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114
Fig. 6.9 Lichen planus.
Extensive involvement of
the perianal area
Fig. 6.10 Vaginal
involvement by LP in a
premenopausal woman.
Note the presence of
inammation and
parabasal cells (phase
contrast microscopy, 400×)
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concurrent steroid-treated LP [36], thus highlighting that these women may have
increased risk of vulvar cancer through the two pathways (dermatoses and HPV).
6.2.4 Psoriasis
Psoriasis is a chronic inammatory skin disease with a prevalence of approximately
2% in the general population. This disease has a bimodal onset, but vulvar manifes-
tations can occur in patients of all ages [37].
On physical examination, bright red, sharply demarcated lesions can appear
above the surrounding normal skin (Fig.6.11). Differently from the typical lesions
of psoriasis in other areas, the silver scales are often absent and can only be apparent
in the mons pubis [38]. The presence of psoriatic lesions on other areas (knees,
elbows, gluteal cleft, scalp) suggests the diagnosis. Köebner or isomorphic phenom-
enon can also be apparent in genital psoriasis. The biopsy should be considered only
in difcult cases without a typical presentation and to exclude malignant lesions.
The treatment should stop the itch-scratch cycle, as it contributes to more inam-
mation. Low to medium potency topical steroids, in combination with steroid-
sparing agents, are often used to reduce the inammation. Second-line treatments
Fig. 6.11 Psoriasis
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include emollients, topical vitamin D analogues, and calcineurin inhibitors [38]. In
severe cases systemic therapy, including immunosupressants and biologics, may be
considered.
6.2.5 Atopic andContact Dermatitis
Dermatitis or eczema is a poorly demarcated, erythematous, and usually itchy rash
that can be found in 20–60% of patients with chronic vulvar symptoms [39].
Atopic dermatitis (AD) is a chronic pruritic skin disorder with multiple clinical
presentations according to the age, but the vulvar involvement can be seen both in
children and adult women. The true prevalence of vulvar AD is not known. A history
of other atopic diseases, suchas asthma, can be present. Vulvar manifestations arise
from a combination of factors that make this area particularly sensitive to eczema or
irritant contact dermatitis when exposed to irritants, such as a decient skin barrier
function and a thin epidermis. The principal symptom referred is pruritus. On physi-
cal examination, acute eczema is characterized by erythema, oedema, and vesicles/
Fig. 6.12 Atopic
dermatitis
J. Lyra and P. Vieira-Baptista
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papules (Fig.6.12), whereas in chronic eczema, there are excoriations and dry scaly
lichenication of the vulva. The presence of typical atopic eczema in other areas sug-
gests the diagnosis. The diagnosis is clinical. Regarding the treatment, median
potency topical steroids are the rst option. Calcineurin inhibitors may also be used.
Contact dermatitis (CD) may be associated with repeated contact with an irritant
or due to sensitization and contact allergy to a specic allergen. A are-up of the
rash after specic exposure should raise the diagnostic suspicion. The main symp-
toms are pruritus and pain. On physical examination, erythema, vesicles, oedema,
and erosions can be found.
Irritant contact dermatitis is the most frequent form of CD, and several factors
(e.g. urinary incontinence, detergents, surfactants) have been implicated in causing
vulvar eczema. Women with AD are at increased risk for contact dermatitis. One
frequent form of irritant contact dermatitis, in middle-age women, is intertrigo. It is
caused by increased moisture and friction in the intertriginous areas and that may
affect the vulva. Obesity, sweating, poor hygiene, and urinary incontinence are
some of the factors associated with it. Intermittent symptomatic treatment with topi-
cal corticosteroids is advised.
Allergic contact dermatitis could be nonsystemic or systemic. In the nonsystemic
form, many allergens are implicated, and the identication requires a dermatologi-
cal evaluation with patch testing. Women with vulvar dermatosis have a higher risk
of secondary contact sensitization due to locally applied medications (including
topical steroids (Fig.6.13)) and can react with a are-up vulvar eczema due to con-
tact with products containing the allergen. The systemic form is an allergic type IV
reaction in women previously sensitized to a specic allergen, when it is inhaled or
injected, resulting in an eczematous reaction. Some of these identied allergens are
nickel, chromium, and cobalt that are present in food products as oats, soy, choco-
late, nuts, and cocoa.
The therapy for both irritant and allergic contact dermatitis is based on eliminat-
ing irritants and/or allergens [40].
Fig. 6.13 Allergic contact dermatitis (clotrimazole+dexamethasone cream)
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6.3 Menopause andVulvar Atrophy
The urogenital tract is dramatically affected by the hormonal changes that charac-
terize menopause. With lower levels of oestrogens, not only the vagina but also the
vulva suffers many changes. In the vagina, mucosal thinning, loss of vaginal rugae,
reduced vaginal discharge, shortened vaginal length and width, and elevated vaginal
pH (associated with a marked decrease in lactobacilli and an increased diversity of
species) can be observed. In the vulva, the skin and vestibular mucosa become thin-
ner, subcutaneous fat decreases, the introitus becomes more lax, sensitivity dimin-
ishes, and there is a reduction in the width of the labia minora, with preserved
length—contrary to what can be seen in lichenoid dermatosis, in which there is a
reduction of both width and length [4].
Some of these changes may also be seen in women with vulvar dermatosis, and,
on the other hand, the latter are more common in postmenopausal women [14].
Altogether, this makes the differential diagnosis between vulvar dermatosis and
natural changes due to menopause a difcult task.
One of every two postmenopausal women will have vulvovaginal symptomatol-
ogy attributable to menopause, such as dryness, irritation, dyspareunia, dysuria, and
noninfectious vaginal discharge. Those symptoms can appear long after other
menopausal symptoms have resolved, and 10–25% of women using systemic hor-
mone therapy can still have urogenital symptoms [41].
Treatment may be initiated according to patient preferences and severity of the
symptoms. Avoidance of contact irritants, use of vaginal moisturizers, and low-dose
vaginal oestrogen preparations can be used. Vaginal oestrogen application (daily for
1–2weeks and then two times weekly) has been shown to be safe and effective in
the relief of genital symptoms than oral formulations [42].
Conict of Interest No conicts of interest to declare.
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© Springer Nature Switzerland AG 2019
F. R. Pérez-López (ed.), Postmenopausal Diseases and Disorders,
https://doi.org/10.1007/978-3-030-13936-0_7
R. Almeida Pinto (*)
Department of Urology, Hospital de S.João, Porto, Portugal
Faculty of Medicine of Porto, Porto, Portugal
i3S (Institute of Innovation and Investigation in Health), Porto, Portugal
7
Bladder Pain Syndrome/Interstitial
Cystitis
RuiAlmeida Pinto
7.1 Bladder Pain Syndrome/Interstitial Cystitis Introduction
Bladder pain syndrome/interstitial cystitis (BPS/IC) is a chronic visceral painful
condition of unknown etiology that affects millions of people worldwide. Symptoms
can be so severe that patients with BPS/IC may have quality of life with lower
scores than those treated for end-stage renal disease [1].
It was previously known as interstitial cystitis, later as painful bladder syndrome,
and since 2008 as bladder pain syndrome/interstitial cystitis in an attempt to include
and classify all patients with pain related to the bladder, not necessarily with inam-
mation coursing the bladder. The European Society for the Study of Interstitial
Cystitis (ESSIC) and the Bladder Pain Syndrome Committee of the International
Consultation on Incontinence dened BPS/IC as chronic (more than 6months) pel-
vic pain, pressure, or discomfort perceived to be related to the bladder, accompanied
by at least one other urinary symptom such as persistent urge to void or increased
daytime and nighttime voiding frequency, with the exclusion of confusable dis-
eases, namely, infection [2, 3]. The term interstitial cystitis (IC) should be reserved
for patients that have typical cystoscopic ndings like Hunner’s lesions and glo-
merulations as well as histological evidence of bladder inammation [2, 3].
Patients with the non-ulcerative phenotype, traditionally viewed as more benign,
tend to be younger, have lower urinary frequency, and have shorter duration of
symptoms before diagnosis. Pain is frequently described in the literature as more
intense in patients with ulcerative phenotype, the more aggressive form. Although
attractive it is yet to be shown that the ulcerative form of BPS/IC represents a pro-
gression of the non-ulcerative disease or a distinct disease within BPS/IC [4–6].
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7.2 Bladder Pain Syndrome/Interstitial
Cystitis Epidemiology
Based on population studies, the prevalence of BPS/IC shows enormous variations.
These variations have been attributed to different factors such as denition used,
diagnostic tools applied, and population surveyed [3].
The prevalence of BPS/IC ranges between 0.57 and 12.6% depending upon the
use of the O’Leary-Sant (OLS) or Pain and Urgency/Frequency (PUF) question-
naires, respectively [7]. BPS/IC has also 30–50 times higher prevalence with these
screening tools/questionnaires than with conrmed physician medical history and
physical examination [8].
Using OLS questionnaire, prevalence between countries varies, being so low as
20–30 per 100,000 women in Japan and the Netherlands and 300–450 per 100,000in
Austria, Taiwan, Finland, and the USA [9, 10]. Up to 12% of women experience
some symptoms during their lifetime [3]. Typically, BPS/IC age of onset is bimodal:
between 21–45 and 66–75years old [8]. Expert opinion leans to accept an average
prevalence of 300 per 100,000 women [3]. The prevalence among rst-degree rela-
tives of BPS/IC patients can be 17 times higher than in non-related individuals [11].
7.3 Bladder Pain Syndrome/Interstitial
Cystitis Pathogenesis
Etiology remains unknown and pathophysiology is probably multifactorial. Up to
50% of BPS/IC patients exhibit chronic inammation on bladder biopsy [12].
Typical histological ndings include abundant inammatory inltrates in the blad-
der urothelium with thinning or erosion, detrusor mastocytosis, granulation tissue,
and intrafascicular brosis [2]. The presence of mast cell migration is one of the
diagnostic criteria for BPS/IC from the National Institute of Diabetes and Digestive
and Kidney Disease (NIDDK).
The hypotheses for etiologies of BPS/IC range from unknown infection, immu-
nologic abnormality, autonomic dysfunction, to pelvic oor dysfunction and even
sexual abuse [12].
Since the early 1920s and 1930s, bacterial infection was and still is thought to be
a signicant cause of the changes observed in BPS/IC.However, until now, studies
failed to conrm one of the putative bacteria [13].
There is an association of systemic lupus erythematous and Sjogren syndrome
with BPS/IC. This fact strengthens the autoimmune disorder as the initial insult
[14]. An abnormal expression of HLA-DR molecules by the urothelium and activa-
tion of T-helper lymphocytes in patients with BPS/IC may enable these cells to
cause destruction of the urothelium [15]. However, no consistent prole of immune
activity has been reported.
BPS/IC patients also have increased resting heart rates [16] and increased sensitivity
to ischemia [17]. This autonomic dysfunction can be explained by the raise of sympa-
thetic tone without corresponding activation of the hypothalamic-pituitary-adrenal axis
R. Almeida Pinto
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[18]. Moreover, BPS/IC patients have been shown to exhibit high levels of urinary
catecholamines and an increase in the number of sympathetic bers coursing the blad-
der [19, 20].
BPS/IC patients are often found to have an increased prevalence of conditions
such as allergies (up to 70% higher in BPS/IC patients), Sjogren syndrome, or even
other somatic or visceral pain syndromes, namely, irritable bowel syndrome, bro-
myalgia, dyspareunia, pelvic oor dysfunction, chronic pelvic pain, vulvodynia,
and complex regional pain syndrome [21, 22]. The incidence of inammatory bowel
disease was found to be 30 times more common in BPS/IC patients with Hunner’s
lesions than in general population.
BPS/IC also has been associated with psychiatric illness such as panic disorder.
Recently, attention has been drawn to the high prevalence of child abuse in patients with
BPS/IC.This is a life event known to be linked with chronic pain development [23].
Higher prevalence of previous pelvic surgery has also been demonstrated among
BPS/IC patients [24]. It is therefore possible that, in many patients, surgeries or
other unrecognized pelvic insults may be the trigger mechanism to initiate the dys-
function of the pelvic region, mainly in postmenopause patients.
After the initial insult, pathophysiology of BPS/IC involves several modica-
tions. Although histological evidence of edema has never been documented, urothe-
lium suffers several changes, namely, altered permeability, decreased tight junction
formation, decreased proliferation, and increased apoptosis [12]. The glycosamino-
glycan (GAG) layer is disrupted, thus allowing the adherence of microorganisms
and the contact of urinary noxious elements with the urothelium, generating pain
[25]. Altered bladder permeability is commonly attributed to reduced tight junction
formation. Decreased proliferation and reduced tight junction formation are usually
related to increased urinary levels of antiproliferative factor (APF) [26]. In addition,
increased apoptosis was also reported, mostly due to an upregulation of inamma-
tory signals mediated by p38 and TNF-α [27].
Proliferation of sensory nerve bers also occurs in BPS/IC.In fact, some authors
suggested that inammation and tissue injury generate a signicant peripheral sprout-
ing of peptidergic, sympathetic, and parasympathetic bers, which could be the mech-
anism responsible for sensitization of the bladder, potentiating pain [
28–30]. These
phenomena could be correlated with the high levels of vascular endothelial growth
factor (VEGF) and nerve growth factor (NGF) found in BPS/IC patients [31].
7.4 Bladder Pain Syndrome/Interstitial Cystitis Assessment
As previously stated, BPS/IC is a condition characterized by chronic pelvic pain,
pressure, or discomfort perceived to be related to the bladder. Associated symptoms
could be persistent urgency and increased daytime and nighttime voiding frequency.
Pain is believed to be the driving symptom for other lower urinary tract symptoms
that commonly afict BPS/IC patients like frequency and nocturia [2]. Pain could
be described as a pressure, burning, discomfort, feeling of fullness/distension, sore-
ness, sharp, stabbing, spasm, or dull sensation related to the bladder. Usually related
7 Bladder Pain Syndrome/Interstitial Cystitis
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