Sjögren syndrome

Source: Wikipedia, the free encyclopedia.
(Redirected from
Sjögren's syndrome
)
Not to be confused with Sjögren–Larsson syndrome and Marinesco–Sjögren syndrome.
Sjögren's syndrome
Other namesSjögren's syndrome, sicca syndrome
Tissue biopsy, blood tests[2]
Differential diagnosisMedication side effect, anxiety, sarcoidosis, amyloidosis[5]
TreatmentArtificial tears, medications to reduce inflammation, surgery[4]
PrognosisNormal life expectancy[6]
Frequency~0.7%[7]

Sjögren syndrome or Sjögren's syndrome (SjS, SS) is a

long-term autoimmune disease that affects the body's moisture-producing glands (lacrimal and salivary),[4] and often seriously affects other organ systems, such as the lungs, kidneys, and nervous system.[8]

Symptoms

Overview and importance to patients

In a 2021 poll of Sjogren's patients, a majority of respondents stated that eight Sjogren's symptoms had a major or moderate impact on their life: fatigue (79%); dry eyes (75%); dry mouth (73%); joint pain (65%); trouble sleeping (64%); eye discomfort (60%); muscle pain (56%); and brain fog (54%).[9][10][11]

Symptoms

Primary symptoms are dryness (

thyroid problems.[4] Those affected are also at an increased risk (15%) of lymphoma.[2][7]

Characteristic dryness appears at a number of locations, such as the tongue, face, and eyes. Marked at left are the salivary glands (which may be swollen), not a facial rash.

The hallmark symptom of Sjögren syndrome is

Vaginal dryness, dry skin, and dry nose may also occur.[13] Other organs of the body may also be affected,[14] including the kidneys, blood vessels, lungs, liver, pancreas, and brain.[13][15]

In some people with SS, skin dryness may be the result of

skin glands. The symptoms may develop insidiously, with the diagnosis often not considered for several years because sicca may be attributed to medications, a dry environment, or aging, or may be regarded as not of a severity warranting the level of investigation necessary to establish the presence of the underlying autoimmune disorder.[16]

Sjögren's syndrome can damage

urinary concentrating defect, and distal renal tubular acidosis.[17]

Complications

Among the complications discussed above, women with anti-Ro/SS-A and anti-La/SS-B antibodies who become pregnant have an increased rate of

pacemaker.[18] Type I cryoglobulinemia is a known complication of Sjögren's syndrome.[19]

Sjögren's syndrome can affect such organs as the liver, pancreas, kidneys, lungs, and central nervous system.[20]

Associated conditions

Sjögren's syndrome is associated with a number of other medical conditions, many of which are

autoimmune thyroiditis, multiple sclerosis and spondyloarthropathy,[23] and several malignancies, principally non-Hodgkin lymphoma.[23][24]

Sjogren's is the second most common cause of dysautonomia.[25][26][27][28]

Causes

While the exact cause is unclear, it is believed to involve a combination of

antibodies.[2] On biopsy there are typically lymphocytes within the glands.[2]

The cause of Sjögren's syndrome is unknown, but it may be the influence of a combination of genetic, environmental, and other factors, as is the case with many other autoimmune disorders.[29] Around 20 autoantibodies could be involved.[30]

Genetics

The observation of high rates of autoimmune disorders in families with a history of Sjögren's syndrome is linked with a genetic predisposition to the syndrome.[31] Studies on the polymorphisms of human leukocyte antigen (HLA)-DR and HLA-DQ gene regions in Sjögren's patients show differential susceptibility to the syndrome as the result of different types of the resulting autoantibody production.[31]

Hormones

Since Sjögren's syndrome is associated with a high prevalence in women,

autoantigens, inducing Sjögren's-like symptoms.[31]

Microchimerism

self-tolerance.[32]

Environment

human T-cell leukemia virus-1 are among the most studied infectious agents in Sjögren's syndrome.[32] To date, no direct cause and effect relationship has been identified between these pathogens and the development of Sjögren's syndrome. Damaged self-structures targeted for apoptosis may be mistakenly exposed to the immune system, triggering autoimmunity in exocrine glands, which are often prone to autoimmune responses.[32]

Pathogenesis

The

exocrinopathy. Although the numerous factors contributing to the progression of this disease have made discovering the exact origin and cause difficult, major advances over the past decade have contributed to a proposed set of pathogenic events that occur prior to the diagnosis of Sjögren's syndrome.[31]

Sjögren's syndrome was originally proposed as a specific,

lacrimal fluid), it does not explain the more widespread systemic effects seen in the progression of the disease.[citation needed
]

In the presence of a susceptible

plasma cells, causing glandular dysfunction in the salivary and lacrimal glands.[31]

Sjögren's syndrome is associated with increased levels in

systemic sclerosis.[citation needed
]

Genetic predisposition

The

T-cell activation owing to HLA susceptibility and the IL-12-IFN-γ-axis.[37]

Patients of different ethnic origin carry different HLA-susceptibility

salivary glands of Sjögren's patients suggests their imperative role in the pathogenesis of SS.[40]

Beyond genetics,

histone acetylation, or microRNA expression probably has a key role in the pathogenesis of autoimmune diseases, including Sjögren's syndrome, though research in this area is very limited.[41]

Environmental triggers

Environmental factors, such as glandular

lesions of patients with Sjögren's syndrome, and which specific molecular mechanisms are involved in the process of viral reactivation, remain to be clarified.[43]

Inflammation

Epithelial cells in Sjögren's syndrome lesions are active participants in the induction and perpetuation of the inflammatory process. Environmental and hormonal factors, in concert with an appropriate genetic background, are believed to trigger Sjögren's syndrome, which

lymphomagenesis (origin of lymphoma).[31]

Programmed cell death

Dysregulation of

epithelial cells of Sjögren's patients compared to healthy people.[45][46] In situ studies did not show increased apoptosis among glandular epithelial cells, but did show reduced apoptosis among infiltrating mononuclear cells. Reduced apoptosis was also implicated in the accumulation of autoreactive B-cells found in the glands. The relationship of autoantibodies expressed in Sjögren's syndrome with apoptosis is still being researched.[29]

Hormonal factors

hypothesized that androgen administration to the ocular surface may serve as an effective therapy for dry eyes.[49]

Diagnosis

While Sjögren's syndrome[50] is one of the most common auto-immune diseases, it has no specific and non-invasive diagnostic tests.

Diagnosing Sjögren's syndrome (SS) is complicated by the range of symptoms that a patient may manifest, and the similarity between symptoms of Sjögren's syndrome and those of other conditions. Also, patients with SS symptoms approach different

specialities
for treatment, which can make diagnosis difficult. Since dry eyes and dry mouth are very common symptoms, and frequently occur in people over 40, affected people may believe that the symptoms are age-related, so ignore them. Some medications can cause symptoms similar to those of Sjögren's syndrome.

Tests

The combination of several tests, which can be done in a series, can eventually diagnose Sjögren's syndrome.[33][51]

Blood tests

Main antinuclear antibody patterns on immunofluorescence.[52] Individuals with Sjögren syndrome usually have a speckled or homogeneous pattern, and rarely a centromere pattern.[53]

Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as

SSB/La, of which anti-SSB/La is far more specific; anti-SSA/Ro is associated with numerous other autoimmune conditions, but is often present in SS. However anti-SSA and anti-SSB tests are frequently not positive in SS.[citation needed
]

Rose bengal test

The

nontoxic dye rose bengal on the eyes. The dye's distinctive colour helps in determining the state and functioning of tear film and the rate of tear evaporation. Any distinctive colour change can indicate SS, but confirming the condition requires many related diagnostic tools.[51]

Schirmer test

slit-lamp examination can reveal dryness on the surface of the eye.[citation needed
]

Use of Schirmer strips to test oral dryness are possible.[54][55]

Saliva flow tests

Symptoms of dry mouth and dryness in the oral cavity are caused by the reduced production of saliva from the salivary glands (parotid gland, submandibular gland, and sublingual gland). In unstimulated whole saliva flow collection, the person spits into a test tube every minute for approximately 15 minutes. A resultant collection of less than 1.5 ml (0.053 imp fl oz; 0.051 US fl oz) is considered a positive result.[56] [51] In a stimulated saliva flow test the person sucks on a sugar free sweet, whilst collecting saliva. An unstimulated salivary flow rate of 0.1 to 0.2 ml/min and a stimulated flow rate of 0.7 ml/min or less is considered to be abnormally low flow rates indicative of salivary gland hypofunction.[57]

Unstimulated saliva production reduces by 40 to 70% between the age of 20 and 80 years, but stimulated saliva production is not affected.[58]

Lip biopsy

A lip/salivary gland biopsy takes a tissue sample that can reveal lymphocytes clustered around salivary glands, and damage to these glands from inflammation. This test involves removing a sample of tissue from a person's inner lip/salivary gland and examining it under a microscope. On such biopsies, the single most important test result in the diagnosis of the oral component of Sjögren syndrome is likely the focus score, which is the number of mononuclear cell infiltrates containing at least 50 inflammatory cells in a 4 mm2 glandular section.[59] The Chisholm-Mason grades are also widely used for salivary gland biopsies (see table).[60]

Ultrasound

Salivary gland ultrasonography is not invasive, and may help reduce unnecessary biopsies in anti-SSA-negative patients. [61][62][63][64]

Other tests

A radiological procedure is available as a reliable and accurate test for Sjögren's syndrome, in the form of a

sialogram. A contrast agent is injected into the parotid duct, which opens from the cheek into the vestibule of the mouth opposite the neck of the upper second molar tooth. The test is intended to detect any blockage in the salivary gland ducts (i.e. parotid duct) and the amount of saliva that flows into the mouth.[51]

For Sjögren's syndrome, sudomotor function through electrochemical skin conductance may help in the diagnosis process.[65][66]

Autoimmune comorbidity

People with Sjögren's may also have other autoimmune conditions.[67][68][69]

Exclusions

Sjögren's syndrome may be excluded in people with past head and neck

acquired immunodeficiency syndrome, pre-existing lymphoma, sarcoidosis, graft-versus-host disease, and use of anticholinergic drugs.[citation needed
]

Prevention

No prevention mechanism exists for Sjögren's syndrome (SS) because of its complexity as an autoimmune disorder.

However

risk factors related to developing SS or reduce the severity of the condition for patients who have already been diagnosed.[citation needed
]

Diet is strongly associated with the inflammation seen in many autoimmune related diseases, including SS. An experimental study concluded that SS patients often show high sensitivity to gluten that directly relates to inflammation.[70]

Moderate exercise is also helpful in SS patients, mainly reducing the effect of lung inflammation.[71][citation needed]

Treatment

Overview

Treatment is directed at managing the person's

antihistamines, may also be stopped.[4]
The most specific extant diagnostic test requires lip biopsy.

Treatments

Neither a cure nor a specific treatment for Sjögren's syndrome is known to permanently restore gland secretion. Instead, treatment is generally symptomatic and supportive.[72][73]

Eye care

Moisture replacement therapies such as

ocular surface for a longer time.[74]

Additionally,

Salagen, a manufactured form of pilocarpine, can be used to help produce tears, as well as saliva in the mouth and intestines.[75] It is derived from the jaborandi plant.[76]

Vaginal dryness

In women with Sjögren's syndrome,

personal lubricants are recommended to help lessen irritation or pain that may result from dryness in the vaginal and vulval areas.[51]

Musculoskeletal

infections
.

Systemic

For systemic symptoms, including fatigue, joint pain, myositis and

B-cell pathology are often used and have less toxic profiles than traditional immunosuppressive regimens.[citation needed
]

Dental care

topical fluoride application to strengthen tooth enamel and frequent teeth cleanings by a dental hygienist. Existing cavities must also be treated, as cavities that extend into the tooth cannot be effectively treated by teeth cleaning alone, and are at a high risk of spreading into the pulp of the tooth, leading to the loss of vitality and need for extraction or root canal therapy. This treatment regimen is the same as for all xerostomia patients, such as for those undergoing head and neck radiation therapy, which often damages the salivary glands; these glands are more susceptible to radiation than are other body tissues.[citation needed
]

Fatigue

A small study showed possible efficacy of vagus nerve stimulation for Sjogren's fatigue reduction.[78]

Prognosis

Organ-related impacts

Non-Hodgkin lymphoma

Results from a number of studies indicate that, compared to other autoimmune diseases, Sjögren's syndrome is associated with a notably high incidence of

lymphoid malignancy.[79] Patients with severe cases are much more likely to develop lymphomas than patients with mild or moderate cases.[80] The most common lymphomas are salivary extranodal marginal zone B cell lymphomas (MALT lymphomas in the salivary glands)[81] and diffuse large B-cell lymphoma.[80]

Lymphomagenesis in primary Sjögren's syndrome patients is considered as a multistep process, with the first step being chronic stimulation of autoimmune B cells, especially B cells that produce

oncogenic mutation, leading to any dysfunction at checkpoints of autoimmune B-cell activation to transform into malignancy. A study's finding has concluded the continuous stimulation of autoimmune B cells, leading to subtle germinal abnormalities in genes having specific consequences in B cells, which underlies the susceptibility to lymphoma.[84]

Other organs

Apart from the notably higher incidence of malignant NHL, Sjögren's patients show only modest or clinically insignificant deterioration in specific organ-related function.

Burden of illness

Sjögren's syndrome is associated with a high burden of illness,

quality of life (QoL),[86] with a significant impact on ability to work resulting from increased rates of disability.[87][88][89] The reduction in QoL is similar to that seen in other chronic conditions such as rheumatoid arthritis, lupus and fibromyalgia.[88]

Mortality

Published studies on the survival of Sjögren's syndrome patients have been limited in varied respects, perhaps owing to the relatively small sample sizes, and the fact that secondary Sjögren's syndrome is associated with other autoimmune diseases. A 2010 study found a slight increase in mortality rates of Sjögren's patients in comparison with the remainder of the population.[31] A 2016 study found that primary Sjögren's was not associated with an increase in all-cause mortality as compared with the general population, but that a subset of patients with extraglandular involvement, vasculitis, hypocomplementaemia and cryoglobulinaemia may be at increased risk of mortality.[90] A 2021 metaanalysis showed a 46% increase in mortality, with significantly greater mortality risk in patients with older age, male gender, vasculitis, interstitial lung disease, low complements, positive anti-La/SSB and cryoglobulinaemia.[91]

Among those without other autoimmune disorders, life expectancy is unchanged.[6]

Epidemiology

Sjögren's syndrome (SS) is the third-most common rheumatic autoimmune disorder, behind rheumatoid arthritis and

systemic lupus erythematosus.[16]

There are no geographical differences in the rates of SS.[92] Sjögren's syndrome has been reported in all areas of the world, although regional rates have not been well studied.[92][93]

Depending on the criteria for determining prevalence, studies estimate the prevalence of SS at between 500,000 and two million people in the United States. Broader studies of SS prevalence range widely, with some reports of up to a prevalence of 3% of the population.[16] A few studies have reported that the incidence of the syndrome varies between three and six per 100,000 per year.[16][94] Between 0.2 and 1.2% of the population is affected, with half having the primary form and half the secondary form.[7] It is around 10 times more common in women than in men.[3] Though the disease commonly begins in middle age, people of any age can be affected.[2][3]

Nine out of 10 SS patients are women.[29][93] In addition to prevalence in women, having a first-degree relative with an autoimmune disease and previous pregnancies have been identified as epidemiological risk factors.[95] Despite the lower risk for men, primary SS in men tends to represent a more severe form of the disease.[96] The role of race and ethnicity in the prevalence of the disease is unknown.[citation needed]

Although Sjögren's syndrome occurs in all age groups, the average age of onset is between ages 40 and 60, although as many as half of all cases may be left undiagnosed or unreported.[29][16][97][98] The prevalence of SS generally increases with age.[16]

Sjögren's syndrome is reported in 30-50% of people with rheumatoid arthritis and in 10-25% with systemic lupus erythematosus.[29]

History

Overview

The disease was described in 1933 by Henrik Sjögren, after whom it is named, but a number of earlier descriptions of people with the symptoms exist.[3]

History

misdiagnosis of Mikulicz's syndrome. Many conditions, such as tuberculosis, infections, sarcoidosis and lymphoma present with similar conditions to those ascribed to Mikulicz's syndrome.[51] Nevertheless, the term "Mikulicz's syndrome" is still used occasionally to describe the appearance of lymphocytic infiltrates on salivary-gland biopsies.[51]

In 1930,

doctoral thesis describing 19 females, most of whom were postmenopausal and had arthritis, showing clinical and pathological manifestations of the syndrome.[99] Sjögren clarified that keratoconjunctivitis sicca, resulting from water deficiency, had no relation to xerophthalmia, resulting from vitamin A deficiency.[99] Sjögren's thesis was not well received as the Board of Examiners criticized some clinical aspects.[100]

After extensive research and data collection, Sjögren published an essential paper in 1951, describing 80 patients with

keratoconjunctivitis sicca, 50 of whom also had arthritis.[100] His subsequent follow-up conference trips pertaining to his paper led to an international interest in Sjögren's syndrome.[100] The term "keratoconjunctivitis sicca" was coined by Sjögren himself and began to be identified as Sjögren's syndrome in literature,[100]
although it can now have more general usage.

Research

Singer-actress Carrie Ann Inaba is the national awareness ambassador and spokesperson for the Sjögren's Syndrome Foundation.

Research into multifactorial autoimmune diseases such as SS focuses on expanding the knowledge surrounding the disorder, improving diagnostic tools and finding ways to prevent, manage and cure the disorder. The

clinical trials and genetic studies of Sjögren's syndrome and is open to those wishing to participate in research studies and to researchers studying the disease.[101]

As with other autoimmune diseases, susceptibility to Sjögren's syndrome is greatly influenced by the human leukocyte antigen.

Greek and Israeli patients.[104] Multiple genome-wide association scans may be conducted in the future to identify key risk variants.[102]

human immunodeficiency virus (HIV), hepatitis delta virus (HDV) and hepatitis C virus (HCV).[104][105][106]

Some research has shown that a paucity of vitamin A and vitamin D are associated with the disease.[104] Vitamin D deficiency was found to be related to neurological manifestations and the presence of lymphoma among patients, but vitamin A levels were inversely associated with extraglandular manifestations of the disease.[104]

Saliva is a potential diagnostic tool for Sjögren's syndrome because the salivary component is changed after onset of the disease.

lab on a chip, the diagnosis can be more convenient.[107]

With regard to therapeutics, multiple

IFN-α seemed less effective.[108]

In 2014, the Sjögren's Syndrome Foundation announced a five-year goal to halve the disease's average time to diagnosis.[109]

Notable cases

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  • Some of the original text for this article was obtained from a public domain resource at NIH

Further reading

External links

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