Drug Naming Games (2.7.2025) Save

It's 02/07/2025. This is the RheumNow podcast. Hi. I'm Jack Cush, executive editor of roomnow.com. February 7.

That means tomorrow, February 8, is Patrick's birthday. Happy birthday, Patrick. You know who you are. This week, a lot of interesting things happening in the wild world of rheumatology. One of the shocking ones was a Medscape survey.

You know, they do those surveys at Medscape about the lives of physicians, our income, and, you know, who's best, who's least, whatever, based on their surveys of thousands of doctors. And they came up with their who's the happiest specialist survey. They do this once a year, and you know, for years we've talked about rheumatologists being amongst the happiest of the subspecialties. Sort of like in Norway, they're supposedly the happiest people, and I heard one joke was that's because the expectations are so low, in Norway because it's so cold. I don't know if that's true.

I've never been to Norway. Please invite me. I would love to find out why people in Norway are happy. But anyway, rheumatologists are really happy, but not this time around. We dropped like a lead bullet.

I mean, my goodness. So at one point, you know, we were number one and number two, and now we're fifth from the bottom at the top of the mix, you know, as far as, you know, are you very happy or whatnot? Allergy, ninety four percent said yes. Pathology eighty eight percent. Dermatology eighty seven percent.

You know, like the top five are also like, you know, the top five income subspecialties. In the bottom, you know, fifth from the bottom, 67% rheumatology. We're just one point better than internal medicine at 66%. How is that? Well, I looked at the survey on Medscape, you can look at it too.

The only fault I have with it is that, only 1% of the people they surveyed were rheumatologists. So, do they have an adequate sample is one thing. Has life changed in rheumatology? Rheumatology is older. There's a lot of burnout in rheumatology.

A lot of, you know, the deluge of white haired, retiring rheumatologists, and maybe you're adding to the negativity. I don't know that we really are that unhappy, or relatively unhappy compared to other people. I'm happier than all the allergists, pathologists, and dermatologists I know. But nonetheless, your ranking drops. So wear a smile, do good things.

The FDA has made some decisions this week about drugs. Maybe the major one was last at the end of last week, they approved a new drug for pain relief. It's to treat moderate to severe pain in adults. The drug is called Jornavix, j o u r n a v x. The generic is Suzeitrigine.

Suzeitrigine, s u z e t r I g I n e. You know, so we're pronouncing these names. It's kinda hard, isn't it? I mean, I gotta look at it. I gotta study it.

I gotta recite it in the mirror like I'm studying my lines. I gotta make it sound like it's easy when it's not easy. And then, you know, the the word the letters don't go together. What you know, of course, all the words are taken. If you wanna name a website these days, you can.

You know, you can't come up with something like Starbucks or or Yahoo because it's everything's taken. You gotta put five letter five words together. Well, here they put words and letters together that don't make any sense. You know, Jorbanax, it's a pain medicine, first in class non opioid analgesic. It reduces pain by targeting, sodium channels in in the nervous system somehow.

Not sure how that works. You got to welcome another pain medicine. It's a non opioid solution. That's great. I have no experience with this.

I have great hope for it. But I'm really perplexed by the names. Suzetra gene, the generic, has got like 10 letters, five vowels. The trade name Jorvnavix has got eight letters and only three vowels. I think there's something there.

Don't you think? The trade name meant to get attention. It's got more consonants, less of those vowels. Generic, nobody cares about. There's always way too many, vowels in the in the generics and making them, maybe a little easier, although they are longer in words.

You know, naming drugs is a real pain in the neck. We'll see with the next report. It's another drug name that's gone bad. So, you know, actually, at some companies, they have competitions when they're coming up. You know, they got a new drug.

It's called KP nine zero seven zero seven. And what are we going to call it? And it comes up with a generic, and then they have company competitions where everybody from the janitor to the, you know, CEO can put in a name. And sometimes that works better than hiring, you know, multimillion dollar ad agencies, because the ad agency is gonna get you a name like Vioxx. You know, v's and x's and t's and, you know, you know, that gets attention.

Right? Those hard consonants. You know, there ain't no great drugs with an h in it at the at the front as their first letter. What I'm Halcyon. Actually, it sounds like a name that would put you to sleep.

But lots of vowels. Right? Hard vowels. And limit those I'm sorry, lots of consonants, hard consonants. Limit the vowels.

The next one: there was a new biosimilar approved, a tocilizumab biosimilar. It's the third biosimilar approved by the FDA from Celtreon. They've got seven biosimilars in the market. They're taking over, or are they not? This one is called, was in development, was called CTP-forty seven.

Its generic name is Tocilizumab e I e I o, you know, the FDA they add on four letters at the end, and this is a n o h for tocilizumab. But the trade name is Avtozma. Avtozma, a v t o z m a. What's that? Eight seven letters, only two vowels.

And it's got a v and a z and, you know, and a t and starts with an av. You know, gets attention. Tocilizumab is like, what, 11 letters and it's got four vowels in it. Well, two more if you add on the extension. Again, this name thing and this naming thing in medicine is is getting to the point of being crazy.

But anyway, this third is this is the third tocilizumab biosimilar. The first one was approved in '23 from Biogen called Tophidense, and then earlier this year, Frenzius Kabi has one called Tyene, t y e n n e. This one, Avtosma, is IV and Sub Q. It's approved for all the things that tocilizumab is approved for. That includes RA, polyarticular JIA, giant cell arteritis, Still's disease, COVID-nineteen, etc.

Okay? So that's good news if you're in the biosimilar biz. Another report this week that affirms that which we all know obesity and overweight increase the risk of chronic inflammatory diseases. This is a TriNetX survey or a study of electronic health record data on over three million people showing that being overweight or obesity increases Let's see For any of the chronic inflammatory diseases Let's see Obesity and overweight was twenty eight-twenty nine percent, whereas in controls, it was only seventeen point six percent. So this is what we know that, you know, obesity is a risk factor for the development of disease.

It may also worsen disease. It may also make drug responsiveness less. But why does it increase the risk of getting chronic inflammatory diseases? It's been seen in RA, in lupus, in JIA, in SPA, in PSA. Why?

It's not simply wear and tear and more pounding on the joints with higher weight. That leads to degenerative disease. We're talking about developing inflammatory disease de novo. So it's either that, there's something stimulatory about bad diets. It's either that bad diets lead to bad microbiomes.

It's either that bad diets directly lead to or indirectly lead to immune dysfunction. If that were the case, maybe obesity would be also linked to some cancers, and I think that actually has been seen many times. So, I think it's really simple. You know, if you look at the pre clinical disease model that Kevin Dean and others have come up with, Mike Hall was Kevin Dean, it says that you're genetically susceptible. There's an environmental trigger that with genetic susceptibility and environmental trigger, you get autoimmunity.

Autoimmunity and one more, you know, one more tick, one more factor will get you into disease progression. What's the environmental triggers? I think bad diet is pollution. It's the same as environmental pollution. This week at RheumNow Live in tomorrow, actually, it's gonna be on Sunday, Karen Costenbatter is giving, a TED talk like, we call them step talks at at RheumNow Live on environmental rheumatology.

And this is just this should be big. I've talked about this recently. I think this is a big thing. How we get disease is largely from the hazards that are in our environment. Bad diet is pollution.

You can quote me on that. A study from the University of Minnesota looked at the the risk of of I'm sorry, not the risk, but actually mortality figures in young adults ages 25 through 44. So that's young and middle aged adults looking at mortality, and they show that from '20 11 to 2020 three, the risk of mortality in this segment of the population has gone up disproportionately so. And in this JAMA article, this excess mortality in adult in younger adults is a societal thing. The biggest contributor to that number was thirty two percent with drug poisoning.

That's not surprising. But also all the other things that you would expect, and that includes transportation deaths, alcohol related deaths, homicides. Suicide was on the list, but not not in the top five. That's obviously a bigger issue with younger adults 25. So, I think this is a disquieting.

I mean, we don't see anything about rheumatology diseases or autoimmune diseases in this population as a cause of death. That wasn't covered in this paper. But I think that this is an important statistic that we need to keep in mind. A study on how you get from psoriasis to psoriatic arthritis. Another lecture at RheumNowLive tomorrow, from Alexis Ogde, where she's looked at this in many different ways, showing that some studies show it, some studies don't.

This particular study is another one of those, I believe this is No, this is not the Trinetics. This is actually a study about factors that are different between those who transitioned from psoriasis to psoriatic arthritis, and the median time frame for that was nine years, right? And that goes along with what's been published before. So they looked at people who were transitioning before nine years, with less than nine years of symptoms before they got psoriatic arthritis, or after. And they found that the late transition group had lower disease activity, less DMARD use, but no differences in radiographic progression.

So, are differences in those that will maybe get there sooner versus those that will get there later. I'm not sure how this is going to change treatment. What Alexis Oggie is going to, address at her lecture is whether aggressive treatment of psoriasis, for instance with either biologics or targeted synthetics, aggressive effective treatment of psoriasis may lessen the risk of psoriatic arthritis. And again, I think that the pre message here is that there are some studies that show it and they're often methodologically flawed, there are a few studies that don't show it. So, maybe it's hard to say and there could be channeling bias.

But anyway, that's my next report, a TriNetX report, which again looks at, you know, millions and millions of people from the electronic health records. And it looks at retrospective data. And in this study, they just compared patients with psoriasis who were either treated with an IL-twenty three inhibitor or an IL-seventeen inhibitor. And in this retrospective, real world EHR data comparing about two thousand three hundred patients on either drug or either class of drugs, that the IL-twenty three inhibitor patients had a slower risk of developing PSA with about a forty percent lower risk. A hazard ratio of 0.6 with confidence intervals of 0.44 to 0.82 and that being very significant.

This was a little higher or significantly higher if we're looking only at 41 to 65 year olds with psoriasis, where the hazard ratio went down to 0.42, which means that that's a fifty eight percent reduced risk. Is this real? It's hard to know. It's manufactured data. You know, the Trinetics, there's problems of propensity matching.

It's not easy to do. It's often not well done. So these are very fast and loose comparisons. But short of head to head studies, how are we going to know? Anyway, I'm going show up and see if Doctor.

Agbe addresses this in her lecture on Can you prevent psoriatic arthritis in psoriasis patients? So, is about a unique study design issue using the TriNetX database on EHR data. Another interesting data analysis thing that we're seeing are these target trial emulation studies, you take a large cohort of people and you emulate a particular trial and the characteristics of a trial and select those patients out. So, this is a target trial emulation study from U Star. This is a study, a U Star is a data set that studies systemic sclerosis.

And in this one, they looked at two zero eight patients with early diffuse systemic sclerosis, and wanted to ask the question: does adding glucocorticoids to immunosuppressive therapy changed skin scores, as measured by the modified Rodnan skin score, MRSS, named for its inventor Doctor. Gerald Rodnan at University of Pittsburgh. And they showed that adding PO steroids up to to twenty milligrams per day to existing immunosuppressives did not make any difference in the modified Rodnan Skin scores. They were similar as far as how they change when followed over time over twenty four months. Both groups dropped minus 2.7 versus minus 3.1.

No significant difference, not any different if they had a high modified Rodden Skin score or a low modified Rodden Skin score. They use a cutoff of 22. I think that's kind of high actually. But nonetheless, I think that it answers the question of if you see early, progressing systemic sclerosis of the diffuse type, will you blast them with steroids? I have done that, because that's been suggested, but you got to worry about, you know, renal crisis in those patients and whatnot.

This data suggests that maybe it doesn't do anything. But then again, this data again, target trial emulation study the mean dose of steroids that they're looking at here is about five milligrams. It wasn't 20. It wasn't a medrol dose pack. It wasn't sixtyforty twenty ten over ten days, something like that.

So, I still think this is an open issue, but I'd like to know what Dinesh Khanna thinks. I'm gonna ask him when I see him. A Danish study looked at the influence of systemic glucocorticoid exposure to women who were pregnant. So, this is a study of a million infant births, and compared those who were exposed to unexposed during the prenatal period, and they showed that glucocorticoid exposure was associated with a higher risk of mental disorders. Autism increased fifty percent, a relative risk of one point five.

These are significant. Intellectual disabilities one point three, thirty percent increased risk. ADHD also one point three. Mood anxiety disorders one point three. Of the one million infant births, about two hundred and ninety thousand were born to mothers with autoimmune or inflammatory diseases.

The exact same numbers were seen: that steroid use may have a downstream effect on the unborn child. Mechanistically, how does that work? I don't know. Making a baby, it's a black box, you know, and that's just a that's a male talking, so, a single and even worse, a single male talking. You figure it out, let me know.

UK has also done cohort analyses of their lupus populations who are hospitalized with an alarming figure. So, in 2023 and 2024, their figures by NICE and the National Health Service shows that hospitalizations for SLE were eight times higher in their black population. That's sixty two point six per 100,000 hospitalizations compared to whites, which was only seven point eight per 100,000. What? It was a little higher in Asians, twenty six.

But even still, blacks are more than double the Asians and about nine times more than than the whites. They found that lupus hospitalizations have increased fifty percent in the last four years from six thousand three hundred to over eight thousand in twenty three-twenty four. Why is this inequality being seen in this population? Is it from and they don't really have the answers, these are just hospitalization numbers. Is it is there any quality of care?

Is it a lack of access? Is it a delay in diagnosis? Clearly, in The UK and NICE are going to need to address this with public policy. That's how we we do this kind of research to see if we can do something about public policy. We've talked about fibromyalgia and lupus recently.

This is a cross sectional study of fifty lupus patients. It's a small study. Twenty four percent had fibromyalgia fibromyalgia. Eighteen percent had widespread pain. Fibromyalgia.

Why don't we just call it fibromyalgia instead of turning it into an adverb or whatever you would call fibromyalgia? The point being that, you know, two out of six, you know, at least of my patients, maybe one out of six lupus patients are going to have fibromyalgia, complicating your management, complicating your assessments. I like this AI report this week. Another interesting thing at RheumNow, Jeff Kerr is going to be talking about AI and rheumatoid arthritis. This is a machine learning algorithm that was developed in a large primary health care data set to see if they could identify early undiagnosed RA.

And they went through, I think they had 29 variables, they actually narrowed it down to 11 features that in a test set and then in a validation set showed great performance in identifying early RA. The 11 features used by AI through machine learning that diagnosed it was rheumatoid factor, CRP, sed rate, uric acid, hemoglobin, platelets, morning stiffness, age, tender joint counts, swollen joint count, and deformity if they're mentioned anywhere in these electronic records. What they found was a 96% specificity, 96% sensitivity, 96% area of the curve. Yeah, AI is gonna make us smarter. It's gonna it's not gonna make decisions for you, but it's gonna be a tool that you will use in your practice or in your research.

I'm fully behind it. I like this report this week. I think it was from Lancet Rheumatology, shows that using a TNF inhibitor if you've got cancer does not change the outcome. I've been yelling and screaming about this all the time. Many of you become adversely handicapped when the patient has cancer, develops cancer, has cancer, and you don't know if you can use your drugs.

And the ACR rules guidelines say if it's a solid cancer, use whatever you're to use. It doesn't really matter. They got a bunch of things wrong when it's a hematologic or lymphoproliferative disorder, but we're not going to talk about that. In this study, three cohorts of patients with either colorectal cancer, five hundred patients lung cancer, eight sixty four prostate cancer, six zero five. Either twelve to twenty percent of these cancer patients were on a TNF inhibitor.

And it turns out their overall survival was not different, meaning these were not worse. In fact, they're less, but the confidence intervals overlap one, so they're not truly inferior. But again, the hazard ratio on colorectal cancer was zero point seven two, confidence intervals of 0.43 to 1.21, lung was 0.7, prostate 0.8. So they don't go up. If anything, they might go down or trend down a little bit.

Oh, by the way, in contrast, steroid use was associated with a significantly worse survival. Now that could be just a surrogate marker for people with worse disease. People with worse disease are going to die. And I'm not saying what's the worst disease? It could have been their arthritis is worse, their cancer is worse, no one knew it was worse, but nonetheless not surprising that they would have worse survival.

But again, this is sobering and good information for you who want to know what to do when your cancer patients are seen by you. Treat them as if they didn't have cancer is my advice. I like this last report that was in J Rheum, with a nice commentary editorial by Hani Gebawi and others: Is rheumatoid arthritis becoming milder? And this is a Canadian Ontario province study where they were enrolling patients in the early undifferentiated polyarthritis study. They got lots and lots of patients, tons of patients, and they divided them up.

I think it was about I want to say it was two thousand patients that were enrolled and these are people who had rheumatoid arthritis, they were enrolled from '98 to 2004, before biologics generally, or soon thereafter with the new criteria from 2000 and five-twenty ten, two sixty six patients, and then the last decade or so, 2010 to 2022, 03/29. That looks like about a thousand patients overall that were analyzed. And what they've seen is, while they looked at those cohorts at baseline, the vast majority of things were not different. Demographics were not different, tender joint count, swollen joint count, shared epitope, etc, right? But there were things that did differ and did change over time.

Over time, since 2005, RA has become less seropositive. It's become less inflammatory as measured by CRP. It's become less erosive at baseline as measured by x rays in these in these many patients. But it's also, at the same time, those are good things that say: Oh, maybe milder? I don't know.

Maybe worse? It's hard to say, but seronegative with inflammation and erosions. I've talked before about seronegative patients aren't necessarily milder. They often are in fact worse. But they've also had more comorbidity, more smoking, and more steroid use.

On the whole, you could say that one, RA is changing. Is it becoming milder? I don't know. I think it may be coming worse with more comorbidity, more inflammation, more erosions. But they're not getting more DMARDs, right?

And their TJCs, SJCs are not worse. Another piece that goes along with it, this, comes from the Mayo Clinic, Doctor. Mayasadova there and her friends, they looked at flare rates in RA showing that over time flare rates have gone down in RA. And I think it might relate to this trend in more seronegatives. Flare rates are higher with seropositive patients compared to seronegatives, with less seronegativity and lower flare rates.

You can look at that paper, the citation is online. You can see that, and by the way, I'll be talking about flare rates at RheumNow Live tomorrow and this weekend in Dallas. It's not too late to register at rheumnow.live if you want to attend virtually or show up and participate in the great fun that we're going to have. You can check out these citations and more on the website. Have a good week.