We discuss the pathophysiology, presentation, and available and emerging treatment for patients with spinal muscular atrophy. We are joined by Diana Castro, MD, Associate Professor of Pediatrics and Neurology at UT Southwestern and Children’s Health Dallas.
Dr. Neeta Goli:
Welcome to Newborn News, a podcast where we discuss educational topics for medical professionals who care for newborns. I'm your host, Dr. Neeta Goli, a pediatrician in the UT Southwestern Newborn Nursery. Welcome back to the podcast. In today's episode, we will be discussing spinal muscular atrophy, or SMA. We are recording remotely due to the ongoing COVID pandemic. We are joined today by Dr. Diana Castro, Associate Professor of Pediatrics and Neurology at UT Southwestern and Children's Health, Dallas.
Dr. Diana Castro:
Hello.
Dr. Neeta Goli:
Hi, Dr. Castro. Thanks for joining us today.
Dr. Diana Castro:
Hi, how are you? Thank you for inviting me.
Dr. Neeta Goli:
So spinal muscular atrophy is an inherited lower motor neuron disorder which, if left untreated, can lead to progressive muscle weakness, and morbidity and mortality associated with that. Now, and on the horizon, we have lots of exciting new technologies to both screen for and treat this disease. So today, we'll discuss the pathophysiology, diagnosis, and management of this disorder. Dr. Castro, could you please start by helping us localize the lesion, so to speak, in neurology terms?
Dr. Diana Castro:
Sure. So, spinal muscular atrophy. The big problem with the disease is, it's concentrated in anterior horn cell located in the spinal cord. The anterior horn cell is where the motor nerves are going to come out. So, the anterior horn cell gets affected, the nerve gets affected, and subsequently, you're going to have all sorts of problems with the neuromuscular junction on the muscle. But the main issue is going to be in the spinal cord.
Dr. Neeta Goli:
So what is the etiology? How is it inherited?
Dr. Diana Castro:
This is inherited in autosomal recessive pattern, so it's 25% chance for each pregnancy. What we have seen actually is with more experience and more patients that we have, it almost looks like after you have had one kid with SMA, even though it's autosomal recessive and even though should it be 25%, it's almost like it gets into a dominant pattern. So we have families with three, four kids with SMA. The problem, really the etiology, is the lack of a protein called survival motor neuron. This protein is produced by a gene called SMN. The SMN is duplicated in our body, so we have SMN1 and SMN2. Everybody has those two. Humans. But the problem in these patients is that they don't have the main gene that is SMN1. So because they lack the main gene, they really depend only on the backup copy, in the SMN2 gene.
Dr. Neeta Goli:
So does SMN2 have to be mutated as well for the full manifestations of SMA to present?
Dr. Diana Castro:
Not really. That's a very good question. No. The problem is that SMN1 produces a hundred percent of the protein, because when you go from, when do you do translation, transduction and the protein gets formed, it forms as a full-length, 100% protein. For the SMN1. But this SMN2 most of the times has the natural mutation where it causes the C to T transition in exome seven. And this is natural, meaning it happens in all of us. And so for that reason, it only produces 10% of full length protein; the other 90% is useless, right?
Dr. Diana Castro:
But again, because we have the SMN1, we don't depend on the backup SMN2 really, but for these patients, they do depend on the SMN2, that's the only thing they have to work with. So if they only have the SMN2 gene, depending on how many copies of the gene they have, it will correlate pretty well with the phenotype. So if you have only two SMN, two copies, you're going to have most likely a more severe patient, a more severe presentation compared to, if you have four copies of SMN2, you're going to have probably more a patient with type three, a patient that is able to walk and is able to do all their things.
Dr. Neeta Goli:
Okay, so let's get into that. What are the different classifications of SMA?
Dr. Diana Castro:
So I'll start by saying that the classification is going to have to start changing. Now we're working on that because as you know, now we have therapies that are changing the landscape completely. So at this moment, right now, that classification that we still use, it is determined by two factors. One, when did the patients start having symptoms at what age, and two, what is the maximum motor function, the patient reached? So if you have a baby that's having symptoms less than six months of age, and the baby's never able to sit independently or to do anything else, that's a type one. And usually those babies have two copies of SMN2. So that's a good correlation.
Dr. Diana Castro:
Then you have the type two. Type two kids usually present between six to 18 months of age. They are able to sit, but they cannot walk. And usually those patients have three copies of SMN2.
Dr. Diana Castro:
Then you have a type three who is older than 18 months of age, who is able to walk independently. And usually those patients will have between three to four copies of SMN.
Dr. Diana Castro:
There is a type four that presents in twenties and thirties, but obviously I don't see those patients. And then there is a type 0. That is the type that neonatologists may see because these are kids that are born completely, completely weak, hypotonic with difficulties feeding and difficulties breathing right after they are born. They usually will have only one copy of SMN2.
Dr. Neeta Goli:
And can you actually explain us a little bit, what exactly does the SMN protein do? What is its role?
Dr. Diana Castro:
So the survival motor neuron, as the name maintains anterior horn cells functional, right? It's what it helps them develop, what it helps them maintain them alive. And if your anterior horn cell, it's alive and it's working well, your motor nerves are going to work well. And if your nerve works well, the muscle will develop well. So it is cascade, before people used to think about spinal muscular atrophy as only affecting the anterior horn sell, but it really ends up affecting the whole pathway all the way down to muscle. But that's why these patients have very atrophic and very small nerves. They have problems in the neuromuscular junction. So they have fatigue related to their disease and then their muscle doesn't develop, or it gets atrophic with time. So to the name, muscular atrophy. The muscle continues getting smaller and the muscles continue getting weaker and hypotonic.
Dr. Diana Castro:
So it's really a condition that will affect the whole pathway. So survival motor neurons. That's what it does, it’s really maintaining that anterior horn cell alive. These babies, if I can make a comment that actually we know that the process of those anterior horn cells, the death of those anterior horn cells starts happening between the second and the third trimester. So changes are happening already when the baby's born, and for a type one that is why it’s so important that the patients get treated within the first six weeks of life, because that is the time where you're going to have more anterior horn cell death and obviously more weakness and more atrophy and more bulbar symptoms and so on. So for a type one, it's extremely important to get them diagnosed early for that reason, because the changes are happening between the second and third trimester and continue happening. So for the first weeks of life.
Dr. Neeta Goli:
And in order to help get the diagnosis earlier, SMA was actually added to the national recommended universal screening panel for newborns in 2018. Texas plans to begin screening for SMA on the routine newborn metabolic screen, I believe later this year in July of 2021 is what I've heard. How will the screening be done?
Dr. Diana Castro:
Yeah. So this was after a fight from all of us. I mean, it's specialists and, and also families’ foundations, trying to make them understand how important it was to diagnose these babies right away. There are some families who have had babies already with SMA. So when they have a new pregnancy, they can do amniocentesis and the baby can get diagnosed intrauterine. Whenever we diagnose somebody, we always test the mother and the father for their carrier status. Now with the newborn screening, that will be part of their regular newborn screening with the dried blood spot. That results with things that we're going to get it around the same time you get newborn screening results. So within the first day of life, right after it’s done, after the patient comes positive for, or there's a possibility of this patient having SMA, we're going to have to do a confirmatory test.
Dr. Diana Castro:
So we will be looking for the deletion of SMN1, because 95% of the patients will have a homozygous deletion of SMN1. And then we also will be looking at the copy number of SMN2, to kind of determine what's the phenotype that patient will have. So those are the first steps. There is something that is extremely, extremely important is that some patients, you're not going to be able to find them within that first screening. So we're going to be able to catch 95% of the patients. There is a 5% of patients are going to be lost, that we're not going to be able to check.
Dr. Neeta Goli:
So for those 5% of patients who are not detected on the newborn screen, how might we expect SMA to present when they're, in the neonatal period, infants, or later in childhood, I know you mentioned earlier, potentially a delay in gross motor milestones, delay in sitting, walking, things like that.
Dr. Diana Castro:
So the presentation will be exactly the same as the deletion of the patients that have homozygous deletion, but with the caveat that there are some patients that may have in one allele, they may have a deletion. And in the other allele, they may have a mutation. This is not, there is not a lot of papers about this, but we have been working with other universities to put the cases together. When we found patients that have a deletion on one side of the gene and the mutation, and these patients may have a milder phenotype. So they present a little bit later. But if you have a patient with regular mutations and there are known modifier mutations, because some patients may have also modify mutations that may cause the phenotype to be less aggressive. What you are going to see is a baby that is born completely normal.
Dr. Diana Castro:
I always tell my residents, my fellows, it's the baby that you open the door and you have this beautiful face looking everywhere, completely awake and alert, with a body that does not correspond to the face. It's a body that is going to be very low tone with a lot of weakness with hyporeflexia or areflexia. That's something that we have to be careful because obviously reflexes may still be present, but it is that this course is that face that does not go with the body let’s say because again, the face is not affected.
Dr. Diana Castro:
So you have normal eye movements, you have normal facial expression. With time, you're going to have bulbar involvement. So difficulty feeding and breathing around three to four months of life. And with time, they're going to lose complete, obviously a motor function of their extremities and their trunk. And also later on, the face will be affected, but the face will be affected later on. It's not one of the first changes that you see. So I always say that if you find a baby that does not correlate, like the face does not go well with the body, that's a baby that likely has spinal muscular atrophy. They do not have cognitive delays. They are quite bright little kids.
Dr. Neeta Goli:
And then, why is there so much variation in the phenotype even potentially among patients who have the same mutation?
Dr. Diana Castro:
That's also a very good question. It's something that we're still working on because it is like I say, there are a couple of mutations in the SMN2 gene that can make the phenotype less aggressive. That we know. There are two mutations that are described, that can cause the phenotype to be less aggressive. But then there is a lot of variation. Even between siblings, you have siblings that are, one is type 3 and the other one is type 2. Even before we start treating them and why they have this variation in expression, phenotypic expression, even though they have the same genetics. And that's something that we're still trying to understand, because the genes that are around the SMN complex have been studied.
Dr. Diana Castro:
There are another three genes that are part of the SMN complex, but they haven't been able to find really a good correlation of any other mutation in any other of those genes, that will cause the phenotype to be more severe or less severe. So it's something that we're still working on it. We don't have good biomarkers yet. And that also is something that obviously is not helping us to understand what will be their response for treatment, for example. That's another point, but it's something important that we still have to work on. There is a lot of work that needs to happen, still in spinal muscular atrophy. Even though we have three medications already, but we don't understand many things.
Dr. Neeta Goli:
Is there any clear understanding as well of why an autosomal recessive disease would potentially, like you mentioned, seem to have some sort of autosomal dominant penetrance in some families?
Dr. Diana Castro:
Not really, no. This is an observation and it's something that all of my colleagues, all SMA experts in the country will tell you. But there is really not a good explanation why some families tend to have more kids with SMA after they have the first one. It's almost like it's dominant in families. I had a family with six kids with SMA. I have families with three and four kids with SMA. So you will think that if it's a recessive condition, it shouldn't affect so many kids of the same couple, but it happens. So again, another thing that we still have to try to understand, there has to be something else. There has to be some other modifying genes that are changing the phenotype somehow, but things are still not clear in that area.
Dr. Neeta Goli:
Interesting so lots more research to be done. If SMA is suspected either based on symptoms or newborn screen results, what is your initial evaluation?
Dr. Diana Castro:
So if it is suspected, if you got a newborn screening, the first thing is sending the confirmation testing, right? That can be done stat, meaning 48 hours. So in 48 hours, we should have results to go ahead and start therapy. So at that point, obviously the patient will be referred to us to neurology, specifically the neuromuscular physician. But if, if a pediatrician is seeing, any physician seeing a patient that they think it is spinal muscular atrophy, there is actually free testing that can be performed. So it's better to be on the safe side, if there's any question, it’s better to send it. It’s sent to a company that is sponsored by one of the pharmaceutical companies. So we get results really quick, within three to four days.
Dr. Diana Castro:
But again, there is a stat test that can be done. I think at that point, if you have that concern, it's much better to give me a call or give us a call and let's start the process. Let's start moving on with scheduling in the clinic and so on. Because even while we get the confirmation, we can be working on other things. We can be looking at their lungs. We can be looking at their lung function. We can be looking at the feeding capacity. We can start doing motor function testing. So there are a lot of things that we still have to do even before we get to the confirmation. So it will be much better to get them referred early. And that's something that, I don't know if it's here in Texas, it's probably not, I think probably many other places that their referral time it is, it's really prolonged, it takes months for these patients to get to our clinic. And every day with spinal muscular atrophy, matters in function, it really matters, every single day. It's a big deal for these babies to get treated.
Dr. Neeta Goli:
Is the confirmatory testing, would that be like a FISH for the SMN1 gene?
Dr. Diana Castro:
Yeah. It will be looking at the SMN1, but it also will tell you the copy number of SMN2. In the past, 10 years ago when I was doing this, we used to do only SMN1, looking for the deletion or mutation in the gene. But now we do the gene copy, the SMN2 copy number because it is also important. But at the time we need to choose, or we need to get therapy. The insurance companies have specific rules about who can be treated really and who cannot. So some companies will not approve treatment for babies with one copy of SMN2. That will be the one that is the newborn, kind of the intrauterine onset. Those are the ones that are born with arthrogryposis and difficulty feeding and breathing right from the first day. So most companies will not cover treatment for those patients. One, because their prognosis is really poor and two, because nothing has been done in terms of research for those patients. So it is important to know the copy number.
Dr. Neeta Goli:
For us. If we are trying to order the test in the computer, is it something that if we type in SMN, it would show up in the electronic medical record or in the computer system, or is it something that we have to go to their website to order?
Dr. Diana Castro:
It is a miscellaneous send-out and it sends to one of the companies that we use a lot is called Invitae, probably you know that company and you send as SMN testing, you can just put “SMN testing” to Invitae and they know. And then the other one is with Athena and Athena has a 48 hour turnaround, so it’s stat. You can send SMN analysis stat to Athena, also as a miscellaneous send out because you're not going to find the order right away.
Dr. Neeta Goli:
Okay. And we have no financial disclosures, but just to say that those are the two tests that are available.
Dr. Diana Castro:
Yeah. I don't have anything to do with those companies. So it's just that it is available. And that, which people will know that it's very easy to, for instance, just send out and send it a lavender top tube, I believe, and then just put it in the mail and send it. It's a test that will come back right away quick. They Invitae one will come back between three to four days. Athena will come back in 48 hours.
Dr. Neeta Goli:
Okay. And how would you recommend we as either newborn nursery hospitalists, or general pediatricians, counsel these families, if we have the suspicion before they were able to see you in neurology?
Dr. Diana Castro:
I think that, I mean counseling, I will say is to make them understand the importance of if this is the diagnosis, we are really against time. We're really against the clock. So make them understand that this is something that they cannot hold on, on. Many times you tell the families, do something and they may take months to do the test. But in these cases, we're not talking about months. We're talking really about days. So just the importance of pushing the system, getting their appointments, making sure it's somebody not calling them, making sure they call the clinic and they get scheduled and they get to be seen as soon as possible.
Dr. Diana Castro:
And then the other part will be the genetic counseling. Because many times I have had families that were diagnosing the baby that is born, you know, like a newborn and that the mom is pregnant already. Or she's going to get pregnant really soon. And it just happened to us recently, we diagnosed one and the mom was just recently pregnant. So the genetic counseling is important to let them know that there is a risk. And if both are carriers, the risk is really high in these cases.
Dr. Neeta Goli:
And then once they do make it to the appointment with you in neurology, what is your current standard of care for treatment?
Dr. Diana Castro:
So if we talk first about standard of care, so standard of care for these patients goes pretty much from head to toe. We make sure that the feeding part is evaluated. So we do a video swallow study for the patients. Many times we do sleep studies when they get a little bit older, or if they're going to start initiating spinraza early. I do send them to cardiac evaluation, cardiac screening, even though these patients, they rarely will have cardiac abnormalities. There was review paper, they got 300 patients with SMA with all type of rhythm abnormalities and structural abnormalities. So to me, I think it's important to send them for a screening.
Dr. Diana Castro:
And then they get to see pulmonology again, to look into the restrictive lung disease that they will develop. These patients cannot use their intercostal muscles. Their intercostal muscles are extremely, extremely weak. So they only use their diaphragm to breathe. That's why they are belly breathers. So they have to be seen really quick because the progression is within weeks, sometimes months, two months, that they will deteriorate, in terms of the respiratory part. Then the other part, like I said, video swallow study, that comes to say, if the patient doesn't pass this video swallow study, do they need a G-tube? And many times G-tube comes with a Nissen to prevent the reflux. We do the evaluation, like the motor function evaluation that is done by physical therapy and occupational therapy. We get them braces if they're needed, we give them hand splints.
Dr. Diana Castro:
We help the families. For example, we don't recommend babies, little babies with SMA to leave the newborn unit in a regular car seat. You know, this is one of the things that people have to be informed about that, they have to leave in a car bed, or they have to leave on one of those car seats that recline completely, because you will try to avoid putting them in that, in that kind of position that is going to push their diaphragm and it's not going to let them breathe. So my PT and OT helped me with all of that area. Nutrition is a very important part of what we do. We do not recommend to have these patients above 25%ile of weight because we don't want them to be too heavy, more fat, more weight means more difficult if moving. And then the other part is the orthopedic part, because with time they will develop scoliosis. They will develop contractures and so on. So I think that it's a lot of pieces that we evaluate a lot of organs, that we evaluate in the clinic.
Dr. Neeta Goli:
And then once we get to treatment, what kind of treatments are currently used as mainstays? And then what kind of treatments are under development and investigation?
Dr. Diana Castro:
So for approved treatments, we have three of them. And I will start with the first one that was approved in December of 2016. And it's called Nusinersen or Spinraza. This is an intrathecal injection that is given every four months for the rest of their lives. At the beginning, I give them four doses in two months as a loading dose. And then after that, it will be every four months afterwards. This medication is approved for all patients from newborn to adults. So it's really, for all types of SMA, the mechanism of action of that medication is working with the SMN2 gene that the patient has because they don't have SMN1, we have to work with what we have. So in this case, SMN2 gene. So it modified the slicing of the SMN2 gene, making these exome seven, that it's most of the time skipped or not included, to be included in the sequence and be able to produce more of the functional protein.
Dr. Diana Castro:
So like they said at the beginning, these patients, even though they have the SMN2, the SMN2 is not functional because most of the time they escape that exome seven. So this medication will help including that exome seven, again in the sequence and increase those levels. It is a great medication. We have trials on all different ages. We have treated patients in the pre symptomatic, that we call, less than six weeks of life. Symptomatic, all the way from six weeks of life to, in terms of trials, we have patients on those 22 years of age, but because it is commercial, patients in all ages have been treated, are treated around the world. So we have a lot of experience with that one. Side effect profile is pretty good. It's mostly related to the lumbar puncture, not really to the medication. That's the first one.
Dr. Diana Castro:
The second one that was approved, was approved in May of 2019. And this medication is called. Zolgensma, or onasemnogene. Zolgensma is a gene transfer therapy and it's given IV and it's times one. So you receive it one time and that's it. It is only approved for kids less than two years of age, because it is given intravenous. There was some studies that was looking at an intrathecal injection of this gene transfer therapy, but it's currently on hold because they animal models show that there could be some possible dorsal ganglia inflammation. So right now the only thing we have approved is for less than two years of age IV. How does it work? It is being transferred. So you're packing the SMN1 gene in an AAV9, and you're giving it to the patient in around an hour.
Dr. Diana Castro:
The only problem for this one is that if the patient has AAV9 antibody, we're not going to be able to use that as a therapy because of the immunologic response. And we also have to start them on prednisone the day before of the infusion. And we keep them on prednisone for around three months. That's number two.
Dr. Diana Castro:
And number three, the latest one approved in August of 2020. And this is called Risdiplam or Evrysdi and Risdiplam is an oral medication. So it's given by mouth or by G tube. It is given daily. It has a very similar mechanism of Nusinersen, of the first one I mentioned, because it modified the splicing on the SMN2 gene. So it improves or increases the levels of SMN protein. This is the newest one, but even though it's the newest one, there has been research trials in around, 500 people around the world. They have very good experience from two months up. So it's approved for babies two months and above. For babies two months under, we can not use Risdiplam yet because the trial is still in progress.
Dr. Diana Castro:
So those are the options we have. All of them are great. The point is start them early. If you start early, you're going to get the best results. And when I say early, it is hopefully in the pre-symptomatic time, meaning the first six weeks of life. You were asking about investigational, and I can mention maybe one of them that we're doing on children that is, it's a myostatin inhibitor. It’s an IV infusion given once a month. If you inhibit myostatin, it will allow the muscles to grow. So it's not targeting exactly the SMN gene, but it's targeting another area that is affected, in this case, the muscle.
Dr. Neeta Goli:
And for our listeners. Can you clarify what AAV9 is?
Dr. Diana Castro:
Oh yeah. Its a Adenovirus. It's an inactivated virus that is in the family of the Parvovirus. AAV has been used for different types of treatments. In this case, AAV9 is the one that is used for SMA. And we're doing research using another type of AAV, there has been AAV8 or AAVrh for Duchenne muscular dystrophy for example. So it's just different strains of the parvovirus.
Dr. Neeta Goli:
And can you speak to the cost of these medications?
Dr. Diana Castro:
Yes, that's where the biggest problem is, is usually the cost, it is extremely high. Nusinersen. It's $125,000 per vial. So like I said, you need four doses in the first two months, and then one every four months. So you can make, the numbers, that's a lot of money because it’s for the rest of your life. The second one, the one that is approved for less than two years, it's Zolgensma, it's $2.2 million, it’s times one, but still a lot of money. And then the last one Risdiplam or Evrysdi . The one that is given oral, it is around $350,000 a year per patient.
Dr. Diana Castro:
These are covered by the insurance and it is a lot of money. But when you start thinking about the number of hospitalizations for these patients without treatments that we had before, the number of ICU stays, the equipment that is needed, the nursing, and everything else. That is all the costs that goes around a patient with spinal muscular atrophy. I think it's worth it. Obviously my patients are worth it and the expense is worth it, but it is a lot of money still. I think that hopefully one day we'll have more reasonable prices for these medications.
Dr. Neeta Goli:
Absolutely. And then with appropriate treatment, early treatment, hopefully caught in the pre-symptomatic period. What is the long-term prognosis for children with SMA?
Dr. Diana Castro:
It depends really the time of treatment. We have studies for Nusinersen in pre-symptomatic babies, less than six weeks of age. And we have studies in pre-symptomatic babies treated with the Zolgensma medication, the gene transfer therapy. And the prognosis for those babies is amazing. These kids are holding their head, sitting, standing, walking. Some of them are running. Most of them don't require any respiratory support or any gastrostomy tube or anything else. So it is amazing that type of response that we see is really amazing for both medications. Again, if you use them in less than six weeks of age. If you use them after that, in my personal opinion, if you use them between six weeks and six months of age, you still have a pretty good chance to make a baby with type 1 who is not going to be able to hold their head or sit or use their arms to now being able to hold their heads, sit up and use their arms pretty well.
Dr. Diana Castro:
I cannot promise they're going to walk, for a type one. I can't promise that. And I always tell the family, and these are the first goal then to try to get her sitting, holding their head, and using their arms because functionally, you're talking, that's a completely different patient. If you are treating patients after six months, I think the prognosis is more, it's more difficult to figure out. It depends how affected is the patient by that point, because by six months a baby with type 1 is pretty weak already. So it depends.
Dr. Diana Castro:
And then for type 2's, who are the ones that can sit, who we call the sitters, the main prognosis for them is to keep their arm function, to be able to use both arms, you know, reach above their shoulders, being able to do their activities of daily living, brushing their teeth, doing their stuff by themselves. And keeping their body also their trunk, more stable, without much of the scoliosis and the weakness they will develop. Because type 2, even though they can sit and use their arms, with time will lose that ability. So when they're in their twenties, thirties, they cannot use their arms much. So we're trying to conserve that and to keep that function.
Dr. Diana Castro:
And for the type 3, these are the walkers. My goal is always to not lose ambulation because these patients, even though they can walk, they will lose ambulation. Most of them will stop walking. So our goal is to try to keep them ambulating so they really don’t develop the other complications you're going to get once you're sitting in a wheelchair.
Dr. Neeta Goli:
And then to end the episode today, do you have any advice for our listeners while they care for newborns?
Dr. Diana Castro:
I think that my advice and something that I didn't mention was the creatine kinase. And it's something that I always have everybody to order one. One creatine kinase in these patients may be normal, but maybe also minimally elevated. So for us, the number in our head is up to 300 is normal. But if you have a patient with 350, 400, 500, think about SMA, because he could be one of those patients. If you have a patient with low muscle tone, with weakness, with difficulty with breathing and with a pretty normal looking face, think about SMA, even if you get some reflexes, think about SMA and send the testing because again, it’s free, we don't have to get a pre-authorization for genetic testing through insurance. We just can send it right away. So why not send it and changing pretty much, changing the life of that patient, changing the outcome completely.
Dr. Neeta Goli:
Thanks again for joining us today, Dr. Castro.
Dr. Diana Castro:
Thank you so much for the invitation and please contact us. I'm always open to talk to anybody. If anybody has any doubt about this. I love what I do. This is my passion, and if I can help, I'll be more than happy.
Dr. Neeta Goli:
Thanks for listening to Newborn News. We hope you join us next time. If you like what you hear, make sure to subscribe and leave us a review. If you have questions, comments, feedback, or suggestions for future episodes, please email me at NewbornNews@utsouthwestern.edu. As a reminder, this content is educational and is not meant to be used as medical advice. Views or opinions expressed in this podcast are those of myself and my guests, and do not necessarily reflect the views of the university.