Derm: Pemphigoid Gestationis: Free MSRA Podcast

⚕️ FREE MSRA PODCAST – Pemphigoid Gestationis
🎧 A clear, high-yield breakdown of this rare autoimmune blistering condition in pregnancy – perfect for exam prep and clinical diagnosis confidence.

🧠 Key Learning Points

📌 Definition
• Pemphigoid Gestationis (PG) is a rare autoimmune subepidermal blistering disorder that occurs during pregnancy, usually in the 2nd or 3rd trimester.
• It involves IgG1 autoantibodies attacking the basement membrane zone of the skin.

📌 Causes & Risk Factors
• Pregnancy-related immune shifts (autoimmune trigger)
• Linked to hydatidiform mole or choriocarcinoma
• HLA-DR3 and HLA-DR4 associations
• Family or personal history of autoimmune disease
🧠 Mnemonic: “GHOST” – Gestation, HLA-DR3/4, Onset late, Skin attack, Thyroid risk

📌 Pathophysiology
• IgG1 antibodies bind to antigens in the lamina lucida → activate complement (C3)
• Leads to inflammation and dermal-epidermal separation
• Creates subepidermal bullae
• Shares antigenic similarities with bullous pemphigoid

📌 Symptoms
• Severe pruritus – hallmark feature, often before rash
• Begins with urticarial plaques (esp. periumbilical) → evolves into tense blisters
• Spares face, palms, soles, and mucosa in most cases
• Often worsens postpartum, but resolves over weeks/months
• May recur with future pregnancies, OCPs or menstruation

📌 Differential Diagnosis
• PUPPP (more common, lacks blisters)
• Bullous pemphigoid
• Linear IgA dermatosis
• Dermatitis herpetiformis
• Pruritic folliculitis of pregnancy
• Erythema multiforme

📌 Diagnosis
• Clinical picture + skin biopsy (from lesion edge)
• Direct immunofluorescence (DIF): linear C3 deposits at basement membrane
• Indirect immunofluorescence (IDIF): circulating IgG autoantibodies (PG factor)
• HLA-typing (supportive, not diagnostic)
🧠 Tip: DIF = deposits in skin, IDIF = antibodies in blood

📌 Management
• Oral corticosteroids (prednisolone 0.5–1 mg/kg/day) – mainstay
• Antihistamines – symptomatic relief for pruritus
• Emollients for skin comfort
• Severe/resistant cases: consider plasmapheresis or immunoadsorption
• Multidisciplinary care: dermatologist + obstetrician + paediatrician

📌 Complications
• Preterm labour (~20%)
• Small-for-gestational-age (SGA) infants
• Neonatal blisters (5–10%): transient, due to maternal IgG crossing placenta
• Psychological distress, sleep disruption from pruritus

📌 Prognosis
• Self-limiting postpartum, but may recur in future pregnancies or hormonal shifts
• Increased lifelong risk of autoimmune disease (e.g. Graves’, Hashimoto’s, Pernicious anaemia)
• Important for long-term autoimmune screening and counselling

📎 More MSRA Resources for Pemphigoid Gestationis
📝 Revision Notes:
https://www.passthemsra.

Episode Transcript

(00:00):
Welcome to the Deep Dive. This is where we take your
source material, notes, articles, whatever you've got,
and really drill down to pull out the most crucial high yield
information. Today we're zeroing in on a
specific condition, Pemphigoid Gestaciones, and this session is
really designed for you, listener to give you a sharp,

(00:20):
focused revision based directly on the material provided.
Exactly. We're looking at pemphigoid
gestacionis or PG. It's, well, it's not common, but
it has some really distinct features and importantly,
implications that arise because it happens during pregnancy.
Will unpack the key info together OK.
Let's dive straight in then. Pemphigoid gestacionis PG.

(00:40):
First things first, what exactlyis it?
Can you give us that core definition?
Right. So the material defines it as an
autoimmune bolus disease, key things, autoimmune blistering
and happens specifically in pregnancy.
Underlying it all is this process where complement and
sometimes immunoglobulin gets deposited in a very specific
place, the lamina lucido, which is part of the skin's basement

(01:02):
membrane zone. Autoimmune.
So the body is attacking itself essentially.
Precisely. The immune system mistakenly
targets part of the skin, and there's an interesting
historical quirk mentioned in the sources.
It used to be called herpes gestaciones.
Herpes gestaciones. It sounds confusing.
It really was, and the material stresses this.
Despite that name, it has absolutely nothing to do with

(01:23):
the herpes virus 0 connection. It was named purely based on the
appearance of the blisters. Kind of a morphological thing,
not the cause. Wow.
OK, Good thing that name's gone mostly.
Well, it's a lot of unnecessary worry I imagine.
So autoimmune blisters in pregnancy?
What makes someone susceptible? Any known triggers or risk
factors? Well, the information links PG

(01:46):
sometimes with high data form mole or even choriocarcinoma, so
there's an association there to be aware of.
OK. So specific pregnancy related
conditions, potentially anythingelse.
Does having PGI don't indicate anything bratter about a
person's health? Yes.
And this is actually a really crucial point from the material
high yield for you to remember. It states quite clearly that

(02:06):
patients who've had PG have a significantly higher risk of
developing other autoimmune diseases later on in life.
Ah, right, that connects back tothe autoimmune definition,
doesn't it? Suggests maybe a general
predisposition. Exactly, it's like the PG
episode might be the first sign of an underlying tendency
towards autoimmunity. That's a key takeaway then.
It's not just isolated to the pregnancy.

(02:28):
What kind of other autoimmune conditions are we talking about?
Does the source list examples? It does.
The specific examples given are Hashimoto's thyroiditis and
pernicious anaemia and later on when discussing prognosis,
Graves' disease is also mentioned.
So think thyroid issues and B12 absorption problems.
Hashimoto's pernicious anaemia. Graves is OK, so PG acts almost

(02:49):
like a a warning sign for the future immune system behaviour.
Got it. Let's get into the how then.
What's actually happening pathologically?
What's the mechanism causing theblisters?
OK, pathophysiology. So patients develop these
specific antibodies, mainly IgG one class.
And these antibodies target components within the skin's
basement membrane, they bind there.

(03:11):
That binding sets off an immune response, brings in complement
inflammation, and the end resultis a separation between the
epidermis and the dermis that creates the space for fluid to
collect, forming those subepidermal vesicles and
blisters. So the antibodies stick to the
glue holding skin layers together, trigger inflammation
and cause separation. Blisters form in the gap.

(03:34):
That makes sense. Yeah, that's a good way to think
about it. The sources also note there's
some antigenic overlap, meaning the target looks similar to the
antibodies found in bullous pemphigoid, another autoimmune
blistering condition. Right.
And do we know why these antibodies form in the 1st place
during pregnancy? What's the initial trigger?
That's the $1,000,000 question, really.
The exact trigger isn't fully known, but the material suggests

(03:54):
a leading theory involves cross reactivity, maybe between some
placental tissue components and similar looking components in
the skin's basement membrane. The immune system gets confused
if you like. Interesting.
The immune system's complexity during pregnancy is just
fascinating. OK, so we know what it is
broadly how it happens, but how often do we actually see this?

(04:14):
Is PG common? No, definitely not common.
Actually it's quite rare. The figures quoted in the
sources vary a bit, but put the incidence somewhere between 1
and 50,000 pregnancies all the way up to maybe 1 and 2,000,000
pregnancies in some populations.Well, one in 50,000 is already
pretty uncommon, but one in 2 million?
That's incredibly rare compared to something like, say, PUPP.

(04:37):
This is way down the list in terms of frequency, right?
Absolutely, way down. The incident seems to be
influenced by the prevalence of certain HLA types in a
population. The material specifically
mentions a higher incidence in Caucasians and links this to
HLAD R3 and HLAD R4 haplotypes being more common in those
affected. So a genetic component
contributing to its rarity and distribution.

(05:00):
Given it is so rare, being able to spot it clinically becomes
even more important. What does it actually look and
feel like for the patient? Key clinical features.
Right. The clinical picture is vital.
High yield stuff here. Typically it appears in the
second or more commonly the third trimester.
OK, late pregnancy. Yes, often with a pretty sudden
onset. And the absolute hallmark
symptom, the thing patients complain about most intensely,

(05:23):
is the itch piratus. It's described as extremely
severe, debilitating even, not just a bit itchy.
Right, intense itch. Got it.
What about the rash itself? What are we looking for?
It usually starts as these red urticarial papules and plaques,
so raised red patches, a bit like hives or nettle rash, often
starts around the umbilicus, thebelly button area.

(05:45):
Then these patches evolve, oftenquite quickly, into tense
vesicles and belay proper blisters filled with fluid and
quite firm or tense to the touch.
OK, so start like hives maybe around the belly button, then
boom, tense blisters. Where does it typically spread?
Is there a pattern? Yes, the distribution is a
really helpful clue. It typically begins on the

(06:05):
abdomen and trunk, then spreads outwards to the limbs.
But crucially, and this is a keypoint the sources emphasise, it
characteristically spares certain areas the face, the
palms of the hands and the solesof the feet.
That sparing is important. Face, palms, soles usually
clear. What about inside the mouth
mucosal areas? Generally spared too.

(06:27):
Mucosal involvement is uncommon,reported in less than 20% of
cases, according to the material.
So you're mainly looking at the trunk and limbs, avoiding those
specific sites. OK, that pattern is very
distinctive. What about the timeline?
Does it just keep getting worse until delivery?
It can fluctuate. Interestingly, the symptoms
sometimes improve a bit in the last few years before delivery,

(06:48):
but then there's often a flare up quite soon after the baby is
born postpartum. The good news is it usually
resolves completely on its own within weeks to months after
childbirth. But as it come back like in
future pregnancies. Yes, recurrence is definitely a
feature. The sources mentioned it can
recur in subsequent pregnancies,quite commonly in fact, and
sometimes it can even be triggered later in life by

(07:09):
things like starting oral contraceptives or even just with
menstruation, which again suggests that hormonal link.
Right. So let's try a quick clinical
snapshot then, based on what you've said.
Third trimester patient, sudden onset, incredibly icky rash that
started as red patches near her navel and now has tense blisters
spreading on her arms and legs. But her face, palms and soles

(07:30):
look fine. Bemfigo adjustatanus has to be
high on the list. Right, absolutely.
That combination, the timing, the intense itch, the
morphology, urticaria to tense blisters and that classic
distribution with sparing is very strongly suggestive of PG.
Recognising that pattern is key.Definitely, but pregnancy rashes
can be tricky. What other conditions should be

(07:51):
on our differential diagnosis list?
What else could look like this or cause severe itching or
blisters in pregnancy? Good point.
The differential is important. The sources list several key
ones, Obviously other autoimmuneblistering diseases like bolus
pemphigoid itself or psychotricial pemphigoid.
Then there are the more common pregnancy specific dermatosis,
especially pruritic urticarial papules and plaques of pregnancy

(08:14):
or PUPP that's much more common and itchy but usually lacks the
big tense blisters of PG. Also need to consider things
like linear IGA, dermatosis, dermatitis herpetiformis maybe
erythema multiform papular dermatitis of pregnancy and
pruritic folliculitis of pregnancy.
It's quite a list. Yeah, some blistering, some just
itchy. It really highlights why you

(08:36):
need to confirm the diagnosis properly.
So how do we do that? How do we nail down PG and rule
out the others? What investigations are key?
Well, First off, the sources sayroutine blood tests like a full
blood count or basic chemistry aren't really helpful for the
diagnosis itself. OK, so standard bloods don't
help much. What does?
It's really a combination. You need that characteristic
clinical picture we just discussed.

(08:58):
Then a skin biopsy is essential.You take a small sample of skin,
usually from the edge of a blister or an affected area.
And what does the biopsy show? For Histology, looking under the
microscope, you'd see that characteristic subidermal split
or blister formation, but the really crucial tests are the
immunofluorescence studies. Right immunofluorescence.
There are two types mentioned. Are there DIF and IDF?

(09:20):
Exactly. Direct immunofluorescence or DIF
is done on a fresh skin biopsy sample, usually taken from skin
right next to a blister paralesional skin.
It directly looks for those immune deposits, the complement,
specifically C3 and sometimes IgG stuck along the basement
membrane zone in the skin itself.
OK, so DIF finds the evidence atthe scene of the crime, so to

(09:42):
speak. Yeah, finds the C3 stuck in the
skin. Precisely.
Then there's indirect immunofluorescence, or idaf
that's done on the patient's blood serum.
It's looking for the circulatingauto antibodies, the PG factor
or IgG antibodies that are floating around in the blood
ready to attack the skin. So IDF finds in the antibody in
the bloodstream. Makes sense.
DIF for deposits in skin, IDF for antibodies in blood.

(10:05):
That's the core of it. Finding that linear C3 deposit
along the basement membrane on DIF is considered the gold
standard diagnostic finding for PG.
The sources also mentioned HLA typing can be supportive.
Finding HLAD R3 or DR4 increasessuspicion, but it's not
diagnostic on its own. Oh, and a small caution from the
material, sometimes the DAF pattern in PG can look similar

(10:28):
to bolis pemphagoid or another station called epidermolysis
bolosa Aqua Zeta. So you always interpret the lab
results alongside the clinical picture.
It's not just about the test result in isolation.
Right. Clinical picture plus Histology
showing the split plus the crucial immunofluorescence
results, especially DAF showing C3 confirmed diagnosis.
OK, so we've confirmed it's PG. How do we treat it?

(10:49):
What's the management approach? The mainstay of treatment, and
this is based on UK practise mentioned in the sources, is
oral corticosteroids, usually prenis alone.
That's the go to for controllingthe inflammation and
importantly, that awful itch. Prenis alone and that's used
during pregnancy and postpartum if needed.
Yes, both during pregnancy and often continued or restarted

(11:10):
postpartum if there's a flare. The typical starting dose range
given is around .5 to 1 milligramme per kilogramme per
day. OK, steroids are key.
What about just managing the itch symptomatically?
Absolutely. Antihistamines are used pretty
routinely alongside the steroidsto help provide some relief from
the severe puritis. Emollients might help soothe the

(11:30):
skin too. And what if it's a really severe
case or doesn't respond well to the steroids?
Are there other options? For those tougher cases, the
material mentions things like plasmapheresis or amino
adsorption could be considered, but these are definitely second
or third line treatments, much less common.
One thing the source has really emphasised for management is the
need for a team approach. Collaborative care involving the

(11:53):
obstetrician, a dermatologist and also a paediatrician is
recommended. Yeah, that makes total sense.
You've got implications for the mum's skin, the pregnancy itself
and potentially the baby needs everyone on the same page.
Definitely it's managing both mother and potential foetal
outcomes. OK, so Speaking of outcomes,
what is the overall prognosis? We know it's usually self

(12:14):
limiting after birth, but are there any complications or long
term issues for the mother or the baby we need to be aware of?
Well, the most reassuring news first, the sources state there's
no increased risk of maternal orinfant mortality directly from
PG. So it's not typically life
threatening in that sense. That's.
Good to know, but are there other impacts on the pregnancy

(12:35):
or the baby's health? Yes there are.
There's a documented higher rateof premature births.
The sources mentioned around 20%risk of preterm labour and also
a higher chance of babies being born small for their gestational
age or SGA. OK.
So increased risk of prematurityand growth restriction important
for obstetric monitoring. Does the baby ever get the rash?
Sometimes, yes. In about 5 to 10% of babies born

(12:58):
to mothers with PG, they might develop a mild, transient,
blistering rash themselves. Why does that happen?
It's thought to be because the mother's IgG antibodies, the
ones causing her rash, can crossthe placenta and get into the
baby circulation. But because the baby isn't
producing them, as the maternal antibodies get cleared from the
baby's system over days to weeks, the rash just fades away

(13:20):
on its own. No specific treatment usually
needed for the baby's rash. OK, so a transient rash in a
small minority resolves spontaneously.
Good. Now circling back to the mother,
what about her long term health?We touched on this earlier.
Yes, and it bears repeating because it's a significant long
term consideration highlighted in the material that increased
lifetime risk of developing other autoimmune diseases.

(13:42):
The list again. Hashimoto's thyroiditis, Graves'
disease, Pernicious anaemia. So having PG is a definite red
flag for a future autoimmune follow up for the mother.
That's a really crucial counselling point, isn't it?
If a patient has had PG, she needs to know about this
increased future risk. Absolutely.
It's a key part of the long termpicture.
So main complications, prematurity risk, 20% SGA risk,

(14:05):
potential transient baby rash and that significant long term
maternal risk of other autoimmune conditions.
OK, it really shows how PG, while rare, sits at this
interesting intersection of dermatology, obstetrics, and
immunology. It really does.
You see the interplay between the hormonal changes of
pregnancy, the immune system's response and how it manifests on

(14:26):
the skin. It's quite fascinating, even if
challenging for the patient. Absolutely.
Well, this has been a really focused deep dive into
pemphigoid justicionis. We've covered its definition as
an autoimmune blistering diseaseof pregnancy, the link to future
autoimmunity, the classic clinical signs like intense itch
and blistering, sparing the facebone soles, the key
diagnostic role of immunofluorescence management

(14:49):
mainly with steroids, and the important outcomes for both
mother and baby. Hopefully this run through has
been a really useful high yield revision session for you.
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