Personality, depression and anxiety in primary Sjogren's syndrome

Personality, depression and anxiety in primary Sjogren's syndrome
Personality, depression and anxiety in primary Sjogren's syndrome - Association with sociodemographic factors and comorbidity.

Mood, sleeping and several neuro-psychologic domains such as cognition are affected by pSS. Specifically, difficulties with attention, focusing, memory and new learning are commonly reported problems
Moreover, the personality traits of pSS patients can potentially interact with the subjective dryness symptoms and treatment outcome. Psychological factors may influence the ability of patients to cope with fatigue and its consequences including negative cognitions such as catastrophizing, avoidance of psychical activity and lack of social support or overprotection.


Patients with primary Sjögren's Syndrome (pSS) have diminished health quality and fatigue, arthralgia along with dryness of the mouth and eyes have major impact on their psychological and social aspects of life. 
The purpose of this study was to determine psychological features of patients with pSS. 
We analyzed personality, depression and anxiety of patients with primary Sjögren's Syndrome (pSS) in comparison with patients with rheumatoid arthritis (RA) and healthy controls (HC) and assessed their association with sociodemographic factors and comorbidity.


In 105 pSS patients (mean age 51.34 years, mean disease duration 5.98 years), 52 RA patients (mean age 51.37 years, mean disease duration 8.10 years) and 54 HC (mean age 51.35 years) clinical and sociodemographic characteristics were determined and results analyzed. 
At enrollment patients and controls completed the Revisited NEO Personality Inventory Five-Factor model (NEO-PI-R), the Zung Self-Rating Depression Scale and the Zung Self-Rating Anxiety Scale. Statistical analyses were performed using SPSS [Version 16.0]. The relative size of the effect was assessed based on standardized estimates of effect size (d).


Patients with pSS, similarly to RA patients had higher scores of Neuroticism and lower scores of Extraversion and Openness for experience  compared to HC. 
There was no significant differences between pSS group and HC in the depression. However, patients with pSS had higher anxiety in comparison to HC.

We confirmed that pSS patients have psychological profiles and levels of anxiety different to healthy subjects. 
In our study, patients with pSS were emotionally unstable, introverted, and more anxious than healthy controls. 
Education and satisfaction with family relationships were significant predictors for psychological characteristics of patients, independently of clinical diagnosis. 
The better understanding of personality dimensions in patients with pSS may provide adequate help by professionals in overcoming adaptation problems which have been observed in these patients.

See Full report on this study 


Diagnosis, treatment, and follow-up of autoimmune hepatitis

Autoimmune Hepatitis Clinical Practice Guidelines (2019)

Diagnosis, treatment, and follow-up of autoimmune hepatitis

The guidelines on the diagnosis, treatment, and follow-up of autoimmune hepatitis were released on January 1, 2019, by the Hellenic Association for the Study of the Liver.

Clinical Characteristics

Autoimmune hepatitis (AIH) should be considered a possibility in any individual with acute or chronic hepatitis, particularly in those with high immunoglobulin G (IgG) levels.
Untreated AIH carries high morbidity and mortality rates, so early and accurate diagnosis is mandatory.
Screening for concomitant autoimmune diseases can be considered in patients with AIH (particularly autoimmune thyroiditis), as AIH is associated with various other autoimmune-mediated conditions.
Cirrhosis should be suspected upon AIH diagnosis, since nearly one-third of adults and half of children with AIH are at the stage of cirrhosis at AIH diagnosis.
The presentation of acute AIH can take one of two clinical forms, as follows:
  • Acute worsening of previously undiagnosed or misdiagnosed AIH
  • Original acute-onset AIH without chronic lesions on liver histology
AIH can be classified as either (1) AIH-1, antinuclear (ANA), smooth muscle (SMA), and/or soluble liver antigens/liver pancreas antibody (anti-SLA/LP)–positive or (2) AIH-2, anti-liver/kidney microsomal antibody type-1 (anti-LKM1), anti-liver/kidney microsomal antibody type-3 (anti-LKM3), and/or liver cytosol type-1 antigen (anti-LC1)–positive.


Patients with AIH-related cirrhosis should undergo ultrasonography every 6 months to monitor for hepatocellular carcinoma (HCC).


All children with AIH should undergo magnetic resonance cholangiopancreatography (MRCP) at minimum to rule out autoimmune sclerosing cholangitis.
Patients who have AIH with cholestatic features should undergo testing for primary biliary cholangitis (PBC).
Interface hepatitis, hepatocyte rosetting, and emperipolesis strongly support but do not confirm AIH.
In daily clinical practice, the 2008 simplified score should be used for AIH diagnosis.
The 1999 revised score can help diagnose difficult AIH cases, since it incorporates treatment response as an important parameter.
Diagnosis of AIH-PBC and AIH–primary sclerosing cholangitis (PSC) variants should not be based on diagnostic scores, but they may be used cautiously in the diagnosis of childhood AIH and acute or fulminant disease.


The goal of AIH therapy is to achieve complete biochemical and histological remission to prevent disease progression.



Just 20 minutes of exercise to reduce inflammation

Just 20 minutes of exercise to reduce inflammation
As little as 20 minutes of exercise could have anti-inflammatory effects, according to this study.

Research, published in the journal Brain, Behavior and Immunity, investigates the benefits of 20-minute exercise sessions on the body's immune system.

Researchers from the University of California-San Diego School of Medicine - led by Suzi Hong, Ph.D., from the Department of Psychiatry and the Department of Family Medicine and Public Health - hypothesized that exercise would improve the body's anti-inflammatory response by activating the sympathetic nervous system.
The sympathetic nervous system helps to increase heart rate, blood pressure, and breathing rate. Physical exercise activates this system to help the body keep up.
During this time, the body releases hormones such as epinephrine and norepinephrine into the bloodstream, which activate the adrenergic receptors of immune cells.

Analyzing the body's immune response to exercise

More specifically, the researchers tested the hypothesis that a single 20-minute session of exercise would be enough to trigger sympathoadrenergic activation, which, in turn, would suppress the production of monocytic cytokines.
Monocytes are a type of white blood cell, or immune cell, that help to fight off bacteria and infections. Cytokines are a type of protein that help other cells to become so-called effector cells, which, in turn, kill off cancerous or infected cells.
TNF is one of these cytokines. TNF can induce cell differentiation and proliferation, but also cell death, including cancerous ones. TNF also has pro-inflammatory properties, which help the body to bring its inflammatory cells to the site of the injury, creating an immunological response.
Inflammation is a necessary part of the body's immune response, but too much inflammation can lead to disease. Chronic inflammation may contribute to diabetesobesityceliac diseasearthritisfibromyalgia, or bowel diseases such as Crohn's disease or ulcerative colitis.
To test their hypothesis, the researchers asked 47 participants to walk on a treadmill for 20 minutes at an intensity rate adjusted to suit each individual's fitness level. Hong and team took blood samples from the participants both before and immediately after the exercise sessions.

As little as 20 minutes of exercise reduces inflammation

The results revealed that a 20-minute session of moderate exercise can have anti-inflammatory effects.
The study confirmed the researchers' hypothesis. Exercise did seem to produce an anti-inflammatory cellular response, which could be seen in the reduction of the cytokine TNF.
"Our study shows a workout session does not actually have to be intense to have anti-inflammatory effects. Twenty minutes to half an hour of moderate exercise, including fast walking, appears to be sufficient. Feeling like a workout needs to be at a peak exertion level for a long duration can intimidate those who suffer from chronic inflammatory diseases and could greatly benefit from physical activity." - Suzi Hong


What is the lymph system?

What is the lymph system?

Our bodies have a network of lymph vessels and lymph nodes. (Lymph is pronounced limf.) This network is a part of the body’s immune system. It collects fluid, waste material, and other things (like viruses and bacteria) that are in the body tissues, outside the bloodstream.

Lymph vessels are a lot like the veins that collect and carry blood through the body. But instead of carrying blood, these vessels carry the clear watery fluid called lymph.
What is the lymph system?
Lymph fluid flows out from capillary walls to bathe the body’s tissue cells. It carries oxygen and other nutrients to the cells, and carries away waste products like carbon dioxide (CO2) that flow out of the cells. Lymph fluid also contains white blood cells, which help fight infections.
Lymph fluid would build up and cause swelling if it were not drained in some way. That’s the role of the lymph vessels. Lymph vessels draw up the lymph fluid from around the cells to send it towards the chest. There, lymph fluid collects into a large vessel that drains into a blood vessel near the heart.

Lymph nodes and what they do

Lymph vessels route lymph fluid through nodes throughout the body. Lymph nodes are small structures that work as filters for harmful substances. They contain immune cells that can help fight infection by attacking and destroying germs that are carried in through the lymph fluid.
There are hundreds of lymph nodes throughout the body. Each lymph node filters the fluid and substances picked up by the vessels that lead to it. Lymph fluid from the fingers, for instance, works its way toward the chest, joining fluid from the arm. This fluid may filter through lymph nodes at the elbow, or those under the arm. Fluid from the head, scalp, and face flows down through lymph nodes in the neck. Some lymph nodes are deep inside the body, such as between the lungs or around the bowel, to filter fluid in those areas. The lymph fluid slowly flows in from all around the body, making its way back to the chest. At the end of its journey, the filtered fluid, salts, and proteins are dumped back into the bloodstream.

Swollen lymph nodes

When there’s a problem, such as infection, injury, or cancer, the node or the group of lymph nodes in that area may swell or enlarge as they work to filter out the “bad” cells. This may be called lymphadenopathy (LIMF-ad-uh-NOP-uh-thee). Swollen lymph nodes tell you that something is not right, but other symptoms help pinpoint the problem. For instance, ear pain, fever, and enlarged lymph nodes near your ear are clues that you may have an ear infection or cold.
Some areas where lymph nodes commonly swell are in the neck, groin, and underarms. In most cases, only one area of nodes swells at a time. When more than one area of lymph nodes is swollen it’s called generalized lymphadenopathy. Some infections (such as strep throat and chicken pox), certain medicines, immune system diseases, and cancers like lymphoma and leukemia can cause this kind of swelling. The health care provider will look for more information to figure out the cause of the swelling. Lymph node swelling is often caused by something other than cancer.


Innovative approaches in the treatment of multiple sclerosis

Innovative approaches in the treatment of multiple sclerosis
By Will Frostick, Senior Associate Consultant Will Frostick delves into the MS treatment landscape and explores some of the cutting-edge treatments on the horizon.

Innovative approaches in the treatment of multiple sclerosis. Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), leading to progressive and permanent disability.

It is estimated that 2,500,000 people across the world suffer from MS. Click to Tweet

The disease impacts everyone differently, with the symptoms ranging from fatigue and vision problems to mental health issues and mobility problems, along with issues with speech and swallowing, and loss of bladder function (to name a few). Sadly, the age of onset is typically 20-40 years and MS is the leading cause of nontraumatic neurologic disability in young people.

The pathogenesis of MS consists of two key components: focal inflammatory demyelination, and neurodegeneration. Nerve function is dependent on the ability of electrical signals to flow through the wire-like axons of neurons, which are wrapped in and insulated by myelin sheaths. In the central nervous system (CNS, which includes the brain, optic nerves and spinal cord), myelin extends from octopus-like arms of oligodendrocytes. This myelination supports neuronal signal conductance and the survival of the neurons themselves.

However, in MS, lymphocytes mount an auto-immune attack on myelin, leading to damage of the myelin sheath. The demyelinated neurons can then no longer function properly and begin to atrophy and degenerate, causing the symptoms of MS.2 As damage can occur anywhere in the CNS, symptoms are highly varied.

There are two main clinical presentations of MS – Relapsing Refractory MS (RRMS) and Progressive MS (PMS).

In RRMS symptoms are intermittent but relapses gradually become more frequent, severe and longer-lasting as the disease progresses. However, PMS is characterised by a progressive worsening of symptoms between flareups, without remission. Pathophysiologically, the disease courses of both types overlap. As a result, patients can transition between the types of MS, making monitoring and treating the disease more challenging.

For example, PMS is characterised by focal inflammatory lesions (an area of damage or scaring in the CNS, also referred to as plaques) in the early stages only, with more diffuse damage becoming common later on. Focal inflammatory lesions are also a feature throughout RRMS, and it is also possible for RRMS patients to show progressive symptoms in the later stages of the disease.



Is sonoelastography a helpful method of evaluation to diagnose Sjögren's syndrome?

Is sonoelastography a helpful method of evaluation to diagnose Sjögren's syndrome?

Sonoelastography is a diagnostic ultrasound technique that provides a noninvasive means of estimating soft tissue elasticity and stiffness. Within the last decade, sonoelastography has gained an increasing amount of attention because it is a noninvasive way of estimating tissue stiffness.

The study, “Is sonoelastography a helpful method of evaluation to diagnose Sjögren’s syndrome?,” was published in the International Journal of Rheumatic Diseases.

At this point in time Sjogren's Syndrome is diagnosed by looking at the eye and mouth symptoms and damage, by evaluating levels of autoantibodies in the blood, and tissue biopsy analysis. A less-invasive, quicker and low-cost procedure that accurately identifies patients affected with Sjögren’s syndrome is needed.

A new sonoelastography technique – virtual touch tissue quantification of acoustic radiation force impulses (ARFI) – offers a promising method for measuring tissue rigidity. 

The aim of this study was to assess the usefulness of ARFI for diagnosing Sjögren's syndrome (SS).


Acoustic radiation force impulses sonoelastography can assist diagnosis of SS, and is a non‐invasive and fast method of detecting pathological changes to the parotid and submandibular glands.


Assessment of xerostomia (dry mouth) in Sjogren's patients - a comparison between three tools

Assessment of xerostomia (dry mouth) in Sjogren's patients

Correlation between Xerostomia index, Clinical Oral Dryness Scale, and ESSPRI with different hyposalivation tests.

Ola Hijjaw, Mohammad Alawneh, Khaled Ojjoh, Hazem Abuasbeh, Ahmad Alkilany, Nabeel Qasem, Mohammad Al-Essa, Saif Aldeen AlRyalat

Department of Internal Medicine, The University of Jordan, Department of Ophthalmology, The University of Jordan, Amman 

Background and objective: Xerostomia is a subjective measure of dry mouth, while hyposalivation is an objective measure of reduced saliva flow rate. In this study, we aim to assess the association between commonly used xerostomia scoring systems, with different hyposalivation measures among Sjogren Syndrome (SS) patients.

Methods: In a cohort of SS patients, we assessed xerostomia using Xerostomia index, clinical oral dryness scale (CODS), and the European League Against Rheumatism SS Patient-Reported Index (ESSPRI), and we assessed hyposalivation using unstimulated whole saliva flow (UWS), stimulated whole saliva flow (SWS), and stimulated parotid flow (SPF). We analyzed the association between xerostomia and hyposalivation using association tests in SPSS.

Results: We included a total of 49 patients in this study, of which 34 (68%) had primary SS, and 15 (32%) had secondary. CODS was significantly correlated with SWS (P=0.048), with a negative correlation coefficient of 0.216, and with SPF (P=0.009), with a negative correlation coefficient of 0.291. The dryness domain of ESSPRI was significantly correlated with UWS (P=0.031) with a negative correlation coefficient of 0.233.

CODS is the scoring system with the highest correlation with hyposalivation, particularly SWS and SPF, followed by ESSPRI dry domain, which is correlated with UWS. Xerostomia index is not correlated with hyposalivation.

Sjogren’s syndrome (SS) is a chronic autoimmune disease affecting mainly the exocrine glands, especially the lacrimal and salivary glands. It is the second most common autoimmune rheumatic disease. Its prevalence ranges between 0.1% and 4.8% with a female to male ratio of 9:1, mostly in the age of 40–60 years. Generally, SS is classified into primary SS, which occurs alone without any other associated disease, and secondary SS, which is associated with other diseases such as rheumatoid arthritis and systemic lupus erythematosus. SS has a wide variety of presentations and can affect almost any organ, but it typically presents with dryness of eyes and mouth.
Xerostomia and hyposalivation are two concepts used in the diagnostic criteria of SS, which are distinguishable from each other. Xerostomia is a subjective measure, when the patient reports a daily feeling of dry mouth, while hyposalivation is an objective quantifiable measure of reduced saliva flow rate. 

Multiple scoring system has been developed to assess xerostomia and several tests for hyposalivation. Three scoring systems we will discuss in our study include Xerostomia index (XI), clinical oral dryness scale (CODS), and the European League Against Rheumatism SS Patient-Reported Index (ESSPRI). Other scoring systems include Profile of Fatigue and Discomfort (PROFAD) and Sicca Symptoms Inventory (SSI). The idea behind PROFAD and SSI development was that the main symptoms of patients with SS are dryness, pain, somatic, and mental fatigue, so these scores were developed to assess these symptoms – PROFAD for fatigue and discomfort and SSI for evaluation of dryness features.
On the other hand, hyposalivation can be assessed either without saliva stimulation (unstimulated whole saliva flow [UWS]) or with saliva stimulation (stimulated whole saliva flow [SWS] and stimulated parotid flow [SPF]), each of which has its own characteristic features. For instance, stimulated flow is less subjected to variation more than unstimulated tests, while stimulated tests are sometimes difficult to obtain. Although the main concern for clinical practitioners is xerostomia rather than hyposalivation, previous studies stressed on the strong relationship between hyposalivation and general health. In this study, we aim to find the association of commonly used xerostomia assessment scores, including XI, CODS, and ESSPRI, with different hyposalivation tests.
This study’s data were obtained from the randomized controlled trials that studied the effect of sialendoscopy on salivary gland function in patients with SS, registered at the US National Institutes of Health (; number: NCT02112019).
This study included patients aged 18–75 years who were diagnosed with SS based on the 2002 American–European Consensus Group classification criteria. 
Variables studied
Upon enrolment, each patient provided his/her demographic data regarding age and gender, and underwent the following tests to assess hyposalivation:
  1. UWS: patients were instructed to start collecting saliva immediately after an initial swallow, and subsequently expectorate into a pre-weighed container every 30 seconds for a 5-minute period.
  2. SWS: patients were asked to chew a 5×5 cm sheet of paraffin (Parafilm M, Pechiney, Chicago, IL, USA) and expectorate into a pre-weighed container every 30 seconds during a 5-minute period.
  3. SPF: collected in plastic tubes from each parotid gland using modified Lashley cups. Stimulation with citric acid (2% w/v) was applied with a cotton wool swab to the lateral border of the tongue at 30-second intervals.
  4. Patients were instructed to refrain from eating/chewing, drinking, brushing teeth, and smoking for 90 minutes prior to these tests.
    Also the following questionnaires were used to assess xerostomia:
    1. Xerostomia inventory: an 11-item score with responses from “Never” to “Always” in a Likert scale. A high total score indicates extremely dry mouth.
    2. Clinical Oral Dryness Scale: a 10-point clinical scale, with a score of 1 assigned to each item. A high total score indicates increased xerostomia severity.
    3. European League Against Rheumatism SS Patient-Reported Index: a 10-point scale for each of oral dryness, pain, and fatigue domains. As we are comparing xerostomia assessment questionnaires, only dryness domain was included. A high total dryness domain score indicates increased xerostomia severity.
  5. Conclusion
    This study provided a comparison between three tools used in the assessment of xerostomia in SS patients. The newly developed CODS is associated with stimulated salivary flow tests (ie, SWS and SPF). XI is not correlated with any objective hyposalivation tests. Finally, ESSPRI dryness domain is associated with the UWS. This is the first study to compare the three tools together, which will guide prospective researchers in choosing the best tool according to their study aim.


Sjögren's syndrome linked to increased cardiovascular comorbidity

Sjögren's syndrome linked to increased cardiovascular comorbidity

Primary Sjögren’s syndrome is associated with increased cardiovascular comorbidities, according to data published in Arthritis Care & Research.
“Patients with chronic autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus are at increased risk of cardiovascular disease, largely because of the systemic inflammation,” Aurelie Beltai, MBBS, of the University of Montpellier, France, and colleagues wrote. “In RA, the cardiovascular disease is the main cause of death. [Primary Sjögren’s syndrome] publications show different estimations of the incidence of cardiovascular complications. This heterogeneity of data led us to conduct a systematic review of this topic.”
To analyze the association between primary Sjögren’s syndrome and cardiovascular morbidity and mortality, Beltai and colleagues conducted a meta-analysis of studies that estimated cardiovascular events with primary Sjögren’s syndrome compared with control groups. The researchers performed a systematic review of articles in Medline and the Cochrane library, as well as abstracts from U.S. and European meetings, focusing on randomized, controlled studies.

Out of 484 articles and abstracts identified, the researchers included 14 in their final analysis. These 14 studies included 67,124 patients with primary Sjögren’s syndrome. Beltai and colleagues recorded relative risk values for cardiovascular morbidity and mortality associated with primary Sjögren’s syndrome in a meta analysis with a random effects model by using Review Manager.

According to the researchers, the risk for coronary morbidity was significantly increased among the primary Sjögren’s syndrome populations, compared with those in control groups. Patients with primary Sjögren’s syndrome also demonstrated significantly increased risks for cerebrovascular morbidity, heart failure rate, and thromboembolic morbidity. However, there was with no statistically significant increased risk for cardiovascular mortality among patients with primary Sjögren’s syndrome.
“This meta-analysis confirms that patients with [primary Sjögren’s syndrome] show increased risk of cardiovascular disease as compared with the general population,” Beltai and colleagues wrote... rheumatologists should be aware of this increased risk in order to propose screening for cardiovascular comorbidities and specific preventive interventions for patients with [primary Sjögren’s syndrome].” – by Jason Laday


Could this widely used food additive cause celiac disease?


Could this widely used food additive cause celiac disease?

Myths about gluten are hard to bust. Intolerance, allergy, sensitivity, hypersensitivity. What is what? 

Celiac disease is none of these things. It is an autoimmune disorder, where gluten triggers the immune system to attack the gut. It is common, lifelong, and can seriously harm health -- but nobody knows for sure what causes it. Now a review in Frontiers in Pediatrics says a common food additive could both cause and trigger these autoimmune attacks, and calls for warnings on food labels pending further tests. 

Environment causes celiac disease -- but only in susceptible individuals 

Gluten-free diets have become popular despite little or no evidence of benefit for most people. But for the 1 in 100 with celiac disease, even a mouthful of bread can trigger an immune response that damages the small intestine, impairing nutrient absorption. 

Exactly what causes this autoimmune reaction to gluten -- a protein found in wheat, rye and barley -- is uncertain. Specific mutations in an important immunity-related gene called HLA-DQ seem to be necessary for developing celiac disease, with one of two HLA-DQ variants present in virtually every sufferer -- but insufficient, as these variants are also present in about 30% of the general population.

 As a result, myriad environmental factors have proposed to interact with genetic risk to cause celiac disease. These span infections, food and toxins; vaccination, drugs and surgery. Most recently, food additives have been suggested to contribute. Among these, microbial transglutaminase -- a bacterial enzyme heavily used in industrial processing of meat, dairy, baked and other food products -- has emerged as a likely culprit, according to the new review. 

How a food binder could be our undoing 

"Microbial transglutaminase can glue together proteins, so it's used to improve food texture, palatability and shelf-life," says co-author Aaron Lerner, visiting professor at the Aesku.Kipp Institute in Germany. "This enzyme functions like the transglutaminase produced by our body, which is known to be the target of autoimmunity in celiac disease." 

 There is a direct positive correlation between rising use of industrial enzymes in bakery products and rising incidence of celiac disease in the last four decades, according to Lerner and co-author Dr Matthias Torsten of the Aesku KIPP Institute, Germany. But if transglutaminase is produced normally in our tissues -- and by our own gut microbes -- what difference should a little more in our diet make?

What links gluten, transglutaminase, HLA-DQ genes and autoimmunity? 

Gluten is tough to break down completely. This is useful for helping baked goods to rise and keep their shape, but in celiac sufferers presents a problem. 

 "The gluten protein fragments or 'peptides' that remain after digestion are highly susceptible to transglutaminase, which modifies them to make a variety of new peptides" Lerner explains. "These unusual peptides are particularly likely to resist further breakdown, and to be recognized as 'foreign' by HLA-DQ immune receptors inside the gut wall -- but only in those carrying the HLA-DQ variants associated with celiac disease." 

Compounding this, components of gluten also loosen the connections between cells lining the gut, allowing more gluten-derived proteins -- as well as microbial transglutaminase -- to breach this barrier and interact with immune cells. 

 "Microbial transglutaminase itself could also increase intestinal permeability by directly modifying proteins that hold together the intestinal barrier," adds Lerner. 

 Human studies implicate microbial transglutaminase 

 This all begs the question: if it is gluten-derived proteins that stimulate immune cells, why does the immune response target transglutaminase? And are microbial and human transglutaminase recognized interchangeably by the immune system? 

 "In one of our own studies, we tested antibodies from the blood of celiac patients. We found that more antibodies were active against complexes of transglutaminase bound to gluten fragments, than against either component alone. The anti-complex antibody count was also the best predictor of intestinal damage in these patients. This was true of both microbial and human transglutaminase complexes, for which there were similar antibody counts." 

 In other words, microbial transglutaminase (bound to gluten fragments) could in fact be the target of the immune response in celiac disease -- and the attack on our own transglutaminase merely a case of mistaken identity. Microbial transglutaminase present in processed foods is therefore a potential environmental cause of celiac disease. 

Is microbial transglutaminase safe? 

 But according to Lerner, the jury is still out. "Ultimately all we have so far are associations between microbial transglutaminase and celiac disease. To test whether this enzyme causes or triggers immune damage in celiac disease will require experimenting with exposure in animal models, intestinal cell lines or biopsies." 

 Nevertheless, with no known cure for celiac disease, treatment depends on preventive measures -- namely, adhering to a gluten-free diet. 

 "Until there is a clearer answer, we recommend transparency and vigilance with regards to labeling of foods processed using microbial transglutaminase." In Switzerland for example, such products must be labelled as unsuitable for persons with celiac disease.

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