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 4. The Future of ADH1 - Looking at Emergent Treatments


CASR and ADH1: Integrating Biology and Genetic Screening 

THE FUTURE OF ADH1 - LOOKING AT EMERGENT TREATMENTS

The Future of ADH1 - Looking at Emergent Treatments


CASR AND ADH1: INTEGRATING BIOLOGY AND GENETIC SCREENING 

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CASR AND ADH1: INTEGRATING BIOLOGY AND GENETIC SCREENING 

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CASR AND ADH1: INTEGRATING BIOLOGY AND GENETIC SCREENING 

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Announcer:
Welcome to CME on ReachMD. This episode is part of our MinuteCE curriculum.

Prior to beginning the activity, please be sure to review the faculty and
commercial support disclosure statements as well as the learning objectives. 

Dr. Schweiger: 
Hello, everybody. Thank you for joining us today. My name is Michelle Schweiger.
And I'm the Director of Pediatric Endocrinology here at Cedars Sinai Medical
Center. And it's with great pleasure to have Dr. Michael Levine, from Children's
Hospital of Philadelphia as our speaker here today as well.

Dr. Levine: 
Greetings from Philadelphia, everybody. It's a pleasure to be here. And I look
forward to our discussion, Michelle.

Dr. Schweiger: 
And our topic for today is the biology of calcium-sensing receptor mutations.

So, Dr. Levine, we know that the calcium-sensing receptor is a member of the
super family of heptahelical transmembrane receptors that are coupled to G
protein-dependent signaling pathways. Can you please tell us about the
calcium-sensing receptor, where it is expressed and how it functions?

Dr. Levine: 
That's a great question, Michelle. The calcium-sensing receptor is a very large
protein with over 1,000 amino acids. It is, as you point, out a G
protein-coupled receptor, so it's part of his super family of receptors that
bind ligands, such as TSH, PTH, ADH, and many other hormones and
neurotransmitters. So, the signaling mechanism of the calcium-sensing receptor
to use a G protein as a signal transducer is a well-known paradigm in
endocrinology and in many other areas of biology.

The calcium-sensing receptor exists as a dimer, and it's ubiquitously expressed,
although it's important to note that it's most highly expressed in the
parathyroid cells, particularly the chief cells, as well as in the kidney,
particularly along the thick ascending limb. The native ligand for the
calcium-sensing receptor is, no surprise, calcium.

And this was really a high watermark in the field of bone and mineral metabolism
when, a number of years ago, Ed Brown and his colleagues identified the
calcium-sensing receptor as a receptor for calcium. And this expanded the
repertoire of biological processes that we associate with calcium. Not only is
calcium important in neuromuscular physiology as a cofactor for many enzymes and
clotting factors, also important for stimulus contraction coupling in muscle
cells, as well of course, as being involved in calcification of the skeleton.

But now we can consider calcium as a ligand and as an endocrine hormone. And
binding of calcium to the calcium-sensing receptor leads to activation of a
number of G proteins, most importantly, Gq and G11, which coupled to
phospholipase C type beta. And activation of phospholipase C leads to hydrolysis
of membrane-bound phospho inositol 4,5 bisphosphate, which yields two important
products, diacylglycerol as well as IP3. And the diacylglycerol activates
protein kinase C, which then activates an entire repertoire of signaling events
that are coupled to protein kinase C. And the IP3 will bind to specific
receptors on the endoplasmic reticulum that allows stored calcium to be released
into the cytosol, thereby increasing cytosolic calcium levels. So, binding of
the calcium-sensing receptor to its receptor outside the cell leads to increases
in cytosolic calcium inside the cell, but that calcium comes from storage pools
within the cell. And as cytosolic calcium levels increase within the parathyroid
cell, there is inhibition of production of PTH, as well as inhibition of PTH
secretion.

Now, in addition to all of these, I think, marvelous signaling properties, it's
important to note that this is a very different mechanism by which calcium is
affecting release of a hormone. In the parathyroid cell, increased cytosolic
calcium decreases secretion of PTH, the hormone that's stored in the cell,
whereas in nearly every other cell, an increase in intracellular calcium leads
to an increase in secretion of the stored hormone. And the basis for this
contrasting physiology, the parathyroid versus the rest of the endocrine world,
remains an unsolved mystery.

Now, the calcium-sensing receptor on the parathyroid chief cell provides an
exquisitely sensitive mechanism for the parathyroid cell to sense the level of
extracellular ionized calcium. And there's a sigmoidal curve with a very steep
portion that describes the relationship between increasing levels of
extracellular ionized calcium and decreasing secretion of PTH. And the
recognition of the central role of the calcium-sensing receptor in controlling
not only PTH production, but also PTH secretion, really, I think encouraged
study of the calcium-sensing receptor as a therapeutic target for manipulating
or controlling the release of PTH from the parathyroid glands. So, this opened
up a whole new field of pharmacology with the calcium-sensing receptor as a
target molecule.

The other thing we should remember is that, in the kidney, particularly in the
thick ascending limb of the nephron, the calcium-sensing receptor can inhibit
reabsorption of calcium, sodium, and water. So, we have to think of it as more
than just inhibiting the reabsorption of calcium. And together, if we think of
the two major targets, the calcium-sensing receptor in the parathyroid and in
the kidney, the activation of signaling in these two tissues, explains the low
level of PTH, the decrease in secretion of parathyroid hormone with hypocalcemia
and the increase in urinary calcium excretion, both can be completely explained
by the gain of function in the calcium-sensing receptor.

So, the excess of urinary calcium excretion in patients with ADH1, which is a
hallmark of this condition and differentiates it from other forms of
hypoparathyroidism, really represents a sort of double whammy, if you will, the
loss of PTH, which can increase reabsorption of calcium, and the activation of
the calcium-sensing receptor, which now decreases calcium reabsorption. So, the
loss of calcium in the kidney is the result of two different lesions.

Dr. Schweiger: 
Thank you. That was really very helpful. So, some of the key points on that is
the intricacies of the calcium-sensing receptor, both on the kidney and in the
parathyroid gland. And just kind of any kind of gain of function mutation or
loss of function mutation can really kind of alter the calcium secretion and PTH
function. Thank you.

Dr. Levine: 
Exactly, exactly.

Dr. Schweiger: 
So, the next question that I had is, we know that the calcium-sensing receptor
is also implicated in familial hypercalcemia hypercalciuria. Tell us how this
same receptor can be involved in ADH1 and familial hypocalcemic hypercalciuria,
which are remarkably contrasting disorders of mineral metabolism?

Dr. Levine: 
That's a great question, Michelle. This is an example of what I think is an
exceedingly pleasing bit of biological symmetry. And there are many other G
protein coupled receptors, as well as G proteins that can have mutations that
lead to either a gain or function or loss of function, and which result in
contrasting phenotypes, which I think is really quite remarkable. I'm always
reminded of Gs alpha, where the loss of function leads to
pseudohypoparathyroidism and resistance to PTH and TSH, and then McCune-Albright
syndrome, where the gain of function can lead to overactivity in some of the
same tissues that are affected by the hormones in which this resistance and
pseudohypoparathyroidism. So, this is a well-worn paradigm.

In FHH, familial hypocalciuric hypercalcemia, there is a loss of function
mutation that leads to an inability of the parathyroid cell to sense
extracellular calcium. And in this scenario, the parathyroid cell thinks that
the serum calcium level is too low, and this leads to increased secretion of PTH
and hypercalcemia. In the kidney, the loss of activity of the calcium-sensing
receptor leads to increased reabsorption of calcium, so there's very little
calcium in the urine in patients who have FHH. This whole mechanism is amplified
in patients who have neonatal severe hyperparathyroidism, due either to dominant
negative mutations in an allele of the calcium-sensing receptor, that leads to a
loss of activity not only in the pathogenic allele but also in the protein made
by the normal allele. Or even in those cases where there are biallelic
mutations. Here, the complete loss of calcium-sensing receptor proteins leads to
an inability of the parathyroid cell to detect calcium. And babies are born with
very high levels of PTH, life-threatening hypercalcemia, severe metabolic bone
disease that often impairs their ability to breathe because of the effect of
high PTH on the ribcage. So, FHH and neonatal severe hyperparathyroidism
represent one end of the spectrum of calcium-sensing receptor disorders. In this
case, there is a loss of function.

And in the other case, ADH1, we have the gain of function. And again, the target
molecule here is the calcium-sensing receptor. And this is led and encouraged
work to use the calcium-sensing receptor as a therapeutic target. And we know
that using calcium mimetics type 2 allosteric regulators of the calcium-sensing
receptor can, in many cases, reduce secretion of PTH, normalize serum calcium
levels. And as we'll hear in a little bit, the calcilytic drugs have also been
used now in preclinical and emerging clinical studies to decrease sensitivity of
the calcium-sensing receptor, shift the curve to the right. And by reducing
activity of the calcium sensing receptor, you can actually increase secretion of
PTH, thereby normalizing serum levels of calcium.

Dr. Schweiger: 
Thank you. The next question I had was the discovery that mutations that
activate the calcium-sensing receptor are the basis for ADH1 provides us with a
molecular testing strategy. Please tell us how you screen for mutations in the
calcium-sensing receptor, and how genetic testing can be used to diagnose ADH1?

Dr. Levine: 
That's a great point, Michelle. And I think that the availability of molecular
genetic testing has really changed the way that we approach the diagnosis of
complex and difficult clinical disorders these days, particularly in
endocrinology, where we have been fortunate to elucidate the molecular cause of
so many of the diseases that we treat. And using a molecular genetic strategy,
either knowing a gene or using a panel of genes can enable us to quickly
determine what the root cause of the disorder is, and then begin to develop a
therapeutic management plan based on knowledge of the underlying genetic defect
and the pathways that are affected.

For the calcium-sensing receptor, over 400 mutations have been identified in
patients with familial hypocalcemic hypercalcemia, FHH, or in patients with
autosomal dominant hypocalcemia type 1, ADH1. And the vast majority of these
mutations are small point mutations that can be identified by sequencing
strategies such as Sanger sequencing, or the newer technologies called next
generation sequencing.

So, I think an early appreciation that genetics can provide us with the proper
diagnosis in patients with hypoparathyroidism, really means that we want to be
doing genetic testing earlier rather than later, once we've made a diagnosis of
hypoparathyroidism. And because ADH1 is a condition that reflects a germline
mutation in the calcium-sensing receptor, the mutation will be present in all
the cells of a patient. This means that the patient may have inherited the
mutation and certainly means the patient can transmit mutation. And again,
because it's a germline mutation, and the mutation is present in DNA from all
cells, you can use DNA from a variety of different cells to do the analysis. So,
cells that are present in saliva, or even in peripheral blood samples, are very
useful sources of DNA for the kinds of analyses that we need to do in order to
identify the mutation in the calcium-sensing receptor.

Now, I should mention that Calcilytix and PreventionGenetics have formed a
partnership to provide no-cost sponsored genetic testing for patients in the
United States and Canada, who have a diagnosis of hypoparathyroidism or
hypocalcemia. That's non-surgical in its basis. And this free testing uses next
generation sequencing to interrogate a panel of nearly 30 different genes, which
includes the calcium-sensing receptor. And the testing is extremely useful. It's
sensitive, it looks at all the exons in the calcium-sensing receptor, as well as
10 to 20 bases in the introns that flank each exon. And the results are reported
as a standard clinical report with an interpretation provided by
PreventionGenetics, that is consistent with ACGM guidelines.

Using this, one can identify mutations in patients with ADH1. And not only is
this important for them guiding the appropriate treatment of patients with ADH1,
but it also now enables family testing to occur. And although 80% of patients
with ADH1 will have an effective relative who has ADH1, only about 25% of
patients with ADH1 are identified because of family screening. So, once you've
identified the genetic defect in the calcium-sensing receptor, it's easy then to
screen all the other first-degree relatives with a serum calcium and a genetic
test, looking for the mutation.

This is also critically important because there's a very long gap in diagnosis
of ADH1. The median age which patients with ADH1 are diagnosed with
hypoparathyroidism is 4 years. But the median age at which ADH1 is diagnosed is
25 years of age. So, we can close this gap by going to earlier genetic testing
in order to identify patients with calcium-sensing receptor mutations.

And I would add to that, that the other important part of doing the family
screening is that many patients will be asymptomatic, and they would not have
been identified as having this condition without doing some kind of family
screening. And you know, people ask the question all the time, why screen
asymptomatic patients? How do you make the asymptomatic patient feel better? And
it turns out as with many other chronic endocrine disorders, once you treat a
patient, they realize that they were not asymptomatic, and they begin to feel
much better with treatment. So, I think that provides yet another incentive for
us to identify patients with ADH1 who may consider themselves to be asymptomatic
because treatment can make them feel better.

Dr. Schweiger: 
Sounds good. So, it sounds, you know, that we need to have a heightened
awareness not only for our symptomatic patients with autosomal dominant
hypoparathyroidism, but also being on the lookout for these asymptomatic
patients that might not be so readily available as far as diagnosis is easy to
tell. Because in these patients, they also have an increased risk for basal
ganglia calcifications, seizure disorders, and nephrocalcinosis. And so, if we
can, you know, evaluate these patients early and get them diagnosed, we can help
prevent some of these complications.

Dr. Levine:
Correct.

Dr. Schweiger:
Thank you, everyone, for joining us today. Wishing everyone a very great day
from here in sunny California. Thank you.

Dr. Levine: 
And bye-bye from Philadelphia.

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You have been listening to CME on ReachMD.  This activity is jointly provided by
Global Learning Collaborative (GLC) and TotalCME, LLC. and is part of our
MinuteCE curriculum.

To receive your free CME credit, or to download this activity, go to
ReachMD.com/CME. Thank you for listening.

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 * OVERVIEW
   
   Autosomal Dominant Hypocalcemia Type 1 (ADH1) is caused by gain-of-function
   variants of the CASR gene encoding the calcium-sensing receptor (CaSR),
   resulting in hypocalcemia, inappropriately low parathyroid hormone levels,
   and hypercalciuria. While this has been defined and reported upon, the role
   CaSR plays in maintaining calcium homeostasis and the potential role it might
   have in different patient types (from pediatric to adult population) is not
   well understood clinically. Furthermore, with newly published data imminent
   surrounding encaleret, providers must be knowledgeable about the implications
   associated with the new literature and the implications it has towards the
   practice of hypoparathyroidism. 


 * TARGET AUDIENCE
   
   This activity has been designed to meet the educational needs of
   endocrinologists, nephrologists, neurologists, pediatricians, geneticists,
   physician assistants, nurse practitioners, as well as other clinicians
   involved in the management of patients with hypoparathyroidism. 


 * LEARNING OBJECTIVES
   
   After participating in this educational activity, participants should be
   better able to: 
   
    * Discuss CASR gene mutations and their role in hypoparathyroidism 
    * Assess future treatments for ADH1 in hypoparathyroidism


 * ACCREDITATION AND CREDIT DESIGNATION STATEMENTS
   
   In support of improving patient care, this activity has been planned and
   implemented by Global Learning Collaborative (GLC) and Total CME, LLC. GLC is
   jointly accredited by the American Council for Continuing Medical Education
   (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the
   American Nurses Credentialing Center (ANCC) to provide continuing education
   for the healthcare team.
   
   This activity was planned by and for the healthcare team, and learners will
   receive 1.0 Interprofessional Continuing Education (IPCE) credit for learning
   and change.


 * DISCLOSURE OF RELEVANT FINANCIAL RELATIONSHIPS
   
   Disclosure Policy
   In accordance with the ACCME Standards for Integrity and Independence, Global
   Learning Collaborative (GLC) requires that individuals in a position to
   control the content of an educational activity disclose all relevant
   financial relationships with any ineligible company. GLC mitigates all
   conflicts of interest to ensure independence, objectivity, balance, and
   scientific rigor in all educational programs. 
   
   The following faculty have disclosed:
   
   Michael A. Levine, MD, FAAP, MACE, FACP, faculty for this educational event,
   receives research grant and manages funds for Shire and Calcilytx; and
   receives consulting fees for Shire.     
   
   B. Michelle Schweiger, DO, MPH, faculty for this educational event, has no
   relevant financial relationships with ineligible companies


 * PLANNERS AND MANAGERS DISCLOSURE LIST
   
   The following planners/reviewers/managers have disclosed:
   
   William Mencia, MD, FACEHP, CHCP, reviewer for this educational event, has no
   relevant financial relationships with ineligible companies.
   
   Total CME, LLC., planners, and managers have no relevant commercial
   relationships to disclose.
   
   All the relevant financial relationships for these individuals have been
   mitigated.


 * DISCLAIMER
   
   The views and opinions expressed in this educational activity are those of
   the faculty and do not necessarily represent the views of GLC and Total CME,
   LLC. This presentation is not intended to define an exclusive course of
   patient management; the participant should use their clinical judgment,
   knowledge, experience, and diagnostic skills in applying or adopting for
   professional use any of the information provided herein. Any procedures,
   medications, or other courses of diagnosis or treatment discussed or
   suggested in this activity should not be used by clinicians without
   evaluation of their patient's conditions and possible contraindications or
   dangers in use, review of any applicable manufacturer’s product information,
   and comparison with recommendations of other authorities. Links to other
   sites may be provided as additional sources of information. Once you elect to
   link to a site outside of MedEd On The Go, you are subject to the terms and
   conditions of use, including copyright and licensing restrictions, of that
   site.
   
   Reproduction Prohibited
   Reproduction of this material is not permitted without written permission
   from the copyright owner.


 * PROVIDER(S)/EDUCATIONAL PARTNER(S)
   
   Jointly provided by Global Learning Collaborative (GLC) and Total CME, LLC.


 * COMMERCIAL SUPPORT
   
   This activity is supported by an independent educational grant from
   Calcilytix Therapeutics.


 * INSTRUCTIONS FOR COMPLETION
   
   During the period 03/22/2024 through 03/22/2025, registered participants
   wishing to receive continuing education credit for this activity must follow
   these steps:
   1. Read the learning objectives and faculty disclosures.
   2. Answer a pre-program question.
   3. View the program.
   4. Complete the post-test with a score of 100%. 
   5. Complete activity evaluation.
   6. Apply for credit and either bank your credits or print your certificate.
   
   For Pharmacists: Upon successfully completing the post-test with a score of
   100% and the activity evaluation form, transcript information will be sent to
   the NABP CPE Monitor Service. This may require you to add or update the
   e-profile ID/date of birth information saved in your account.


 * SYSTEM REQUIREMENTS
   
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    * Recommended Internet Speed: 5Mbps+
   
   


 * PUBLICATION DATES
   
   Release Date: 03/22/2024
   
   Expiration Date: 03/22/2025
   
   


Michael A. Levine, MD, FAAP, MACE, FACP
B. Michelle Schweiger, DO, MPH
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Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

Managing Myelofibrosis with a Patient-Centered Approach

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Schedule30 Sep 2024
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