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26.2.2.2 Hidradenitis Suppurativa
Hidradenitis suppurativa (HS) is a chronic inammatory disease that courses clinically with episodes of abscesses and very painful nodules which are foul-smelling
and recurrent, the formation of sinus tracts and scar tissue. It affects typically
densely populated areas with apocrine glands, mainly the axillae, groin, buttocks
and the perianal and submammary areas. It usually appears during puberty and
tends to affect females more than males. Having this disease is usually associated
with a reduction in the patient’s quality of life, leading to frustration, depression,
social isolation, and difculty establishing social relationships. Treatment for
hidradenitis includes general measures (weight loss, quitting smoking), drugs (antibiotics, isotretinoin, nasteride, prednisone, cyclosporine, etc.) and surgery (incision and drainage, closure by secondary intention, etc.). In the last 5 years the
efcacy of biological drugs of the iniximab family (chimeric monoclonal antibodies) that act by inhibiting the proinammatory action of TFN-α has been
demonstrated.
Obesity is related both to HS and OSA, in which the intermittent obstruction of
the pharyngeal airways causes hypoxia during sleep. The shared immunologic
mechanisms may predict OSA risk of in patients with HS [55–57]. As in HS, the
proinammatory state in sleep apnea is characterized by the activation of nuclear
factor-kappa b and IL-17 signaling, together with increased concentrations of
inammatory cytokines such as TNF-α and IL-6. The incidence of OSA in a cohort
of patients with this disease was 3.5% compared to 2.5% in an obese control population. The risk was even higher in women and the youngest patients [58] (Fig.26.2).
Epidemiologic studies report the prevalence of OSA in patients with HS as being
higher than in healthy control populations [58]. One prospective trial used formal
sleep studies to assess the prevalence of OSA in HS.All patients completed validated questionnaires to evaluate the prevalence of sleep apnea, including the Berlin,
STOP-Bang, and Epworth sleep questionnaires. The patients with HS were more
likely to be obese and smokers [59], with a well-known risk factor for OSA development [60]. Furthermore, both HS and OSA are associated with elevated serum
levels of TNF-α and immune dysregulation [56, 61].
Thirty-eight percent (n=6/16) of the patients with HS who underwent outpatient
sleep tests had an AHI of >5 and were diagnosed with OSA.There was a positive
Fig. 26.2 Thirty-twoyear-old woman with
obesity and obstructive
sleep apnea. Abscessied
lesions and stulas in the
axillary region, compatible
with hidradenitis
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relationship between giving positive for OSA and stages 2 and 3in the Hurley system (a scale of the severity of the disease) (r=0.49, P=0.05), and between giving
positive for OSA and DLQI (quality of life) scores (r=0.56, P=0.03).
OSA is associated with elevated systemic inammation [56, 61]. In a series of
patients, those with a higher C-reactive protein level were more likely to be at risk
for OSA (v2=4187; P=0.04). Patients with severe HS were also at greater risk for
OSA (OR 4.6; P=0.02). However, this relationship continued to be signicant even
after controlling for other risk factors [62]. This study [62] shows that the prevalence of OSA in patients with HS is more signicant than that suggested in epidemiologic studies [58].
26.2.2.3 Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS), also known as functional ovarian hyperandrogenism, chronic hyperandrogenic anovulation or reproductive metabolic syndrome is a metabolic and endocrine dysfunction with a high prevalence. It is the
commonest cause of hyperandrogenism, with an incidence of 3% in adolescent and
adult women. It is estimated to be present in 75% of hirsute women and in 10% of
premenopausal women. Its presence should be suspected in any adolescent or
woman of child-bearing age with hirsutism or other skin manifestations of hyperandrogenism, irregular menstrual periods, and obesity. Its etiology is uncertain, and it
manifests by various symptoms and signs, especially irregular menstrual periods,
skin manifestations of hyperandrogenism (acne, alopecia, seborrhea, and hirsutism), obesity, infertility, insulin resistance and the polycystic aspect of the ovaries
on ultrasound examination (Fig. 26.3). Furthermore, most women with PCOS
(60%–68%) present insulin resistance and compensatory hyperinsulinemia which
may also be present in subjects of normal body weight. Insulin resistance plays a
predominant role in the long-term metabolic consequences of the syndrome, among
which type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease
should be noted.
Fig. 26.3 Twenty-threeyear-old woman diagnosed
with polycystic ovary
syndrome. Acne lesions on
forehead
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Women with PCOS are more likely to be insulin resistant than controls of the
same weight. They have an exceptionally high prevalence of early onset type 2 diabetes and a substantially greater risk of hypertension, dyslipidemia, heart disease
and other vascular disorders.
Evidence from small studies suggests that PCOS is independently associated
with greater risk and severity of OSA [63–68].
It is known that the greater risk of OSA in patients with PCOS is related to obe-
sity, insulin resistance, and hyperandrogenemia. Obesity has been identied as an
independent risk factor for OSA [69].
The current literature provides associative but not pathophysiologic links
between PCOS and OSA.The fact is that women with PCOS have the highest rates
of obesity and, as they age, they have a greater risk of developing OSA.Therefore,
physicians who treat obese women with PCOS should very clearly suspect the presence of OSA, mainly because both OSA and PCOS are independently associated
with greater cardiometabolic risk and treatment of the OSA may reduce this risk
[70–72].
Although most studies that have used matched groups or statistical adjustment
have found OSA in patients with PCOS to be more prevalent and severe, two crosssectional studies which analyzed the prevalence of OSA in women with PCOS
found no increased risk of PCOS/OSA when using a validated questionnaire [73] to
detect the disorder and polysomnography [74].
Lin etal. performed a longitudinal analysis using data from the Taiwan National
Health Insurance Research database between 1998 and 2009 [75], which covers
almost 98% of the entire population of Taiwan. The researchers identied 4595
women with PCOS aged 18years or older (mean age 28.0±6.79years) using the
relevant International Classication of Diseases (ICD-9-CM) code. These women
did not have any concurrent diagnosis of sleep apnea before enrolling in the study.
An equal number of female controls without PCOS or sleep apnea who were
matched for age and time of enrollment were selected. The diagnosis of OSA was
made after patients underwent polysomnography. The authors found that women
with PCOS had a greater incidence of OSA than controls (1.71 vs. 0.631000
person- years P < 0.001). Even after adjusting for age, level of urbanization,
income and comorbidities, there was still a signicant relationship between PCOS
and OSA risk (HR: 2.71, 95% CI: 1.62, 4.53). This study had various strengths,
with the rst and most important being the large sample size and its longitudinal design.
Another recent study [76] which analyzed 328 patients with PCOS, found that
the prevalence of OSA was 40% (131/328) and that 6 cases (5%) were severe.
Univariate analysis showed that body mass index and blood pressure were signicantly higher in patients with OSA than in those without OSA (P<0.05). At the
same time, the anti-Mullerian hormone was lower in patients without OSA.As for
glucose metabolism and lipids, glycosylated hemoglobin, fasting plasma glucose,
and fasting insulin levels were signicantly higher in patients with PCOS and
comorbid OSA than those without OSA (all P<0.05). The patients with OSA also
had higher levels of triglycerides, low-density lipoprotein cholesterol,
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high- sensitivity C-reactive protein levels, and lower levels of high-density lipoprotein cholesterol (HDL-C) (P<0.05). Logistic regression analysis revealed that a
higher body mass index, elevated serum testosterone, and lower HDL-C were correlated with the appearance of OSA (P<0.05).
OSA in patients with PCOS is associated with multiple abnormalities in repro-
ductive endocrine and metabolic disorders.
Anecdotally, a report has been published of a 15-year-old girl [77] with severe
acanthosis nigricans of the neck and axillae with severe obesity (a body mass index
of 46.7kg/m2) and many other medical comorbidities, who presented progressive
worsening of OSA over 2years. The patient showed evidence of insulin resistance,
hypertension, dyslipidemia, PCOS, and nonalcoholic fatty liver disease. In this
case, the multiple morbidities, probably mediated by severe obesity, seems to be the
basis of the acanthosis nigricans and the OSA, but it is likely that the acanthosis
nigricans and OSA are unrelated.
Common acne is one of the skin manifestations of adolescent and young adult
women with PCOS.An open single-arm trial evaluated the use of 0.5mg/kg of
isotretinoin in subjects with common severe acne [78]. The authors assessed the
severity of the acne, depression, excessive daytime sleepiness and the sleep variables of the participants using polysomnography before and after 1month of treatment. The participants experienced improved sleep latency and efciency but no
change in AHI.
A retrospective case series relates keloid acne to OSA [79]. Keloid acne of the
neck (KAN) is an inammatory skin disease characterized by scarring of the hair
follicles in the posterior aspect of the neck and scalp and is attributed to mechanical
causes such as the use of razors or helmets and other external sources [80].
After studying 1.5 million patients, a study identied concomitant KAN and
OSA in 17 individuals. Sixteen (94%) were male and 9 (53%) were white. OSA
diagnosis was made before that of KAN in 10/17 individuals (58.8%). Eight patients
(47%) had received treatment with positive pressure for several years before the
diagnosis of KAN, which suggests that chronic follicular occlusion of the CPAC
could contribute to the development of KAN.In two cases (11.7%), there was
explicit evidence of the use of CPAC as a precipitating or exacerbating factor of the
lesions.
Metabolic syndrome, a condition commonly associated with OSA, has been
implicated in the pathogenesis of the disease due to chronic follicular occlusion.
It is believed that the proinammatory cytokines driven by the insulin resistance
contribute to abnormal follicular keratinization, which increases the risk of common acne and hidradenitis suppurativa [81]. Through similar mechanisms, the
metabolic abnormalities observed in OSA may also increase the likelihood of
developing KAN in white patients, where the disease is less prevalent than in
black patients.
Other rare diseases exist with skin manifestations that are associated with
OSA due to the link with obesity, such as Elephantisis Nostras Verrucosa
(chronic lymphedema) [82] and Klinefelter syndrome (ulceration of the lower
extremities) [83].
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26.2.3 Skin Disease Related toMechanical Obstruction
oftheUpper Airways
26.2.3.1 Lipodystrophies
Lipodystrophy, an abnormal redistribution of fat, has also been linked to a greater
risk of OSA due to mechanical obstruction of the upper airways in patients with
Klinefelter syndrome.
Familial Partial lipodystrophy type 2 (also known as thick neck syndrome) is
due to mutations in the LMNA gene, which encodes the lamins A and C, components of the nuclear lamina (MIM 151660). Patients are healthy at birth, but around
puberty, they selectively lose fat deposits in the extremities and buttocks while visceral, facial, and neck fat deposits are conserved and may increase with excessive
calorie intake. Using polysomnography OSA has been documented in 2 women
with this disease [84].
Lipodystrophy resulting from antiretroviral treatment for HIV is another
causal factor [85]. Protease inhibitors are a vital part of antiretroviral therapy in
patients infected with HIV.Long-term use of these drugs may cause lipodystrophy,
characterized by peripheral lipoatrophy and accumulation of central fat, which may
increase the risk of developing OSA.Thus, some patients develop an extensive collection of adipose tissue around the neck and pharynx (the so-called “buffalo
hump”), which could explain why 7% of patients with HIV have OSA as compared
to 2%–4% of the normal population [86]. The increase in the circumference of the
neck, body mass index with overweight or obesity and lipodystrophy are potential
risk factors for OSA in patients with HIV.In general, they are patients of normal
weight but with a fat content that is notably increased, particularly in the trachea
area. This suggests that the association could be related to adipose tissue distribution that is characteristic of patients with this type of lipodystrophy.
One recent retrospective cohort study with 54 patients found no signicant association between the length of use of protease inhibitors and OSA severity [87].
Multiple symmetric lipomatosis, also known as Launois–Bensaude syndrome,
is another rare condition associated with OSA [88]. Blistering diseases which progressively compromise the upper airways may also cause OSA.A case series of 142
patients with cicatricial pemphigoid, a chronic blistering disease of the mucosa
which frequently courses with subsequent scarring, reported that 24% of the participants had nasal manifestations, and 79% had subsequent nasal obstruction [89]. Of
these patients, two were diagnosed with OSA.Lesions in the larynx were found in
9% of patients and in the oropharynx and hypopharynx in 8% of patients. Cicatricial
pemphigoid may be a direct cause of OSA given the obstruction of the upper
airways.
Anecdotally, there has been one report of severe OSA in two children, ages 10
and 14, with hypertrophic scarring after severe burns in the face and upper part of
the body probably due to restriction of movement of the thoracic wall due to the use
of a close-tting garment, with signicant oxygen desaturation [90]. Both children
experienced an improvement in OSA symptoms once the tight-tting garments
were removed.
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There are multiple studies of cases of OSA as a consequence of the obstruction
of the upper airways secondary to localized tumors, postradiotherapy of the upper
airways, and urticaria or angioedema affecting the uvula.
P. Redondo
26.2.4 Skin Disorders Related toHypoxia
26.2.4.1 Skin Cancer andOSA
Recently OSA has been shown to be associated with a greater prevalence, incidence, and mortality from skin cancer [91]. The systemic inammation due to the
hypoxia-reoxygenation cycles in OSA may activate several mechanisms which
enhance tumor progression [92, 93]. Specically, two recent studies have shown the
existence of a relationship between OSA and the aggressiveness of cutaneous melanoma [94, 95].
Melanoma is a malignant tumor derived from melanocytes, dendritic cells originating from the neural crest and responsible for the synthesis of melanin. It may
spread both through the lymph nodes or the bloodstream and may become established on normal skin. When it appears on an existing nevus, the main criteria which
give rise to the suspicion of the diagnosis of melanoma are changes in size and
uneven pigmentation. Although it has not been fully demonstrated, several sources of
evidence indicate the fundamental role of ultraviolet (UV) radiation in the development of at least two-thirds of all melanomas. It has been veried that there is a statistically signicant relationship between melanoma and intermittent sun exposure
(odds ratio [OR]=1.71), especially if this is accompanied by sunburn (OR=1–91)
and that the incidence and mortality from melanoma are higher in regions close to the
equator where the intensity of UV radiation is greater. The risk of developing melanoma is higher in white patients, those of Nordic or Celtic origin and is lower among
natives of Asia, Africa and South America and in dark-skinned subjects from the
Mediterranean region. The danger is greater when the UV radiation interacts with a
genetically determined phenotype characterized by subjects having fair skin that
burns easily (phototypes I and II) and multiple nevi, especially if they are atypical.
Although melanoma represents 10% of all skin cancers, at least 65% of the
deaths related to skin cancer can be attributed to melanoma. However, unlike nonmelanoma skin cancer, this tumor is diagnosed at an earlier age (mean age of
55years). It reaches the highest specic incidence by age in individuals over 65.
A cohort study conducted at the national level in the United States on 5.6million
people using data from a national health insurance database for employees found a
greater likelihood of melanoma in patients with OSA (OR 1.14, IC 1.10–1.18) [91].
Some studies have also evaluated the possible mechanisms of the association. A
Spanish cohort study of 350 patients recently diagnosed with melanoma and stratied
by AHI, the researchers measured serum levels of biomarkers related to hypoxia and
tumoral adhesion (VEGF), IL-8, intracellular adhesion molecule (ICAM) and vascular intracellular adhesion molecule (VCAM-1), and markers of tumor aggressiveness
(S100 calcium-binding protein B, S100B) and melanoma inhibitory activity (MIA).
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Levels of VEGF, IL-8, ICAM-1, S100B, and MIA were not related to the severity
of OSA although VCAM-1 levels were higher in patients with OSA than in those
without the disease (mild OSA: odds ratio (OR) 2.07, P=0.021; moderate to severe
OSA: OR 2.35, P=0.013). In patients with cutaneous melanoma, OSA may contribute to tumorigenesis through the adhesion produced by this integrin [96].
In a Spanish prospective cohort study of 376 patients with cutaneous melanoma
who underwent polysomnography, intermittent nocturnal hypoxia, calculated by the
desaturation index, was found to have a weak association with HIF-1α (OR 1.03,
95% CI: 1.01–1.06), but not with VEGF [97]. Furthermore, in 436 consecutively
enrolled patients, the aggressiveness of the cutaneous melanoma, as evaluated using
well dened criteria such as the Breslow index increased in a markedly and independent fashion in patients with OSA, especially if they were younger [98].
A recent study with 56 patients consecutively diagnosed with melanoma [94]
shows that the frequency and severity of respiratory disorders during sleep were
independently associated with a greater rate of melanoma growth and greater tumor
thickness, higher mitotic index, and more ulceration. These features are associated
with a poor prognosis in cutaneous melanoma.
Multivariate analyses were used to examine the independent relationship between
the severity of sleep respiratory disorders (AHI) and indices of nocturnal oxygen
desaturation (ODI3% vs. ODI4%) and measures of aggressiveness of the cutaneous
melanoma. All of these factors were independently associated with a higher rate of
melanoma growth. 60.7% of patients had respiratory disorders during sleep (AHI
≥5) and 14.3% severe OSA (AHI ≥30) [94]. Other factors involved included oxida-
tive stress and a high degree of systemic inammation in OSA [99].
A recent meta-analysis including six studies with a combined cohort of more
than 5million patients suggests that patients with OSA are at greater risk for melanoma in comparison to those without OSA.This effect continued to be signicant
between the studies with at least 5years of follow-up but lost importance for prospective studies and subgroups adjusted for obesity [100].
Related to pathophysiologic mechanisms, several factors need to be considered:
Firstly, the hypoxia in OSA may favor melanoma development by increasing
tumorigenic biomarkers such as HIF [101], which coordinate the expression of the
genes that promote tumor adaptation and survival, such as efcient angiogenesis
metastasis and resistance to treatment [102].
Secondly, hypoxia may contribute even further to the tumorigenesis of the melanoma by promoting proliferation, the ability for self-renewal and the chemoresistance of the melanoma mother cells [103, 104].
Thirdly, the intermittent hypoxia and sleep fragmentation of OSA may enhance
tumor growth by altering the host immune response. The macrophages associated
with the tumor are an essential component of the tumor stroma and polarize into two
functionally different phenotypes, M1 (tumor inhibitors) and M2 (tumor promoters)
[105]. In addition, the intermittent hypoxia and sleep fragmentation of OSA may
change the polarity of the macrophages toward the M2 phenotype, which enhances
tumoral proliferation, migration, and invasion.
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Fourthly, the increase in sympathetic activity due to OSA may favor melanoma
development as the increase in beta-adrenergic receptors promotes angiogenesis
[106, 107]. Some studies show that beta-adrenergic receptor antagonists may mitigate the progression of melanoma [108].
P. Redondo
26.2.4.2 Others
Another possible association between skin diseases and OSA suggests that
androgenetic alopecia or male pattern baldness is related to hypoxia. In a crosssectional study of 932 men, those with OSA and a family history of hair loss
were seven times more likely to have male pattern baldness than those who had
neither risk factor (IC 3.70–12.56). The authors hypothesize that this phenomenon could be related to the chronic-intermittent hypoxia of OSA which interrupts the normal division of hair follicles and leads to iron deposition in tissues,
which is associated with a reduction in the saturation of transferrin which in
turn leads to the inadequate availability of iron to support the division of the
follicles [109].
OSA may also be considered a risk factor for the survival of skin aps in breast
reconstruction [110].
26.3 Skin disease related to Treatment withCPAP
26.3.1 Local Skin Effects Secondary totheUse ofVentilation
withNoninvasive Positive Pressure
OSA is often treated with various types of masks that administer noninvasive continuous positive pressure to the airways during sleep. In one study, up to 50% of
CPAP users reported skin allergy, air leaks, or abrasions. However, these factors are
not sufciently serious to limit the use of the treatment [111]. In addition, the masks
can cause several types of dermatitis.
Allergic contact dermatitis is associated with itching, redness, and, if sufciently severe, blisters. In rare cases, the silicon component of the CPAC may be an
allergen that triggers allergic contact dermatitis. One study evaluated the effect of
the composition of the CPAP mask in adult patients undergoing treatment with
CPAP for OSA and compared individually molded masks (71%) with industrial silicone masks (28%) [112]. The individually molded masks reduced nasal abrasions
and red eyes and caused fewer contact allergic reactions than the silicone masks
(13% vs. 5%). However, using a humidier did not change the rate of adverse effects
in the two groups. In the presence of eczematous lesions in the cephalic pole of
patients with CPAC, the dermatologist must rule out allergic contact dermatitis
using a standard battery of contact tests [113].
Patients with dry and easily irritable skin are at greater risk of presenting irrita-
tive dermatitis or seborrheic dermatitis (Fig.26.4). Treatment with humectants
before to the use of CPAP may protect the face from irritative dermatitis induced by
the CPAP mask. The incorrect use of CPAP masks also increases the risk of patients’
skin becoming dry due to air leaks from the mask.
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Fig. 26.4 Thirty-sevenyear-old male with obesity
and obstructive sleep
apnea. Eczematous lesions
compatible with seborrheic
dermatitis in the central
facial region and beard
area, which worsen with
the use of CPAP
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An automated retrospective research study showed that patients with rosacea
have a signicantly higher risk of OSA [114].
Rosacea is a chronic inammatory dermatosis characterized by the appearance
of erythema, telangiectasias, papules and pustules in the centrofacial area. The
etiology of the disease is unknown although the involvement of several factors
such as vascular reactive disorders and an immunologic response to microorganisms such as Demodex folliculorum and Helicobacter pylori has been postulated.
As a result of the limited knowledge of the physiopathology of the disease, therapeutic options are not directed against the pathogenic mechanisms and are not
curative. Treatment is based on the use of antibiotics, anti-inammatories, and
retinoids administered topically or systemically, vascular laser, and, in severe
cases, surgical techniques. Rosacea is a disease that typically affects subjects aged
between 30 and 50. In Europe, it is estimated that it affects between 1.5% and
10% of the population.
A recent study reports that ve patients with OSA developed rosacea or experienced worsening of the disease symptoms after using a CPAP mask that covered the
nose and mouth. Two patients exhibited centrofacial symptoms restricted to the
shape of the CPAP mask, and three patients had cutaneous nasal symptoms. It was
postulated that the effect of the CPAP mask, which increases the humidity and
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temperature of the skin, may induce lesions in patients with an underlying sensitivity to rosacea. This could have implications for the choice of the CPAP mask and the
topical therapeutic options for the rosacea. Furthermore, OSA and its metabolic/
cardiovascular comorbidities may also play a role in the development of rosacea
symptoms [115].
P. Redondo
26.3.2 Systemic Skin Benefits Following theUse ofVentilation
withNoninvasive Positive Pressure
It is essential to highlight that CPAP may also be a therapy for the skin as adequately
treated OSA may improve wound healing. In a case study, the use of CPAC was
associated with the resolution of a dyshidrosis, an endogenous eczema of the hands.
The authors speculate that improved oxygenation of the tissues and a reduction in
sympathetic tone (due to fewer nocturnal awakenings) was the reason for the
improvement [116]. It was found that two patients with OSA had yellow nail syndrome and the discoloration of the nails resolved with the use of CPAP [117].
Another adult had onychophagy and treatment with positive pressure, improved bot
only the parasomnia improved, but also, the nail biting with resolution of the onychodystrophy [117].
In line with this, CPAP also seems to improve excessive nocturnal sweat-
ing. Sweating is controlled almost entirely by the sympathetic nervous system,
and its primary function is to increase heat loss and maintain thermoregulation [118].
Habitual snoring in children is associated with OSA [119]. In a study of 1760
third grade German children, chronic snoring was more frequently associated with
sleep hyperhidrosis (OR=3.6, 95% CI 1.2–10.8) [120].
Two Icelandic studies have examined the relationship between OSA and sleeprelated sweating in adults [118, 121]. In the rst, with 15 patients with moderate to
severe OSA, core body temperature, skin temperature and electrodermal activity (a
measure of sweating) were evaluated in patients untreated for OSA (mean HAI
45.3±3.9). At the beginning of the study, electrodermal activity was correlated with
an increase in morning and evening systolic blood pressure and less rapid eye movement sleep. After treatment with CPAP for 107±19days, during which mean AHI
dropped to 4.5±0.9, electrodermal activity fell from 131.9±22.4 to 78.5±17.7.
Treatment was also correlated with reductions in evening systolic and diastolic
blood pressure reductions while rapid eye movement sleep increased. The second
study [121] evaluated the effect of CPAP on sleep-related sweating in 700 participants from the Icelandic Sleep Apnea Cohort followed over 2years. Frequent nocturnal sweating was observed in 30.6% of males and 33.3% of females with OSA
compared to 9.3% of males and 12.4% of women from the general population
(P<0.001). In addition, the prevalence of frequent night sweating decreased after
the full CPAP treatment from 33.2% to 11.5% (P<0.003). Hyperhidrosis may be
an index of sympathetic activation and dysregulation of the autonomous nervous
system in OSA.
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