141. Acute Hepatic Porphyria: Beware the Zebra (CE)

Rare Disease Day takes place on the last day of February every year. More than 30 million people in the United States are affected by over 7,000 rare diseases. Acute hepatic porphyria (AHP) is one of these rare diseases and carries with it a substantial disease burden. Delayed diagnosis, misdiagnosis and missed diagnosis frequently occur in the journey of the person living with AHP, with the average time from symptom onset to diagnosis being 15 years.

On today’s episode, nurse practitioners (NPs) Drs. Laurie Connors and Paula Tucker discuss the clinical presentation and symptoms that are associated with AHP as well as management, attack prevention and treatment strategies. NPs are important members of the collaborative care team for people living with this condition and their families.

A participation code will be provided at the end of the podcast — make sure to write this code down. One you have listened to the podcast and have the participation code, return to this activity in the CE Center. Click on the "Next Steps" button of the activity and

1. Enter the participation code that was provided.
2. Complete the post-test .
3. Complete the activity evaluation.

This will award your CE credit and certificate of completion. 0.75 CE, 0.25 RX, will be available through Feb. 28 , 2026.

 

This activity is supported by an independent educational grant from Alnylam.

Episode Transcript

(00:13):
- From the American Associationof Nurse Practitioners,
I'm the host of today'sspecial edition episode, nurse
practitioner and educationspecialist Patty Scalzo.
And this is NP Pulse, thevoice of the nurse practitioner.
Welcome to NP Pulse, AANP’s podcast,

(00:36):
bringing you uniquenurse practitioner voices
and expertise on issues thatmatter to NPs and our patients.
As always, be sure to subscribeto this podcast, share
with your colleagues, and check back often
for new conversationswith nurse practitioners
and healthcare leadersfrom across the nation.
NP Pulse podcast listenersmay claim CE credit

(00:58):
for this program through February, 2026.
After you listen to the podcast,
view aanp.org/cecenter
register for this activity.
Enter the participation code
provided at the end of this podcast
and then complete thepost-test and evaluation.
Rare Disease Day takes placeon the last day of February

(01:20):
every year. A rare diseaseis defined as a disease
or condition that affectsfewer than 200,000 people in
the United States.
Acute hepatic porphyria isone of these rare diseases
and it is associated withsubstantial disease burden.
On today's podcast, we're joinedby nurse practitioners
Dr. Laurie Connors and

(01:41):
Dr. Paula Tucker to discussacute hepatic porphyria
and why it is so important
to keep this conditionin your differential.
The average time from the onsetof symptoms to diagnosis is
15 years,
and this delay preventspeople from receiving timely
treatment and can lead toworsening of complications.

(02:01):
Dr. Laurie Connors is anassociate professor at the
University of South Floridain the College of Nursing.
Dr. Connors is triple board certified
as a family nurse practitioner
and advanced practice nursein both genetics and oncology.
Her commitment to nursing science
and translational genomics isevident in a successful NIH

(02:22):
funded research program and leadership
as the past president ofthe International Society
of Nurses in Genetics.
Dr. Paula Tucker is a clinicalassociate professor at Emory
University, Nell HodgsonWoodruff School of Nursing,
where she is the specialty director
of the emergency nursepractitioner program.

(02:42):
In addition to herteaching responsibilities,
Dr. Tucker currently practices
as an emergency nursepractitioner at a level one trauma
center in Atlanta, Georgia.
It is my pleasure to welcomeour nurse practitioner experts,
Laurie and Paula.
- Thank you for that introduction.
I'm honored to share in hostingthis podcast titled Acute

Hepatic Porphyria (03:03):
Beware the Zebra with my NP colleague, Dr.
Laurie Connors.
As an emergency nurse practitioner,
I often have the privilege of caring
for patients in acute conditions.
Having the opportunity toprovide awareness on this rare
and often misunderstoodcondition is truly a privilege.

(03:24):
You see, as clinicians, we'retaught early on to think
of horses, not zebras, particularlywhen we hear hoof beats.
In other words, when a patientpresents with symptoms,
we focus on the most common
and likely causes ratherthan rare diseases.
But sometimes that approach leads us
to miss something crucial,

(03:44):
and that's exactly what happens
with acute hepatic porphyrias.
And for the remainder ofthis podcast, I will refer
to this acute hepaticporphyria as AHPs, a group
of rare genetic diseases
that affect fewer than 200,000people in the United States.
Because they are uncommon,AHPs often remain undiagnosed

(04:08):
or misdiagnosed for yearsleaving patients struggling
with unexplained symptomsand repeated hospital visits
before anyone evenconsiders the possibility.
AHPs can affect anyoneregardless of race or gender.
But here's something criticalfor clinicians to know.
80% of cases occur in womenbetween the ages of 15 and 45.

(04:31):
This means that when ayoung female presents
with severe unexplainedabdominal pain, we need
to expand our differential
beyond the usual suspects likeappendicitis, pancreatitis,
cholecystitis, irritable bowel syndrome.
If we don't, we riskoverlooking a potentially
life-threatening condition.

(04:52):
The challenge with AHP is
that it doesn't fit neatlyinto the single specialty.
It presents with a mix ofgastrointestinal, neurological,
and even autonomic systems,
which means patients often bounce
between gastroenterologists,neurologists, psychiatrists,
and emergency providers, eachtreating different aspects

(05:15):
of their illness withoutever connecting the dots.
And that's why raising awareness
among nurse practitioners is so important.
So what exactly is AHP?
I'm going to turn it overto my colleague, Laurie,
to break it down for us.
Laurie, take it away.
- Thanks, Paula. Yes,my name's Laurie Connors,

(05:35):
and as a genetic nursepractitioner, I'm so honored
that we can be here today.
As Paula mentioned,this is a rare disease,
but that means low awareness.
Our goal is to create awarenessand elevate diagnosis.
So what are AHPs?
AHPs are primarily causedby a genetic mutation

(05:55):
that we now say genetic variant.
This occurs in one of theenzymes involved in heme
biosynthesis in the liver.
This may sound complicatedIn simple terms, one
of the enzymes in the hemepathway does not work properly.
Heme is essential to our body
and is necessary for the liverto function. In the liver

(06:19):
the heme pathway is controlled
by the enzyme ALAS1.
With AHP disease,
what happens is there's anaccumulation of ALAS1
and the enzyme is not able to keep up.
This leads to an accumulationof neurotoxin intermediates,

(06:41):
a buildup of toxins calledporphyrins in the liver.
The two main porphyrins we willtalk about are ALA and PBG.
There are different types.
The most common is acuteintermittent porphyria.
This is caused by a pathogenicvariant in the HMBS gene.

(07:04):
The next type is hereditary coproporphyria,
which is caused by avariant in the CPOX gene.
The third is variegateporphyria, which is caused
by a variant in the PPOX gene.
These three are all inheritedin an autosomal dominant
pattern, and we will discuss
that a little bit later inthe podcast, what that means

(07:26):
for the individualpatient and their family.
The fourth subtype is ALA deficiency porphyria
and is caused by avariant in the ALA gene.
This is a very rare subtypeand is autosomal recessive.
Next, Paula is gonna talk
to us about acute attacksin clinical presentation

(07:47):
of this disease.
- Thanks, Laurie, for setting the stage.
Now let's dive into the history
and clinical presentation of AHPs.
These rare conditions canbe incredibly challenging
to recognize, butunderstanding the patterns
and key features is critical
for early diagnosis and intervention.

(08:08):
So let's start with acuteattacks. The hallmark of AHP.
For most patients, theseattacks are infrequent
and intermittent.
They may only have oneor two in their lifetime,
but for about 10% of patients,these attacks are recurrent,
meaning they happen fouror more times a year.

(08:29):
This small group carries amuch higher disease burden
with frequent hospitalvisits, significant pain
and reduced quality of life.
Now, what are thetriggers of these attacks?
There are several well-documentedtriggers clinicians
should be aware of.
First, let's talk about medications.
Some drugs are known toprecipitate AHP attacks

(08:52):
because they increaseenzyme activity in the heme
synthesis pathway.
These include sulfonamides,barbiturates, rifampin,
and metoclopramide.
And this is why it's so important
to carefully review medicationsin patients with known
or suspected AHP.
Next is alcohol and cigarette smoking.

(09:15):
Alcohol disrupts metabolic pathways,
and smoking introduces toxins
that exacerbate oxidative stress, both
of which can trigger an acute episode.
Hormonal changes are another big one,
especially in women of childbearing
age. Fluctuations during the luteal phase
of the menstrual cyclecan precipitate attacks,

(09:38):
which is particularlysignificant since 80%
of AHP cases occur inwomen between the ages
of 15 and 45.
Then there's stress.
And this can take on many forms,
physical stress like infections, surgery
or trauma, emotional stress,
or even dietary changes such as fasting

(10:00):
or extreme dieting.
Any of these can destabilizethe metabolic balance
and lead to an attack.
And here's an interesting point.
Not every attack has an obvious trigger.
Some episodes occur withoutany clear precipitating factor,
making it even harderto predict or prevent.

(10:20):
Now let's talk about thesigns and symptoms of AHP.
During an attack. AHP hasa classic triad of symptoms
that can help guide our diagnosis.
The first is severediffuse abdominal pain,
which happens in about 90% of cases,
and this pain is often out of proportion

(10:41):
to the physical exam findingsor even imaging results.
The second is peripheral neuropathy,
which can affect the autonomic, central
and peripheral nervoussystems leading to numbness,
tingling, or even paralysis.
And the third is centralnervous system dysfunction,
which can manifest as confusion,agitation, hallucination,

(11:03):
or even seizures.
But the presentation doesn't stop there.
Patients can also experiencepain in other regions
of their body, such as the lower back
or extremities, nausea,vomiting, and hypertension
or tachycardia, often as partof the autonomic instability.
Electrolyte imbalances likehyponatremia are also common.

(11:28):
In severe cases, patientsmay develop seizures
or psychiatric symptoms suchas agitation or hallucination.
And in the subtypes of AHPknown as varigate porphyria
and hereditary coproporphyriapatients can also develop
cutaneous symptoms like blistering

(11:48):
and photosensitivityfollowing sun exposure.
So without treatment, AHPattacks can progress rapidly,
and in the most severe cases,
respiratory paralysisbecomes a very real risk,
which makes timely recognitionand intervention critical.
So now that we've exploredhow AHP presents, Laurie,

(12:11):
can you walk us through the complications
and diagnosis of AHP? It's all yours,
- Certainly, Paula.
This is a chroniccondition and undiagnosed
there can be chronic complications.
These patients have intermittentepisodes of abdominal pain,
so they have chronic pain,sleep disorders, fatigue,

(12:34):
and they also have moodand affective disorders.
Because of the chronic pain,they tend to have high rates
of opioid use.
As you might imagine,
the toxicity within the livercan create an inflammatory
response, and these repeatedepisodes causing this
inflammation significantlyincreases an individual's risk

(12:56):
of primary liver cancer.
In fact, their risk of primaryliver cancer is 38 times
higher than the general population.
Other potential sequelaeinclude non hepatic cancers,
neuropathies, hypertension,and chronic kidney disease.
Prognosis is fairly good,generally comparable

(13:18):
to the non HP population.
Assuming they do not have problems
with respiratory depression.
Diagnosis is a challenge.
Diagnosis is oftendelayed, misdiagnosis
or missed diagnosis altogether.
The average time from symptom onset

(13:40):
to establishing definitivediagnosis is 15 years.
Consider how many episodesthis individual has experienced
in order to get to that diagnosis.
Many of these individualshave unnecessary surgical
treatment and other treatments
because they're presentingwith an acute abdomen.

(14:02):
Certainly we need to ruleout a surgical abdomen
and evidence of intestinal obstruction.
However, we also need
to have you consider AHP inyour differential diagnosis.
When that patient presentswith acute abdominal pain.
The testing is fairly straightforward.

(14:23):
Remember, there are theseneurotoxins in the liver
that are eventually excretedin the urine.
So you can check the levelof porphyria in the urine.
You can also specificallycheck PBG and ALA.
That is in the acute setting.
If you wanna find theexact subtype of AHP,

(14:45):
you would need to do genetic testing.
For example,
if acute intermittent porphyriais in your differential,
you would wanna testspecifically for the HMBS gene.
For most intents and purposes,
most nurse practitioners arenot going to go down the route
of genetic testing,
but certainly urine testingis very easily accessible

(15:09):
and can establish the diagnosis and
therefore get this patientto the necessary treatment.
- Now, let's shift our focuson the management, both
for the short term during an acute attack
and over the long term toimprove patient's quality of life
and prevent future attacks.

(15:31):
AHP management is complex
and patients may present forcare in a variety of settings.
So it's important for clinicians across
specialties to be prepared.
Patients with AHP mightfirst show up in the emergency
department, often during an acute attack
with severe abdominal pain,nausea, or neurologic symptoms.

(15:53):
But they may also initiallypresent in primary care
with more subtle non-specificcomplaints like fatigue
or chronic pain.
Others might find themselvesreferred to specialists such
as gastroenterologists,hematologists, hepatologists,
or geneticists, especially ifsymptoms remain unexplained
after multiple events, no matter

(16:15):
where these patients present.
The key is recognizing the condition early
so we can intervene appropriately.
So let's talk aboutthe goals of treatment,
which fall into three main areas.
First, we aim to treat acuteattacks, stopping symptoms,
and stabilizing the patient.
Second, we focus on reducingthe risk of future attacks,

(16:37):
which means helpingpatients avoid triggers
and using preventivetreatments when needed.
Finally, we look atpharmacotherapies to prevent attacks
for patients with recurrent symptoms along
with cascade screening
and genetic counseling
to help family membersunderstand their risk.
Now, when it comes tomanaging acute attacks,

(16:59):
the cornerstone treatmentis IV hemin therapy.
This drug has been around since the 1980s
and has a long history of success
according to multiple studies. Hemin works
by blocking the productionof ALA synthase,
which is the enzyme thatdrives the buildup of toxic
heme precursors.

(17:20):
It's administered as a three
to four milligram per kilograminfusion over four days
and is most effective whengiven early in an attack.
But here's an important tip.
Hemin should always be reconstituted
with human serum albumin
to reduce infusion related side effects.
Now, in addition to hemin, the use

(17:41):
of symptom directed treatments
to address the patient'simmediate needs are also provided.
So for example, painmanagement is often necessary,
and in many cases, opioids are required
to control severe pain. Antiemetics
to help relieve nausea and vomiting.
We also need to keepan eye on electrolytes,

(18:04):
particularly sodium and magnesium.
Since hyponatremia
and hypomagnesemia arecommon during acute attacks
and can complicate therecovery. For mild cases,
IV glucose can sometimessuffice to stop the attack.
But for moderate to severe attacks,
hemin is the gold standard. For patients

(18:25):
with recurrent AHP attacks
the focus shifts to prevention.
While IV hemin is indicatedto treat the symptoms
of acute attacks of AHP, itis sometimes used off-label
for prophylactic management,even though it's effectiveness
for this is less clear.
This approach has been shownto reduce the frequency

(18:45):
of attacks, but it does come with risk.
For example, patientsreceiving regular infusions may
develop iron overload
or face infection risk ifthey require a central line
for administration.
Now, Laurie, will you share
with us a newer therapy onthe market for managing AHP?
- Certainly, Paula, this isan exciting time in genetics.

(19:09):
It has been discovered that the inhibition
of ALAS1 can reduce the accumulation
of these neurotoxins in the liver.
ALA and PBG are the reasonswhy we see the clinical
manifestations in AHP.
So this medication givosiran.

(19:29):
This is a treatment approved for AHP
and it lowers ALAS1 level,
thereby reducing PBG and ALA production
and reducing acute attack rates.
How does it work?
This medication is a small interfering RNA
that targets hepatic ALAS1 messenger RNA.

(19:54):
The downregulation of ALAS1 messenger
RNA prevents the accumulation
of the neurotoxins fromdeveloping in the first place.
The givosiran molecule,
the small interfering RNA is conjugated
to a delivery system.
The delivery system isselective for hepatocytes

(20:14):
by selectively bindingtransmembrane receptors
found on these cells.
Downregulation of ALAS1 messenger RNA,
prevents accumulation of the neurotoxins.
That is the take home message.
We now have a treatmentto prevent these attacks.
The dosing and administrationis fairly simple.

(20:36):
It is administered viasubcutaneous injection in an office
setting once a month.
But certainly there needs
to be education on lifestyle counseling
and multidisciplinary management.
Patients need to beengaged in their healthcare
and be counseled on the useof a medical alert bracelet,
avoidance of triggers thatcan exacerbate the attacks

(20:58):
and when to seek medicalcare for acute symptoms,
recognizing and respondingto prodromal symptoms
before an attack, knowingwhat medications to avoid,
how to treat their pain, andcertainly support groups.
- So now that we've exploredthe key features of AHP,
let's bring it to life with a case study.

(21:21):
So we have Sarah, a 23-year-old female
who presented multiple timesto the emergency department
with severe crampy abdominalpain that seemed out
of proportion to any physical findings.
She also experienced nausea,vomiting, tachycardia,
and occasional confusion.
Her initial workup includedCT scans of the abdomen

(21:42):
and pelvis, which repeatedlycame back normal ruling out
appendicitis, cholecystitis,
and other common causes of abdominal pain.
As part of the diagnostic process,
Sarah was prescribed severalmedications over the course
of her visits, includingantispasmodics, antiemetics,
and even antibioticsfor presumed infections.

(22:05):
However, none of these treatmentsprovided lasting relief
and her symptoms persisted.
At one point, she was prescribeda medication containing
sulfonamides, which unknowinglytriggered an acute attack,
worsening her condition.
Sarah's symptoms includedthe classic triad,
which is seen in AHP. Severediffuse abdominal pain,

(22:27):
which she described as unrelenting
and unlike any pain she'd experienced
before. Peripheral neuropathy,which caused numbness
and tingling in her extremities.
Central nervous systemdysfunction, which included periods
of confusion and agitation.
In addition to the triad, Sarahalso exhibited hypertension

(22:47):
and hyponatremia duringher acute episodes,
which were further clues pointing to AHP.
After a nurse practitionerconsidered AHP in the
differential, a thorough historyrevealed several potential
triggers for her attacks.Alcohol consumption
during social events. A crash diet

(23:08):
she had tried to lose weight rapidly.
Recent use of sulfonamidecontaining medication
for a presumed infection
and emotional stress that wasrelated to work deadlines.
A urine PBG ALA
and porphyrin test was ordered,
which returned markedly elevated levels,

(23:30):
confirming the diagnosis of AHP.
Genetic testing followed,
identifying a specific mutation
responsible for her symptoms.
Once Sarah was stabilized with IVglucose
and hemin therapy, her careshifted to long-term management
and prevention of future attacks.
Her team provided extensivelifestyle counseling,

(23:53):
which included avoiding theknown triggers such as alcohol,
cigarette smoking,
and fasting, educating herabout medications to avoid
with a comprehensive list of unsafe drugs
provided for a reference,
recommending a medic alert bracelet
to alert healthcare providersto her diagnosis in case

(24:13):
of emergencies, encouragingher to seek early medical care
for any symptoms, especiallyif she experienced severe pain,
neurologic changes orautonomic instability,
and even connecting her tosupport groups for patients
with AHP, allowing herto share experiences
and learn coping strategies from others
with similar challenges.

(24:34):
And then discussing theimportance of genetic testing
for family members
and provide appropriatecounseling and monitoring.
With these changes, Sarahexperienced far fewer attacks
and regained control of her life.
She became more aware of her triggers
and was empowered to advocate
for herself in healthcare settings.

(24:54):
Her involvement in a support group also
provided emotional reassurance
and practical advice fromothers living with AHP.
So the key to managing AHP lies not only in timely
recognition and acute treatment,
but also in holistic patient-centered care
that addresses lifestylefactors, prevention,

(25:15):
and long-term support.
So now that we've explored Sarah's journey
and the clinicalpresentation of AHP, Laurie,
will you guide us throughthe diagnostic process
and genetic testing
and what cliniciansshould keep in mind when
evaluating these patients?
Laurie, over to you.
- Thanks, Paula. Youmentioned person-centered care

(25:38):
and AHP is a great example.
Most hps are inherited in anautosomal dominant pattern,
meaning that eachoffspring has a 50% chance
of inheriting the disorder.
So if you recall in biology,if you have a genetic variant
in a gene and you have a child,

(25:59):
there's a 50 50 chance that
that child will inherit the condition.
They will inherit the genotype,
but they might not developsymptoms of the disease.
Gene variants that cause AHPhave variable expressivity,
meaning many people have apathogenic variant for AHP,

(26:22):
but they have what's called latent disease
and never developsymptoms with the disease.
Therefore, even though thoseoffspring can inherit the
pathogenic variant, it may not be known.
So this information, thisdiagnosis, is not only key
for the person experiencingthe acute attack
to determine the type of AHP

(26:44):
and the causative genetic variant.
It is also important fortheir at-risk family members
to consider cascade testing.
Why? Because we now have a new drug
that can be used in thissetting for chronic disease.
So over five years ago now, in 2019,

(27:05):
the FDA approved treatment
for AHP based on efficacydata from the Envision trial.
The Envision trial was arandomized double-blind,
placebo controlledmultinational trial involving 20
different countries.
Patients were randomized
to receive once monthlysubcutaneous injections of givosiran

(27:26):
or placebo duringsix month period of time.
The primary efficacy endpointwas the rate of attacks
that required hospitalization,urgent healthcare visits,
or the administration of IV hemin at home.
On average, this is significant,
patients with AHP

(27:48):
in the treatment armexperienced 70% fewer
attacks compared tothose in the placebo arm.
This was groundbreakingthat we now have a treatment
for this chronic disease
and is such an example ofhow the NP can collaborate
with specialty care teamsto manage these types

(28:08):
of individuals as well astheir at-risk family members.
Back to you, Paula.
- Thank you, Laurie.
You know, managing AHP iscertainly a team effort.
Nurse practitioners play a keyrole in recognizing the signs
of AHP, initiating timely treatment,
and collaborating with specialists

(28:30):
to ensure the best outcomes for patients.
Let's talk about how nursepractitioners can collaborate
effectively with the specialty care team
and provide resources to patients.
As nurse practitioners,we're often the first point
of contact for patientsexperiencing symptoms of AHP,
whether it's in the emergencydepartment, primary care,

(28:52):
or urgent care settings.
But diagnosing and managing AHP doesn't just stop with us.
It requires close collaboration
with specialists likehematologists, genetic counselors,
and gastroenterologists.
So what is our role?
Recognizing the need for specialty input.
So once a urine PBG test

(29:14):
and other urine test confirms,
AHP, hematology is usuallyconsulted for acute management,
including hemin therapy.Coordinating long-term care,
this involves working with hepatologists
or genetic specialists forcascade screening, surveillance
for complications likehepatocellular carcinoma,

(29:35):
and starting new therapies like givosiran.
Ensuring communication, NPsact as a bridge, ensuring
that patients understand theirdiagnosis, treatment plan,
and follow-up schedule.
Managing AHP can feel quiteoverwhelming for both patients
and providers, but there arefantastic resources available.

(29:58):
The American Porphyria Foundation
and other organizationsprovide ED guidelines
or emergency department guidelines
to help clinicians recognizeand manage acute attacks.
These include informationon symptoms, testing,
and the administration
of IV hemin in the emergency department.
Having these guidelineson hand can be lifesaving

(30:20):
during acute episodes.
The American PorphyriaFoundation offers a wealth
of information for patients and providers.
It includes educationalmaterials, support groups,
and updates on the latesttreatment advances.
And the Global PorphyriaAdvocacy Coalition is another
excellent resourceconnecting patients worldwide

(30:41):
with advocacy tools and community support.
As nurse practitioners,we should be prepared
to guide patients toward theseresources, empowering them
to understand their condition
and take an active role in their care.
So finally, let's bring it all together.
When should we think about AHP?

(31:01):
If a patient presentswith severe abdominal pain
that doesn't fit typical patterns
and imaging rules outconditions like appendicitis,
cholecystitis, or pancreatitis,
AHP should be on yourdifferential diagnosis.
You also wanna be alert forsymptoms that don't align
with other GI conditions,such as nausea, vomiting,

(31:23):
or constipation, reddishcolored urine, tachycardia
or hypertension, hyponatremia
or neurologic symptoms likesensory loss or confusion,
and then pain in other areas of the body,
like the lower back or extremities.
Think about AHP when there aresubtle hints, like a history

(31:44):
of porphyrinogenic drug use,such as barbiturates
or sulfonamides. Symptoms that are worse
during the premenstrualphase of the cycle, exposure
to those known triggerslike alcohol, fasting,
or physical stress.
So the takeaway here is thatwhen you encounter a patient
with severe unexplained,recurrent symptoms,

(32:06):
especially women inthe 15 to 45 age group,
consider AHP.
The earlier we recognize it,
the better the outcomes for the patient.
AHP may be a zebra in the diagnostic
field, but it's a zebra
we all need to watch for.With greater awareness,
collaboration, and the use

(32:27):
of resources we can help these patients
get the care they need.
I wanna thank you for joining us,
and Laurie, thank you
for co-hosting thispodcast, Exploring Acute
Hepatic Porphyria:
Beware of the Zebra.
Do you have anything elseyou wanna share with us
before we close out?
Thanks, Paula. This has been wonderful.

(32:47):
You know, as a nurse practitioner
in family practice for over 25 years
and now having certifications in oncology
and genetics, this is justsuch an important area because
although it's a rare disease,I really have to wonder if
that is because of lowawareness and low diagnosis.
And I think today, ourgoal to create awareness

(33:09):
and elevate diagnosis, I thinkwe've reached that, Paula,
and I think this is gonna behuge so that we can impact
that 15 years from onsetof symptoms to diagnosis.
Thank you for allowing me to contribute.
- Well, thank you so much, Laurie and Paula.
It's been an absolutepleasure listening to you

(33:29):
and gaining your perspective
and insights on this extremely important
topic. To our listeners,
I hope you found this episode educational
and can apply some of what wasdiscussed to your practice.
Join your NationalProfessional Association
and add your voice to over 120,000
of your NP colleagues nationwide.
I urge you to becomean AANP member today.

(33:52):
Membership gives youaccess to so many benefits,
including tools andresources for your practice.
And the AANP CE Center,
which offers a comprehensivelibrary of CE activities
for NPs of all specialties
and experience levels.Exclusive discounts
and many free activities areyours as an AANP member

(34:12):
to help you complete statelicensure requirements
and earn the creditsneeded for recertification.
Remember, you can claimCE credit for this program
through February, 2026,
by logging into the CE center at aanp.org/center.
Register for this program.

(34:33):
Enter the participation code AHP2025.
Again, that's AHP2025, andthen complete the post-test
and evaluation.
Be sure to subscribeto this podcast, share
with your colleagues, and checkback often for new episodes.
Thank you for listening.