QD Clinic - Week 6 Save

Welcome to QD Clinic brought to you by RheumNow live, the best meeting for NPs and PAs. I'm Jack Cush from RheumNow. Today's case is the NP says this patient needs help and flares off of therapy. So the story here is a 53 year old seropositive rheumatoid arthritis patient has had RA for since 1986, a long time, has been treated with a lot of different comes in and she's doing really poorly. Actually, had done the same thing about three or four months ago, came in both times then and now.

She's been off of her abetacept for more than four weeks and is now flaring badly. This particular patient has a history of hypothyroidism, a little bit of fibromyalgia and some poor sleep. She's currently taking five milligrams of prednisone, two thousand milligrams of sulfasalazine, and she's on abetacept. Previously, the patient has been treated with and failed a number of different medicines including, Kineret, Symphony, Plaquenil, sulfasalazine, methotrexate, prednisone, Humira, and probably leaving one or two out. So this time she comes in and the question is, is she flaring because she's off of the abatacept or because she has another problem like fibromyalgia and poor sleep.

Often that can be easy, sometimes it's not. This particular patient says that she's been off of therapy this time for about two months, missed a total of about eight shots and just started a week ago. She says that she's doing really badly. She thinks that it's her RA is really acting up. When you question her, she tells you about nerve pain hurting all over her shoulders, her arms, her legs, her knees, elbows, her fingers, etc.

She thinks it's RA. I'm thinking it may be fibromyalgia and her poor sleep, which she says it's poor on the survey form. However, when you examine the patient, see she has 14 tender, 10 swollen, a number of tender points. Her C. I.

Score which is really high, it's 30. Last visit it was 24, she was failing then. But when you look back at her, she's actually never had a really good C. Dye score in the last year, suggesting that even when she was on the abatacept, she wasn't getting a complete response. The lowest she got to was a C.

Dye at 15. And so the question here is what are you going to do? You're just going to restart the abatacept, the biologic and hope she gets control of the disease or whether you should move on. So the nurse practitioner and I were discussing this, she knows the patient maybe a little better than I do. She believes the patient's really quite compliant but the problem has been the abatacept has been interrupted multiple times by changing insurance and by pharmacy problems and through no fault of her own she was without medicine.

So she believes that if I put her back on abatacept which we did four months ago, three months ago, we might be in the same situation next time she comes. So the question is do you move on or not and I think that that's really the question that we were talking about and for me it was easy. Let's move on. The question is what do you move on to? I think you have to first ask the question was the patient controlled or not on the therapy that was being interrupted?

She was never controlled it's easy to move on. The next question is what does the patient want? You know, she's been on a lot of biologics, a lot of injectables, she's been on some pills. Does she want a pill or does she want an injectable? Does that seem to, either one seem to fit into her work, lifestyle, etc.

This patient was a little, was okay with whatever we suggested but really wanted to lean more towards a pill. And then lastly, you do some defensive prescribing in many of these people getting around to the ninth or tenth or seventh or fourth different DMAR that you're going to use hopefully in combination. And by defensive prescribing I mean, wouldn't use a TNF inhibitor in someone who had a history of TB, latent TB, fungal infection or recurrent severe infection. It's just too problematic and you're answering a question about the drug and infection too many times. It's easier to move on to other therapies.

Similarly, someone had a history of Hepatitis B treated or untreated, you wouldn't use a TNF inhibitor, rituximab or even abatacid. They had a history of severe coronary artery disease, heart failure, and MI, you wouldn't use it on steroids and And lastly, if they had a history of diverticulosis, GI perforations, lower GI perforations, you wouldn't use tocilizumab or an IL-six inhibitor or one of the JAK inhibitors, can also cause lower intestinal GI perforations. In this particular patient, she chose to go with a JAK inhibitor. We kept her on her sulfasalazine, her low dose prednisone, we told her on a JAK inhibitor, she should have an early response, could be two to four, maybe even six weeks, but we're gonna know in six weeks. And so we brought her back for a return visit at that time point.

And if she's not hitting a home run, we're moving on to our next best therapy. This is how my nurse practitioner and I resolved this issue. So again, why is RheumNow live the best meeting for nurse practitioners? So far our registration, is really doing quite well, it's getting quite busy. We have 10 to 15% of the registrants are nurse practitioners and physician assistants.

We have pre learning assignments that you're going to see before you come. We have handouts that you can download both during the meeting and before the meeting. There's a lot of Q and A at this meeting. Again, over 25 of the time or four hours of the sixteen hours of CME is going to be devoted to Q and A and there's a lot more that's going to happen just spontaneously. It's a great chance for networking given the large number of NPs and Ps are going to come to the meeting.

Check it out at roomnow.live. We'll talk to you more this week about these Welcome to QD clinic brought to you by roomnow.live. This is the best meeting for NPs and their physicians to go to. Today's case is when to stop the anakinra. This case is a 43 year old male who has a diagnosis of adult onset Still's disease and more recently OA of the knee or meniscal tear of the knee with some early OA changes.

He was diagnosed over ten years ago when he had the systemic onset of many features that made the diagnosis. High spiking fevers of 105, evanescent rashes, an itchy rash and hives, polyarthritis with swollen joints, many swollen joints, pleuritic chest pain, myalgias, sore throat, leukocytosis, hyperferonemia as high as I think thirty four thousand, anemia, hypoalbuminemia, increased LFTs. He was seronegative for rheumatoid factor and ANA. He has ultimately developed fusion of his left wrist and responded dramatically to steroids and then later to Anakinra also known as Kineret. This gentleman has been managed over the last ten years by me and he intermittently has had flares of his disease so stills can be polycyclic or monocyclic.

He's had polycyclic systemic disease cycles of inflammatory disease again somewhere between twenty five and forty percent of patients after they've had their systemic disease will settle down into chronic inflammatory arthritis that gets treated just like rheumatoid arthritis. It's a seronegative RA polyarticular treat them with anything from gold methotrexate TNF inhibitors whatever you want to use. Same thing you use in RA, would use in those people who have chronic articular disease. However, the cycles of systemic disease, fevers, rash, serositis, incredibly high white counts, ferritins, CRPs, all that kind of stuff, that needs steroids, methotrexate and an IL-one or an IL-six inhibitor. So in his recurrences of his systemic disease ten years ago and again four years ago he received somewhere between six and ten months of systemic therapy, the ones I just mentioned.

He recently had a flare about a year ago, actually around eight or nine months ago, and at the last visit two months ago, I said it's time to go off the Kineret. So what we did was we said take the, just so you know and your labs look good and it looks like it's safe to stop, take the Anakinra every other day for a month. He was very worried about this. Take it every, and actually I think I said a few weeks, take it every three days for a few weeks and if you are taking it every three days and there's no recurrence of disease, you can probably stop the drug. Well, he's back two months later and he's still on the drug because he's worried.

Because when he got out to three days, he just didn't feel like himself. He got a little sore throat. He was a little achy and he thought his disease was coming back because those were the features he had when he first started. Did he make the right choice? No.

He was dealing with worry symptoms and not the hard symptoms of systemic JIA or Still's disease. So it was explained to him that when you're going through the great thing about Anakinra or Kinneret is that when you stop it, again about, I don't know, close to a hundred percent of patients are going to flare within three to seven days after they stop their Kinneret. It's almost always around seventy two hours. And they'll get the recurrence of the features they got when they started the disease, but importantly, they have to have the features of systemic disease. High fever, not 99, 101.2, 100.

Two, I'm saying 102 to 106 fevers starting three days after or rashes, again the evenescent rashes that come and go including the itchy rashes or swollen joints. They can start out with some tender joints but they should become, they should persist, they should not come and go, and they should be associated with swelling. Two out of three of those, and it should be backed up by the lab showing inflammation ongoing. So that's when they know that their disease is still active. So let's look at this from the flip side.

How do you know when to take them off therapy? And I think you should look at all the symptoms. Do they have those systemic symptoms or not? And again arthritis can be treated differently but even arthritis can be counted. So if they have no fever, sore throat, rash, no joint pain and no joint swelling and their labs are normal, white counts normal, CRP is normal, sed rate is normal, ferritin is normal and aldolase is normal.

Many patients with an active inflammatory disease will have an elevated aldolase and a normal CPK. It's part of their liver activation. It's a very good biomarker, maybe the best biomarker in managing patients with adult Still's or systemic JIA. So if all those are normal, now you have an open door on stopping therapy and you can wean them off the end of counter just as I said, every two days for a few weeks, every three days for a few weeks, and then stop. But while you're doing that weaning, might be good to give them the safety net of either taking acetaminophen, I like Tylenol arthritis, two or three pills a day, or a low dose of a non steroidal or some anti inflammatory assuming they can take safely take an anti inflammatory with or without PPI protection, and let them go off of it.

Again, if they can go beyond a week and have no symptoms, they're scot free and clear. If the symptoms recur after two or three weeks or two months or whatever, you might want to rethink the diagnosis of Still's disease into something else, something else like traps or, familial fever or something like that, you might want to rethink the diagnosis. But again, you should be able to go off if all those clinical and lab parameters are normal, you should be able to stop. What if someone's on, another drug like Anakinra? First off, if they're on Kineret and Anakinra and prednisone, the symptoms are going to recur within three days.

If they're on Actemra, Tocilizumab or another IL-six inhibitor, it's going to be longer, it's going to be more like four to six weeks before they get that same flare. Again, fever, prodromal sore throat, serositis, swollen joints, rash that comes and goes, again a visible rash that comes and goes. Those are the features of Still's disease in the systemic phase being active. So in our fellows case, was he not having a flare of systemic disease. His labs were normal when we checked them.

He is being told to stop his Kineret today and I put him on meloxicam seven point five once a day or twice a day. He already takes Prilosec, and he should do fine going forward. There are more elaborate and investigative ways looking for an IL-one signature, with microarrays. That's been very helpful for us here, but that's not commercially available. This was an easy case for me because I see a lot of but this is hopefully good information for you.

Tune in for more QD videos. This is QD clinic brought to you by RheumNow Live, a great meeting for nurse practitioners and physician assistants. Our case today is rheumatoid arthritis and the question of how and when to optimize methotrexate. So our patient is a 56 year old female who's had rheumatoid arthritis since 2006, and she was put on at that time methotrexate and etanercept and has done incredibly well ever since. She started that medicine with another doctor.

She moved to see me I believe sometime around 2012, 2013, has been in remission for many, many visits. But in the last year, the patient actually has had more joint pain. So if you look at her CDAI scores, again, a combination of measures, it's been, you know, 1 1030111 for a long time, but really like in the last six visits, which is like last three years, half of them were in remission, three or less. One was in LDAS of low disease activity state from, four to eight, and the others were eight and fifteen suggesting high activity. And so the question is, she needs a change in therapy.

She's on methotrexate. She's on etanercept, or does she need to fix things? She says that she's doing swell. She likes how she's doing except she says she's had more pain in her hands. And again, the last few visits, this is what she says.

She has more this, more that. She's not quite perfect, but she's kind of happy where she is. So we discussed the options of maybe changing therapy or modifying therapy or giving a short course of prednisone for a flare. Again, usually the patient wants to minimize things. In this case, we're going to talk about optimizing methotrexate.

This particular patient is taking six pills of methotrexate once a week, and that's always well for her. She has been on on as high as eight in the past and, somewhere along the line it was weaned down to six and she's done very well, but maybe she's not. So the question is, what do you do in optimizing methotrexate? The first decision is, do you need to optimize it for toxicity or efficacy? We'll start out by talking about efficacy.

Would you do better by changing this patient to parenteral? And clearly, would. Basically, changing from the same dose of fifteen milligrams oral to fifteen milligrams parenteral is an upgrade in therapy and should be tried in patients who wanna do the sub q, route. Now the problem with parenteral, many of you make this change thinking that it's gonna help you manage the toxicity, the oral, the GI, the CNS, and in fact, it worsens it because you're giving more drug. You know, when you give parenteral, they get a hundred or sub q, they get a 100% of what you give them.

When you give it orally, you get almost a 100%, but once you start approaching fifteen milligrams per week or six pills a week, is variable absorption. And so when you change them to more pills, you still have more of the same but still variable absorption. If you switch them to parenteral, you get more drug. More drug means more side effects. LFTs, oral, GI, etcetera.

So the move of going to parenteral a shot, to deal with the toxicity is wrong. You're gonna get more toxicity. So I like sticking on oral and I like what Mike Weinblatt and others have taught me, which is splitting the oral dose. When you split your oral dose from six pills once a week to three pills BID on Tuesday, as opposed to six pills at night on Tuesday, you get a much higher rate of absorption because your lower levels of the drug as delivered to the GI tract gives you much greater absorption, almost between 80100%. So you approach levels that you would get if you went to a parenteral administration.

So when I get the fifteen milligrams of methotrexate a week, and I want to pay to the patient to do better, I split the dose to three pills bid on the same day, once a week. So three pills bid on Tuesday or Wednesday, it doesn't really matter. The same thing for four or five or six even bid. But I really am only gonna give ten ten pills or twenty five milligrams my top dose that I'll do. That's the second issue.

You can increase the dose from whatever you're using up and you can go in two or five two point five or five milligram increments up to, twenty five milligrams a week. You can make that change five milligrams every four weeks, to see how they tolerate it and see how it goes. And again, if you split the dose, you're gonna get more drug delivery, which means you could get more nausea, GI, oral ulcers, diarrhea, mental fog, all that kind of stuff that can happen when you go to split oral dosing as well. If you want less of that stuff, have to lower the dose or find another drug. So, the other deal would be how to manage toxicity.

Again, the main toxicities here are oral ulcerations. The answer is not folic acid. If you look at the Cochrane review on folic acid tells you if you take folic acid, you reduce the amount of LFT elevations, you reduce the number of drug discontinuations, you can improve some GI symptoms, says nothing about improving oral ulcers. Okay? And oral ulcers will not improve it and again if you think you have, do the research, you won't find any improvement.

The trick is vitamin A and this really works very well. Vitamin A eight thousand units once a day prevents oral ulcerations in at least seventy seventy five percent of patients. Believe me, I've been doing this for many years, it works. Learned this from a folate scientist who showed that if you take methotrexate and inject it down the mouth of a rat, you get hemorrhagic enterocolitis. If you pretreat them with vitamin A, you get nothing.

So it really works really, really well. The second trick is to use dextromethorphan, Robitussin DM, Mucinex DM for patients who have queasiness, even nausea, and especially the mental fog. The next day, the thirty six hours after methotrexate, they feel flu like, they feel like a dish rag, they lay around, they change their dosage, they they sleep it off. That is, you know, a base of the fog of of fibromyalgia. That is due to the breakdown of homocysteine into excitogenic amines that are taken up by NMDA receptors in the brain that can be blocked by dextromethorphan.

How do you do it? Pretty simple. You give the methotrexate on Friday night and you take a Mucinex DM, which has got guaifenacin and I think thirty milligrams of dextromethorphan in it. So you take it with the methotrexate When you take the methotrexate, and if you split the methotrexate, you can take it the next day. But I tell people take two doses about twelve hours apart with the methotrexate and twelve hours later.

Sometimes they need a third, but usually they don't need a third dose. Do that every week. It takes care of the CNS manifestations, it takes care of the queasiness, which I used to think was a GI manifestation that we managed by the vitamin A, it's actually better managed by the dextromethorphan. That's how you can optimize methotrexate. If you have any questions about that, look at the blog we have on methotrexate on RheumNow.

I think you'll find it really helpful in managing patients. We're gonna talk about this patient in our next QD clinic video, and talk about, should I change therapies? Hope you enjoyed it. Hey, this is QD clinic brought to you by RheumNow Live, where we're changing minds and practice one practitioner at a time. So our case today is change or not?

We talked about this patient under optimizing methotrexate, and the patient is a 56 year old with rheumatoid arthritis since 2006, managed for the last twelve years with methotrexate and etanercept and doing really well in remission most of that time. However, in the last few visits, she comes in with a more nuisance complaints. Her pain is a two. Her C. Dye score is an eight at this visit.

She has six tender joints and one swollen joint in MCP, and she says she's having problems with her hand on the right side, and she thinks it's from walking the dog and she's got some kind of excuse for it, but it could be just her rheumatoid arthritis not under great control. So in the last video we talked about maybe you should optimize methotrexate. Let's talk about, let's say she has a week you can't optimize methotrexate, you're maxed out on methotrexate. Now it's a matter of sticking with what you've got or adding on another DMARD or adding on prednisone or changing biologics. So in this particular case, I think you should recognize that most patients don't want to change and there's really several good reasons for this.

They're very fearful of what they don't know. Fred Wolf's got a great paper in J. Rheum from about ten, twenty years ago, ten, fifteen years ago looked at why patients change. This is looking at the National Data Bank, why patients change and the top reason why patients won't change is they're very fearful of what may happen with a new therapy. Even when you tell them there's a guaranteed improvement to be expected, they're likely to accept low levels or manageable levels of discomfort, inconvenience and whatnot, as opposed to changing to something new, cool, wonderful, you know, there's all kinds of risks for them.

They might be financial risk, there are side effect risks, they're very fearful of that and so you actually have to be, you know, a very good salesman to explain why this change might be warranted in this particular patient. Here, are we gonna change for one swollen joint? Not at this one visit, but realize in the last six visits, more than half of her visits have not been in low disease activity or in remission, but have been in sort of low level CDAI scores between eight and fifteen. So the issue is here we could have the discussion on changing her etanercept to another biologic. She can't, let's say, increase her methotrexate for one reason or another.

The other option is adding in prednisone, which she's taken before. Some patients will accept a low dose of prednisone, maybe even as little as two point five milligrams to do very, very well without the added inconvenience and it costs and worry of a new biologic. So that's a reasonable option. I'm personally not in favor of adding on another Plaquenil or sulfasalazine, but you could do that as well. That seems to work if you could convert her to triple DMARR therapy, and that would be cheaper and maybe even better for some patients.

Patients prefer pills. So the first question is, you know, should I change or not? And really to make this decision, you really need to be a metrics driven individual, which means that you need to do tender joint counts, swollen joint count, and then some measure of a score. You need to do a rapid score, which is something the patient does by themselves and you don't have to do a joint exam. I don't know why a rheumatologist would not do a joint exam on every patient at every visit, that escapes me.

But if you want to save time and couldn't do a joint exam this time, you could get by with a rapid score, you can do the joint count, the swollen joint count, tender joint count and calculate a C die or an S die score. I do a joint count, a pain score, a HAC score. My score is called a gas score, a global arthritis score. It's a 28 joint tender count, plus their pain score, plus their HAC score. And actually it correlates almost incredibly well with a CDAI score.

So I rely on tender joint counts as opposed to swollen joint counts because everybody can do a tender joint count, only a world expert like me and you can do a swollen joint count. So it's very reproducible, but having the metric lets you see what the trends are and don't and you don't have to rely on what's happening here and now with this one or two swollen joints today, and the patient wants to live with it. So I think the idea here is you need to find out what they want and how they're willing to operate. So I think that in my patient, you know, this is gonna be her second biologic after taking etanercept. I think, you know, ask her what's ideal.

Does she want an injection or she only want to deal with pills? And I think in choosing your next biologic, you can go with the ideals, things that you recommend, something she's heard about, maybe your aunt was taking this, you know, that sort of thing. And I think that, you know, when they're motivated to take something, give them their option, you're gonna increase the odds of of improvement. However, if this is now gonna be their third or fourth or subsequent biologic or DMAR combination, now patient choice becomes a little bit less of a of a consideration, and now you're tending to back into what you can reasonably do based on what the patient experienced before. So I call this defensive prescribing.

So if they've had hepatitis before, really can't do, you know, give them certain drugs like methotrexate or Rava. Maybe even if they had LFT elevations with a JAK inhibitor, should probably shouldn't use Actemra in those people. Same thing for other things like infections, TB, chronic lung disease, recurrent infections, cancer, those are things that tend to make you defensively prescribe where you back into the one or two options that are safest for that patient and you can sell that reasonably well, and the patient's willing to accept that. So I think having a threshold, I think that the data I want to impart upon you is very good data. It's very as much as great rheumatologists are great at managing RA and diseases like RA, and doing so without even having the metrics, there's pretty damning data about how many rheumatologists do not change therapy, DMARR therapy in the face of active disease.

This comes from large cohort studies, large longitudinal registries that are based in practices like, corona and whatnot that show even when you measure, even when you declare the patient to be moderate or severely active, the number of patients that you, the rheumatologist, change is really shockingly low. Meaning that with six months or more of moderate disease, only a third are changing DMARDs. To get to a majority, you have to go out one year before over sixty three percent of patients will in fact change their DMARD. And that means a conventional DMARD or a biologic DMARD change. That's pretty bad.

In my book, should we be making these decisions about success or failure in therapy every six weeks. Unless you're talking about gold, penicillin, and rituximab, you're gonna know in six weeks whether or not you're hitting a home run with whatever new drug you prescribe. Decisions need to be made definitively based on hard facts, and you should push it because left up to the patient they may not want to change. So I think again, patient buy in, having the discussion are all important factors in making these hard decisions about whether to change or not. Tune in for more QD videos.

Go to roomnow.live to see what's the, what's going on. The faculty looks amazing. Hi. This is QD video brought to you by RoomNow live where it's not about the dots and the data. It's about connecting the dots.

Imagine that. Today's case is rules for pregnancy. So I just finished seeing a 27 year old gal who is nulliparous until recently and she had just delivered her baby. She had a healthy young girl, while taking, tocilizumab. And this brings up the issue of how to manage patients with inflammatory arthritis, who are on DMARDs and biologics and or those who want to get pregnant.

Think the smartest thing actually I heard, at last year's ACR is if you have a woman of childbearing age in your clinic, you need to have the discussion at every visit about what's your plan for getting pregnancy, getting pregnant. They need to have a plan, they need to know that you have a plan, and towards that end the ACR, is coming out with a three part manuscript on guidelines for patients with rheumatic disease and their reproductive health. It's going to talk about, contraception, lactation, the use of drugs. It's going to cover all rheumatic diseases, inflammatory disease, lupus, etc. So look for that.

It's going to be voluminous. It's going to be really instructive. There should be a lot of education around it. And you can develop your own rules based on that guideline when it comes out. Let me give you my guideline for what happens.

What's interesting about this patient is she was told by the many doctors saw her before me when she had a febrile undiagnosed disease, when she was diagnosed with Still's disease, and she had, you know, spiking fevers to 105, even as in rashes, polyarthritis, serositis, lymphadenopathy, splenomegaly, the whole package. When she was diagnosed they told her never get pregnant. You may not ever get pregnant, that it would be dangerous to get pregnant. And of course all that's just goofy and wrong. So that's the first thing I told her when I saw her and she was on methotrexate and I put her on a biologic, in this case we put her on tocilizumab, she did really well, she stopped her methotrexate, was doing very well tocilizumab and she asked, now can I get pregnant?

And I told her, of course, you have to be off methotrexate to consider that. Now she was doing great, she was in remission and I said, get pregnant, let's see what happens and we'll manage it after that. Soon after got pregnant, stayed on the drug. She stopped the drug for about three or four weeks around the time that she was delivering and she resumed the drug after delivery and is now breastfeeding on the drug. So here are the rules.

Number one, you need to be in, and this applies to people with an RA, psoriatic arthritis, inflammatory arthritis, these are not necessarily rules for other autoimmune diseases like lupus. Number one, you need to be in remission to get pregnant. When you're in remission and you've been in remission for a while, you're safe to get pregnant, you're just gonna have the best outcome. You have to have a health a healthy mama to make a healthy baby. Number two, if you're not quite in remission and your low dose activity, you need to be on some therapy to get pregnant.

So and of course, you should be on therapy that's compatible with pregnancy. You should not be on leflunomide, mycophenolate and methotrexate. Of those three, the most dangerous, fetotoxic drug is mycophenolate, not methotrexate. So yes, you can get switch over to any other DMARD or biologic. Preferred biologics to get pregnant on if you're gonna be don't wanna get pregnant would be first cerdulizumab and two etanercept because mainly because they have a short half life and I can manipulate those much better.

I think all other biologics like my patient on Actemra are fine. There's growing amounts of data suggest that they you can conceive on those medicines and can take them throughout pregnancy. Remember, there's a big wide area or a big voluminous area of research from the GI world where Crohn's and UC patients actually have a lot of flares, during pregnancy. They need to be managed and they stay on these biologics almost uniformly often with DMARDs and 6MP and other therapies and they do very, very well. So you can stay on another biologic.

I don't want to be pushing, being on either rituximab or a JAK inhibitor, rituximab because there's long half life JAK inhibitor because I don't think we have enough evidence yet, but you can be on any one, pregnant and if you're in remission at the time you are beta hCG positive and you have already conceived, and you're in remission and doing well, you can stop the biologic. If you're not in remission, you should continue it throughout the pregnancy. So what do you do during the pregnancy? Just continue it and you can continue throughout. Again, on how well they're doing, you could stop it midway through or the last trimester if they're sailing through, but many people can safely take that.

Again, roughly about twenty percent of rheumatoid might need to be on, a biologic although I think that, more, than that percentage are actually going to have activity during pregnancy. Again, issue really here is the mother. If this is their first pregnancy, they're hell bent on being off of all drugs. If this is their fourth pregnancy, they're like, give me all the drugs you need. I know I can make a baby.

If they get, if they're gonna deliver, you could stop and basically rules there on stopping a biologic that they're on, they're gonna deliver is you don't want them to be have peak drug levels of that drug at the time of delivery. You wanna minimize any risk of of infection. So if they're on an infusible like infliximab, you wouldn't do an infliximab infusion and deliver on the next day or Tuesday. You'd wanna wait till the till six or eight weeks later. Same thing for adalimumab, or any other injectable that has a longer half life.

You want to be maybe off for a week or two or as long as you can, and then you can resume it soon after you know, they're at home and the baby's breastfeeding, you can resume it right away. If you think the patient needed it during pregnancy, they're probably going to need it postpartum. I wanted to make a statement about what to do during the pregnancy while they're still pregnant. You know, after eight weeks, certainly after twelve weeks of pregnancy, you can use any drug you want. You can use fetotoxic drugs, you can use cyclophosphamide, you can use chemotherapy, you can use Coumadin, colchicine, you name it, any drug almost because the baby's already made, organogenesis is done.

You might want to change some things, certainly no nonsteroidals, in the last six weeks or so, before delivery because that has issues with the, patent ductus arteriosus that that can prematurely close under the influence of prostaglandin inhibition. But other than that, you can use almost any drug in the later in the second and third trimester drug. I've had patients recently with complex disorders who were taking multiple drugs, know, a DMARDs, like I think one patient was on two DMARDs taking abatac at the same time. And then another one was thinking, know, so really can use any kind of combination at that point without any real risk. At delivery, again, you should try to be off the drug at the time of delivery and then you can resume during breastfeeding.

You could pretty much use every drug during breastfeeding. There's very little evidence that any of it gets in the breast milk and if it does get in the breast milk, there's almost no evidence that's gonna get into the child's bloodstream. So those are my rules on managing pregnancy. I hope you find them health health helpful, and we'll talk to you at the next QD video.