Showing posts with label AutoimmuneDisease. Show all posts
Showing posts with label AutoimmuneDisease. Show all posts

Saturday, October 17, 2026

How Psychological Stress Can Trigger Arthritis Flares Via An Inflammatory Pathway

How psychological stress triggers arthritis flares via an IL-6-dependent pathway

Psychological stress has long been associated with worsening symptoms in rheumatoid arthritis (RA). However, the underlying mechanism connecting psychological stress to the occurrence of joint inflammation has remained poorly understood. In particular, how psychological stress can trigger inflammation in joints that were previously affected, even after the disease has gone into remission, remains an important unanswered question………Continue reading….

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Source: Medical Xpress

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Critics: 

Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Pain and stiffness often worsen following rest. Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body. The disease may also affect other parts of the body, including skin, eyes, lungs, heart, nerves, and blood. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart.

Fever and low energy may also be present. Often, symptoms come on gradually over weeks to months. While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves the body’s immune system attacking the joints. This results in inflammation and thickening of the joint capsule. It also affects the underlying bone and cartilage.

The diagnosis is made mostly on the basis of a person’s signs and symptoms. X-rays and laboratory testing may support a diagnosis or exclude other diseases with similar symptoms. Other diseases that may present similarly include systemic lupus erythematosus, psoriatic arthritis, and fibromyalgia among others.

The goals of treatment are to reduce pain, decrease inflammation, and improve a person’s overall functioning. This may be helped by balancing rest and exercise, the use of splints and braces, or the use of assistive devices. Pain medications, steroids, and NSAIDs are frequently used to help with symptoms. Disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the progression of disease.

Biological DMARDs may be used when the disease does not respond to other treatments. However, they may have a greater rate of adverse effects. Surgery to repair, replace, or fuse joints may help in certain situations. RA affects about 24.5 million people as of 2015. This is 0.5–1% of adults in the developed world with between 5 and 50 per 100,000 people newly developing the condition each year. Onset is most frequent during middle age and women are affected 2.5 times as frequently as men.

It resulted in 38,000 deaths in 2013, up from 28,000 deaths in 1990. The first recognized description of RA was made in 1800 by Dr. Augustin Jacob Landré-Beauvais (1772–1840) of Paris. The term rheumatoid arthritis is based on the Greek for watery and inflamed joints. RA primarily affects joints, but it also affects other organs in more than 15–25% of cases. Associated problems include cardiovascular disease, osteoporosis, interstitial lung disease, infection, cancer, feeling tired, depression, mental difficulties, and trouble working.

Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function.

The fibroblast-like synoviocytes (FLS), highly specialized mesenchymal cells found in the synovial membrane, have an active and prominent role in these pathogenic processes of the rheumatic joints. RA typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and typically lasts for more than an hour.

Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, such as osteoarthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are less prominent. The pain associated with RA is induced at the site of inflammation and classified as nociceptive as opposed to neuropathic.

The joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical. As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may develop almost any deformity depending on which joints are most involved.

Specific deformities, which also occur in osteoarthritis, include ulnar deviation, boutonniere deformity (also “buttonhole deformity”, flexion of proximal interphalangeal joint and extension of distal interphalangeal joint of the hand), swan neck deformity (hyperextension at proximal interphalangeal joint and flexion at distal interphalangeal joint) and “Z-thumb.”

“Z-thumb” or “Z-deformity” consists of hyperextension of the interphalangeal joint, fixed flexion and subluxation of the metacarpophalangeal joint and gives a “Z” appearance to the thumb. The hammer toe deformity may be seen. In the worst case, joints are known as arthritis mutilans due to the mutilating nature of the deformities. Worldwide, RA affects approximately 1% of the adult population and occurs in one in 1,000 children. Studies show that RA primarily affects individuals between the ages of 40–60 years and is seen more commonly in females.

A family history of RA increases the risk around three to five times; as of 2016, it was estimated that genetics may account for 40–65% of cases of seropositive RA, but only around 20% for seronegative RA. RA is strongly associated with genes of the inherited tissue type major histocompatibility complex (MHC) antigen. HLA-DR4 is the major genetic factor implicated – the relative importance varies across ethnic groups. Genome-wide association studies examining single-nucleotide polymorphisms have found around one hundred alleles associated with RA risk. 

Risk alleles within the HLA (particularly HLA-DRB1) genes harbor more risk than other loci.The HLA encodes proteins that control recognition of self- versus non-self molecules. Other risk loci include genes affecting co-stimulatory immune pathways—for example CD28 and CD40, cytokine signaling, lymphocyte receptor activation threshold (e.g., PTPN22), and innate immune activation—appear to have less influence than HLA mutations.

Despite the strong genetic components of the disease, identical twin studies have shown only 12-15% concordance for twins raised in separate households. This indicates that rheumatoid arthritis most likely results from a combination of genetic and environmental factors, in a majority of cases.

Ancient DNA Helps Solve Multiple Sclerosis Mystery in Europe

(MICROGEN IMAGES/SCIENCE PHOTO LIBRARY/Getty Images)

The secrets of our ancestors might hold the key to why multiple sclerosis (MS) is more common among white, northern Europeans than among Europe’s more southern populations. While scientists have found hundreds of genes to date that are associated with MS, up to a fifth of northern Europeans have a genetic variant, called HLA-DRB1*15:01, that conveys a threefold higher risk of developing the autoimmune disease. Where this variant came from and why it persisted and spread is a mystery. An international team of researchers, led by William Barrie from the University of Cambridge, now thinks they are on to a new lead…..…Story continues…

By: Carly Cassella

Source: ScienceAlert

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Critics:

Multiple sclerosis (MS) is an autoimmune disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. Being a demyelinating disease, MS disrupts the ability of parts of the nervous system to transmit signals, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems.

Symptoms include double vision, vision loss, eye pain, muscle weakness, and loss of sensation or coordination. MS takes several forms, with new symptoms either occurring in isolated attacks (relapsing forms) or building up over time (progressive forms). In relapsing forms of MS, between attacks, symptoms may disappear completely, although some permanent neurological problems often remain, especially as the disease advances.

In progressive forms of MS, bodily function slowly deteriorates once symptoms manifest and will steadily worsen if left untreated. While its cause is unclear, the underlying mechanism is thought to be either destruction by the immune system or failure of the myelin-producing cells. Proposed causes for this include immune dysregulation, genetics, and environmental factors, such as viral infections. MS is usually diagnosed based on the presenting signs and symptoms and the results of supporting medical tests.

No cure for multiple sclerosis is known. Current treatments are aimed at mitigating inflammation and resulting symptoms from acute flares and prevention of further attacks with disease-modifying medications. Physical therapy and occupational therapy, along with patient-centered symptom management, can help with people’s ability to function.

The long-term outcome is difficult to predict; better outcomes are more often seen in women, those who develop the disease early in life, those with a relapsing course, and those who initially experienced few attacks. Multiple sclerosis is the most common immune-mediated disorder affecting the central nervous system. Nearly one million people in the United States had MS in 2022, and in 2020, about 2.8 million people were affected globally, with rates varying widely in different regions and among different populations.

The disease usually begins between the ages of 20 and 50 and is twice as common in women as in men. MS was first described in 1868 by French neurologist Jean-Martin Charcot. The name “multiple sclerosis” is short for multiple cerebro-spinal sclerosis, which refers to the numerous glial scars (or sclerae – essentially plaques or lesions) that develop on the white matter of the brain and spinal cord.

As multiple sclerosis (MS) lesions can affect any part of the central nervous system, a person with MS can have almost any neurological symptom or sign referable to the central nervous system. Fatigue is one of the most common symptoms of MS. Some 65% of people with MS experience fatigue symptomatology, and of these, some 15–40% report fatigue as their most disabling MS symptom. Autonomic, visual, motor, and sensory problems are also among the most common symptoms.

The specific symptoms are determined by the locations of the lesions within the nervous system, and may include focal loss of sensitivity or changes in sensation in the limbs, such as feeling tingling, pins and needles, or numbness; limb motor weakness/pain, blurred vision, pronounced reflexes, muscle spasms, difficulty with ambulation (walking), difficulties with coordination and balance (ataxia).

Problems with speech or swallowing, visual problems (optic neuritis manifesting as eye pain & vision loss, or nystagmus manifesting as double vision), fatigue, and bladder and bowel difficulties (such as urinary or fecal incontinence or retention), among others. When multiple sclerosis is more advanced, walking difficulties can occur and the risk of falling increases. Difficulties thinking and emotional problems such as depression or unstable mood are also common.

The primary deficit in cognitive function that people with MS experience is slowed information-processing speed, with memory also commonly affected, and executive function less commonly. Intelligence, language, and semantic memory are usually preserved, and the level of cognitive impairment varies considerably between people with MS.

Uhthoff’s phenomenon, a worsening of symptoms due to exposure to higher-than-usual temperatures, and Lhermitte’s sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS, although may not always be present.

Another presenting manifestation that is rare but highly suggestive of a demyelinating process such as MS is bilateral internuclear ophthalmoplegia, where the patient experiences double vision when attempting to move their gaze to the right & left. Some 60% or more of MS patients find their symptoms, particularly including fatigue, are affected by changes in body temperature.

The main measure of disability and severity is the expanded disability status scale (EDSS), with other measures such as the multiple sclerosis functional composite being increasingly used in research. EDSS is also correlated with falls in people with MS. While it is a popular measure, EDSS has been criticized for some of its limitations, such as relying too much on walking.

The condition begins in 85% of cases as a clinically isolated syndrome (CIS) over a number of days with 45% having motor or sensory problems, 20% having optic neuritis, and 10% having symptoms related to brainstem dysfunction, while the remaining 25% have more than one of the previous difficulties.

Regarding optic neuritis as the most common presenting symptom, people with MS notice sub-acute loss of vision, often associated with pain worsening on eye movement, and reduced colour vision. Early diagnosis of MS-associated optic neuritis helps timely initiation of targeted treatments.

However, it is crucial to adhere to established diagnostic criteria when treating optic neuritis due to the broad range of alternative causes, such as neuromyelitis optica spectrum disorder (NMOSD), and other autoimmune or infectious conditions. The course of symptoms occurs in two main patterns initially:

Either as episodes of sudden worsening that last a few days to months (called relapses, exacerbations, bouts, attacks, or flare-ups) followed by improvement (85% of cases) or as a gradual worsening over time without periods of recovery (10–15% of cases).A combination of these two patterns may also occur or people may start in a relapsing and remitting course that then becomes progressive later on.

Relapses are usually unpredictable, occurring without warning. Exacerbations rarely occur more frequently than twice per year. Some relapses, however, are preceded by common triggers and they occur more frequently during spring and summer. Similarly, viral infections such as the common cold, influenza, or gastroenteritis increase their risk. Stress may also trigger an attack.

Many events have been found not to affect rates of relapse requiring hospitalization including vaccination, breast feeding, physical trauma, and Uhthoff’s phenomenon.

How Psychological Stress Can Trigger Arthritis Flares Via An Inflammatory Pathway

Psychological stress has long been associated with worsening symptoms in rheumatoid arthritis (RA). However, the underlying mechanism connec...