M. Daboubi, T. Maaita, M. Al-Ruhaibeh

Herpes Gestationis: A Case Report
Moh’d K. Daboubi MD*, Tagreed J. Maaita MD**, Maysoon K. Al-Ruhaibeh MD^
ABSTRACT
We report a case of a 34 year old pregnant female patient who presented with herpes gestationis in her second
trimester. She was gravida 5, para 4 with skipped or uninvolved pregnancies and was managed at Queen Alia
Military Hospital. This autoimmune bullous dermatosis is very rare and usually persists during the postpartum
period.
Key words: Herpes Gestations, Pregnancy, Histopathology
JRMS July 2010; 17(Supp 2): 94-97
Introduction
Herpes gestationis, also known as Pemphigoid
gestations, is a rare recurrent vesiculobullous
autoimmune disease of pregnancy and the
postpartum period. Most cases resolve within few
months of delivery. The disease is characterized by
intense pruritic skin eruptions and may result in
increased fetal morbidity. Its incidence ranges from
1:50,000 to 1:500,000 pregnancies. (1) The
interaction of this rare pathology with pregnancy is
underestimated by obstetricians. (2)
Case Report
A 34-year-old Jordanian lady gravida 5, para 4, all
her previous pregnancies ended in normal vaginal
deliveries. The patient attended King Hussein
Medical Centre at nine weeks gestation and had
regular follow up for a singleton pregnancy. At 26
weeks gestational age she suddenly developed
severe intensely itchy urticarial papules and plaques
which later became vesiculobullous lesions, starting
mainly around the umbilicus (Fig. 1) and then
spreading to involve the whole body (Fig. 2) sparing
the face, mucous membranes, palms and soles
When the patient’s history was reviewed it was
noted that she developed the same lesions in her
second and fourth pregnancies, both started in the
second trimester around the 26 th week of gestation
and developed when she took oral contraceptive
pills after her third pregnancy. During each attack
she was admitted and a skin biopsy was taken and
herpes gestationis was confirmed. She was treated
with prednisolone tablets with a good response in
few days.
On this admission two-skin biopsies from her left
arm were taken, one from lesional skin for
histopathology examination and the other one from
peri-lesional skin for direct immunoflourescence.
The first one demonstrated sub epidermal vesicles
with focal spongiosis, a heavy perivascular
lymphohistiocytic infiltrate and esinophils in the
dermis and in the bullae (Fig. 3 & 4). Direct
immunoflourescence demonstrated heavy linear C3
deposits while IgG, IgM, IgA and fibrinogen were
negative.
She was started orally on 40mg prednisolone
tablets per day, in addition to topical steroid
ointment and systemic antihistamine. She responded
well to this treatment in few days, and was
discharged home after eight days on 40mg
prednisolone daily; two weeks later the dose was
gradually decreased to 30mg per day. She attended
From the Departments of:
*Gynecology and Obstetrics, IVF Unit, King Hussein Medical Centre (KHMC), Amman-Jordan.
**Dermatology, Queen Alia Military Hospital (QAMH), Amman-Jordan.
^ Histopathology
Correspondence should be to Dr. M. Daboubi, P. O. Box 620812 Amman 11162 Jordan, E-mail: mdaboobi@hotmail.com
Manuscript received April 3, 2006. Accepted August 31, 2006
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Fig. 1. Pruritic urticarial lesions developing a periumbilical
pattern on the abdomen
Fig. 2. Annular erythema on the fore arm
Fig. 3. Dense peri-vascular dermal lymphohistiocytic
infiltrate and esinophils
antenatal clinic and the dermatology clinic as well
regularly every two weeks.
She delivered vaginally at 39 weeks a baby boy
weighing 3.150 kilograms who was healthy without
abnormalities or skin lesions. She had two very
small skin lesions at time of delivery.
The patient experienced a postpartum flare-up on
the third day while she was still in the hospital;
prednisolone dose was increased to 50mg per day
and she was discharged five days later on 40mg per
day. Later the dose was decreased gradually till it
was stopped at the 14 th week post partum.
It is important to notice that the first and the third
pregnancies were free of the disease.
Discussion
Herpes gestationis is one of the specific
dermatoses of pregnancy like Papular dermatitis of
pregnancy. It is characterized by intense pruritic
urticarial papules and plaques with the development
of tense vesicles and bullae, and it tends to recur
with subsequent pregnancies and with the use of the
Fig 4. Sub epidermal vesicle containing lymphohistiocytes
and esinophils
oral contraceptive pill. Herpes gestationis is clearly
hormonally modulated, since the rash flares
premenstrually, (3) however skipped or uninvolved
pregnancies occur in 8% of reported cases. (4,5) The
same occurred with our patient, which is important,
because this is very rare and explanation of why
skipped pregnancies occur remains uncertain. It is
not due to the mother and the fetus being compatible
at the DR locus (as there is an association of Herpes
gestationis with HLA DR3 and DR4 antigens), nor it
is due to a change in partner. (4)
It tends to occur any time from first trimester to
the immediate post partum period but mostly it
begins in the second or third trimester.
Exacerbation at the time of delivery or post partum
period occurs in 75% of the patients and most
patients recover within 14 weeks after delivery. (6)
Persistence up to 28 months post partum has been
frequently reported, (6,7) and exceptionally long
persistence for eight years has been reported in one
case. (6) Herpes gestationis occurs in pregnancy and
in trophoplastic tumors.
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Herpes gestations must be differentiated from
other pruritic skin diseases such as prurigo
gestationis, impetigo herpetiformis and pruritic
urticarial papules and plaques of pregnancy. (8) The
histopathology of Herpes gestationis shows
edematous papillae with sub epidermal vesicles and
dense dermal eosinophilic infiltrate forming
eosinophilic spongiosis. (4)
Direct Immunofluorecence of peri-lesional skin
demonstrated linear deposits of C3 at basement
membrane; IgG deposits may be found in 40-50% of
reported cases. (4,7)
The cause of Herpes gestationis may be related to
abnormal expression of major histocompatibility
complex class П Ag within the placenta that initiate
an allogenic response to the placenta basement
membrane which cross react with skin. (9,10) This
theory is based on an association of Herpes
gestationis with HLA DR3 and DR4 antigens. (1,11,12)
Fabbri et al. suggested that an inflammatory
infiltrate is involved in the production of
Pemphigoid gestationis bullous lesions assuming
that Th2 cells (T helper type 2 cells) might be
implicated in the very early stages of autoimmune
response and may exercise a broad influence in
blister formation in this disease. (13) Jenkins reported
that 13.8% of patients with Herpes gestations had
associated autoimmune disease. (4)
Our patient delivered a full term baby with no
congenital abnormality or cutaneous lesions and
with a normal birth weight. There is no clear
evidence that Herpes gestationis poses significant
risk to either mother or child, (14) in Jenkins study of
278 cases there was 16% spontaneous abortions and
only 2.8 % of infants had evidence of skin lesions. (4)
Cutaneous involvement of the neonate occurs in 2-
10%. (15) In our case no cutaneous involvement
occurred. Neonates should be evaluated for adrenal
insufficiency when affected mother has received
steroids for prolonged periods. (14)
Systemic steroids are the treatment of choice to
relieve pruritus and to suppress the eruption; in
severe reluctant cases intravenous Immunoglobulins
may be needed for few days to initiate remission.
Chlorpheniramine appeared to suppress pruritus,
also topical steroids help. Azathioprine, dapsone,
pyridoxine are used as adjuvant therapy and one
case was helped with goserelin for continuing
disease several years post partum with only initial
success. (16)
Immunoblotting and ELISA are sensitive tools for
the detection of auto antibodies to bullous
pemphigoid antigen (17) 180 KD in patients with
pemphigoid gestations; the ELISA is useful to
monitor auto antibody serum levels.
Conclusion
Herpes gestationis is a pregnancy specific
dermatosis, which usually recurs with each
pregnancy with more severe course and earlier
onset, but disease-free pregnancies may occur.
The disease usually flares up in the early
postpartum period. Early diagnosis and
management may help to prevent maternal and fetal
complications.
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