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P. Ch al em
Table 8.1 Systemic
autoimmune disease and
obstructive sleep apnea
Systemic autoimmune diseases related to obstructive sleep
apnea
1. Rheumatoid arthritis
2. Ankylosing spondylitis
3. Systemic lupus erythematosus
4. Sjögren’s syndrome
5. Systemic sclerosis
6. Inammatory myopathies
7. Vasculitides
Fig. 8.1 Complex relationship between obstructive sleep apnea, autoimmunity and obesity
autoimmune diseases? (2) Are systemic autoimmune diseases a predisposing factor
for developing obstructive sleep apnea? (3) Can obstructive sleep apnea predispose
to systemic autoimmune diseases? Existing literature does not provide a satisfactory
answer to these questions but sheds some light on the matter (Fig.8.1).
8.1 Common Pathophysiological Pathways Between
Obstructive Sleep Apnea andSystemic
Autoimmune Diseases
Episodes of intermittent apnea result in decreased airow (and therefore oxygen)
through the airway, leading to tissue hypoxia. The consequence of this “intermittent
hypoxia” is increased oxidative stress and lipid peroxidation. This leads to a state of
chronic inammation, which is characterized by the expression of cytokines such as
tumor necrosis factor alpha (TNF-α), interleukin (IL)-6 and IL-8, among others
[5, 13].
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This inammatory state is also characterized by the activation of transcription
factors such as the hypoxia-inducible factor (HIF) and the nuclear factor kappa beta
(NF-ƙB). HIF plays a role in angiogenesis processes that take place in inammatory
phenomena. In turn, NF-ƙB induces the transcription of genes related to proinammatory cytokines (TNF-α, IL-1, IL-2, IL-6, IL-8, IL-12), promotes the proliferation
of immune system cells and has an antiapoptotic effect on some of these cells
[5, 13–16].
Additionally, alterations in sleep patterns that necessarily accompany obstructive apnea lead to changes in the immune system, such as a decrease in natural
killer cells and an increase in proinammatory cytokines such as IL-1 and
IL-2 [5].
There is a complex interrelationship between obesity, obstructive sleep apnea
and autoimmune diseases. The link between obesity and obstructive sleep apnea is
well known, as it has been demonstrated that the accumulation of adipose tissue in
the walls of the pharynx can cause a reduction in the caliber of the upper airway.
Moreover, obesity is linked to proinammatory states that may, in turn, favor inammation and upper airway narrowing. Indeed, adipose tissue is responsible for producing adiponectin, TNF-α and IL-6, among other cytokines, which clearly further
predispose to the onset of systemic autoimmune diseases. Therefore, this may lead
to a multidirectional process whereby adipose tissue promotes the appearance of
apnea and systemic autoimmune diseases, conditions that will reinforce each other
(Fig.8.1) [5, 17, 18].
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8.2 Systemic Autoimmune Diseases asaPredisposing
Factor forObstructive Sleep Apnea
Several publications show that obstructive sleep apnea occurs more frequently in
patients with systemic autoimmune diseases when prevalence gures are compared
with the general population [7, 9, 10].
This raises the possibility of a causal relationship between systemic autoimmune
diseases and obstructive sleep apnea. This could occur through several possible
mechanisms, some of which were addressed in the paragraphs above. Inammatory
activity mediated by cytokines and transcription factors is common in several diseases. Moreover, factors specic to each disease may explain a greater predisposition to the onset of obstructive sleep apnea. Thus, alterations of the cervical spine
(in rheumatoid arthritis and ankylosing spondylitis), retrognathia (in rheumatoid
arthritis) or weakness of the pharyngeal muscles (in inammatory myopathies) are
local factors that can lead to upper airway obstruction and subsequent apnea
(Figs.8.2a–e). In other inammatory diseases (such as Sjögren’s syndrome, systemic sclerosis, vasculitides, systemic lupus erythematosus), the local mechanisms
that may cause or worsen obstructive apnea are not very clear (Table8.2) [5, 11,
14, 19–21].
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a b
3
1
2
4
5
P. Ch al em
c
d
e
Fig. 8.2 (a) Lateral X-ray of the normal cervical spine (neutral position). Some anatomical struc-
tures are indicated: C1 vertebra (1), C2 vertebra (2), nasopharynx (3), oropharynx (4) and laryngopharynx (5). (b and c). In a normal cervical spine, both in the neutral position and in exion, the
anterior arch of C1 (red line) and the odontoid process of C2 (yellow line) are united and the
nasopharynx retains its caliber (white circle). (d and e). When dislocation between C1 and C2
occurs in rheumatoid arthritis, the separation of the rst two vertebrae (separation of the red and
yellow lines) is accentuated by exion of the cervical spine and may be accompanied by a decrease
in the caliber of the nasopharynx (white circle)
Table 8.2 Local factors leading to upper airway obstruction in systemic autoimmune diseases
Disease Local factor leading to upper airway obstruction
Rheumatoid arthritis C1–C2 damage (dislocation, impaction, C2 erosion or
fracture)
Rheumatoid arthritis Subaxial luxation (below C2)
Rheumatoid arthritis Temporomandibular damage (causing retrognathism)
Ankylosing spondylitis Cervical spine involvement
Inammatory myopathies Involvement of respiratory and pharyngeal muscles
Sjögren’s syndrome Cytokine-mediated narrowing of the upper airway
Sjögren’s syndrome Lymphoid inltration of the upper airway
Sjögren’s syndrome Increased viscosity of respiratory secretions
a
These mechanisms are less clear than in other diseases
a
a
a
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8.3 Obstructive Sleep Apnea asaPredisposing Factor
forSystemic Autoimmune Diseases
Existing studies in populations of patients with systemic autoimmune diseases have
demonstrated the increased prevalence of obstructive sleep apnea in these groups.
Furthermore, studies in cohorts of patients with obstructive sleep apnea have concluded they face a higher risk of developing systemic autoimmune diseases.
In 2016, Chen etal. published a retrospective study using nationwide databases
in Taiwan. Data were obtained from 105,846 adults diagnosed with obstructive
sleep apnea between 2002 and 2011. Patients with a previous history of autoimmune disease were excluded from this retrospective analysis. The study included
a control group with 423,384 participants without obstructive sleep apnea.
According to the results, patients with obstructive sleep apnea face an increased
risk of suffering from autoimmune diseases, particularly rheumatoid arthritis (HR
[95% CI]: 1.33), Sjögren’s syndrome (HR: 3.45) and Behçet’s disease (HR: 5.33).
This study did not nd an increased risk of developing systemic lupus erythematosus or systemic sclerosis among patients with obstructive sleep apnea [22].
In a smaller cohort, also from Taiwan, Kang and Lin report similar ndings: the
risk of developing rheumatoid arthritis was higher in patients with obstructive sleep
apnea than in the control group (HR [95% CI]: 1.66) [23].
Even though a solid relationship between obstructive sleep apnea and the
development of psoriatic arthritis or other spondyloarthritis has not been rmly
established, a surprising link has been identied with the onset of cutaneous psoriasis. In Taiwan, Yang etal. found that a prospective cohort of patients with
obstructive sleep apnea diagnosed by polysomnography faced an increased risk of
developing psoriasis (HR [95% CI]: 2.30). Cohen etal. also established an association between obstructive sleep apnea and psoriasis in a cohort of nurses in the
United States (RR [95% CI]: 2.19). However, this study does not specify the criteria (probably very heterogeneous) that enabled them to diagnose obstructive
sleep apnea [24, 25].
8.4 Obstructive Sleep Apnea inRheumatoid Arthritis
It is estimated that more than a third of patients with rheumatoid arthritis suffer from
obstructive sleep apnea, a prevalence much higher than in the general population.
The risk factors are the same as those described for individuals without arthritis:
age, obesity and neck circumference. However, two circumstances specic to rheumatoid arthritis have been associated with obstructive sleep apnea: involvement of
the cervical spine (Figs.8.2a–e) and retrognathism associated with temporomandibular joint involvement [6, 26].
Rheumatoid arthritis frequently affects the cervical spine and causes lesions
mainly at the level of the atlantoaxial joint (C1–C2 dislocation) and the odontoid
apophysis of C2 (which can suffer erosions and even fractures). Additionally, atlantoaxial impaction or basilar impaction (due to damage to the atlantooccipital joints
or the C1–C2 joints at the level of the lateral masses of the atlas) is also described.
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Finally, subaxial subluxation can occur, a less frequent form in which the intervertebral joints at multiple levels below C2 are affected (Table8.2) [27].
In a Japanese series, Shoda etal. describe 29 patients with cervical spine lesions
without other factors that could increase the risk of obstructive apnea (such as obesity,
adenoid hypertrophy, nasal obstruction, cricoarytenoid arthritis or temporomandibular involvement). Obstructive sleep apnea was found in 79% of cases. None of the
patients had apnea of central origin, possibly because of the absence of signicant
spinal cord lesions. The authors suggest that obstructive apnea is determined by an
interaction between the mechanical properties of the upper airway and neurological
alterations in the regulation of muscle tone. Indeed, cervical spine lesions cause the
spine to shorten, reducing the caliber of the upper airway and favoring its obstruction.
In addition, the authors speculate that occipitocervical lesions could be associated
with alterations of cranial nerves V, VII, IX, X and XII, responsible for controlling the
muscles that dilate the airway, generating its collapse [28].
Surgical treatment of cervical spine deformities that corrects kyphosis associated
with atlantooccipital and atlantoaxial joint disorders has been shown to increase
airway patency, improving obstructive apnea [29].
The involvement of the temporomandibular joints is widely known in rheumatoid arthritis. Severe damage to these joints may cause retrognathism, leading to the
reduction in the caliber of the upper airway and its obstruction. CPAP treatment has
been proposed in these rare cases. Tracheostomy proved to be the solution in an
extremely severe case. Surgical interventions on the temporomandibular joint have
also been considered (Table8.2) [30–33].
Regardless of the evident cause–effect relationship between the anatomical alterations described in patients with rheumatoid arthritis and obstructive sleep apnea, it
should be noted that in most cases, apnea is related to systemic inammatory phenomena. Therefore, systemic treatment with disease-modifying drugs that act on
proinammatory cytokines may be useful to improve respiratory alterations.
Although there is not enough evidence in this regard, the impact of pharmacological
treatment of arthritis on obstructive sleep apnea should be the subject of future
research [34].
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8.5 Obstructive Sleep Apnea inAnkylosing Spondylitis
A retrospective study was carried out in Taiwan with a cohort of 2210 patients diagnosed with ankylosing spondylitis between 2003 and 2013 and a control group of
8840 adults (Tsao etal. 2019). The study found an adjusted hazard ratio (aHR) of
2.826 (95% CI: 3.169–19.792) for developing obstructive sleep apnea. Indeed, during the 11-year follow-up period, 30 patients with ankylosing spondylitis (1.36%)
developed obstructive sleep apnea compared to 40 controls (0.46%) [7].
Wiginder etal. found different results in Sweden. Using home sleep monitoring
devices, the authors compared 46 ankylosing spondylitis patients with 179 controls.
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Approximately half of the subjects in both groups (47.8% and 50.8%, respectively)
had obstructive sleep apnea. It is possible that the sample size did not allow nding
differences between the two groups [35].
It is well known that the inammatory activity of certain systemic diseases can
cause tiredness and produce sleep disturbances, further worsening the symptoms of
fatigue. Obstructive apnea can also manifest itself in daytime tiredness, independent
of the inammation. Manifestations of the systemic inammatory activity of ankylosing spondylitis may sometimes be confused with sleep disorders [36–38].
It has been proposed that cervical spine involvement in ankylosing spondylitis
may cause upper airway stenosis, favoring the development of obstructive apnea. It
is also important to consider the role of inammation mechanisms on the mucosa
and lymphoid tissue adjacent to the airway, which could contribute to obstructive
phenomena (Table8.2) [39, 40].
The treatment of obstructive sleep apnea in patients with ankylosing spondylitis
does not differ from the usual treatment (sleep hygiene, avoiding certain medications, weight loss, postural measures, using a CPAP). Furthermore, it has been suggested that anti-TNF and other anti-inammatory agents can reduce apnea symptoms
and improve sleep quality, although there is no agreement in this regard [39–41].
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8.6 Obstructive Sleep Apnea inInflammatory Myopathies
As inammatory myopathies (polymyositis, dermatomyositis and inclusion body
myopathy) are low-prevalence diseases, there are fewer publications on the relationship with obstructive sleep apnea than other systemic autoimmune diseases.
Selva-O’Callaghan etal. published a case series of 16 patients with inammatory myopathies (12 with dermatomyositis, 2 with polymyositis and 2 with inclusion body myopathy) who underwent polysomnography. The mean apnea–hypopnea
index (AHI) was 28.7, and sleep apnea (dened as an AHI higher than 5) was documented in 14 of the 16 patients (87%). Episodes of apnea of central origin were
detected only occasionally. Treatment with CPAP in four patients showed very good
results [11].
Rodríguez Cruz etal. published their experience with 15 patients with inclusion
body myopathy. Using home sleep monitoring devices, the authors diagnosed sleep
apnea (AHI higher than or equal to 5) in 100% of the patients. The mean AHI was
23.4; ve patients had mild apnea (AHI: 5–15), six had moderate apnea (AHI:
15–30) and four had severe apnea (AHI higher than 30) [42].
Based on the available literature, no specic guidelines can be established
regarding the treatment of obstructive sleep apnea in inammatory myopathies. In
addition to the treatments currently described (including positive pressure
devices), pharmacological treatment—immunosuppressants and glucocorticoids—is essential to achieve recovery of the respiratory and pharyngeal muscles
(Table8.2).
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8.7 Obstructive Sleep Apnea inSjögren’s Syndrome
A retrospective study in Taiwan included 12,926 patients diagnosed with Sjögren’s
syndrome between January 1, 2002, and December 31, 2011. The control group
consisted of 51,704 individuals without autoimmune diseases. The diagnosis of
sleep apnea was made by polysomnography. After adjusting for age, sex and comorbidities, obstructive sleep apnea incidence was signicantly higher in patients with
Sjögren’s syndrome than in controls (0.61% and 0.33%, respectively). The risk of
developing obstructive sleep apnea was found to be increased, with an aHR of 2.48
(95% CI: 1.89–3.24) [12].
Karabul etal. published a prospective study on 44 patients with Sjögren’s syndrome, consecutively recruited between April 1, 2019, and December 31, 2020. All
patients underwent a polysomnography study and 84% (37 of 44) were diagnosed
with obstructive sleep apnea, reecting a higher prevalence than the general population. Of the patients diagnosed with obstructive sleep apnea, 12 (27%) suffered a
mild form, 19 (43%) a moderate form and 6 (14%) a severe form. Comparing
Sjögren’s syndrome patients with and without obstructive sleep apnea revealed a
statistically signicant association between apnea and age, higher body mass index,
overweight and obesity. There was no relationship between apnea and lung involvement associated with Sjögren’s syndrome [9].
The mechanisms by which Sjögren’s syndrome is associated with obstructive
sleep apnea are unclear. There are several possibilities, which could contribute
simultaneously. As mentioned above, cytokine-mediated proinammatory states
can promote inammation and narrowing of the upper airway. Additionally, lymphoid inltration of the upper airway contributes to a decrease in airway caliber.
The increased viscosity of respiratory secretions associated with the sicca syndrome
may also contribute to airow obstruction. Simultaneously with airway dryness, an
increase in the surface tension of the liquid layer lining the mucosa has been
described. This increase in surface tension favors airway collapse, requiring a signicant increase in intraluminal pressure to achieve reopening. However, it has not
been corroborated that the upper airway in Sjögren’s syndrome patients is systematically more prone to collapse (Table8.2) [43].
8.8 Obstructive Sleep Apnea inSystemic
Lupus Erythematosus
Chronic fatigue is undoubtedly one of the common nonspecic symptoms in
patients with systemic lupus erythematosus. It could reect the inammatory activity of the disease, its sequelae, the presence of depression, the side effects of medications or alterations in sleep patterns [44, 45].
Valencia-Flores etal. compared 14 systemic lupus erythematosus patients with
11 healthy controls of similar age but with a lower body mass index (26.78kg/m2 on
average in the lupus patients versus 20.85kg/m2 in the controls). The number of
respiratory events per hour (apneas and hypopneas) was quantied, determining the
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respiratory disturbance index (RDI). The mean RDI in the patients with lupus erythematosus was 8.84 and 1.89in controls. Half of the patients had mild or moderate
apnea: moderate apnea (RDI >10 and <30) was diagnosed in 3 of the 14 patients
with lupus (21.5%), and mild apnea (RDI >5 and <10) was diagnosed in 4 patients
(28.6%). Additionally, a signicant increase in abnormal limb movements was
found in lupus patients with and without respiratory disorders [8].
Iaboni etal. also reported sleep disturbances in a group of 35 patients with lupus.
The AHI was higher than 5in 20 of the 35 patients (57%). Nine patients (25.7%)
with obstructive sleep apnea were found to have an AHI higher than 10; the average
AHI in this group was 19.3. Even though this article does not specify the AHI of the
control group of 17 healthy individuals, it compares other parameters (sleep efciency, awakening/hours of sleep), nding sleep disturbances in patients with lupus
that could partly explain the frequently reported fatigue [45].
As in other systemic autoimmune diseases, obstructive sleep apnea is frequently
found in patients with systemic lupus erythematosus. It has been postulated that
chronic use of glucocorticoids may partially explain sleep disturbances, but this has
not been sustained. No mechanisms specic to lupus have been described to explain
the higher frequency of obstructive sleep apnea, but the previously mentioned
inammatory mediators probably play a role [8, 18, 19, 45–47].
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8.9 Obstructive Sleep Apnea inSystemic Sclerosis
Medical literature describes two main types of systemic sclerosis (scleroderma): the
limited and diffuse cutaneous forms. The former usually presents itself without pulmonary parenchymal involvement, but pulmonary hypertension is a frequent manifestation. In the latter, both pulmonary hypertension and interstitial involvement are
frequent manifestations. The increase in pulmonary artery diameter allows for estimating pulmonary hypertension. Yakut etal. used home sleep monitoring devices to
evaluate 62 patients (58 women). Obstructive sleep apnea was diagnosed when AHI
≥15/h. Interstitial involvement and pulmonary artery diameter were assessed using
computed axial tomography. Obstructive sleep apnea was documented in 20 patients
(32%): 17/42 (40%) with the limited form and 3/20 (15%) with the diffuse form.
There were no differences in lung parenchyma involvement between patients with
and without apnea. An increased pulmonary artery diameter was found in 10/20
patients (50%) with obstructive sleep apnea. This nding was evident in only 6/17
(14%) patients without apnea. The authors concluded that in patients with systemic
sclerosis, obstructive sleep apnea is associated with an increased risk of pulmonary
hypertension, regardless of lung parenchymal involvement, with an odds ratio (OR)
of 4.7 (95% CI: 1.06–20.88) [48].
Two additional studies found that the prevalence of obstructive sleep apnea
(dened as AHI ≥5/h) in patients with systemic sclerosis is approximately 50%.
One of these studies included 38 patients with interstitial lung disease. The other
study included 39 patients, nding no relationship between interstitial lung disease
and obstructive sleep apnea [10, 49].
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Obstructive sleep apnea is a frequent manifestation in patients with systemic
sclerosis, both in the diffuse and the limited variants. It most likely contributes to
pulmonary hypertension and does not seem to correlate with interstitial lung disease. The diagnosis and treatment of obstructive sleep apnea should be part of the
comprehensive management of patients with systemic sclerosis.
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8.10 Obstructive Sleep Apnea inSystemic Vasculitides
The vasculitides are a highly heterogeneous group of low-prevalence diseases characterized by the inammation of the blood vessel wall and occlusion of the vascular
lumen with subsequent tissue ischemia. The clinical manifestations of vasculitides
are highly diverse. Except for Behçet’s disease, no studies were found on obstructive sleep apnea.
A retrospective study in Taiwan included 1221 patients diagnosed with Behçet’s
disease and followed up between January 1, 2002, and December 31, 2011. The
control group consisted of 4884 individuals without autoimmune diseases.
Polysomnography was used to diagnose sleep apnea. After adjusting for age, sex
and comorbidities, the incidence of obstructive sleep apnea was signicantly higher
in patients with Behçet’s disease than in controls (1.23% and 0.33%, respectively).
The risk of developing obstructive sleep apnea was found to be increased, with an
aHR of 1.99 (95% CI: 1.06–3.72) [12].
Tascilar et al. studied 51 patients with Behçet’s disease without neurological
involvement and compared them with 21 healthy controls. Polysomnography was
performed on 40 Behçet patients and all controls. The AHI was signicantly higher
in Behçet patients than in the control group. However, when patients with active and
inactive Behçet’s disease were compared, no difference was found in the frequency
of sleep alterations [50].
Obstructive sleep apnea is more frequent in patients with Behçet’s disease than
in the general population, although it does not seem to worsen disease activity or be
caused by it. Likewise, it seems evident that obstructive sleep apnea contributes to
Behçet patients’ fatigue and impaired quality of life. The correct diagnosis and
treatment of obstructive sleep apnea should be part of the comprehensive management of patients with Behçet’s disease.
8.11 Conclusions andFuture Perspectives
Obstructive sleep apnea is more frequent in patients with systemic autoimmune
diseases than in the general population. Sleep disorders may be partially responsible
for fatigue and impaired quality of life in patients with autoimmune diseases, highlighting the need to actively assess the presence of these disorders. Current treatment does not differ from that used in patients without autoimmune diseases (sleep
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hygiene, avoiding certain medications, losing weight, postural measures and positive pressure devices). An adequate understanding of the complex pathophysiological mechanisms (still to be determined) will allow for better treatment of autoimmune
diseases and sleep disorders.
Take-Home Message
• Patients with systemic autoimmune diseases such as rheumatoid arthritis, anky-
losing spondylitis, inammatory myopathies, Sjogren’s syndrome, systemic
lupus erythematosus, systemic sclerosis, and vasculitides suffer from obstructive
sleep apnea more frequently than the general population.
• There are common pathophysiological pathways between obstructive sleep
apnea and systemic autoimmune diseases (activation of transcription factors and
induction of the transcription of genes related to the production of proinamma-
tory cytokines).
• Early diagnosis and timely treatment of sleep disorders in patients with autoim-
mune diseases will improve their quality of life and long-term prognosis.
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