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Pemphigus Vulgaris
DOI: http://dx.doi.org/10.5772/104814
. Antibody-dependent cytotoxicity, which consists of activation of NK cells
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through binding the human Fc portion of Rituximab to the FcRIII receptor:
this activates NK cells to release cytotoxic mediators, including perforins
and granzyme B, which induces caspases-dependent cell death in the target
lymphocyte.
. Antibody-dependent phagocytosis, in which neutrophils, monocytes and
macrophages bind Rituximab opsonized B-cells through the Fcγ
Receptor.
Recently, a new mechanism referred to as trogocytosis, or shaving has been
characterized. In trogocytosis, macrophages remove Rituximab-CD complexes by transferring plasma membrane; this triggers cell death through a yet-to-be
identified mechanism [].
Despite being used in the treatment of pemphigus since the early s, anti-
CD monoclonal antibodies such as rituximab are still considered third-line agents
in the European Academy of Dermatology and Venereal Diseases guidelines published
in []. Recently, anti-CD antibodies have been recommended as the first
choice only for moderate to severe and/or resistant pemphigus. Following administration of rituximab, a rapid and sustained decrease in circulating and tissue B lymphocytes is observed, lasting at least to months. Recent evidence suggests that it also
affects T lymphocytes []. Rituximab treatment reduced the total corticosteroid
dose required for clinical remission, thus reducing side effects secondary to long-term
high-dose corticosteroids. A recent retrospective case-control study involving
patients showed that patients previously treated with rituximab treated with conventional therapy were able to reduce their monthly prednisone dose by from a
median of .mg/month to .mg/month [].
It should be administered IV as a slow infusion (four to hours). There are no
standardized protocols for the use of rituximab in autoimmune bullous diseases.
There is much debate about the optimal dose of Rituximab in pemphigus. Two main
protocols are used: the rheumatoid arthritis protocol, which consists of two ,mg
infusions two weeks apart, and the lymphoma protocol, which consists of four
mg once-weekly infusions []. No differences in percent remission and diseasefree time were observed in either protocol. They can be used alone or in combination with intravenous immunoglobulin, plasmapheresis and immunoadsorption. It
can also be applied to patients already taking prednisone and immunosuppressive
drugs; dose reduction and suspension of the latter should be accelerated, due to the
increased risk of infection [].
Intravenous Immunoglobulin (IVIg); derived from a pool of donors, IVIg
consists of human plasma-derived IgG, sugars, salts and solvents []. It is thought
that IVIg functions by saturating the neonatal Fc receptor, thereby increasing the
catabolism of the patient’s serum antibodies containing pathogenic autoantibodies
[]. IVIg is mostly used in patients resistant to corticosteroid and immunosuppressive treatments. gr/kg is applied in each session. In studies, it has been shown that
the application of .g/kg/day for consecutive days is effective in the treatment
[, ]. It can also be combined with rituximab. Slow –.hour infusions can
minimize infusion reactions []. A major benefit of IVIg is its few side effects.
The most common side effects are headache, dyspnea, tachycardia, and abdominal
discomfort. The most serious adverse events are aseptic meningitis and cerebrovascular accidents, occurring in < of PV patients treated with IVIg []. It can be
used on pregnant women.
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TNF-α inhibitors; TNF-α is one of the cytokines involved in acantholysis.
Although the use of Infliximab and Etanercept as a case report appears to be effective
in the treatment of PV, there are conflicting results [].
Topical treatment; PV is largely managed with systemic therapy, but skin and
mucosal care are extremely important. For this purpose, topical corticosteroids and,
if there is a risk of infection, antibiotic creams are often added to the treatment. It has
also been reported that tacrolimus and pimecrolimus, pilocarpine gel , nicotinamide gel , . sulfadiazine creams are also beneficial [].
During the treatment period, patients should be followed closely for diabetes,
hypertension, heart failure, myopathy, osteoporosis, avascular bone necrosis,
glaucoma, cataract due to corticosteroids, infections, especially respiratory tract
infections, hepatitis, CMV reactivation or hematological abnormalities (anemia,
leukopenia) as a result of immunosuppression.
Future Therapies; CAAR-T Therapy, BTK inhibitor and pMAPK inhibitor are
included.
CAAR-T Therapy; T cells expressing chimeric autoantibody receptors (CAAR-T
cells) that target antibody-producing B cells are one of the latest proposed avenues for
treating for autoimmune conditions.
Bruton tyrosine kinase (BTK) Inhibitor; Bruton tyrosine kinase (BTK) is
expressed in B cells and innate immune cells, acting as an essential signaling element in multiple immune cell pathways. Selective BTK inhibition has the potential
to target multiple immune-mediated disease pathways. Rilzabrutinib is an oral,
reversible, covalent BTK inhibitor designed for immune-mediated diseases [].
One of the new potential treatments for pemphigus, the BTK inhibitor rilzabrutinib
(PRN) was recently tested in patients with PV in a phase II trial and controlled
– of lesion activity in patients in a mean of weeks []. Thus, inhibition of
kinases such as BTK shows promising potential for future treatment of PV.
pMAPK inhibitor (SB); In a murine model of pemphigus, pMAPK
inhibition prevented blister formation. On the other hand, in a study, the formation
of blisters in the mucosa could not be prevented by a pMAPK inhibitor, and they
claimed that, unlike the epidermis, the ultrastructural changes of blister formation
and desmosomes were independent of pMAPK in the oral mucosa [].
. Prophylaxis against side effects in prolonged corticosteroid
Basic screening and prophylaxis of osteoporosis, ophthalmological evaluation,
vitamin D and calcium supplementation during corticosteroid therapy, treatment
with bisphosphonates (ie alendronate, risedronate) in patients at risk of developing
osteoporosis (postmenopausal women and>years and>months on corticosteroid treatment), clinical systemic antifungals, antiviral and antibiotic therapy if
needed, use of H-blockers or proton pump inhibitors, antithrombotic prophylaxis
in case of high thrombosis risk, psychological support if necessary, physiotherapy if
long-term corticosteroid therapy is required [].
. Prognosis
The mortality rate of PV is estimated about –. Death is mainly a result of
corticosteroid and immunosuppressant side effects. In particular, patients with
Pemphigus Vulgaris
DOI: http://dx.doi.org/10.5772/104814
persistent PV may develop serious infections secondary to high-dose corticosteroid
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use. Most patients with relapsing forms of the disease require a long course of treatment of years or more [].
. Pemfigus vulgaris in children
PV is the most common type in the pediatric group among all pemphigus types,
excluding endemic pemphigus foliaceus []. The pediatric variant is divided into
two, childhood PV (–years) and adolescent (juvenile) PV (–years) [].
Most patients have mucocutaneous involvement, both in childhood and in the juvenile
form. Oral, nasal, ocular and anal mucous membranes are involved. The frequency
of genital involvement is high in both groups []. The clinical picture is similar to
that in adults. Loose bullae on intact or erythematous skin open easily and become
eroded and crusted lesions. Antibody titrations can be detected in the serum in most
of patients []. Nikolsky’s sign is positive.
Systemic steroid as in adults, is the cornerstone of treatment []. Systemic side
effects develop in two-thirds of patients treated with systemic steroids. The most
common side effects are; Cushing’s syndrome (), growth retardation ()
and infection (). Prednisone dose is started at –mg/day, when new lesion
growth stops, it is gradually reduced and adjuvant therapy is added. Many adjuvant
agents such as AZA, dapsone, mycophenolate mofetil, cyclophosphamide, methotrexate, cyclosporine, plasmapheresis, IVIg and rituximab have been used in the
treatment of children as in adults. Data on the use of rituximab therapy in pediatric
patients are limited. The youngest case treated with rituximab was a -year-old girl
[]. There are partial and complete remission reports in the literature. There is no
standard dosing regimen in children. The lymphoma protocol was used in most of the
published cases. Treatments usually last –years and the prognosis is better than in
adult patients [].
. Pemfigus vulgaris during pregnancy
PV is extremely rare in pregnancy. On the other hand, pregnancy may accelerate
or increase PV, as reported in well-known autoimmune diseases such as systemic
lupus erythematosus []. Babies of mothers with pemphigus may be affected by the
disease in many different ways, from stillbirth to transient PV lesions in newborns,
due to transplacental transmission of pathogenic anti-Dsg antibodies []. The more
uncontrolled the disease in the mother and the higher the titers of Dsg antibodies in
the mother’s serum or umbilical cord blood, the worse the possible outcomes []. PV
seen during pregnancy can affect the mother, delivery and fetus. While the disease
exacerbates mostly in the first, second trimester and postpartum periods, it calms
down in the third trimester []. The reason for this is probably the increase in the
endogenous chorionic corticosteroid hormone and the resulting immunosuppression
[, ]. However, no change is observed in some patients during pregnancy, and
these patients may remain in remission []. The postpartum disease worsens in all
pemphigus patients who are not treated during pregnancy []. If the disease worsens
in the first trimester, medical termination of pregnancy may be considered. If the
worsening of the disease occurs in the second or third trimester, steroids are a safe
treatment option [].
Wound Healing - Recent Advances and Future Opportunities
In the publications on the treatment of autoimmune bullous diseases in pregnancy,
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it is stated that topical/systemic steroids and AZA can be used safely. In a small
number of case reports, it has been reported that rituximab, IVIg, and dapsone may
also be safe []. AZA is the most commonly used non-steroidal immunosuppressant
in pemphigus. If it is necessary to give, the lowest dose should be preferred to prevent
fetal damage []. The pregnancy category is D. Cyclosporine is believed to be less
effective in the treatment of pemphigus but is the most reliable agent in pregnancy
[]. MMF, cyclophosphamide, and methotrexate are drugs that are not preferred or
even contraindicated during pregnancy [].
. Vaccination in pemphigus patients
Administration of live vaccines is contraindicated when using adjuvant immunosuppressants and rituximab. Vaccination against seasonal influenza, HN, tetanus
and pneumococci are recommended in patients receiving oral corticosteroids or
immunosuppressives. During systemic immunosuppression, the level of protection
after vaccination raises question marks []. On the other hand, it has been reported
in the literature that pemphigus vulgaris is seen after tetanus diphtheria, hepatitis B
and influenza vaccine applications, and that the disease exacerbates after influenza
vaccine use []. We do not have any data on which patients vaccination will cause
disease reactivation [].
Although COVID mRNA vaccines may cause autoimmune bullous disease activation, it is recommended not to abandon the vaccination and to treat the existing
picture in case of disease activation [].
Based on vaccination experience, when vaccines for COVID- are available,
dermatologists may advise vaccination –weeks after completion of a treatment
cycle with rituximab or extend dosing intervals so that a minimum time of weeks
precedes the next drug infusion [].
Limited data suggest that patients with autoimmune bullous disease receiving
immunomodulatory therapies are not primarily at risk for serious or fatal
COVID- [].
Pemphigus Vulgaris
DOI: http://dx.doi.org/10.5772/104814
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Chapter 8
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Diagnosis and Treatment of
Venous Leg Ulcer
VesnaKaranikolic and AleksandarKaranikolic
Abstract
Venous leg ulcer (VLU) represent a pathological tissue change in the form of a
defect in the lower leg which occurs as a complication of chronic venous insufficiency.
The prevalence of VLUs varies between .– in the total population and – in
persons over the age of . Venous ulcer is usually localized on the inner side of the
lower third of the leg, oval, circular or irregular in shape. It is usually fibrous or covered with fresh granules that bleed heavily to the touch. It is very important to have a
comprehensive clinical examination at the very beginning. Subsequent non-invasive
and sometimes invasive tests may be indicated for diagnosis and treatment planning.
Inadequate diagnosis results in inadequate therapy. The goal of therapy is complete
restitution of the tissue defect and prevention of recurrence. The three basic elements
of VLUs therapy are: local therapy, compression therapy and surgical treatment. If
VLUs do not heal despite the application of standard therapeutic modalities, there
are opportunities to apply new treatment technologies. The modern approach to the
treatment of VLUs is based on the application of various biophysical interventions
and medical devices.
Keywords: venous disease, venous leg ulcers, wound healing, diagnosis, venous leg
ulcers treatment
. Introduction
Venous leg ulcer (VLU) represent a pathological tissue change in the form of a
defect in the lower leg which occurs as a complication of chronic venous insufficiency
(CVI) []. Chronic ulceration is defined as ulceration on the lower leg that lasts (does
not heal) within weeks, and is caused by various etiopathogenetic factors [].
Venous leg ulcers often heal slowly and result in long-term suffering and intensive use
of health care resources [, ]. A VLUs represent a growing health problem, and they are
a condition that is very expensive to treat for both the health system and patients.
A VLUs endangers the patient’s normal life. Treatment of VLUs requires dedication
and cooperation between the patient and the doctor. The health-related impact of VLUs
is increasingly recognized as a valuable outcome measure for assessing interventions,
especially when complete cure is unlikely []. Adults with VLUs often have multiple disabling symptoms, including pain, sleep disturbance, depression, swelling of the lower
extremities, fatigue and symptoms associated with inflammation of lower leg (redness,
localized heat, discomfort due to high exudate levels and itching) [].
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The prevalence of VLU varies between .– in the total population and –
in persons over the age of []. Studies have shown that – of the adult population either has or has had venous ulceration []. The prevalence of VLU in Western
European countries in the population over the age of is .–. [].
It is very important to point out that a certain number of VLUs heal very slowly
or not at all. In a period of about months with the application of adequate therapy, about of VLUs heals [, ]. However, about of VLUs do not heal even
after years from the beginning of treatment, and about even after years
from the beginning of treatment []. At the annual level, the recurrence rate of
VLUs ranges from – []. The risk of recurrence over a period of year ranged
from – [].
Risk factors for VLUs are numerous, and most patients have more than one.
Most of these factors are immutable and this group includes being female, elderly,
having previous venous thrombosis of the legs, pulmonary embolism, multiparity, musculoskeletal and joint diseases [, ]. Obesity and sedentarianism are risk
factors that can be influenced on []. The genetic traits of an individual can also
be emphasized as a predisposing factor [, ], but the specific gene or set of genes
responsible for the occurrence of this disease has not been determined so far. In
people with varicose veins, Forkhead box C, located on chromosome q [],
was isolated.
Despite the application of different standard treatment modalities for VLUs, a
certain percentage of venous ulcers do not heal. Studies have shown that prolonged
healing time or refractoriness to applied therapy may be due to an increase of T
lymphocytes and granulocytes, lack of oxygen, growth factor and cytokine imbalance []. For this reason, we are working on the development of modern therapeutic
modalities, while the number of new techniques for the VLUs care has increased in
recent years and is constantly improving [].
. Symptomatology
Venous ulcer is usually localized on the inner side of the lower third of the leg,
oval, circular or irregular in shape. The surface of the ulcer depends more on the
degree of development than on the etiology. It is usually fibrous or covered with fresh
granules that bleed heavily to the touch (Figure ).
The ulcer area is thickened, pigmented and induced, together with subcutaneous
adipose tissue. These changes correspond to lipodermatosclerosis, which is in fact a
pre-ulcerative condition [].
The absence of lipodermatosclerosis in the vicinity of the ulcer surface suggests
that the ulcer may not be of venous origin. The presence of dilated venules, most
often around the maleolus, below the ulcer surface, is also significant as a consequence of the transmission of increased venous tension through insufficient communicating veins. The presence of larger, dilated incompetent communicating veins
is very significant for venous ulcers. An ulcer localized on the lateral side of the lower
leg is often associated with an incompetent saphenous vein []. The presence of
edema, lipodermatosclerosis and varicose superficial veins also supports the venous
ulcer genesis. When examining ulcers, it is necessary to always examine the condition
of the arterial circulation [].
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