The ATLAS trial presented at #ASCO22
-Given design (3 drugs maint, and PFS as endpoint), answer was obvious.
-Low power to detect any survival difference
-No quality of life presented, suspect would be worse if properly measured in KRd arm
-Please don’t adopt in practice! #mmsm
Other thoughts:
-induction suboptimal by US standards, suspect benefit would be even less if len was given. Remember- that len based consolidation helps if induction regimen did not contain len (emn02-h095), but does NOT help if induction regimen contains len (STAMINA trial)
Presenter described treatment as well tolerated. There was a treatment related death in KRd arm. After randomization, 5 patient in len arm withdrew due to “patient decision/other” but 16 withdrew in KRd arm.
That’s informative censoring.And likely because KRd was tough to handle
You can see in here- the censoring going on, much more drop outs in KRd arm.
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Theres a lot of talk about "top 5 or top 10" abstract lists at #asco2022 and a lot of hype.
In this 🧵, I highlight 5 flawed myeloma studies. I mean no offense to the well intentioned investigators, but do this to encourage critical inquiry and debate.
Those that were MRD positive paid the "MRD tax" in a big way- 36 months of coming to the infusion center twice a week.
With an endpoint of PFS and comparison of 3 vs 1, result guaranteed.
Wonder what QOL was in K arm?
2
Dara-RVD for smoldering.
SO PROBLEMATIC.
What does "MRD' negativity even mean in someone with smoldering myeloma? Why should the results of this trial matter any more than the dozens of other duplicative small trials? How can you cure some people who WERE NOT gonna progress?
A commendable point of this trial is that those who were became MRD negative, were taken off KRD maintenance after 8 months of KRD maintenence.
Those who did not achieve MRD negativity (what a punishment)- were subjected to 3 years of maintenance therapy 😟
I have said this before, as have many people wiser than I have.
To change maintenance strategies (especially for standard risk patients)- you have to show an overall survival advantage. You have to show the disease trajectory is changed.
Heres an educational 🧵 about me-too drugs using isatuximab as a case example. Dedicated to patients trying to separate hype from reality, and trainees seeking to make sense of so many new approvals for the disease states they are seeing.
It is a medication that is similar to a pre-existing drug with a similar mechanism of action but some minor tweaks that "may" change efficacy or toxicity.
Why do so many me-too drugs exist?
It is a much safer route for pharma companies to make money by modifying an existing product rather than promoting a brand new drug with a new mechanism of action that may or may not work/be safe.
Prophylactic anticoagulation and risk of DVT in myeloma- a 🧵 on the evidence, a few case vignettes, and some guidance (based on VERY imperfect evidence).
1) DVT is a PROBLEM in MM. Those who develop DVT have 3x risk of mortality compared to those who don't. pubmed.ncbi.nlm.nih.gov/22511493/
2) DVT is COMMON- Incidence varies dramatically based on studies, but ~ 3-15% of patients develop it.
3) DVT risk is HIGHEST within first 6 months of diagnosis.
In an analysis of two large randomized trials including both transplant eligible and transplant ineligible patients, DVT occurred almost exclusively in first 6 months.
In honor of myeloma action month, heres a tweetorial on diagnosis of various plasma cell dyscrasias. It is a long interactive one with polls, so be prepared. It is geared towards trainees, oncologists who don't see a lot of myeloma, and other medicine specialties.
🧵 #mmsm
Also, you wont get CME for this, but I don't get paid for this either. Sometimes the best things in life are free (with no hidden agenda for promoting a drug), and you don't (or shouldn't) get paid for them 😀 There are some simplifications here (given Twitter)
Q1. A 47 yr old M with a creatinine of 2.1 (new/?etiology) is referred to you. Mild proteinuria (500mg/day). CBC normal. SPEP shows M protein of 1.8 g/dl, IFE -ve. Kappa light chain is 200 mg/L, ratio=11,BM biopsy with 5% monoclonal plasma cells. PET/CT -ve. Diagnosis?
Is MGUS more common in patients with osteoporosis? Do patients with MGUS have lower bone density? Should patients with osteoporosis be screened for MGUS? Or patients with MGUS screened for osteoporosis? What does the data (and guidelines) say?
🧵 #mmsm#medtwitter
We know from work done by the gurus of myeloma- that fractures are more common in patients with mgus than general population
But are fractures because of decreased done density or existing osteoporosis? We didn’t know.
More work from the Mayo Group did also show that patients with MGUS had a slightly higher risk of osteoporosis, but you can see- the RR was 1.2 with 95% CI of 1.0-1.4. pubmed.ncbi.nlm.nih.gov/19648385/