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BULLOUS PEMPHIGOID (PEMPHIGOID GESTATIONIS, HERPES GESTATIONIS)

Aimee S. Payne
|
March 13, 2019

ARE YOU CONFIDENT OF THE DIAGNOSIS?

What you should be alert for in the history

Determine if the lesions are pruritic. Bullous pemphigoid (BP) is almost always
pruritic, and itch can be the first presenting symptom or can herald a relapse.

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Ask about aggravating factors or associated conditions, which can include
stress, ultraviolet radiation or radiation therapy, menses or pregnancy (also
known as herpes gestationis), recent vaccinations, and a history of neurologic
disease including dementia, Parkinson’s disease, or cerebrovascular accident.
Bullous pemphigoid has been anecdotally associated with several drugs including
penicillamine, captopril, furosemide, nonsteroidal anti-inflammatory agents, and
antibiotics.

Determine if the patient has a history of inflammatory skin diseases associated
with pemphigoid, including lichen planus or psoriasis.

Ask about a gritty sensation in the eyes, hoarseness, or difficulty swallowing
to evaluate for potential mucosal disease. Mucosal involvement in bullous
pemphigoid is less common, and when present, usually affects only the
oropharyngeal mucosa. If patients have extensive mucosal disease including the
conjunctiva, a diagnosis of mucous membrane (cicatricial) pemphigoid should be
considered.

Characteristic findings on physical examination

There are two primary morphologies of clinical lesions in BP: tense bullae and
urticarial papules and plaques (Figure 1). A classic clinical presentation for
bullous pemphigoid is tense bullae on an erythematous base arising on the lower
extremities in an elderly patient (Figure 1). However, a wide spectrum of
disease exists. Early disease may begin with pruritus, and skin lesions may
appear non-specific, with excoriated papules or eczematous patches. A pompholyx
variant may present with confluent vesicles on the palms and soles. Localized
disease may also occur, most commonly in the pretibial area, sites of
irradiation, or around surgical sites.

FIGURE 1.

Tense bullae, erosions, and urticarial plaques on the legs of an elderly
patient, typical of bullous pemphigoid. (Photo courtesy of Misha Rosenbach, MD)

Lesions heal without scarring and usually without milia, although with
widespread disease milia can occur after healing.

* Expected results of diagnostic studies

Skin biopsy for histology: A punch or shave biopsy for histology should be
obtained from an urticarial plaque or at the lateral edge of a fresh blister.
Biopsy of an old blister can confuse the diagnosis due to necrosis of the roof
of the blister and/or re-epithelialization of the base. Histology of BP will
show a subepidermal blister, most often with prominent eosinophilic/mixed
inflammation in the dermis, epidermis, and blister fluid (Figure 2). Rarely,
cell-poor subepidermal bullae are observed. Biopsy of urticarial lesions will
demonstrate eosinophilic spongiosis.

FIGURE 2.

Histology of bullous pemphigoid showing subepidermal blister with eosinophils
(arrows).

These routine light microscopy findings are histologically non-specific and may
also be observed in allergic contact dermatitis, scabies infestation, and other
inflammatory or immunobullous skin conditions. Autoantibodies to the basement
membrane zone should be documented by direct immunofluorescence, indirect
immunofluorescence (including salt split skin), and/or ELISA.

Skin biopsy for direct immunofluorescence (DIF): A punch or shave biopsy should
be obtained from normal-appearing perilesional skin and submitted in Michel’s or
other appropriate fixative for direct immunofluorescence analysis. BP will
demonstrate linear basement membrane zone staining, classically for C3 greater
than IgG. Dermis always has a strong background on DIF testing due to the high
concentration of IgG in blood, which extravasates into the dermis during the
biopsy, potentially masking the detection of immune reactants at the
dermal-epidermal junction. Incubation of the skin sample in sterile saline at 4
degrees C for up to 24 hours prior to transfer to Michel’s fixative will help to
wash out unbound dermal IgG and increase the sensitivity of DIF detection.

Even if all skin lesions have healed because of recent therapy, DIF should
remain positive for at least several weeks. Immune reactants are typically
destroyed within the blister cavity, leading to false negative results if
samples for DIF are taken from blistered or urticarial skin.

Even with a subepidermal blister and positive DIF result, the diagnosis of BP is
not 100% certain since epidermolysis bullosa acquisita and p200 pemphigoid can
yield similar findings (although the presence of prominent eosinophils on
histology and a classic clinical presentation would be relatively convincing for
BP.) To confirm the diagnosis, indirect immunofluorescence on salt split skin or
ELISA is beneficial.

Serum sample for indirect immunofluorescence (IIF): Serum is incubated with
epithelial substrates (monkey esophagus, normal human skin, or normal human skin
pre-incubated with 1 M NaCl). On non-salt split substrates, IIF for BP will
classically demonstrate C3 greater than IgG basement membrane zone staining
(Figure 3), and will remain positive for at least several weeks after skin
lesions have healed. On salt split skin, IIF for BP will demonstrate linear
staining of the basement membrane zone on the roof or epidermal side of the
blister (sometimes both the epidermal and dermal side are stained).

FIGURE 3.

Indirect immunofluorescence staining of monkey esophagus with bullous pemphigoid
serum demonstrates linear basement membrane zone staining of C3 and IgG

Serum sample for BP ELISA: Antigen-specific ELISAs (BP180 and BP230) are
sensitive and specific for BP and are less subjective than
immunofluorescence-based tests. However, BP ELISA is not always available from
major national reference laboratories. The BP180 ELISA is 84% to 89% sensitive
and 98% to 99% specific. The BP230 ELISA is 72% sensitive and 99.5% specific.
The combination of the two ELISAs is 97.1% sensitive.

Complete blood count will often show peripheral eosinophilia, although the
presence or absence of this laboratory finding does not define or preclude a
diagnosis of BP.

* Diagnosis confirmation

The clinical differential diagnosis for BP is broad and includes epidermolysis
bullosa acquisita, porphyria, p200 pemphigoid, linear IgA bullous dermatosis,
pemphigus vulgaris, Stevens-Johnson syndrome, toxic epidermal necrolysis,
urticaria or urticarial drug reaction, disseminated herpes simplex or zoster,
scabies, and arthropod reaction. Localized disease can also be confused with
allergic contact dermatitis or dyshidrotic eczema.

WHO IS AT RISK FOR DEVELOPING THIS DISEASE?

The incidence of BP ranges from 4.3 per 100,000 person years in the United
Kingdom to 6.6 per million in western Europe. The sex ratio of cases in women to
men averages 1.5:1, except in Kuwait where a 5:1 sex ratio has been reported.
The incidence of BP increases with age, with an average yearly increase in
incidence of 17% in the United Kingdom. Rarely, disease can occur in children.

Women may develop BP during or shortly after pregnancy (also known as pemphigoid
gestationis or herpes gestationis). The disease is histologically and clinically
identical to BP except for its age of onset. Population-based studies have also
shown that bullous pemphigoid is associated with neurologic diseases, including
dementia, Parkinson’s disease, and cerebrovascular accident. In most cases
bullous pemphigoid follows the onset of neurologic disease but in some cases it
precedes the neurologic diagnosis. Although the exact mechanism for this
association is unclear, both BP180 and BP230 are expressed in brain and skin,
leading to speculation that neurologic disease or inflammation may lead to an
autoimmune reaction to one or both antigens.

Several medications have been anecdotally associated with BP, including
furosemide, penicillamine, captopril, ibuprofen, and antibiotics. Disease may or
may not remit with discontinuation of the medication.

The MHC class II allele DQB1*0301 is more often observed in BP patients.

WHAT IS THE CAUSE OF THE DISEASE?

* Etiology

The pathologic target of autoantibodies in BP is type XVII collagen, also known
as bullous pemphigoid antigen 2 (BPAg2) or BP180, a transmembrane protein of the
hemidesmosome. Most autoantibodies bind to the NC16A domain, an extracellular
non-collagenous domain. Both IgG and IgE antibodies have been implicated in
disease pathology, the latter thought to account for urticarial lesions in BP.

Almost all patients with BP demonstrate antibodies to bullous pemphigoid antigen
1 (BPAg1) or BP230. BP230 is a cytoplasmic plaque protein of the hemidesmosome.
Autoantibodies to BP230 likely arise secondary to basal keratinocyte damage and
do not play a direct role in blister formation.

* Pathophysiology

As with most autoimmune diseases, the reasons for the loss of immune tolerance
in BP are unknown. Because human BP autoantibodies do not cross-react with mouse
BP180, it has been more complicated to develop mouse models for study. Our
knowledge of disease pathophysiology has resulted from four models: injection of
human BP IgG into rabbit cornea, passive transfer of serum IgG from rabbits
immunized with mouse BP180 to mice, passive transfer of human BP autoantibodies
to immunodeficient mice bearing human skin grafts, and passive transfer of human
BP autoantibodies to ‘humanized’ mice (BP180-deficient mice that were
subsequently made transgenic for human BP180).

The current working model of disease pathology is as follows: Anti-BP180 IgG
binds to the basement membrane zone. Complement fixation and activation causes
leukocyte chemotaxis and degranulation of mast cells, which promotes chemotaxis
of eosinophils. Release of proteolytic enzymes by inflammatory cells (such as
neutrophil elastase and eosinophil gelatinase) causes cleavage of basement
membrane zone proteins including BP180, leading to blister formation.
Additionally, passive transfer of anti-BP180 IgE recapitulates many aspects of
the urticarial phase of disease. Monovalent (Fab) fragments of BP IgG do not
cause blisters, and mice deficient in components of complement or neutrophil
elastase do not develop blisters, indicating that the effector functions of BP
autoantibodies are required for disease.

SYSTEMIC IMPLICATIONS AND COMPLICATIONS

BP typically affects the skin without systemic involvement. However, one study
in the Czech Republic found a significantly higher incidence of neurologic
disease (primarily stroke and dementia) in BP patients compared with age- and
sex-matched controls. These data are intriguing since an alternatively spliced
form of BP230 is expressed in neural tissue, and mice with a genetic deletion of
BP230 demonstrate defects in epithelial integrity as well as neurodegeneration.

Secondary infection can occur and may be difficult to identify with widespread
urticarial and erosive lesions.

TREATMENT OPTIONS

OPTIMAL THERAPEUTIC APPROACH FOR THIS DISEASE

Class I steroids such as clobetasol can be applied twice daily to new lesions.
Topical tacrolimus ointment may also be considered in areas where chronic
steroid therapy is undesirable. A randomized controlled trial of topical
steroids (20 grams twice daily) and oral prednisone (1.0 mg/kg/day) in severe
cases of BP showed that topical steroids were significantly more effective, had
lower 1-year mortality, and were associated with fewer severe complications as
compared with oral prednisone.

For mucosal disease, dexamethasone elixir, swish and spit 5cc once to twice
daily, is easy to use. Clobetasol ointment or gel can also be applied directly
to mucosal erosions. Dental trays (fitted by oral medicine) facilitate occlusion
of topical steroids to the gingiva at night.

BP (including widespread disease) may respond to tetracyclines plus niacinamide
(tetracycline 2g daily or doxycycline 100 mg twice daily, plus niacinamide 500
mg 3 times daily). This regimen is worth a trial, particularly in elderly
patients with multiple comorbid conditions for whom oral steroids and other
immunosuppressants would be difficult.

With persistent or widespread disease, oral corticosteroids such as prednisone
are indicated. For moderate disease, 0.5 mg/kg/day of prednisone or equivalent
may be sufficient. Doses generally do not need to exceed 1 mg/kg/day of
prednisone. If patients flare on 1 mg/kg/day of prednisone, the dose can be
split to twice daily or three times daily dosing, which increases the
therapeutic efficacy without increasing the total daily dose. Before starting
high dose steroids, tuberculosis screening should be performed (via tuberculin
skin testing or QuantiFeron-TB gold blood assay).

If patients will be on chronic corticosteroids (at least 5 mg daily prednisone
equivalent for at least 3 months), osteoporosis counseling and prevention is
indicated. Additionally, Pneumocystis prophylaxis should be considered for
patients on chronic prednisone, particularly with daily prednisone doses of 15
mg or higher. Patients should remain on high-dose steroids until new lesions
cease to form, and then the dose can be gradually tapered to the minimum
required to control disease. If patients can be managed with 10 mg (or ideally 5
mg) daily prednisone or less, corticosteroid monotherapy is feasible.

Dapsone (100 to 200 mg daily) may be effective to lower the daily corticosteroid
dose in patients with stable disease. Dapsone can be used in addition to
mycophenolate mofetil or azathioprine. As an advantage, dapsone 100 mg daily
provides Pneumocystis prophylaxis. Glucose-6-phosphate dehydrogenase (G6PD)
activity should ideally be measured before starting therapy, particularly in men
of African-American and Middle Eastern descent. Most patients will experience a
1 to 2 gram/dl drop in hemoglobin due to hemolysis, although some patients can
experience a severe pancytopenia with or without systemic hypersensitivity
reaction. Laboratory monitoring should be performed at least every other week
for the first 8 weeks.

In patients requiring greater than 10 mg daily prednisone for control of disease
activity, or in patients with contraindications to systemic corticosteroid
therapy, other immunosuppressants are necessary to reduce or replace systemic
corticosteroids. Mycophenolate mofetil (30 mg/kg/day divided twice daily) is
generally well tolerated, although side effects of fatigue, gastrointestinal
upset, and tremor are not uncommon, particularly at higher doses, and there is a
small long-term risk of lymphoma and fatal infection or reactivation from JC
virus with progressive multifocal leukencephalopathy.

Reduction of corticosteroid dose can be initiated as early as 1 month after
starting mycophenolate mofetil, although maximal effect of mycophenolate mofetil
is not achieved until 2 to 3 months. Azathioprine can be started at 50 mg daily
and titrated upward by 50 mg every 1 to 2 weeks until side effect, therapeutic
effect, or the target dose of 2.5 mg/kg/day occurs. Measurement of serum
thiopurine methyltransferase (TPMT) level prior to start of azathioprine therapy
can be performed, although some studies suggest that TPMT levels do not
correlate with the incidence of adverse effects or efficacy of azathioprine
therapy.

Nevertheless, if serum TPMT levels are very low or very high, azathioprine may
not be a good choice for therapy, due to an increased likelihood for adverse
effects or lack of effect, respectively. The active metabolites for azathioprine
do not significantly accumulate until 6 to 8 weeks after initiation of therapy,
leading to a delayed therapeutic effect.

In patients who have severe or persistent disease that is unable to be
controlled with corticosteroids and/or other immunosuppressives, other therapies
such as rituximab, intravenous immunoglobulin, plasmapheresis, and
cyclophosphamide can be considered. B-cell depletion therapy with rituximab
(anti-CD20 monoclonal antibody) is anecdotally effective for the treatment of BP
and has been proposed by some experts to be considered for first-line therapy
for another autoimmune blistering disease, pemphigus vulgaris.

Both lymphoma (375 mg/m
2 IV weekly x 4 weeks) and rheumatoid arthritis (1000 mg IV on days 1 and 15)
dosing regimens can be used. In vivo studies from lymphoma patients indicate
that peripheral blood B cells disappear from the circulation within days,
although antibody production by plasma cells (which are not well targeted by
rituximab) can persist for months; therefore, maximal results are typically not
observed until 3 to 6 months after infusion, and re-infusion every 6 months may
be required. Fatal infection has occurred with rituximab therapy, including
bacterial sepsis, hepatitis B reactivation, and progressive multifocal
leukencephalopathy from JC virus, although fatal infection is also a potential
side effect of first-line therapies for BP, including prednisone and
mycophenolate mofetil.

Intravenous immunoglobulin (IVIG, 2 mg/kg, divided over 3 to 5 days) is
effective for BP therapy and can be provided by hospital or home infusion. IVIG
is thought to induce catabolism of endogenous serum antibodies and offers the
advantage of being immunoprotective. A disadvantage of IVIG is that the
temporary serum viscosity associated with the infusion can cause stroke or other
complications from clotting. The serum half-life of IVIG has been reported to
range from 8 to 39 days (average 3 to 4 weeks). Treatment guidelines for
autoimmune blistering disease with IVIG suggest an initial frequency of every 4
weeks until disease remits, increasing to 6, 8, 10, 12, 14, then 16 weeks, the
latter being the proposed end point for an initial course of therapy.

Plasmapheresis allows for the rapid removal of antibodies from the circulation,
but must always be used in conjunction with adjunctive immunosuppressants to
prevent new antibody production.

Cyclophosphamide (50 to 200 mg daily) is among the fastest agents for treating
disease. However, its risk of blood count and liver test abnormalities,
infertility, and hemorrhagic cystitis with bladder carcinoma, together with the
advent of other effective therapies such as rituximab, have led to the decreased
use of cyclophosphamide in the management of severe BP.

Case reports and one small case series have shown therapeutic benefit in bullous
pemphigoid patients with omalizumab, a monoclonal antibody that binds and
suppresses IgE.

Treatment options are summarized in Table I.

Topical corticosteroids Tetracyclines plus niacinamide Oral corticosteroids
Mycophenolate mofetil Azathioprine Dapsone Rituximab Intravenous immunoglobulin
Plasmapheresis Cyclophosphamide

PATIENT MANAGEMENT

The goal of treatment is to obtain a complete remission off therapy, although
many patients may only achieve a partial remission off therapy, or a complete
remission on minimal therapy. When starting patients on therapy, risks of
medications should be discussed. There is no systemic medication that is 100%
safe. However, the 1-year mortality of BP has been reported to range from 6% in
the United States to 19% in the United Kingdom to 41% in France; therefore, the
risk-benefit ratio often favors treatment.

Open erosions can become superinfected with Staphylococcus aureus or
herpesviruses; culture of refractory or worsening lesions should be considered.
Remind patients that their skin during active disease is fragile, so crusted
blisters should not be scrubbed.

Patients should receive regularly scheduled dental cleaning from a hygienist
experienced with oral blistering disease. Patients often avoid cleanings due to
painful mucosal disease; however, over time plaque buildup leads to chronic
gingival inflammation that aggravates disease. If necessary, patients can take a
short (1 to 2 week) course of prednisone surrounding their cleanings to prevent
flares of disease.

Whether or not serial BP180 ELISA monitoring is of clinical value to follow
disease activity is unclear. Studies have shown that 65% of remission sera will
still maintain a positive BP180 ELISA index value. However, other studies have
suggested that BP180 ELISA titers parallel disease activity, and one study found
that a BP180 ELISA value greater than 27-IU/mL at the time of clinical remission
was most predictive of disease relapse. Patients should ideally be maintained in
complete remission for at least 1 year before all immunosuppressive therapy is
discontinued. Often patients want to taper off their medications quickly, but
then flare and have to go back on high doses of medications for disease control,
which may reduce the chance for disease remission.

Typically, corticosteroids are tapered off first, then adjunctive
immunosuppressants are slowly tapered over the course of 1 year. However, the
tapering regimen should be tailored for each patient depending on side effects
and response to therapy. It is common for patients to have a small flare with
each dose taper; as long as lesions heal within 1 week and no further lesions
form, the taper can be continued. Recurrence of pruritus often precedes the
development of frank urticarial or bullous lesions and may herald disease
relapse.

The Centers for Disease Control recommends that all patients on
immunosuppressive therapy receive influenza and other regularly scheduled
vaccinations. While on immunosuppressive therapy, patients should be reminded
that they should not receive live vaccines (e.g. nasal influenza or zoster).

UNUSUAL CLINICAL SCENARIOS TO CONSIDER IN PATIENT MANAGEMENT

Pregnant patients who develop BP (also known as pemphigoid gestationis) should
be referred for high-risk obstetrical care. Pregnant patients are usually
treated with prednisone monotherapy, as most other immunosuppressive agents are
pregnancy category D, including mycophenolate mofetil, azathioprine,
tetracyclines, and cyclophosphamide. Dapsone is pregnancy category C. There are
sparse data regarding the safety of immunosuppressives in men whose pregnant
wives can be exposed to drug in seminal fluid. Rare cases of birth defects with
azathioprine use by fathers have been reported. An ongoing registry of male
transplant patients receiving mycophenolate mofetil has shown no significant
increase in birth defects.

In hospitalized patients with severe disease, blood should be cultured so that
bacteremia can be identified and treated. A thin layer of triamcinolone 0.1%
ointment can be spread on sterile linens and wrapped around patients twice
daily. Unfortunately, there is no single consensus regimen among experts about
how to treat severe pemphigoid, owing to the sparsity of randomized controlled
trials in this rare disease. Historically, these patients were treated with
corticosteroids, cyclophosphamide, and plasmapheresis due to their rapid
therapeutic effect.

Several other regimens can be considered for the hospitalized patient,
including:

* intravenous corticosteroids (as high as 60 mg methylprednisolone 4 times
daily), adjunctive immunosuppressant such as mycophenolate mofetil, and IVIG
(which is immunoprotective)

* intravenous corticosteroids (+/- adjunctive immunosuppressant) and rituximab
for long-term control

* intravenous corticosteroids (+/- adjunctive immunosuppressant),
plasmapheresis to immediately remove serum antibodies, followed by rituximab
for long-term control

The timing of certain combinations of medications should be considered. For
example, rituximab infusion should not be administered immediately before
plasmapheresis or IVIG, as the former would clear the rituximab and the latter
may induce its catabolism. However, rituximab is thought to rapidly bind and
deplete circulating B cells (within days), and peripheral B cell counts begin to
recover as early as 8 days after infusion.

Theoretically therefore, plasmapheresis and IVIG could be considered as early as
1 to 4 weeks after completion of rituximab infusion, although studies indicate
that rituximab half-life progressively increases with subsequent weekly
infusions (suggesting saturation of in vivo binding sites), and that a higher
serum concentration is associated with better treatment outcome in B cell
lymphomas. Conversely, plasmapheresis can be performed immediately prior to
rituximab, but the ideal timing of rituximab infusion after a course of IVIG is
unknown, with recommendations ranging from 1 to 6 weeks based on the serum
half-life of IVIG.

WHAT IS THE EVIDENCE?

Stanley, JR, Wolff, K, Goldsmith, LA, Katz, SI, Gilchrest, B, Paller, AS,
Leffell, DJ. “Pemphigoid”. 2011. (A more complete review of the clinical
presentation and management of BP.)

Vodegel, RM, de Jong, MCJM, Meijer, HJ, Weytingh, MB, Pas, HH, Jonkman, MF.
“Enhanced diagnostic immunofluorescence using biopsies transported in saline”.
BMC Dermatol. vol. 4. 2004. pp. 10(An informative visual comparison of Michel's
fixative, snap freeze, and saline for diagnostic immunofluorescence testing with
pemphigus and pemphigoid. Saline is the preferred medium for pemphigoid,
although samples must be processed or otherwise fixed within 24 hours.)

Sakuma-Oyama, Y, Powell, AM, Oyama, N, Albert, S, Bhogal, BS, Black, MM.
“Evaluation of a BP180-NC16a enzyme-linked immunosorbent assay in the initial
diagnosis of bullous pemphigoid”. Br J Dermatol. vol. 151. 2004. pp. 126-31.
(Describes the validation of the BP180 ELISA for pemphigoid.)

Yoshida, M, Hamada, T, Amagai, M, Hashimoto, K, Uehara, R, Yamaguchi, K.
“Enzyme-linked immunosorbent assay using bacterial recombinant proteins of human
BP230 as a diagnostic tool for bullous pemphigoid”. J Dermatol Sci. vol. 41.
2006. pp. 21-30. (Describes the validation of the BP230 ELISA for pemphigoid,
including the increased sensitivity of testing when combining the BP180 and
BP230 ELISAs.)

Joly, P, Roujeau, JC, Benichou, J, Picard, C, Dreno, B, Delaporte, E. “A
comparison of oral and topical corticosteroids in patients with bullous
pemphigoid”. N Engl J Med. vol. 346. 2002. pp. 321-7. (In this study of 341 BP
patients randomized to topical clobetasol [20 grams twice daily] or oral
prednisone [0.5 to 1.0 mg/kg/day depending on disease severity], no difference
in survival, efficacy, or complications was observed with moderate disease, but
in severe disease topical corticosteroids were significantly more effective than
oral prednisone [99% versus 91%], had increased 1-year survival [76% versus 58%]
and had fewer complications [29% versus 54%].)

Beissert, S, Werfel, T, Fieling, U, Bohm, M, Sticherling, M, Stadler, R. “A
comparison of oral methylprednisolone plus azathioprine or mycophenolate mofetil
for the treatment of bullous pemphigoid”. Arch Dermatol. vol. 143. 2007. pp.
1536-42. (Seventy-three [73] patients with BP were randomized to treatment with
oral methylprednisolone [0.5 mg/kg/day] plus azathioprine [2 mg/kg/day] or oral
methylprednisolone [0.5 mg/kg/day] plus mycophenolate mofetil [2 g/day]. Similar
efficacy and cumulative corticosteroid doses were observed in both groups,
although mycophenolate mofetil had significantly lower rates of liver toxicity
compared with azathioprine.)

Fairley, JA, Baum, CL, Brandt, DS, Messingham, KA. “Pathogenicity of IgE in
autoimmunity: successful treatment of bullous pemphigoid with omalizumab”. J
Allergy Clin immunol. vol. 123. 2009. pp. 704-5. (First published case report on
omalizumab treatment of a BP patient refractory to prior corticosteroids,
azathioprine, and minocycline. After a 16-week course, body surface involvement
declined from 50% to 5% with resolution of tense bullae, although small erosions
remained. This report supports an in vivo role for IgE autoantibodies in BP
pathogenesis.)

Ahmed, AR, Dahl, MV. “Consensus statement on the use of intravenous
immunoglobulin therapy in the treatment of autoimmune mucocutaneous blistering
diseases”. Arch Dermatol. vol. 139. 2003. pp. 1051-9. (Provides guidelines for
the use of IVIG, including indications, pre-screening, premedications, dose,
frequency, monitoring, and therapeutic end points.)

Bernard, P, Reguiai, Z, Tancrède-Bohin, E, Cordel, N, Plantin, P, Pauwels, C.
“Risk factors for relapse in patients with bullous pemphigoid in clinical
remission: a multicenter, prospective, cohort study”. Arch Dermatol. vol. 145.
2009. pp. 537-42. (Patients [114] with BP in clinical remission for at least 3
months on less than 10g clobetasol cream per week or 7 mg daily prednisone
equivalent discontinued all topical and systemic therapy and were followed for 1
year. The only factor significantly predicting disease relapse was a BP180 ELISA
titer greater than 27-IU/mL.)

Fischel, F, Barbe, C, Joly, P. “Clinical and immunologic factors associated with
bullous pemphigoid relapse during the first year of treatment: a multicenter,
prospective study”. JAMA Dermatol. vol. 150. 2014. pp. 25-33.

Taghipour, K, Chi, CC, Vincent, A, Groves, RW, Venning, V, Wojnarowska, F. “The
association of bullous pemphigoid with cerebrovascular disease and dementia: a
case-control study”. Arch Dermatol. vol. 146. 2010 Nov. pp. 1251-4. (A study
that showed bullous pemphigoid is significantly associated with cerebrovascular
disease and dementia.)

Brick, KE, Weaver, CH, Savica, R, Lohse, CM, Pittelkow, MR, Boeve, BF. “A
population-based study of the association between bullous pemphigoid and
neurologic disorders”. J Am Acad Dermatol. vol. 71. 2014 Dec. pp. 1191-7.
(Retrospective study of one Minnesota county that confirmed there is an
association of bullous pemphigoid with neurologic disorders, especially dementia
and Parkinson disease.)

Yu, KK, Crew, AB, Messingham, KA, Fairley, JA, Woodley, DT. “Omalizumab therapy
for bullous pemphigoid”. J Am Acad Dermatol. 2014. vol. 71. Sep. pp. 468-74.
(Article that discusses the use of omalizumab in 6 patients that demonstrated
the fact that omalizumab neutralizes the activity of IgE in patients with
bullous pemphigoid and improved 5 of 6 patients' disease activity.)

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provided by Decision Support in Medicine LLC. The Licensed Content is the
property of and copyrighted by DSM.

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