Heart

So much rage and hate

Sweeping thought Egypt's cities

Hope for silent heart

 

 

Love and hate

The heart is missing a beat

Best a silent heart

 

 

Turning and turning

This life is like the seasons

Pacify your heart

 

From the beginning

Your heart has been pacified

Go on silent heart

 

http://chevrefeuillescarpediem.blogspot.de/

Meine Vortragstermine RRZ in Meerbusch

Ich werde in den kommenden Monaten wieder Vorträge im Rahmen der RheumaAkademie halten. Unten stehen die Themen und jeweils eine kurze Einführung sowie der Zeitpunkt. Die Vorträge finden im Rheinischen Rheuma Zentrum (RRZ), Meerbusch-Lank, statt, und zwar im Vortragssaal gegenüber der Cafeteria. Wo das liegt, steht hier: http://www.rrz-meerbusch.de/de/kontakt/so-finden-sie-uns.html. Bitte melden Sie Ihre Teilnahme vorher möglichst an, da der Raum nur Platz für 80-100 Personen bietet, und zwar bei Frau Davids 02150 917-319 oder davids(at)rrz-meerbusch.de.

Aus dem Text zur RheumaAkademie: "Sie finden die bundesweit erste Rheuma-Akademie bei uns am Rheinischen Rheuma-Zentrum in Meerbusch-Lank. Neben Schulungs- und Kursprogrammen finden Sie zahlreiche Angebote im Veranstaltungs- und Fortbildungsbereich." Link: http://www.rrz-meerbusch.de/de/fuer-patienten-besucher/rheuma-akademie.html 

Fibromyalgiesyndrom

Für viele ist Fibromyalgie ein Mysterium. Gezielte Informationen aus psychologischer und medizinischer Sicht erhalten Sie an diesem Abend. Wie entsteht Fibromyalgie? Welche Irrtümer bestehen zur Fibromyalgie? Wie kann man diese Schmerzerkrankung behandeln? Was kann man selbst gegen die Schmerzen unternehmen? Zu diesen Fragen werden die Vorträge Aufschluss geben, außerdem ist anschließend Zeit für Diskussion. Wir werden auch die Therapiemöglichkeiten am Rheinischen Rheuma Zentrum vorstellen.

Termin: Dienstag, 10.09.2013 

Zeit: 19:00-20:30 Uhr
Referenten: 

Sabine Schlösser 

MSc-Psych., Klinische Psychologie 

Dr. med. Lothar M. Kirsch 

Arzt für Innere Medizin, Rheumatologie und Physikalische Therapie, Oberarzt der Abteilung Innere Medizin / Rheumatologie
Mein Vortrag ist hier: http://rheumatologe.blogspot.de/2013/09/fibromyalgiesyndrom-vortrag.html

Wie funktionieren Biologika?

Biologika werden seit über 10 Jahren erfolgreich in der Rheumatologie eingesetzt. Aber was sind Biologika? Wie funktionieren sie? Wie werden sie eingesetzt? Welche Erkrankungen kann man behandeln? Wie sieht es mit unerwünschten Arzneimittelwirkungen aus? Es bleiben doch sehr viele Fragen offen. Nach dem Vortrag hoffentlich nicht.

Termin: Donnerstag, 19.09.2013 

Zeit: 19:00-20:30 Uhr
Referent: Dr. med. Lothar M. Kirsch 
Hierzu ist kein Textauszug vorhanden.

Welche Medikamente werden gerade gegen Rheuma entwickelt?

In den letzten Jahren sind eine Vielzahl von neuen Medikamenten entwickelt worden bzw. sie sind aktuell noch in der Erprobung. Wie Erfolg versprechend sind sie? Was ist von den Neuentwicklungen zu halten? Stimmt die Theorie? Wann stehen sie in der Therapie zur Verfügung? Nach dem Vortrag werden Sie wissen, wovon die Presse in der Zukunft berichten wird.

Termin: Dienstag, 01.10.2013 

Zeit: 19:00-20:30 Uhr
Referent: Dr. med. Lothar M. Kirsch 
Hierzu ist kein Textauszug vorhanden.

Magnete, Salben, Tinkturen,

Wenn man die Illustrierten aufschlägt werden nicht nur Medikamente, sondern auch Magnete, Salben, Tinkturen und weiteres mehr angeboten. Ist ein zusätzlicher Nutzen zu erwarten? Oder wird einem nur das Geld aus der Tasche gezogen? Anhand von Beispielen wird über Sinn und Unsinn diskutiert. Nach dem Vortrag sollten Sie befähigt sein, Anzeigen kritischer zu lesen.

Termin: Donnerstag, 10.10.2013 

Zeit: 19:00-20:30 Uhr
Referent: Dr. med. Lothar M. Kirsch 

Carpe Diem Kamishibai Haibun Cathedral

Seeing the Sagrada Familia reminded me of my last stay in Barcelona, but soon my mind drifted off and I found myself in the Iranian desert.

“In the desert, you can remember your name” is a line out of the lyrics of Horse with no name by “America”. It came to me, when I was looking at the traffic sign, warning drivers about wild or semi wild dromedaries crossing the road. Here it isn’t the horse but the dromedary on which one was supposed to cross sand and dunes of the desert.

Breathing and eating

Dust of the changing desert

Dromedary lives

The sand of the dunes always keeps shifting in the wind or the sun would make it shift by heat. Sometimes there are sounds like a snake approaching, but it’s the wind that surrounds you with or without dust. Sometimes the wind is turning around like enjoying a ride on the carrousel. 

Further away I chanced upon an oasis. It wasn’t waiting there for me. It simply came up from behind the dunes. I spent a little while there with an old man, besides his wife and another man, the rest of a larger population, who had left the oasis long ago. We drank a tea and in an alcove there was still a slightly bleached out photograph of Shah Reza Pahlevi, as if time didn’t pass here.

Clear water

Where does it come from?

The goats just drink it

Through stony valleys, across plains and then again through sand and dust – until the minivan got caught in the sand. But what a nice landscape! I had to walk a couple of hours to reach another oasis to get help.

Stars to guide and light

From sand to gravel to road

Later a cool drink

I've returned back to my friends a couple of hours later with a truck and some men from the oasis to help freeing the minivan in the pitch dark night. A friend thought about helicopters being deployed if we were lost in the desert, but there aren’t any helicopters.

Cool night wind

And the stars rotating

Until the doorstep

http://chevrefeuillescarpediem.blogspot.de/

Fibromyalgia and Yoga

I’ve just looked at a paper in the Oxford Journal of Rheumatology. H. Cramer and Colleagues of the Dept. of Internal and Integrative Medicine in Essen, Germany, reviewed studies on yoga for rheumatic diseases; see link below.

They concluded: “Based on the results of this review, only weak recommendations can be made for the ancillary use of yoga in the management of FM syndrome, OA and RA at this point.”

In their results they talked about two studies on fibromyalgia: “In two RCTs on FM syndrome, there was very low evidence for effects on pain and low evidence for effects on disability.” This complies with the findings leading to the German guidelines. Nevertheless the guidelines recommend the use of Yoga, Tai-Chi or Qi-Gong. Even with low effect size these meditative relaxing and movement techniques can be of use in multimodal therapy settings.

Link:

http://rheumatology.oxfordjournals.org/content/early/2013/08/09/rheumatology.ket264.short?rss=1

03.02.2014:

There's a recent study of J.K. Kiecolt–Glaser and colleagues: "Yoga’s impact on inflammation, mood, and fatigue in breast cancer survivors: a randomized controlled trial". Results: "At 3 months post-treatment, fatigue was lower in the yoga group (P = .002), vitality was higher (P = .01), and IL-6 (P = .027), TNF-α (P = .027), and IL-1β (P = .037) were lower for yoga participants compared with the control group." Conclusion: "Chronic inflammation may fuel declines in physical function leading to frailty and disability. If yoga dampens or limits both fatigue and inflammation, then regular practice could have substantial health benefits."

Link: http://www.ncbi.nlm.nih.gov/pubmed/24470004 

I hope that we'll see more studies like this one to get more confidence in advocationg yoga as a part of therapy in different rheumatic and non-rheumatic conditions.