Zu Abkürzungen von anti-rheumatischen Medikamenten

Ich las den den Artikel von T. Schmeiser et al.[1]. Und da waren sie wieder, die Abkürzungen, die ich so nicht mag. Ich halte es für eine gute Idee, Medikamente mit drei Buchstaben abzukürzen, aber es muss nicht jedes Land seine eigenen Abkürzungen produzieren. Flughäfen haben solche Abkürzungen mit drei Buchstaben. Der Flughafen Köln/Bonn wird CGN abgekürzt und kein Reiseveranstalter käme auf die Idee, plötzlich KLN oder KÖL zu benutzen.

Ich hatte bereits über diese Art von Abkürzungen vor etwa acht Jahren schon einmal berichtet [2].

Bei neun Medikamenten sind Abweichungen zum Gebrauch im Abstract-Band des 2019 ACR Meetings [3] vorhanden.

Bei Abatacept ist die von Schmeiser gewählte Alternative sogar besser, da weniger fehleranfällig gegenüber Adalimumab.

Baricitinib wird in den Studien des 2019 ACR Meeting mit bari abgekürzt. BAR ist prinzipiell in Ordnung, führt einen aber beim Suchen auf „bar“-Diagramme.

Certolizumab mit CMZ abzukürzen ist nur vom deutschen Medikamentennamen (Cimzia) her zu erschließen.

ETA für Etanercept finde ich nicht gut, weil es im Japanischen ein schlechten Beigeschmack hat [4].

Golimumab – warum nur GOM? GOL ist einsichtiger.

Für Infliximab war auch schon IFX in Gebrauch. IFN kann als Abkürzung von Infusion verwechselt werden.

Für SAR als Abkürzung für Sarilumab habe ich noch keinen Beleg. Wäre prinzipiell nichts gegen einzuwenden.

Für Tocilizumab hatte ich früher TOC gefunden, durchgesetzt hat sich TCZ. TOC wäre auch einleuchtender als TOZ.

Selbstverständlich kann jeder seine Abkürzungen so wählen, wie sie dann im Abkürzungsverzeichnis stehen. Verständlicher ist man aber, wenn man einen Konsens für Abkürzungen herstellt.

Links und Literatur:

[1] Schmeiser, T., Broll, M., Dormann, A. et al. Einstellung von Patienten mit entzündlich-rheumatischen Erkrankungen zur immunsuppressiven Therapie im Rahmen der COVID-19 Pandemie – eine Situationsanalyse. Z Rheumatol 79, 379–384 (2020). https://doi.org/10.1007/s00393-020-00800-8 ABC:

[2] https://rheumatologe.blogspot.com/2012/11/abkurzungen-fur-dmards-in-der-s1.html
[3] 2019-Abstract-Supplement.pdf https://acrabstracts.org/download-abstracts/
[4] https://rheumatologe.blogspot.com/2016/12/whats-in-names-of-drugs-in-rheumatology.html
Edward S. Herman, Noam Chomsky: Manufacturing Consent. Pantheon Books, New York 2002.

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WIN-Session SLE beim Kongress der DGRh 2018 in Mannheim

Im Laufe der letzten 25 Jahre wurde die Bedeutung der Antimalariamittel für die Langzeitprognose entdeckt. Mycophenolat Mofetil (MMF) ist eine Alternative zu Cyclophosphamid. Rituximab ist besonders bei Antikörpervermittelten Symptomen hilfreich. Eine konsequentere Kortikosteroid Reduktion muss angestrebt werden. Calcineurininhibitoren sind bei Lupusnephritis wirksam. Belimumab wurde zugelassen.

Konsequenter Sonnenschutz (durch Bekleidung und Sonnenschutzcremes mit LSF über 50). Vitamin D3 mit 2000-5000 IE täglich zu fettreichem Essen. Kalzium diätetisch und durch Substitution  sollte mindestens 1,2 g pro Tag betragen - Vorsicht bei Niereninsuffizienz sowie Nierensteinen. Gute Paitentenaufklärung verbessert die Compliance. Kariovaskuläre Risiken vermidern. Patienten sollten selbstständig Urin mit Teststäbchen untersuchen. Impfungen durchführen lassen.

Off-label: MTX, Leflunomid, Cyclosporin A, Tacrolimus, Rituximab; MMF nur bei Lupusnephritis zugelassen.

Wir benötigen eine Treat-to-Target Strategie mit geeigneten und validierten Aktivitätsscores.

Anifrolumab (IFN-Typ1-Rezeptorblockade) hat in einer Phase 3 Studie den primären Endpunkt verfehlt. Baricitinib, IL-2, Ustekinumab werden zur Zeit untersucht, da bereits positive Daten vorliegen.

Das Makrophagen Aktivierungs Syndrom kann aussehen wie der Schub einers SLE. Red flags sind: hohes Fieber, Erhöung von CRP, Procalcitonin, Ferritin, GOT, LHH, Neutopenie, Myokarditis, Krampfanfälle.

Initial sind hochdosiert Glukokortikoide notwendig, gefolgt von Cyclophosphamid oder Etoposid.

Risikofaktoren vür die Aufnahme auf die Intensivstation sind Thrombozytopenie und hohes CRP.

Es wurde die Frage "Brauchen wir Belimumab?" gestellt und mit: Ja, aber beantwortet.

PLENARSITZUNG

1.1 Wolfgang Amadeus Mozart

08:30 - 10:00 02 | WIN-Session SLE

Vorsitz: Falk Hiepe, Berlin

Bimba Franziska Hoyer, Kiel

08:30 02.01 | … mal ganz praktisch: welche Parameter

für Krankheitsaktivität und Remission helfen im Alltag?

Martin Aringer, Dresden

08:50 02.02 | SLE-Therapie: heute und morgen

Reinhard Voll, Freiburg i. Br.

09:10 02.03 | What you should know about macrophage activationsyndrome

in SLE: new aspects from a French cohortstudy

Thierry Martin, Strasbourg, Frankreich

09:30 02.04 | Brauchen wir Belimumab?

Contra: Hanns-Martin Lorenz, Heidelberg

Pro: Andreas Schwarting, Bad Kreuznach

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Ustekinumab at the EULAR 2013 Meeting

Ustekinumab (Stelara) is a human monoclonal antibody against IL-12 and IL-23. Adverse events include an increased risk of infections (tuberculosis and others) and cancer. There were a couple of studies on Ustekinumab and I've been eager to know, whether these studies confirmed the positive impressions, the drug had made last year. I didn’t see the solution of problems treating psoriatic arthritis in ustekinumab, but thought of getting a new option to treat at least some patients with psoriatic arthritis better than before (ACR 2012). Now let’s switch to the newer studies or new results.

P. Rahman an colleagues presented a study [SAT0264]: "Ustekinumab [UST] improves physical function, quality of life and work productivity of patients with active psoriatic arthritis who were naïve to MTX, despite MTX therapy or previously treated with anti-TNFα: results from PSUMMIT I and PSUMMIT II". Conclusions: "UST improves physical function, improves general, arthritis and skin-related quality of life, and reduces the impact of disease on work productivity in patients with active PsA regardless of current or prior MTX use or prior anti-TNF experience." If you expected differences in patients naïve to anti-TNFα, your're right. In results we find: " In the anti-TNF naïve population, statistically significantly greater improvement in SF-36 MCS was observed in the combined UST 45mg and 90mg group vs PBO."

I. McInnes and colleagues presented [SAT0267]: "Safety of ustekinumab from the placebocontrolled periods of psoriatic arthritis and psoriasis clinical developmental programs". The conclusions as expected: " During the PBO-controlled portion, UST was well-tolerated. Overall safety were consistent between populations & safety event rates were generally comparable between pts receiving PBO & UST within each population."

K. Papp and colleagues looked at long-term safety [SAT0287]: "Long-term safety of ustekinumab: 5 years of follow-up from the psoriasis clinical development program including patients with psoriatic arthritis". Conclusions: "With continuous UST exposure for up to 5yrs and approximately 9000 pt-years of follow-up in the PsO development program, long-term safety in the Overall Population were consistent with previous reports at earlier follow-up and event rates were generally comparable to other currently approved biologic agents. Long-term safety in the sub-group of PsO patients with a history of PsA at baseline were generally comparable to those in the overall study population." Nothing unexpected, but this look on safety makes one feel safe to prescribe the drug later.

C. Ritchlin and colleagues presented the following study [OP0001]: "Maintenance of efficacy and safety of ustekinumab in patients with active psoriatic arthritis despite prior conventional nonbiologic and anti-TNF biologic therapy: 1 yr results of the PSUMMIT 2 trial". The highest ACR70 was reached in the 90 mgs group at 17.9%. Conclusions: "Both UST doses (45/90 mg q12w) yielded significant and sustained improvements in PsA signs/symptoms with favorable and comparable safety profiles. UST was effective in both anti-TNF-naïve and anti-TNF-experienced pts, with greater efficacy in anti-TNF naïve pts and anti-TNFexperienced pts previously treated with 1 or 2 anti-TNF agents."

It seems we're getting a new drug to treat psoriatic arthritis - now let's wait for if and when FDA and EMEA approve ustekinumab.


Link:
ACR 2012 in Washington http://rheumatologe.blogspot.de/2012/12/ustekinumab-at-acr-2012-in-washington.html

Ustekinumab at the ACR 2012 in Washington

I restrict this blogpost to Ustekinumab. Link for EULAR 2012: http://rheumatologe.blogspot.de/2012/07/ustekinumab-and-other-options-in.html.Ustekinumab (Stelara) is a human monoclonal antibody against IL-12 and IL-23. Adverse events include an increased risk of infections (tuberculosis and others) and cancer.

A. Kavanaugh and colleagues presented: "Ustekinumab Improves Arthritis-Related and Skin-Related Quality of Life in Patients with Active Psoriatic Arthritis: Patient Reported Outcomes From Randomized and Double Blinded Phase III Psummit I Trial" (Abstract No. 569). Conclusion: "Ustekinumab improves general as well as arthritis and skin-related quality of life, and reduces the impact of disease on work productivity in patients with active PsA." There is not much on arthritis in this part of the study.

Ch. T. Ritchlin and colleagues presented: "Ustekinumab in Active Psoriatic Arthritis Including Patients Previously Treated with Anti-TNF Agents: Results of a Phase 3, Multicenter, Double-Blind, Placebo-Controlled Study" (Abstract No. 2557). The conclusion looked like this: "UST reduced signs & symptoms, improved physical fxn, enthesitis & improved plaque PsO. Safety profiles were similar between UST & PBO." - Welcome to twitter! (UST, PsO &b PBO) The presentation of results is very eloquent, whereas it is very laconic on the DAS28 response.

Another study (actually all are the same) by A. Kavanaugh and colleagues: " Ustekinumab in Patients with Active Psoriatic Arthritis: Results of the Phase 3, Multicenter, Double-Blind, Placebo-Controlled Psummit I Study" (Abstract No. 2562). Here we have DAS28-CRP responses: 34.5% for placebo, 65.9% for 45 mg, and 67.6% for 90 mg. Conclusion: "In pts with active PsA, UST significantly reduced the signs and symptoms of arthritis, improved physical function, enthesitis and dactylitis, and improved plaque psoriasis vs PBO-treated pts at wk24. Safety profiles were similar between UST-and PBO-treated pts."

And there has been the late breaking poster (Abstract No. L4): Continued Improvement of Signs and Symptoms in Patients with Active Psoriatic Arthritis: Week 52 Results of a Phase 3, Multicenter, Double-Blind,Placebo-Controlled Study." Here we have DAS28-CRP responses: none for placebo, as these patients changed to ustekinumab, 72,7% for 45 mg, and 74,6% for 90 mg. Conclusion has been much the same like above.

Do we have the solution of our problems in psoriatic arthritis? I fear we haven't, but we get a new option to treat at least some of our patients better than before.

Ustekinumab and other options in psoriatic arthritis

F. van den Bosch discussed „how to treat psoriatic arthritis?” Upon failure of methotrexate as a “therapeutic option, approved anti-TNF agents, such as etanercept, adalimumab, infliximab and golimumab, have been shown to improve dramatically the outcomes for patients, often tackling both the rheumatological and the dermatological aspects of the disease.” He didn'd mention leflunomide and cyclosporin A, though. But new agents have been studied or are in development for psoriatic arthritis: abatacept, ustekinumab, and secukinumab as well as small oral molecules (protein kinase inhibitors) such as apremilast or tofacitinib.


D. Wallis and colleagues presented an observational stuy on biologics in psoriatic arthritis. They looked at treatment response, drug survival, and outcome after switching. As switching means switching in the class of TNF inhibitors, the study also shows that we are in desperate need for other modes of action in psoriatic arthritis. Persistance with the first TNF inhibitor has been 70% at 36 months with 87% at 12 months. But persistence with the second biologic agent has only been 53% at 12 months. So it is worth while to switch, but we end up with a resonable number of patients we have to look for new therapeutic options. If the reason for switching has been an adverse event, the chances are higher that the second TNF inhibitor persists.


[AB0928] PSORIATIC ARTHRITIS AND BIOLOGIC THERAPY: TREATMENT RESPONSE, DRUG SURVIVAL AND OUTCOME AFTER SWITCHING – AN OBSERVATIONAL STUDY
D. Wallis1, D. Jadon1, W. Tillett1, N. Waldron1, C. Cavill2, N. McHugh1, E. Korendowych1. 1Royal National Hospital for Rheumatic Diseases; 2Bath Institute for Rheumatic Diseases, Bath, United Kingdom
Conclusions: Persistence with the first biologic agent in this cohort was 87% at 12 months, 74% at 24 months and 70% at 36 months. The response to the first biologic agent was sustained at 24 months across joint, skin, nail and quality of life measures. Persistence with the second biologic agent was 53% at 12 months. Patients who switched to a second biologic agent because of adverse event were more likely to continue with the second agent than those who switched because of secondary inefficacy.


Out of the new drugs let's have a closer look at ustekinumab. There has been a discussion on adverse events, but the study didn't find a significant difference between ustekinumab and placebo. I.B. McInnes and colleagues presented a study of ustekinumab in patients with active psoriatic arthritis. It has been a phase 3, multicenter, double-blind, placebo-controlled study. The results showed an ACR20 response of 49.5% for ustekinumab (22.8 for placebo) and a DAS28-CRP response of 67.6% with 34.5% for placebo. PASI75 response has been 62.4% with 11.0% for placebo. Safety profiles have been similar in all groups.


[OP0158] USTEKINUMAB IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS: RESULTS OF THE PHASE 3, MULTICENTER, DOUBLE-BLIND, PLACEBO-CONTROLLED PSUMMIT I STUDY
I.B. McInnes1, A. Kavanaugh2, A.B. Gottlieb3, L. Puig4, P. Rahman5, C. Ritchlin6, S. Li7, Y. Wang7, A.M. Mendelsohn7, M.K. Doyle7,8, on behalf of the PSUMMIT I Study Group. 1U Glasgow, Scotland, United Kingdom; 2U California, San Diego, CA; 3Tufts Med Cntr, Boston, MA, United States; 4Universitat Autònoma de Barcelona, Barcelona, Spain; 5Memorial U, NL, Canada; 6U Rochester, Rochester, NY; 7Janssen R&D, Spring House, PA; 8U Penn, Philadelphia, PA, United States
Conclusions: In pts w/ active PsA,UST sig reduced the signs and symptoms of arthritis, improved physical function, enthesitis and dactylitis and improved plaque psoriasis vs PBO-treated pts at wk24. Safety profiles were similar between UST-and PBO-treated pts.


All in all ustekinumab will be a real option, but still there will be lots of patients waiting for other therapeutic options. None the less, I'll be looking forward for approval of the drug. And I'll be looking for developments concerning abatacept, secukinumab, apremilast, and tofacitinib.